﻿FN Clarivate Analytics Web of Science
VR 1.0
PT J
AU Black, JD
   Rezvani, K
AF Black, Jennifer D.
   Rezvani, Khosrow
TI Heat Shock Protein 70s as Potential Molecular Targets for Colon Cancer
   Therapeutics
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
DE Heat shock protein; Mortalin-2; Colorectal cancer; Apoptosis; Targeted
   therapy; Chemotherapy
ID METASTATIC COLORECTAL-CANCER; WILD-TYPE P53; NUCLEAR RIBONUCLEOPROTEIN
   K; TUMOR-SUPPRESSOR P53; KINASE-C-ALPHA; HSP70 FAMILY; PHASE-II;
   MITOCHONDRIAL HEAT-SHOCK-PROTEIN-70; HEPATOCELLULAR-CARCINOMA;
   BIOCHEMICAL MODULATION
AB Background: Targeted drugs modulate selective pathways activated or repressed only in cancer cells, resulting in a higher response to chemotherapy with less severe side effects. The use of a selected member of the heat shock protein 70 family (HSP70) as an effective therapeutic target in the treatment of colorectal cancer (CRC) will be the focus of this review.
   Methods: We generated two main questions for this study: 1) What are the current and potential future molecular therapies in CRC? 2) Can selective members of the HSP70 family advance drug design and drug discovery for treatment of CRC patients? We discuss related articles based on their significance and translational contributions to the existing literature.
   Results: The first part of this review discusses molecularly targeted agents that are currently used successfully in the clinic for the treatment of patients with CRC and highlights several novel targeted agents that are being investigated in ongoing trials. The second part of this review focuses on the unique tumorigenic functions of heat shock proteins, particularly mortalin-2, an essential heat shock protein for mitochondrial biogenesis in normal cells and a dominant oncoprotein in colon cancer cells. Basic and clinical studies have justified mortalin-2 as a potential molecular target, and its inhibition could dramatically improve patients' responses to standard chemotherapies.
   Conclusion: Further understanding of the contributions of HSP70 family members to CRC at the molecular level, combined with translation of new concepts into effective targeted therapies, are anticipated to improve clinical outcomes and increase the therapeutic synergy with combination treatment with cytotoxic agents.
C1 [Black, Jennifer D.] Univ Nebraska, Med Ctr, Eppley Inst Res Canc & Allied Dis, Gastrointestinal Canc Res Program,Fred & Pamela B, Omaha, NE USA.
   [Rezvani, Khosrow] Univ South Dakota, Div Basic Biomed Sci, Sanford Sch Med, 414 E Clark St,Lee Med Bldg, Vermillion, SD 57069 USA.
C3 University of Nebraska System; University of Nebraska Medical Center;
   University of South Dakota
RP Rezvani, K (corresponding author), Univ South Dakota, Div Basic Biomed Sci, Sanford Sch Med, 414 E Clark St,Lee Med Bldg, Vermillion, SD 57069 USA.
EM khosrow.rezvani@usd.edu
OI Rezvani, Khosrow/0000-0003-1963-2211
FU startup package (Division of Basic Biomedical Sciences, University of
   South Dakota); National Institute of General Medical Sciences of the
   National Institutes of Health (NIH) award [5P20GM103548]; NIH [DK060632,
   CA191894, CA036727]
FX This work was supported by a startup package (Division of Basic
   Biomedical Sciences, University of South Dakota) and by National
   Institute of General Medical Sciences of the National Institutes of
   Health (NIH) award 5P20GM103548 (Miskimins) to KSR. Research in the
   laboratory of JDB is supported by NIH grants DK060632, CA191894, and
   CA036727.
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BP 3171
EP 3188
DI 10.2174/0929867323666160627105033
PG 18
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
   Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA EB0AV
UT WOS:000387006700004
PM 27356538
DA 2025-01-04
ER

PT J
AU Piastra, V
   Ganci, F
   Sacconi, A
   Pranteda, A
   Allegretti, M
   Bernardini, R
   Serra, M
   Lupo, B
   Dell'Aquila, E
   Ferretti, G
   Pescarmona, E
   Bartolazzi, A
   Blandino, G
   Trusolino, L
   Bossi, G
AF Piastra, Valentina
   Ganci, Federica
   Sacconi, Andrea
   Pranteda, Angelina
   Allegretti, Matteo
   Bernardini, Roberta
   Serra, Martina
   Lupo, Barbara
   Dell'Aquila, Emanuela
   Ferretti, Gianluigi
   Pescarmona, Edoardo
   Bartolazzi, Armando
   Blandino, Giovanni
   Trusolino, Livio
   Bossi, Gianluca
TI Repurposed AT9283 triggers anti-tumoral effects by targeting MKK3
   oncogenic functions in Colorectal Cancer
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Article
DE MKK3/p38MAPK; Drug repurposing; Aurora kinase A; Target therapy;
   Colorectal cancer (CRC)
ID KINASE KINASE 3; SMALL-MOLECULE INHIBITOR; AURORA KINASES; PHASE-I;
   DISCOVERY; POTENT; IDENTIFICATION; BIOLOGY; GROWTH; GAIN
AB BackgroundColorectal cancer (CRC) is the third most common type of cancer and the second leading cause of cancer-related deaths worldwide, with a survival rate near to 10% when diagnosed at an advanced stage. Hence, the identification of new molecular targets to design more selective and efficient therapies is urgently required. The Mitogen activated protein kinase kinase 3 (MKK3) is a dual-specificity threonine/tyrosine protein kinase that, activated in response to cellular stress and inflammatory stimuli, regulates a plethora of biological processes. Previous studies revealed novel MKK3 roles in supporting tumor malignancy, as its depletion induces autophagy and cell death in cancer lines of different tumor types, including CRC. Therefore, MKK3 may represent an interesting new therapeutic target in advanced CRC, however selective MKK3 inhibitors are currently not available.MethodsThe study involved transcriptomic based drug repurposing approach and confirmatory assays with CRC lines, primary colonocytes and a subset of CRC patient-derived organoids (PDO). Investigations in vitro and in vivo were addressed.ResultsThe repurposing approach identified the multitargeted kinase inhibitor AT9283 as a putative compound with MKK3 depletion-mimicking activities. Indeed, AT9283 drops phospho- and total-MKK3 protein levels in tested CRC models. Likely the MKK3 silencing, AT9283 treatment: i) inhibited cell proliferation promoting autophagy and cell death in tested CRC lines and PDOs; ii) resulted well-tolerated by CCD-18Co colonocytes; iii) reduced cancer cell motility inhibiting CRC cell migration and invasion; iv) inhibited COLO205 xenograft tumor growth. Mechanistically, AT9283 abrogated MKK3 protein levels mainly through the inhibition of aurora kinase A (AURKA), impacting on MKK3/AURKA protein-protein interaction and protein stability therefore uncovering the relevance of MKK3/AURKA crosstalk in sustaining CRC malignancy in vitro and in vivo.ConclusionOverall, we demonstrated that the anti-tumoral effects triggered by AT9283 treatment recapitulated the MKK3 depletion effects in all tested CRC models in vitro and in vivo, suggesting that AT9283 is a repurposed drug. According to its good tolerance when tested with primary colonocytes (CCD-18CO), AT9283 is a promising drug for the development of novel therapeutic strategies to target MKK3 oncogenic functions in late-stage and metastatic CRC patients.
C1 [Piastra, Valentina; Ganci, Federica; Sacconi, Andrea; Pranteda, Angelina; Allegretti, Matteo; Serra, Martina; Blandino, Giovanni; Bossi, Gianluca] IRCCS Regina Elena Natl Canc Inst, Dept Diagnost Res & Technol Innovat, Translat Oncol Res Unit, Via Elio Chianesi 53, I-00144 Rome, Italy.
   [Piastra, Valentina; Pranteda, Angelina] Univ Roma Tre, Dept Sci, Rome, Italy.
   [Bernardini, Roberta; Serra, Martina] Univ Roma Tor Vergata, Interdept Ctr Comparat Med Alternat Tech & Aquacul, Rome, Italy.
   [Lupo, Barbara; Trusolino, Livio] Candiolo Canc Inst FPO IRCCS, Turin, Italy.
   [Lupo, Barbara; Trusolino, Livio] Univ Torino, Dept Oncol, Turin, Italy.
   [Dell'Aquila, Emanuela] IRCCS Regina Elena Natl Canc Inst, Div Med Oncol 2, Rome, Italy.
   [Ferretti, Gianluigi] IRCCS Regina Elena Natl Canc Inst, Div Med Oncol 1, Rome, Italy.
   [Pescarmona, Edoardo] IRCCS Regina Elena Natl Canc Inst, Dept Pathol, Rome, Italy.
   [Bartolazzi, Armando] St Andrea Univ Hosp, Pathol Res Lab, Rome, Italy.
C3 Roma Tre University; Italfarmaco; University of Rome Tor Vergata; IRCCS
   Fondazione del Piemonte per l'Oncologia; University of Turin; Sapienza
   University Rome; Azienda Ospedaliera Sant'Andrea
RP Bossi, G (corresponding author), IRCCS Regina Elena Natl Canc Inst, Dept Diagnost Res & Technol Innovat, Translat Oncol Res Unit, Via Elio Chianesi 53, I-00144 Rome, Italy.
EM gianluca.bossi@ifo.it
RI Bossi, Gianluca/B-9394-2017; Piastra, Valentina/AAC-2023-2022; sacconi,
   andrea/J-3669-2018; Trusolino, Livio/A-3896-2011; Allegretti,
   Matteo/B-7030-2016; Ferretti, Gianluigi/ABH-6945-2020; Blandino,
   Giovanni/LLM-1397-2024; Bernardini, Roberta/AAC-1301-2019; Ganci,
   Federica/K-9857-2016
OI Ganci, Federica/0000-0002-8010-2183
FU Italian Association for Cancer Research (AIRC) [18449]; Lega Italiana
   per la Lotta contro i Tumori (LILT) [5X1000 2019]; Italian Ministry of
   Health "Ricerca Finalizzata" [RF-2021-12372851]; Italian Ministry of
   Health
FX This work was financially supported by the following grants to G. Bossi:
   The Italian Association for Cancer Research (AIRC) (ID. 18449 project);
   the Lega Italiana per la Lotta contro i Tumori (LILT ) (5X1000 2019);
   The Italian Ministry of Health "Ricerca Finalizzata" (RF-2021-12372851).
   This work was financially supported through funding from the
   institutional "Ricerca Corrente" granted by the Italian Ministry of
   Health.
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NR 40
TC 0
Z9 0
U1 0
U2 0
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1756-9966
J9 J EXP CLIN CANC RES
JI J. Exp. Clin. Cancer Res.
PD AUG 20
PY 2024
VL 43
IS 1
AR 234
DI 10.1186/s13046-024-03150-4
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA D2I9J
UT WOS:001294485700002
PM 39164711
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Deng, SH
   Gu, JN
   Jiang, ZX
   Cao, YH
   Mao, FW
   Xue, YF
   Wang, J
   Dai, K
   Qin, L
   Liu, K
   Wu, K
   He, QY
   Cai, KL
AF Deng, Shenghe
   Gu, Junnan
   Jiang, Zhenxing
   Cao, Yinghao
   Mao, Fuwei
   Xue, Yifan
   Wang, Jun
   Dai, Kun
   Qin, Le
   Liu, Ke
   Wu, Ke
   He, Qianyuan
   Cai, Kailin
TI Application of nanotechnology in the early diagnosis and comprehensive
   treatment of gastrointestinal cancer
SO JOURNAL OF NANOBIOTECHNOLOGY
LA English
DT Review
DE Gastrointestinal cancer; Nanotechnology; Nanoparticles; Early diagnosis;
   Targeted therapy; Surgical navigation; Tumour imaging
ID METASTATIC COLORECTAL-CANCER; SOLID LIPID NANOPARTICLES; IRON-OXIDE
   NANOPARTICLES; GASTRIC-CANCER; PHOTODYNAMIC THERAPY; DRUG-DELIVERY;
   CONTRAST AGENT; COLON-CANCER; TARGETED DELIVERY; SILICON NANOWIRE
AB Gastrointestinal cancer (GIC) is a common malignant tumour of the digestive system that seriously threatens human health. Due to the unique organ structure of the gastrointestinal tract, endoscopic and MRI diagnoses of GIC in the clinic share the problem of low sensitivity. The ineffectiveness of drugs and high recurrence rates in surgical and drug therapies are the main factors that impact the curative effect in GIC patients. Therefore, there is an urgent need to improve diagnostic accuracies and treatment efficiencies. Nanotechnology is widely used in the diagnosis and treatment of GIC by virtue of its unique size advantages and extensive modifiability. In the diagnosis and treatment of clinical GIC, surface-enhanced Raman scattering (SERS) nanoparticles, electrochemical nanobiosensors and magnetic nanoparticles, intraoperative imaging nanoparticles, drug delivery systems and other multifunctional nanoparticles have successfully improved the diagnosis and treatment of GIC. It is important to further improve the coordinated development of nanotechnology and GIC diagnosis and treatment. Herein, starting from the clinical diagnosis and treatment of GIC, this review summarizes which nanotechnologies have been applied in clinical diagnosis and treatment of GIC in recent years, and which cannot be applied in clinical practice. We also point out which challenges must be overcome by nanotechnology in the development of the clinical diagnosis and treatment of GIC and discuss how to quickly and safely combine the latest nanotechnology developed in the laboratory with clinical applications. Finally, we hope that this review can provide valuable reference information for researchers who are conducting cross-research on GIC and nanotechnology.
C1 [Deng, Shenghe; Gu, Junnan; Jiang, Zhenxing; Cao, Yinghao; Mao, Fuwei; Xue, Yifan; Wang, Jun; Qin, Le; Liu, Ke; Wu, Ke; He, Qianyuan; Cai, Kailin] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Gastrointestinal Surg, Wuhan 430022, Hubei, Peoples R China.
   [Dai, Kun] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Neonatal Intens Care Unit, Wuhan 430022, Hubei, Peoples R China.
C3 Huazhong University of Science & Technology; Huazhong University of
   Science & Technology
RP He, QY; Cai, KL (corresponding author), Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Gastrointestinal Surg, Wuhan 430022, Hubei, Peoples R China.
EM 402294701@qq.com; caikailin@hust.edu.cn
RI cai, kailin/KIA-9950-2024
FU Interdisciplinary program of Wuhan National High Magnetic Field Center
   [WHMFC202113]; Huazhong University of Science and Technology;
   'Fundamental Research Funds for the Central Universities',HUST
   [2021JYCXJJ063]; National Natural Science Foundation of China [82170678]
FX This study was supported by the Interdisciplinary program of Wuhan
   National High Magnetic Field Center (Grant No.WHMFC202113), Huazhong
   University of Science and Technology, `the Fundamental Research Funds
   for the Central Universities',HUST (2021JYCXJJ063) and the National
   Natural Science Foundation of China (No.82170678).
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NR 189
TC 21
Z9 23
U1 9
U2 71
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1477-3155
J9 J NANOBIOTECHNOL
JI J. Nanobiotechnol.
PD SEP 15
PY 2022
VL 20
IS 1
AR 415
DI 10.1186/s12951-022-01613-4
PG 29
WC Biotechnology & Applied Microbiology; Nanoscience & Nanotechnology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Science & Technology - Other
   Topics
GA 4O6FC
UT WOS:000854790300007
PM 36109734
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ciombor, KK
   Bekaii-Saab, T
AF Ciombor, Kristen K.
   Bekaii-Saab, Tanios
TI A Comprehensive Review of Sequencing and Combination Strategies of
   Targeted Agents in Metastatic Colorectal Cancer
SO ONCOLOGIST
LA English
DT Review
DE Colorectal neoplasms; Molecular targeted therapy; Combination drug
   therapy; Investigational therapies; Patient selection; Antineoplastic
   protocols
ID FOLFIRI PLUS CETUXIMAB; RANDOMIZED PHASE-III; OPEN-LABEL; 1ST-LINE
   TREATMENT; 2ND-LINE TREATMENT; REGORAFENIB PLUS; MODIFIED FOLFOX6;
   DOUBLE-BLIND; BEVACIZUMAB; CHEMOTHERAPY
AB The emergence of targeted therapies for the treatment of metastatic colorectal cancer (mCRC) has considerably improved survival, but has also resulted in a dilemma of identifying the optimal sequence and combination of various agents in the mCRC treatment landscape. A number of cytotoxic agents, including irinotecan, oxaliplatin, 5-fluorouracil, capecitabine, and TAS-102, are available for treatment of mCRC. Additionally, whereas patients harboring rat sarcoma viral oncogene homolog (RAS)-wild type mCRC can be treated with the anti-epidermal growth factor receptor antibodies cetuximab and panitumumab or antiangiogenic agents (bevacizumab, ziv-aflibercept, and ramucirumab), patients with RAS-mutant mCRC are limited to antiangiogenic agents as biologic options. Regorafenib, a multikinase inhibitor, can be used in both RAS subgroups. As such, the recommended sequence of therapies that should be received by each subgroup must also be considered separately. This review provides an overview of recent clinical data for approved and investigational targeted therapies that have been studied across different mCRC treatment lines and patient subgroups. It also examines emerging trends in the treatment landscape for mCRC, including treatment with immune checkpoint inhibitors and the utilization of genomic profiling.
   Implications for PracticeCurrently, there are no established guidelines for optimal sequencing of cytotoxic or targeted agents in metastatic colorectal cancer (mCRC). This review provides a snapshot of the current mCRC treatment paradigm and examines the latest clinical data that support the utilization of several targeted agents alone or in combination with backbone chemotherapy across different lines of treatment and patient populations, highlighting recommendations for their usage. Recent advances in the treatment landscape are also summarized, including genomic profiling and preliminary results with immune checkpoint inhibitors.
C1 [Ciombor, Kristen K.] Vanderbilt Univ, Med Ctr, Dept Internal Med, Div Hematol & Oncol,Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
   [Bekaii-Saab, Tanios] Mayo Clin, Canc Ctr, Dept Internal Med, Div Hematol & Med Oncol, 5881 E Mayo Blvd, Phoenix, AZ 85054 USA.
C3 Vanderbilt University; Mayo Clinic; Mayo Clinic Phoenix
RP Bekaii-Saab, T (corresponding author), Mayo Clin, Canc Ctr, Dept Internal Med, Div Hematol & Med Oncol, 5881 E Mayo Blvd, Phoenix, AZ 85054 USA.
EM bekaii-saab.tanios@mayo.edu
RI Bekaii-Saab, Tanios/AGD-6851-2022
OI Bekaii-Saab, Tanios/0000-0001-7721-1699
FU Boehringer Ingelheim Pharmaceuticals, Inc.
FX The authors meet criteria for authorship as recommended by the
   International Committee of Medical Journal Editors. The authors received
   no direct compensation related to the development of the manuscript.
   Writing and editorial support were provided by Lauren Fink, Ph.D., of
   MedErgy, which was contracted and funded by Boehringer Ingelheim
   Pharmaceuticals, Inc. Boehringer Ingelheim Pharmaceuticals, Inc. was
   given the opportunity to review the manuscript for medical and
   scientific accuracy, as well as intellectual property considerations.
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NR 77
TC 56
Z9 58
U1 0
U2 12
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PD JAN
PY 2018
VL 23
IS 1
BP 25
EP 34
DI 10.1634/theoncologist.2017-0203
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FS3DI
UT WOS:000419659100006
PM 29021377
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Fowler, M
   Tobback, H
   Karuri, A
   Fernández-Ortega, P
AF Fowler, Matthew
   Tobback, Helene
   Karuri, Alice
   Fernandez-Ortega, Paz
TI Nursing care and management of adverse events for patients with
   <i>BRAF</i><SUP><i>V600E</i></SUP>-mutant metastatic colorectal cancer
   receiving encorafenib in combination with cetuximab: a review
SO SUPPORTIVE CARE IN CANCER
LA English
DT Review
DE Nursing role; BRAF Mutation; Encorafenib; Cetuximab; Toxicity;
   Colorectal cancer
ID TARGETED THERAPIES; PRIMARY MELANOMAS; MELANOCYTIC NEVI; BRAF;
   TOXICITIES; VEMURAFENIB; INHIBITION; SURVIVAL
AB Encorafenib is a B-Raf proto-oncogene serine/threonine-protein kinase (BRAF) inhibitor, approved in the EU and USA, in combination with the epidermal growth factor receptor (EGFR) inhibitor cetuximab, for the treatment of patients with BRAF(V600E)-mutant metastatic colorectal cancer (mCRC). In the pivotal BEACON CRC trial, patients achieved longer survival with encorafenib in combination with cetuximab vs. conventional chemotherapy. This targeted therapy regimen is also generally better tolerated than cytotoxic treatments. However, patients may present with adverse events unique to the regimen and characteristic of BRAF and EGFR inhibitors, which produce their own set of challenges. Nurses play an essential role in navigating the care of patients with BRAF(V600E)-mutant mCRC and managing adverse events that patients may experience. This includes early and efficient identification of treatment-related adverse events, subsequent management of adverse events and education of patients and their caregivers around key adverse events. This manuscript aims to provide support to nurses managing patients with BRAF(V600E)-mutant mCRC receiving encorafenib in combination with cetuximab, by summarising potential adverse events and providing guidance on how to manage them. Special attention will be paid to the presentation of key adverse events, dose modifications that may be required, practical recommendations and supportive care measures.
C1 [Fowler, Matthew] Univ Hosp Derby & Burton NHSFT, Uttoxeter Rd, Derby DE22 3NE, England.
   [Tobback, Helene] UZ Leuven, Gasthuisberg Campus, Leuven, Belgium.
   [Karuri, Alice] Barts & London NHS Trust, London, England.
   [Fernandez-Ortega, Paz] Inst Catala Oncol, Lhospitalet De Llobregat, Barcelona, Spain.
C3 KU Leuven; University Hospital Leuven; Barts Health NHS Trust; Institut
   Catala d'Oncologia
RP Fowler, M (corresponding author), Univ Hosp Derby & Burton NHSFT, Uttoxeter Rd, Derby DE22 3NE, England.
EM matthew.fowler@nhs.net
RI Fernandez-Ortega, M Paz/H-7881-2019
OI Fernandez-Ortega, M Paz/0000-0001-7957-3909
FU Paige Johnson and Danielle Walsh of Meditech Media and Chrysalis Medical
   Communications; Nucleus Global Ltd; Pierre Fabre
FX Medical writing support was provided by Paige Johnson and Danielle Walsh
   of Meditech Media and Chrysalis Medical Communications, both part of
   Nucleus Global Ltd., and was funded by Pierre Fabre. The authors were
   responsible for all content and editorial decisions.
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NR 56
TC 5
Z9 5
U1 1
U2 3
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0941-4355
EI 1433-7339
J9 SUPPORT CARE CANCER
JI Support. Care Cancer
PD APR
PY 2023
VL 31
IS 4
AR 204
DI 10.1007/s00520-023-07579-9
PG 14
WC Oncology; Health Care Sciences & Services; Rehabilitation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Health Care Sciences & Services; Rehabilitation
GA 9R0IX
UT WOS:000945340400002
PM 36881161
OA Bronze, Green Published
DA 2025-01-04
ER

PT J
AU Takeda, R
   Hirohashi, Y
   Shen, M
   Wang, LM
   Ogawa, T
   Murai, A
   Yamamoto, E
   Kubo, T
   Nakatsugawa, M
   Kanaseki, T
   Tsukahara, T
   Nishidate, T
   Okita, K
   Kutomi, G
   Sato, N
   Takemasa, I
   Torigoe, T
AF Takeda, Rui
   Hirohashi, Yoshihiko
   Shen, Min
   Wang, Liming
   Ogawa, Tadashi
   Murai, Aiko
   Yamamoto, Ed
   Kubo, Terufumi
   Nakatsugawa, Munehide
   Kanaseki, Takayuki
   Tsukahara, Tomohide
   Nishidate, Toshihiko
   Okita, Kenji
   Kutomi, Goro
   Sato, Noriyuki
   Takemasa, Ichiro
   Torigoe, Toshihiko
TI Identification and functional analysis of variants of a cancer/testis
   antigen LEMD1 in colorectal cancer stem-like cells
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Colorectal cancer; Cancer stem cell; LEMD1; Splicing variant;
   Cancer/testis antigen
ID INITIATING CELLS; EXPRESSION; MARKER; TARGET; DNAJB8; GENES
AB Colorectal cancer (CRC) is one of the most common malignancy, and the prognosis is not still satisfactory due to treatment resistance, recurrence and distant metastasis. Cancer stem cells (CSCs)/cancer-initiating cells (CICs) is endowed with higher tumor-initiating ability, self-renewal ability and differentiation ability, and CSCs/CICs are resistant to treatments.nhus, CSCs/CICs are thought to be responsible for recurrence and distant metastasis, and eradication of CSCs/CICs is essential to cure CRCs. However, the molecular mechanisms of CSCs/CICs are remain unknown, and we aimed to elucidate molecular aspects of CR-CSCs/CICs in this study. We screened the transcriptome data of primary human CR-CSCs/CICs that we previously established, and found that LEM domain containing 1 (LEMD1) is preferentially expressed in CR-CSCs/CICs. LEMD1 belongs to cancer-testis (CT) antigen, and has five transcript variants (variant 1 [V1] - variant 5 [V5]). We found that LEMD1 V1, V2 and V3 is expressed in testis and CR-CSCs/CICs, whereas LEMD1 V4 and V5 is ubiquitously expressed. LEMD1 gene knockdown experiments using siRNAs and gene overexpression experiments revealed that LEMD1 has a role in the maintenance of CR-CSCs/CICs. These observations indicate that CR-CSC/CIC-specific LEMD1 variants are reasonable target of CR-CSC/CIC-targeted therapy. (C) 2017 Elsevjer Inc. All rights reserved.
C1 [Takeda, Rui; Hirohashi, Yoshihiko; Shen, Min; Wang, Liming; Ogawa, Tadashi; Murai, Aiko; Yamamoto, Ed; Kubo, Terufumi; Nakatsugawa, Munehide; Kanaseki, Takayuki; Tsukahara, Tomohide; Sato, Noriyuki; Torigoe, Toshihiko] Sapporo Med Univ, Sch Med, Dept Pathol, Chuo Ku, South1 West 17, Sapporo, Hokkaido 0608556, Japan.
   [Ogawa, Tadashi; Nishidate, Toshihiko; Okita, Kenji; Kutomi, Goro; Takemasa, Ichiro] Sapporo Med Univ, Sch Med, Dept Surg, Chuo Ku, South1 West 17, Sapporo, Hokkaido 0608556, Japan.
C3 Sapporo Medical University; Sapporo Medical University
RP Hirohashi, Y; Torigoe, T (corresponding author), Sapporo Med Univ, Sch Med, Dept Pathol, Chuo Ku, South1 West 17, Sapporo, Hokkaido 0608556, Japan.
EM hirohash@sapmed.ac.jp; torigoe@sapmed.ac.jp
RI Wang, Liming/N-9512-2015; Hirohashi, Yoshihiko/AFQ-4227-2022; Kanaseki,
   Takayuki/LKK-0993-2024
OI Torigoe, Toshihiko/0000-0002-9463-5917; Kanaseki,
   Takayuki/0000-0001-7294-6880
FU Ministry of Education, Culture, Sports, Science and Technology of Japan
   [21249025]; program for developing the supporting system for upgrading
   education and research from the Ministry of Education, Culture, Sports,
   Science and Technology of Japan; Health and Labor Sciences Research
   Grants; Ovarian Cancer Research Fund; Suharakinenzaidan Co., Ltd.;
   Northern Advancement Center for Science & Technology of Hokkaido Japan;
   project for development of innovative research on cancer therapeutics
   from Japan Agency for Medical Research and development, AMED;
   Grants-in-Aid for Scientific Research [21249025] Funding Source: KAKEN
FX This study was supported by a Grant-in-Aid for Scientific Research from
   the Ministry of Education, Culture, Sports, Science and Technology of
   Japan (21249025) (to N.S.), program for developing the supporting system
   for upgrading education and research from the Ministry of Education,
   Culture, Sports, Science and Technology of Japan (to N.S.), Health and
   Labor Sciences Research Grants, a grant-in-aid of Ovarian Cancer
   Research Fund (to T.T.), Suharakinenzaidan Co., Ltd. (to Y.H.),
   Grants-in-Aid for Regional R&D Proposal-Based Program from Northern
   Advancement Center for Science & Technology of Hokkaido Japan (to Y.H.
   and T.T.) and the project for development of innovative research on
   cancer therapeutics from Japan Agency for Medical Research and
   development, AMED.
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NR 28
TC 18
Z9 18
U1 1
U2 11
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
EI 1090-2104
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD APR 8
PY 2017
VL 485
IS 3
BP 651
EP 657
DI 10.1016/j.bbrc.2017.02.081
PG 7
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA EQ3ZA
UT WOS:000398011300012
PM 28219643
DA 2025-01-04
ER

PT J
AU Li, RF
   Gao, X
   Sun, HT
   Sun, LX
   Hu, XJ
AF Li, Ruofan
   Gao, Xu
   Sun, Haitao
   Sun, Lixin
   Hu, Xiaojian
TI Expression characteristics of long non-coding RNA in colon
   adenocarcinoma and its potential value for judging the survival and
   prognosis of patients: bioinformatics analysis based on The Cancer
   Genome Atlas database
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Long non-coding RNA (lncRNA); colon cancer; The Cancer Genome Atlas
   (TCGA); bioinformatics analysis
ID AXIS
AB Background: To investigate the expression characteristics of long non-coding RNA (lncRNA) in colon adenocarcinoma (COAD) and its potential value in predicting the prognosis of patient survival.
   Methods: We downloaded COAD-related RNA sequencing (RNA-seq) data and patient survival data from The Cancer Genome Atlas (TCGA). The data were analyzed for lncRNA expression differences, subjected to Cox regression analysis for survival rate, and Kaplan-Meier (KM) survival curves were plotted to analyze the role of the key genes related to prognostic survival by pathway enrichment analysis.
   Results: The data of 494 COAD clinical samples from TCGA were analyzed; 204 lncRNAs were differentially expressed, 156 were up-regulated, and 48 were down-regulated. The 10 genes with the most significant expression differences were Linc02418, Blacat1, ELFNI-AS1, CRNDE, AC002384.1, AL353801.1, LINC01645, AC073283.2, AC087379.1, and LINC00484. Cox regression analysis of 204 lncRNA genes showed that 23 lncRNA genes with significant effects on the prognosis and survival rate of COAD patients were obtained when P<0.05 was used as the threshold. With P <= 0.001 as the threshold, the KM curves of 4 genes (Linc02257, Linc02474, Ac010789.1, Ac083967.1) were statistically significant (P<0.05). The gene Linc02257 was selected for Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, and it was revealed that the inheritance of Linc02257-regulated gene expression was closely related to tumor development, such as collagen-containing extracellular matrix, organogencsis, activity of membrane protein receptors, and ion channel activity. The signaling pathways regulated by Linc02257 were also closely related to tumors, such as neuroactive ligand-receptor interaction, the PI3K-AKT signaling pathway, calcium signaling pathway, and protein digestion and absorption.
   Conclusions: In COAD, lncRNA is differentially expressed and plays an important role in the disease regulation. It has potential application value in the diagnosis, targeted therapy, and prognosis of COAD patients.
C1 [Li, Ruofan; Gao, Xu; Sun, Haitao; Sun, Lixin] Capital Med Univ, Dept Gen Surg, Beijing Luhe Hosp, Beijing, Peoples R China.
   [Hu, Xiaojian] Xian Med Coll, Affiliated Hosp 2, Dept Urol, 167 Fangdong St, Xian 710038, Shaanxi, Peoples R China.
C3 Capital Medical University; Xi'an Medical University
RP Hu, XJ (corresponding author), Xian Med Coll, Affiliated Hosp 2, Dept Urol, 167 Fangdong St, Xian 710038, Shaanxi, Peoples R China.
EM huxiaojian2022@163.com
RI Gao, Xu/LCD-7933-2024; Sun, Lixin/AAT-1932-2020
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NR 32
TC 5
Z9 5
U1 1
U2 5
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD JUN
PY 2022
VL 13
IS 3
BP 1178
EP 1187
DI 10.21037/jgo-22-384
EA MAY 2022
PG 10
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA 2V2IM
UT WOS:000813246900001
PM 35837189
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Mohammadi, C
   Mahdavinezhad, A
   Saidijam, M
   Bahreini, F
   Pashaki, AS
   Gholami, MH
   Najafi, R
AF Mohammadi, Chiman
   Mahdavinezhad, Ali
   Saidijam, Massoud
   Bahreini, Fatemeh
   Pashaki, Abdolazim Sedighi
   Gholami, Mohammad Hadi
   Najafi, Rezvan
TI DCLK1 Inhibition Sensitizes Colorectal Cancer Cells to Radiation
   Treatment
SO INTERNATIONAL JOURNAL OF MOLECULAR AND CELLULAR MEDICINE
LA English
DT Article
DE DCLK1; ionizing radiation; colorectal cancer; radiosensitivity
ID DNA-DAMAGE RESPONSE; STEM-CELLS; RADIORESISTANCE; EMT; MARKER; REPAIR;
   ATM; RADIOSENSITIVITY; MECHANISMS; RESISTANCE
AB Colorectal cancer (CRC) is one of the most prevalent diagnosed cancers and a common cause of cancer-related mortality. Despite effective clinical responses. a large proportion of patients undergo resistance to radiation therapy. Therefore, the identification of efficient targeted therapy strategies would be beneficial to overcome cancer radioresistance. Doublecortin-like kinase 1 (DCLK1) is an intestinal and pancreatic stem cell marker that showed overexpression in a variety of cancers. The transfection of DCLK1 siRNA to normal HCT-116 cells was performed, and then cells were irradiated with X-rays. The effects of DCLK1 inhibition on cell survival, apoptosis, cell cycle, DNA damage response (ATM and gamma H2AX proteins), epithelial-mesenchymal transition (EMT) related genes (vimentin, N-cadherin, and E-cadherin), cancer stem cells markers (CD44, CD133, ALDH1 and BMI1), and beta-catenin signaling pathway (beta-catenin) were evaluated. DCLK1 siRNA downregulated DCLK1 expression in HCT-116 cells at both mRNA and protein levels (P <0.01). Colony formation assay showed a significantly reduced cell survival in the DCLK1 siRNA transfected group in comparison with the control group following exposure to 4 and 6 Gy doses of irradiation (P <0.01). Moreover, the expression of cancer stem cells markers (P <0.01), EMT related genes (P <0.01), and DNA repair proteins including pATM (P <0.01) and gamma H2AX (P <0.001) were significantly decreased in the transfected cells in comparison with the nontransfected group after radiation. Finally, the cell apoptosis rate (P <0.01) and the number of cells in the G0/G1 phase in the silencing DCLK1 group was increased (P <0.01). These findings suggest that DCLK1 can be considered a promising therapeutic target for the treatment of radioresistant human CRC.
C1 [Mohammadi, Chiman; Mahdavinezhad, Ali; Saidijam, Massoud; Bahreini, Fatemeh; Najafi, Rezvan] Hamadan Univ Med Sci, Res Ctr Mol Med, Hamadan, Hamadan, Iran.
   [Pashaki, Abdolazim Sedighi; Gholami, Mohammad Hadi] Mandieh Radiotherapy & Brachytherapy Charitable C, Hamadan, Hamadan, Iran.
C3 Hamadan University of Medical Sciences
RP Najafi, R (corresponding author), Hamadan Univ Med Sci, Res Ctr Mol Med, Hamadan, Hamadan, Iran.
EM najafi2535@gmail.com
RI SedighiPashaki, Abdolazim/L-2781-2018; Mahdavinezhad, Ali/P-8431-2017;
   Gholami, Mohammad/AAO-5886-2020; Najafi, Rezvan/U-8110-2017
FU Hamadan University of Medical Sciences [9611177264]
FX This study was funded by a grant from Hamadan University of Medical
   Sciences (9611177264).
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NR 42
TC 9
Z9 9
U1 1
U2 14
PU CELLULAR & MOLECULAR BIOLOGY RESEARCH CENTER
PI BABOL
PA BABOL UNIV MEDICAL SCIENCES, GANJAFROUZ AVE, BABOL, 4717647745, IRAN
SN 2251-9637
EI 2251-9645
J9 INT J MOL CELL MED
JI Int. J. Mol. Cell. Med.
PD WIN
PY 2021
VL 10
IS 1
BP 23
EP 33
DI 10.22088/IJMCM.BUMS.10.1.23
PG 11
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA TH6AG
UT WOS:000672169900003
PM 34268251
DA 2025-01-04
ER

PT J
AU Hsu, HC
   Chou, WC
   Kuan, FC
   Lee, KD
   Rau, KM
   Huang, ES
   Yang, TS
AF Hsu, Hung-Chih
   Chou, Wen-Chi
   Kuan, Feng-Che
   Lee, Kuan-Der
   Rau, Kun-Ming
   Huang, En-Seng
   Yang, Tsai-Sheng
TI A Phase II study of S-1 plus oral leucovorin in heavily treated
   metastatic colorectal cancer patients
SO CANCER MANAGEMENT AND RESEARCH
LA English
DT Article
DE refractory metastatic colorectal cancer; S-1; oral leucovorin; Phase II;
   survival and safety
ID HIGH-DOSE LEUCOVORIN; SURGICAL ADJUVANT BREAST; ACQUIRED-RESISTANCE;
   1ST-LINE TREATMENT; RANDOMIZED-TRIAL; FLUOROURACIL; OXALIPLATIN;
   IRINOTECAN; THERAPY; 5-FLUOROURACIL
AB Purpose: Fewer treatment options are available for refractory metastatic colorectal cancer (mCRC). In early trials, S-1 monotherapy was effective for mCRC patients after chemotherapy failure and its combination with oral leucovorin therapy offers promising results in untreated mCRC. Hence, we conduct a Phase II trial to assess the efficacy of S-1 plus oral leucovorin (SL) in refractory mCRC that progressed after multiple prior standard therapies.
   Methods: In this open-label, single-arm study, we enrolled the refractory mCRC patients who received fluoropyrimidine, oxaliplatin, and irinotecan treatment and at least one targeted therapy previously. The doses of SL were 40-60 and 30 mg twice daily separately. They were administered for 7 days in a 2-week cycle. Treatment was continued until disease progression.
   Results: Of the 41 enrolled patients, 36 patients were evaluable with 61.1% disease control rate. The median progression-free survival and overall survival were 2.55 and 7.63 months, respectively. Regression change in tumor size stayed 10%-20% in five patients (13.9%) through 18 weeks after treatment, and two patients continued free from tumor progression at 30 and 42 weeks. Compared with moderate heavily pretreated mCRC patient subgroup (<= 4 prior regimens), the severe heavily pretreated subgroup (>= 5 prior regimens) showed similar disease control rate and survival benefit. Grade 3 or higher toxicities were documented only in 11 patients (26.8%).
   Conclusion: SL shows potential as a salvage regimen in refractory mCRC patients especially in the severe heavily pretreated setting and is well tolerated in these patients.
C1 [Hsu, Hung-Chih; Chou, Wen-Chi; Yang, Tsai-Sheng] Chang Gung Mem Hosp Linkou, Dept Internal Med, Div Hematol & Oncol, Taoyuan, Taiwan.
   [Hsu, Hung-Chih; Chou, Wen-Chi; Kuan, Feng-Che; Rau, Kun-Ming; Huang, En-Seng; Yang, Tsai-Sheng] Chang Gung Univ, Coll Med, Taoyuan, Taiwan.
   [Kuan, Feng-Che] Chang Gung Mem Hosp, Div Hematol & Oncol, Puzi, Chiayi, Taiwan.
   [Lee, Kuan-Der] Taipei Med Univ Hosp, Dept Med, Div Hematol & Oncol, Taipei, Taiwan.
   [Lee, Kuan-Der] Taipei Med Univ, Taipei, Taiwan.
   [Rau, Kun-Ming] Chang Gung Mem Hosp, Div Hematol & Oncol, Kaohsiung, Taiwan.
   [Huang, En-Seng] Chang Gung Mem Hosp, Div Hematol & Oncol, Keelung, Taiwan.
C3 Chang Gung Memorial Hospital; Chang Gung University; Chang Gung Memorial
   Hospital; Taipei Medical University Hospital; Taipei Medical University;
   Taipei Medical University; Chang Gung Memorial Hospital; Chang Gung
   Memorial Hospital
RP Yang, TS (corresponding author), Chang Gung Mem Hosp Linkou, Dept Internal Med, Div Hematol & Oncol, 5 Fu Hsing St, Kuei Shan 33305, Taoyuan County, Taiwan.
EM a481124@cgmh.org.tw
RI Chou, Wen-Chi/L-1478-2019; yu, dong/KRO-7922-2024
OI Rau, Kun-Ming/0000-0002-1209-3043; Hsu, Hung-Chih/0000-0002-4719-4143
FU TTY Biopharm Company Ltd. (Taipei, Taiwan)
FX This study was sponsored by TTY Biopharm Company Ltd. (Taipei, Taiwan).
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NR 35
TC 3
Z9 3
U1 0
U2 0
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1179-1322
J9 CANCER MANAG RES
JI Cancer Manag. Res.
PY 2018
VL 10
BP 6061
EP 6070
DI 10.2147/CMAR.S179345
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HC4PR
UT WOS:000451786300003
PM 30538555
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Dunne, EM
   Fraser, IM
   Liu, M
AF Dunne, Emma Maria
   Fraser, Ian Mark
   Liu, Mitchell
TI Stereotactic body radiation therapy for lung, spine and oligometastatic
   disease: current evidence and future directions
SO ANNALS OF TRANSLATIONAL MEDICINE
LA English
DT Article; Proceedings Paper
CT 4th Hong Kong International Oncology Symposium
CY NOV 03-04, 2017
CL City Univ Hong Kong, Hong Kong, HONG KONG
SP Hong Kong Adventist Hosp, ACT Gen, Hong Kong Lung Canc Study Grp, Soc Clin Oncol, Hong Kong Coll Radiologists, Hong Kong Integrated Oncol Ctr
HO City Univ Hong Kong
DE Non-small cell lung cancer (NSCLC); oligometastases; radiosurgery;
   stereotactic body radiotherapy
ID METASTATIC COLORECTAL-CANCER; PAINFUL BONE METASTASES; QUALITY-OF-LIFE;
   EARLY-STAGE; ABLATIVE RADIOTHERAPY; HEPATIC RESECTION; PHASE-II;
   SURGICAL-MANAGEMENT; MULTIPLE FRACTIONS; RANDOMIZED-TRIAL
AB Stereotactic body radiation therapy (SBRT) also referred to as stereotactic ablative radiotherapy (SABR), is a technique which has emerged over the past two decades due to improvements in radiation technology. Unlike conventional external beam radiotherapy (cEBRT) which traditionally delivers radiation in small doses [approximately 2 Gray (Gy) per fraction] over several weeks, SBRT, typically delivered in one to eight fractions, is a technique whereby potentially ablative doses of radiotherapy (usually 7.5-20 Gy per fraction) can be delivered with steeper dose gradients and sub millimetre precision, minimising risk to surrounding normal tissues. The potential benefits of excellent tumor control with low toxicity has led to the increasing use of SBRT in a number of clinical situations. Due to compelling evidence, SBRT is now the treatment of choice for medically inoperable patients with peripherally located stage I non-small cell lung cancer (NSCLC). Controversy remains however as to its efficacy and safety for central or ultra-central lung tumors. The evidence base supporting the use of SBRT as a novel treatment for spinal metastases and oligometastases is rapidly expanding but challenges remain in these difficult patient populations. In an era where targeted therapy and improved systemic treatments for stage IV cancer have resulted in increased disease-free survival, and our knowledge of the oligometastatic state is ever expanding, using SBRT to treat metastatic disease and gain durable local control is increasingly desirable. Several randomized trials are currently underway and are sure to provide valuable information on the benefit and utility of SBRT across many tumor sites including early-stage NSCLC, spinal metastases and oligometastatic disease. Recognizing the evolving role of SBRT in clinical practice, this paper provides a critical review of recent developments in each of these areas particularly highlighting the challenges facing clinicians and discusses potential areas for future research.
C1 [Dunne, Emma Maria; Fraser, Ian Mark; Liu, Mitchell] BCCA, Dept Radiat Oncol, Vancouver, BC, Canada.
RP Liu, M (corresponding author), 600 West 10th Ave, Vancouver, BC V5Z 4E6, Canada.
EM mliu@bccancer.bc.ca
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NR 111
TC 20
Z9 26
U1 0
U2 3
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2305-5839
EI 2305-5847
J9 ANN TRANSL MED
JI ANN. TRANSL. MED.
PD JUL
PY 2018
VL 6
IS 14
AR 283
DI 10.21037/atm.2018.06.40
PG 15
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Oncology; Research & Experimental Medicine
GA GP7PP
UT WOS:000441096800003
PM 30105233
OA Green Published
DA 2025-01-04
ER

PT J
AU Suzuki, SI
   Matsusaka, S
   Hirai, M
   Shibata, H
   Takagi, K
   Mizunuma, N
   Hatake, K
AF Suzuki, Shun-Ichi
   Matsusaka, Satoshi
   Hirai, Mitsuharu
   Shibata, Harumi
   Takagi, Koichi
   Mizunuma, Nobuyuki
   Hatake, Kiyohiko
TI A novel approach to detect KRAS/BRAF mutation for colon cancer: Highly
   sensitive simultaneous detection of mutations and simple pre-treatment
   without DNA extraction
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE colon cancer; KRAS mutation; BRAF mutation; QProbe method
ID METASTATIC COLORECTAL-CANCER; SINGLE NUCLEOTIDE POLYMORPHISMS; RAPID
   DETECTION SYSTEM; KRAS P.G13D MUTATION; AUTOMATED DETECTION;
   PROGNOSTIC-FACTOR; TARGETED THERAPY; K-RAS; CETUXIMAB; INHIBITION
AB It has been reported that colon cancer patients with KRAS and BRAF mutations that lie downstream of epidermal growth factor receptor (EGFR) acquire resistance against therapy with anti-EGFR antibodies, cetuximab and panitumumab. On the other hand, some reports say KRAS codon 13 mutation (p.G13D) has lower resistance against anti-EGFR antibodies, thus there is a substantial need for detection of specific KRAS mutations. We have established a state-of-the-art measurement system using QProbe (QP) method that allows simultaneous measurement of KRAS codon 12/13, p.G13D and BRAF mutation, and compared this method against Direct Sequencing (DS) using 182 specimens from colon cancer patients. In addition, 32 biopsy specimens were processed with a novel pre-treatment method without DNA purification in order to detect KRAS/BRAF. As a result of KRAS mutation measurement, concordance rate between the QP method and DS method was 81.4% (144/177) except for the 5 specimens that were undeterminable. Among them, 29 specimens became positive with QP method and negative with DS method. BRAF was measured with QP method only, and the mutation detection rate was 3.9% (6/153). KRAS measurement using a simple new pre-treatment method without DNA extraction resulted in 31 good results out of 32, all of them matching with the DS method. We have established a simple but highly sensitive simultaneous detection system for KRAS/BRAF. Moreover, introduction of the novel pre-treatment technology eliminated the inconvenient DNA extraction process. From this research achievement, we not only anticipate quick and accurate results returned in the clinical field but also contribution in improving the test quality and work efficiency.
C1 [Suzuki, Shun-Ichi] ARKRAY Mkt Inc, Mkt Div, Shinjuku Ku, Tokyo 1600004, Japan.
   [Matsusaka, Satoshi; Mizunuma, Nobuyuki] Japanese Fdn Canc Res, Canc Inst Hosp, Gastroenterol Ctr, Koto Ku, Tokyo 1358550, Japan.
   [Hirai, Mitsuharu] ARKRAY Inc, Div Res & Dev, Kamigyo Ku, Kyoto 6020008, Japan.
   [Shibata, Harumi; Takagi, Koichi; Hatake, Kiyohiko] Japanese Fdn Canc Res, Canc Chemotherapy Ctr, Clin Chemotherapy, Koto Ku, Tokyo 1358550, Japan.
C3 Japanese Foundation for Cancer Research; Japanese Foundation for Cancer
   Research
RP Matsusaka, S (corresponding author), Japanese Fdn Canc Res, Canc Inst Hosp, Gastroenterol Ctr, Koto Ku, 3-10-6 Ariake, Tokyo 1358550, Japan.
EM satoshi.matsusaka@jfcr.or.jp
OI Hirai, Mitsuharu/0000-0002-7633-9161
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NR 30
TC 5
Z9 5
U1 1
U2 8
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1019-6439
EI 1791-2423
J9 INT J ONCOL
JI Int. J. Oncol.
PD JUL
PY 2015
VL 47
IS 1
BP 97
EP 105
DI 10.3892/ijo.2015.2978
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CK8DG
UT WOS:000356468100011
PM 25936694
OA Green Published, hybrid, Green Submitted
DA 2025-01-04
ER

PT J
AU Kipkeeva, F
   Muzaffarova, T
   Korotaeva, A
   Mansorunov, D
   Apanovich, P
   Nikulin, M
   Malikhova, O
   Stilidi, I
   Karpukhin, A
AF Kipkeeva, Fatimat
   Muzaffarova, Tatyana
   Korotaeva, Alexandra
   Mansorunov, Danzan
   Apanovich, Pavel
   Nikulin, Maxim
   Malikhova, Olga
   Stilidi, Ivan
   Karpukhin, Alexander
TI The Features of Immune Checkpoint Gene Regulation by microRNA in Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE microRNA; immune checkpoint; immunotherapy
ID RENAL-CELL CARCINOMA; COLORECTAL-CANCER; TUMOR-SUPPRESSOR;
   BREAST-CANCER; PD-L1 EXPRESSION; DOWN-REGULATION; ANTITUMOR RESPONSES;
   TARGETING B7-H1; GASTRIC-CANCER; BINDING-SITE
AB Currently, the search for new promising tools of immunotherapy continues. In this regard, microRNAs (miRNAs) that influence immune checkpoint (IC) gene expression in tumor and T-cells and may be important regulators of immune cells are considered. MiRNAs regulate gene expression by blocking mRNA translation. An important feature of miRNA is its ability to affect the expression of several genes simultaneously, which corresponds to the trend toward the use of combination therapy. The article provides a list of miRNAs acting simultaneously on several ICs and miRNAs that, in addition to IC, can regulate the expression of targeted therapy genes. There is dependence of miRNA interactions with IC genes on the type of cancer. The analysis of the accumulated data demonstrates that only about 14% (95% CI: 9.8-20.1%) of the studied miRNAs regulate the expression of specific IC in more than one type of cancer. That is, there is tumor specificity in the miRNA action on ICs. A number of miRNAs demonstrated high efficiency in vitro and in vivo. This indicates the potential of miRNAs as promising agents for cancer immunotherapy. Additional studies of the miRNA-gene interaction features and the search for an optimal miRNA mimic structure are necessary.
C1 [Kipkeeva, Fatimat; Muzaffarova, Tatyana; Korotaeva, Alexandra; Mansorunov, Danzan; Apanovich, Pavel; Karpukhin, Alexander] Med Genet Res Ctr, 1 Moskvorechye St, Moscow 115522, Russia.
   [Nikulin, Maxim; Malikhova, Olga; Stilidi, Ivan] Minist Hlth Russia, NN Blokhin Natl Med Res Ctr Oncol, 24 Kashirskoe Shosse, Moscow 115478, Russia.
C3 Research Centre for Medical Genetics; Ministry of Health of the Russian
   Federation
RP Karpukhin, A (corresponding author), Med Genet Res Ctr, 1 Moskvorechye St, Moscow 115522, Russia.
EM karpukhin@med-gen.ru
RI Malikhova, Olga/AAP-5835-2020; Mansorunov, Danzan/AGL-9048-2022
OI Mansorunov, Danzan/0000-0003-1561-2504; Malikhova,
   Olga/0000-0003-0829-7809
FU Ministry of Science and Higher Education of the Russian Federation
   [FGFF-2022-0011]
FX The research was carried out within the state assignment and funding of
   the Ministry of Science and Higher Education of the Russian Federation
   FGFF-2022-0011.
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NR 199
TC 7
Z9 8
U1 1
U2 9
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD AUG
PY 2022
VL 23
IS 16
AR 9324
DI 10.3390/ijms23169324
PG 20
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 4C7TY
UT WOS:000846651900001
PM 36012588
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Nakamura, Y
   Shitara, K
AF Nakamura, Yoshiaki
   Shitara, Kohei
TI Development of circulating tumour DNA analysis for gastrointestinal
   cancers
SO ESMO OPEN
LA English
DT Review
ID METASTATIC COLORECTAL-CANCER; PICODROPLET DIGITAL PCR; ANTI-EGFR
   THERAPY; CELL-FREE DNA; ACQUIRED-RESISTANCE; KRAS MUTATIONS; RAS
   MUTATIONS; MICROSATELLITE INSTABILITY; PHASE-II; HETEROGENEITY
AB Comprehensive genomic profiling using next-generation sequencing (NGS) enables the identification of multiple genomic biomarkers established in advanced gastrointestinal (GI) cancers. However, tissue-based NGS has limitations, such as long turnaround time and failure to detect tumour heterogeneity. Recently, the analysis of circulating tumour DNA (ctDNA) using polymerase chain reaction-based or NGS-based methods has demonstrated the capability to detect genomic alterations with high accuracy compared with tumour tissue analysis with short turnaround time and identify heterogeneous resistance mechanisms. Furthermore, ctDNA analysis can be repeatedly performed on disease progression to clarify resistant clones. Clinical trials that test the outcome of a selected targeted therapy based on a ctDNA result are ongoing to prospectively evaluate the clinical utility of ctDNA analysis. Furthermore, the improvement of ctDNA analysis beyond current technical limits of mutation-based ctDNA detection methods has expanded the potential for detecting the presence of tumours in patients with no clinically evident disease, such as minimal residual disease and early cancer. Although a careful understanding of the advantages and limitations are required and further prospective studies are needed, the ctDNA analysis has the potential to overcome several challenges in the treatment of various types of cancers at all stages, including GI cancers.
C1 [Nakamura, Yoshiaki] Natl Canc Ctr Hosp East, Biobank Translat Res Support Sect, Translat Res Management Div, Clin Res Support Off, Kashiwa, Chiba, Japan.
   [Nakamura, Yoshiaki; Shitara, Kohei] Natl Canc Ctr Hosp East, Dept Gastroenterol & Gastrointestinal Oncol, Kashiwa, Chiba, Japan.
C3 National Cancer Center - Japan; National Cancer Center - Japan
RP Shitara, K (corresponding author), Natl Canc Ctr Hosp East, Dept Gastroenterol & Gastrointestinal Oncol, Kashiwa, Chiba, Japan.
EM kshitara@east.ncc.go.jp
RI Shitara, Kohei/AAA-3877-2021
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NR 72
TC 22
Z9 22
U1 0
U2 6
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2059-7029
J9 ESMO OPEN
JI ESMO Open
PD MAR
PY 2020
VL 5
SU 1
AR e000600
DI 10.1136/esmoopen-2019-000600
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LN5HH
UT WOS:000532967700003
PM 32830648
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zaaimi, Y
   Aparicio, T
   Laurent-Puig, P
   Taieb, J
   Zaanan, A
AF Zaaimi, Yosra
   Aparicio, Thomas
   Laurent-Puig, Pierre
   Taieb, Julien
   Zaanan, Aziz
TI Advanced small bowel adenocarcinoma: Molecular characteristics and
   therapeutic perspectives
SO CLINICS AND RESEARCH IN HEPATOLOGY AND GASTROENTEROLOGY
LA English
DT Review
ID PROGNOSTIC-FACTORS; PHASE-II; PERIAMPULLARY ADENOCARCINOMA;
   SMALL-INTESTINE; CHEMOTHERAPY; CANCER; SURVIVAL; RISK; MLH1; MANAGEMENT
AB Small bowel cancer represents less than 5% of all gastrointestinal cancers, while small bowel adenocarcinoma (SBA) accounts for about one third of all cancers of the small bowel. Although SBA frequently appears sporadically, some diseases are risk factors, such as Crohn's disease and some genetic predispositions to cancer. Progress in the identification of molecular alterations suggests some similarities in carcinogenesis between SBA and colorectal cancer. Evidence levels for the treatment and prognosis of these tumors are insufficient because of the scarcity of this disease and the absence of randomized trials. Chemotherapy based on fluoropyrimidine plus a platinum salt appears to be the most effective treatment regimen in non-randomized prospective trials for advanced SBA. Targeted therapy, against the angiogenic pathway or the epidermal growth factor receptor (EGFR) pathway, for example, is not yet established, but seems promising given the over-expression of vascular epithelial growth factor (VEGF)-A or EGFR observed in SBA. Phase I and II studies are currently evaluating the safety and efficacy of these targeted therapies in SBA treatment. The low incidence of SBA should promote the development of international collaborations to improve our knowledge of the biological mechanisms underlying these tumors and to set up therapeutic trials. (C) 2015 Elsevier Masson SAS. All rights reserved.
C1 [Zaaimi, Yosra; Taieb, Julien; Zaanan, Aziz] Hop Europeen Georges Pompidou, AP HP, Dept Gastroenterol & Digest Oncol, 20 Rue Leblanc, F-75015 Paris, France.
   [Aparicio, Thomas] Avicenne Hosp, AP HP, Dept Gastroenterol & Digest Oncol, Bobigny, France.
   [Laurent-Puig, Pierre; Zaanan, Aziz] INSERM, UMR S 1147, Paris, France.
   [Laurent-Puig, Pierre; Taieb, Julien; Zaanan, Aziz] Paris Descartes Univ, Paris, France.
   [Laurent-Puig, Pierre] Hop Europeen Georges Pompidou, AP HP, Dept Biol, F-75015 Paris, France.
C3 Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Europeen Georges-Pompidou - APHP; Assistance
   Publique Hopitaux Paris (APHP); Hopital Universitaire Avicenne - APHP;
   Universite Paris Cite; Institut National de la Sante et de la Recherche
   Medicale (Inserm); Universite Paris Cite; Assistance Publique Hopitaux
   Paris (APHP); Universite Paris Cite; Hopital Universitaire Europeen
   Georges-Pompidou - APHP
RP Zaanan, A (corresponding author), Hop Europeen Georges Pompidou, AP HP, Dept Gastroenterol & Digest Oncol, 20 Rue Leblanc, F-75015 Paris, France.; Zaanan, A (corresponding author), INSERM, UMR S 1147, Paris, France.; Zaanan, A (corresponding author), Paris Descartes Univ, Paris, France.
EM aziz.zaanan@aphp.fr
RI ; Laurent-Puig, Pierre/B-2226-2013
OI Zaanan, Aziz/0000-0001-8372-5653; taieb, julien/0000-0002-9955-4753;
   Laurent-Puig, Pierre/0000-0001-8475-5459
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NR 56
TC 31
Z9 33
U1 0
U2 5
PU ELSEVIER MASSON, CORP OFF
PI PARIS
PA 65 CAMILLE DESMOULINS CS50083 ISSY-LES-MOULINEAUX, 92442 PARIS, FRANCE
SN 2210-7401
EI 2210-741X
J9 CLIN RES HEPATOL GAS
JI Clin. Res. Hepatol. Gastroenterol.
PD APR
PY 2016
VL 40
IS 2
BP 154
EP 160
DI 10.1016/j.clinre.2015.09.008
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DI0GY
UT WOS:000373174900007
PM 26547136
DA 2025-01-04
ER

PT J
AU Nie, CY
   Lv, HF
   Chen, BB
   Xu, WF
   Wang, JZ
   Liu, YJ
   Wang, SQ
   Zhao, J
   He, YD
   Chen, XB
AF Nie, Caiyun
   Lv, Huifang
   Chen, Beibei
   Xu, Weifeng
   Wang, Jianzheng
   Liu, Yingjun
   Wang, Saiqi
   Zhao, Jing
   He, Yunduan
   Chen, Xiaobing
TI Microsatellite stable metastatic colorectal cancer without liver
   metastasis may be preferred population for regorafenib or fruquintinib
   plus sintilimab as third-line or above therapy:A real-world study
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE microsatellite stable; immunotherapy; targeted therapy; liver
   metastasis; colorectal cancer
ID IMMUNOTHERAPY; MULTICENTER; NIVOLUMAB; PLACEBO; BENEFIT
AB ObjectivesThe antitumor activity of nivolumab plus regorafenib in colorectal cancer from a phase Ib REGONIVO study is encouraging. The present study was conducted to evaluate the efficacy and safety of regorafenib or fruquintinib plus sintilimab as third-line or above therapy in patients with microsatellite stable (MSS) metastatic colorectal cancer. MethodsPatients with MSS metastatic colorectal cancer who have failed from prior treatment and received regorafenib or fruquintinib plus sintilimab as third-line or above therapy from January 2019 to December 2020 were prospectively analyzed based on real-world clinical practice. The primary end point was progression free survival (PFS). Secondary end points included objective response rate (ORR), disease control rate (DCR), overall survival (OS), and safety. Results42 patients received regorafenib plus sintilimab(RS), and the other 30 patients received fruquintinib plus sintilimab(FS). In the general population, the ORR and DCR were 13.9% and 70.8%, and the median PFS and OS was 4.2(95% CI=2.9-5.5) and 10.5 (95% CI=8.6-12.4) months, respectively. There were no statistically significant differences between RS and FS group in PFS (3.5(2.2-4.8) vs. 5.5(3.5-7.5) months, P=0.434) and OS (11.0(7.0-15.0) vs. 10.5(3.8-17.2) months, P=0.486). Subgroup analysis suggested that patients without liver metastasis responded well to this combination regimen (ORR: 21.4% vs. 9.1%) and obtained better OS (26(8.8-43.2) vs. 10.0(7.4-12.6) months, P=0.016). The incidence of Grade 3-4 adverse events (AEs) was 15.3% and the toxicities were generally tolerable and manageable. ConclusionsRegorafenib or fruquintinib plus sintilimab as third-line or above therapy provide a feasible treatment regimen for MSS metastatic colorectal cancer with tolerated toxicity. Patients without liver metastasis may be the preferred population for this combination regimen.
C1 [Nie, Caiyun; Lv, Huifang; Chen, Beibei; Xu, Weifeng; Wang, Jianzheng; Wang, Saiqi; Zhao, Jing; He, Yunduan; Chen, Xiaobing] Zhengzhou Univ, Henan Canc Hosp, Dept Med Oncol, Affiliated Canc Hosp, Zhengzhou, Peoples R China.
   [Nie, Caiyun; Lv, Huifang; Chen, Beibei; Xu, Weifeng; Wang, Jianzheng; Wang, Saiqi; Zhao, Jing; He, Yunduan; Chen, Xiaobing] Zhengzhou Univ, State Key Lab Esophageal Canc Prevent & Treatment, Zhengzhou, Peoples R China.
   [Nie, Caiyun; Lv, Huifang; Chen, Beibei; Xu, Weifeng; Wang, Jianzheng; Wang, Saiqi; Zhao, Jing; He, Yunduan; Chen, Xiaobing] Henan Engn Res Ctr Precis Therapy Gastrointestinal, Zhengzhou, Peoples R China.
   [Nie, Caiyun; Lv, Huifang; Chen, Beibei; Xu, Weifeng; Wang, Jianzheng; Wang, Saiqi; Zhao, Jing; He, Yunduan; Chen, Xiaobing] Zhengzhou Key Lab Precis Therapy Gastrointestinal, Zhengzhou, Peoples R China.
   [Liu, Yingjun] Zhengzhou Univ, Henan Canc Hosp, Dept Gen Surg, Affiliated Canc Hosp, Zhengzhou, Peoples R China.
C3 Zhengzhou University; Zhengzhou University; Zhengzhou University
RP Chen, XB (corresponding author), Zhengzhou Univ, Henan Canc Hosp, Dept Med Oncol, Affiliated Canc Hosp, Zhengzhou, Peoples R China.; Chen, XB (corresponding author), Zhengzhou Univ, State Key Lab Esophageal Canc Prevent & Treatment, Zhengzhou, Peoples R China.; Chen, XB (corresponding author), Henan Engn Res Ctr Precis Therapy Gastrointestinal, Zhengzhou, Peoples R China.; Chen, XB (corresponding author), Zhengzhou Key Lab Precis Therapy Gastrointestinal, Zhengzhou, Peoples R China.
EM zlyychenxb0807@zzu.edu.cn
RI w0a0n0g, s0a0i/HGB-8344-2022
FU Medical Science and Technique Foundation of Henan Province
   [212102310623, SB201901101]; Young and Middle-aged Health and Technology
   Innovation Leading Talent Project of Henan Province [YXKC2020008]; 1000
   Talents Program of Central plains [204200510023]; Sate Key Laboratory of
   Esophageal Cancer Prevention Treatment [Z2020000X]
FX This work was supported by Medical Science and Technique Foundation of
   Henan Province (No. 212102310623), Medical Science and Technique
   Foundation of Henan Province (No. SB201901101), Young and Middle-aged
   Health and Technology Innovation Leading Talent Project of Henan
   Province (No. YXKC2020008), 1000 Talents Program of Central plains (No.
   204200510023) and the Sate Key Laboratory of Esophageal Cancer
   Prevention & Treatment (No. Z2020000X).
CR André T, 2020, NEW ENGL J MED, V383, P2207, DOI 10.1056/NEJMoa2017699
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NR 30
TC 11
Z9 10
U1 0
U2 5
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD SEP 26
PY 2022
VL 12
AR 917353
DI 10.3389/fonc.2022.917353
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 5Q8BV
UT WOS:000874050900001
PM 36226061
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Dai, MY
   Li, LM
   Qin, X
AF Dai, Meiyu
   Li, Limin
   Qin, Xue
TI Clinical value of miRNA-122 in the diagnosis and prognosis of various
   types of cancer
SO ONCOLOGY LETTERS
LA English
DT Article
DE microRNA-122; cancer; The Cancer Genome Atlas; diagnosis; overall
   survival rate
ID RENAL-CELL CARCINOMA; HEPATOCELLULAR-CARCINOMA; CIRCULATING
   MICRORNA-122; EGYPTIAN PATIENTS; PLASMA MIR-122; LIVER-CANCER;
   EXPRESSION; BIOMARKERS; HEPATITIS; TARGET
AB The present study aimed to systematically analyze the value of microRNA-122 (miRNA-122) in the diagnosis and prognosis of hepatocellular carcinoma (HCC) and other types of cancer. First, the reverse transcription-quantitative polymerase chain reaction method was used to detect the expression levels of miRNA-122 in the serum samples of patients with HCC, benign lesions and healthy volunteers. Next, miRNA-seq data of miRNA-122 from The Cancer Genome Atlas database were used to analyze the differential expression and overall survival rate associated with a variety of types of cancer. Meanwhile, the target gene prediction of miRNA-122 was performed using four different software programs. Finally, 353 significant target genes were identified for Gene Ontology and Kyoto Encyclopedia of Genes and Genomes functional enrichment analysis. Finally, it was demonstrated that the expression levels of miRNA-122 in the HCC group were increased compared with the healthy group (P<0.001), but decreased with respect to the benign group (P<0.001). In addition, the combination of the miRNA-122 and a fetoprotein may further improve the diagnostic accuracy between the HCC and healthy groups (area under the curve, 0.980; 95% confidence interval, 0.958-1.000). It was also demonstrated that miRNA-122 exhibited significantly differential expression and the overall survival rate was predicted for various other types of cancer, including colorectal cancer, renal carcinoma, cholangiocarcinoma, prostate cancer and thyroid carcinoma. Functional enrichment analysis demonstrated that the target genes of miRNA-122 may contribute to the composition of the nucleus and cytoplasm, and regulate a variety of biological processes, including cardiac muscle cell differentiation and glucose metabolic processes via protein biosynthesis, estrogen and glucagon associated signaling pathways. These results revealed that miRNA-122 may be an indispensable biomarker for the diagnosis, prognostic evaluation and targeted therapy in pan-cancer.
C1 [Dai, Meiyu; Li, Limin; Qin, Xue] Guangxi Med Univ, Affiliated Hosp 1, Dept Clin Lab, 6 Shuangyong Rd, Nanning 530021, Guangxi, Peoples R China.
C3 Guangxi Medical University
RP Qin, X (corresponding author), Guangxi Med Univ, Affiliated Hosp 1, Dept Clin Lab, 6 Shuangyong Rd, Nanning 530021, Guangxi, Peoples R China.
EM qinxue919@126.com
RI qin, xue/KQV-3701-2024
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NR 85
TC 26
Z9 27
U1 1
U2 16
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD APR
PY 2019
VL 17
IS 4
BP 3919
EP 3929
DI 10.3892/ol.2019.10024
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HQ8AB
UT WOS:000462644700035
PM 30881509
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Jan, YH
   Lu, CT
   Lam, AKY
AF Jan, Yi-Hua
   Lu, Cu tai
   Lam, Alfred King-yin
TI Comparison of genomic profiling of patient-matched primary colorectal
   and surgical resected distant metastatic (stage IV) colorectal carcinoma
   for drug actionability
SO HUMAN PATHOLOGY
LA English
DT Article
DE Genomic; Distant metastases; Colorectal carcinoma; Tumour mutational
   burden; MSI; RAS
ID TUMOR-CELLS; OPEN-LABEL; CANCER; PLUS; EXPRESSION; NIVOLUMAB; CETUXIMAB;
   TRIAL
AB It is often difficult to obtain adequate tissue for genomic study from distant metastases for assessment of targeted therapy in colorectal carcinomas. The study aims to explore the genomic differences between matched distant metastatic colorectal carcinomas (mCRC) and primary carcinoma using surgical specimens of both with adequate tissue. Thirty-four paired primary and distant metastatic colorectal carcinoma samples (liver, ovary, and lung) were obtained from surgical excisions (not small biopsies) and are microsatellite stable. They were subjected to DNA sequencing using comprehensive next-generation sequencing. This included mutation concordance analysis and mutational signature analysis. The mutation concordance analysis showed 49.6% shared mutations between primary and metastatic tumours, with 23.0% mutations exclusive to primary tumours and 27.4% mutations exclusive to distant metastases. While many patients with KRAS/BRAF mutations had shared mutations, two cases had unique KRAS mutations in the primary tumours only. Additionally, TMB (tumour mutational burden) analysis revealed that half of the TMB-high (>= 7.5 mutations/Mb) metastatic colorectal carcinomas had a low TMB (<7.5 mutations/Mb) in the primary tumours. The mutational signature analysis identified de novo signatures consistent with known single base substitution patterns such as SBS11 (alkylation agents) and SBS30 (base excision repair deficiency) post-chemotherapy. To conclude, this study demonstrates significant genomic variations in resected distant metastasis when compared to primary colorectal carcinomas when adequate tissue is available. This finding underscores the importance of considering these differences and selecting tissue for mutation analysis in planning targeted and effective treatment strategies for mCRC.
C1 [Jan, Yi-Hua] ACT Genom Co Ltd, Taipei 114, Taiwan.
   [Jan, Yi-Hua] Koo Fdn Sun Yat Sen Canc Ctr, Dept Mol Med, Taipei 11259, Taiwan.
   [Lu, Cu tai] Gold Coast Univ Hosp, Dept Surg, Southport, Qld 4215, Australia.
   [Lu, Cu tai; Lam, Alfred King-yin] Griffith Univ, Sch Med & Dent, Gold Coast Campus, Gold Coast, Qld 4222, Australia.
   [Lam, Alfred King-yin] Gold Coast Univ Hosp, Pathol Queensland, Southport, Qld 4215, Australia.
   [Lam, Alfred King-yin] Univ Queensland, Fac Med, Herston, Qld 4006, Australia.
C3 Gold Coast University Hospital; Griffith University; Griffith University
   - Gold Coast Campus; Gold Coast University Hospital; University of
   Queensland
RP Lam, AKY (corresponding author), Griffith Univ, Sch Med & Dent, Gold Coast, Qld 4222, Australia.
EM a.lam@griffith.edu.au
RI Lam, Alfred/C-1652-2008
OI Lam, Alfred/0000-0003-2771-564X
FU ELITE Research Grant Programme of Hong Kong Science & Technology Park;
   ACT Genomics, Co. Ltd, Hong Kong
FX The study was supported by the ELITE Research Grant Programme of Hong
   Kong Science & Technology Park and ACT Genomics, Co. Ltd, Hong Kong.
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NR 24
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0046-8177
EI 1532-8392
J9 HUM PATHOL
JI Hum. Pathol.
PD JUL
PY 2024
VL 149
BP 21
EP 28
DI 10.1016/j.humpath.2024.06.001
EA JUN 2024
PG 8
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA WK7E0
UT WOS:001254819900001
PM 38862093
OA hybrid
DA 2025-01-04
ER

PT J
AU Tavares, TS
   Hofman, J
   Lekesová, A
   Zelazková, J
   Wsól, V
AF Tavares, Tassia S.
   Hofman, Jakub
   Lekesova, Alzbeta
   Zelazkova, Jana
   Wsol, Vladimir
TI Olaparib Synergizes the Anticancer Activity of Daunorubicin via
   Interaction with AKR1C3
SO CANCERS
LA English
DT Article
DE daunorubicin; olaparib; synergistic; anti-proliferative; leukaemia;
   KG1&#945; HepG2
ID ALDO-KETO REDUCTASES; POLY(ADP-RIBOSE) POLYMERASE; CARBONYL REDUCTION;
   REDUCING ENZYMES; PARP INHIBITORS; CANCER-CELLS; IN-VITRO; PHASE-I;
   METABOLISM; DOXORUBICIN
AB Sample summary
   Anthracyclines (ANT) are anti-tumor agents frequently used for the treatment of various cancers. Unfortunately, their clinical success is overshadowed by the emergence of drug resistance. Metabolism by carbonyl reducing enzymes (CREs) represents a critical mechanism of ANT resistance. Here, we have explored possible interactions of CREs with olaparib, an FDA-approved targeted chemotherapeutic. Although olaparib has been demonstrated to potentiate the antiproliferative effect of ANT in experimental models, the causing mechanisms remain unclear. In our study, we demonstrated that olaparib potently inhibits the AKR1C3 reductase at clinically relevant concentrations. Furthermore, we showed that this interaction mediates the reversal of ANT resistance and thus represents a critical mechanism of the synergy between ANT and olaparib. Our observations represent valuable knowledge that could be transformed into the more effective therapy of AKR1C3-expressing tumors.
   Olaparib is a potent poly (ADP-ribose) polymerase inhibitor currently used in targeted therapy for treating cancer cells with BRCA mutations. Here we investigate the possible interference of olaparib with daunorubicin (Daun) metabolism, mediated by carbonyl-reducing enzymes (CREs), which play a significant role in the resistance of cancer cells to anthracyclines. Incubation experiments with the most active recombinant CREs showed that olaparib is a potent inhibitor of the aldo-keto reductase 1C3 (AKR1C3) enzyme. Subsequent inhibitory assays in the AKR1C3-overexpressing cellular model transfected human colorectal carcinoma HCT116 cells, demonstrating that olaparib significantly inhibits AKR1C3 at the intracellular level. Consequently, molecular docking studies have supported these findings and identified the possible molecular background of the interaction. Drug combination experiments in HCT116, human liver carcinoma HepG2, and leukemic KG1 alpha cell lines showed that this observed interaction can be exploited for the synergistic enhancement of Daun's antiproliferative effect. Finally, we showed that olaparib had no significant effect on the mRNA expression of AKR1C3 in HepG2 and KG1 alpha cells. In conclusion, our data demonstrate that olaparib interferes with anthracycline metabolism, and suggest that this phenomenon might be utilized for combating anthracycline resistance.
C1 [Tavares, Tassia S.; Lekesova, Alzbeta; Zelazkova, Jana; Wsol, Vladimir] Charles Univ Prague, Fac Pharm Hradec Kralove, Dept Biochem Sci, Heyrovskeho 1203, Hradec Kralove 50005, Czech Republic.
   [Hofman, Jakub] Charles Univ Prague, Fac Pharm Hradec Kralove, Dept Pharmacol & Toxicol, Heyrovskeho 1203, Hradec Kralove 50005, Czech Republic.
C3 Charles University Prague; Charles University Prague
RP Wsól, V (corresponding author), Charles Univ Prague, Fac Pharm Hradec Kralove, Dept Biochem Sci, Heyrovskeho 1203, Hradec Kralove 50005, Czech Republic.
EM silvatat@faf.cuni.cz; hofmanj@faf.cuni.cz; lekesova@faf.cuni.cz;
   zelazkoj@faf.cuni.cz; wsol@faf.cuni.cz
RI Hofman, Jakub/T-6461-2017; Wsol, Vladimir/K-3476-2016
OI Wsol, Vladimir/0000-0003-3745-7648
FU European Union [CZ.02.1.01/0.0/0.0/18_069/0010046];  [20-20414Y]
FX This research was funded by the InoMed project, grant number
   CZ.02.1.01/0.0/0.0/18_069/0010046 co-funded by the European Union.
   Furthermore, it was supported by the Czech Science Foundation (grant No.
   20-20414Y).
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NR 54
TC 9
Z9 10
U1 1
U2 18
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD NOV
PY 2020
VL 12
IS 11
AR 3127
DI 10.3390/cancers12113127
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OW6JO
UT WOS:000592990800001
PM 33114555
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Ashktorab, H
   Daremipouran, M
   Devaney, J
   Varma, S
   Rahi, H
   Lee, E
   Shokrani, B
   Schwartz, R
   Nickerson, ML
   Brim, H
AF Ashktorab, Hassan
   Daremipouran, Mohammad
   Devaney, Joe
   Varma, Sudhir
   Rahi, Hamed
   Lee, Edward
   Shokrani, Babak
   Schwartz, Russell
   Nickerson, Michael L.
   Brim, Hassan
TI Identification of Novel Mutations by Exome Sequencing in African
   American Colorectal Cancer Patients
SO CANCER
LA English
DT Article
DE APC; Mutation; tumor suppressors; oncogene; cancer pathways
ID CATENIN PATHWAY; READ ALIGNMENT; DNA; GENE; METHYLATION; EXPRESSION;
   DISCOVERY; FRAMEWORK; CELLS; APC
AB BACKGROUNDThe purpose of this study was to identify genome-wide single nucleotide variants and mutations in African American patients with colorectal cancer (CRC). There is a need of such studies in African Americans, because they display a higher incidence of aggressive CRC tumors.
   METHODSWe performed whole exome sequencing (WES) on DNA from 12 normal/tumor pairs of African American CRC patient tissues. Data analysis was performed using the software package GATK (Genome Analysis Tool Kit). Normative population databases (eg, 1000 Genomes SNP database, dbSNP, and HapMap) were used for comparison. Variants were annotated using analysis of variance and were validated via Sanger sequencing.
   RESULTSWe identified somatic mutations in genes that are known targets in CRC such as APC, BRAF, KRAS, and PIK3CA. We detected novel alterations in the Wnt pathway gene, APC, within its exon 15, of which mutations are highly associated with CRC.
   CONCLUSIONSThis WES study in African American patients with CRC provides insight into the identification of novel somatic mutations in APC. Our data suggest an association between specific mutations in the Wnt signaling pathway and an increased risk of CRC. The analysis of the pathogenicity of these novel variants may shed light on the aggressive nature of CRC in African Americans. Cancer 2015;121:34-42. (c) 2014 American Cancer Society.
   We have little knowledge of the phenotypic genetic changes of colorectal cancer in African Americans and their correlation with the DNA changes found in the majority of cancers in this population. Identifying biomarkers in colorectal cancer in African Americans is likely to help determine the key genes involved in the progression of this disease and identify biomarkers for targeted therapy and management in African Americans with colorectal cancer.
C1 [Ashktorab, Hassan; Daremipouran, Mohammad; Rahi, Hamed] Howard Univ, Coll Med, Dept Med, Washington, DC 20060 USA.
   [Ashktorab, Hassan; Daremipouran, Mohammad; Rahi, Hamed] Howard Univ, Coll Med, Ctr Canc, Washington, DC 20060 USA.
   [Devaney, Joe] Children Natl Med Ctr, Washington, DC USA.
   [Varma, Sudhir] Hithru LLC, Silver Spring, MD USA.
   [Lee, Edward; Shokrani, Babak; Brim, Hassan] Howard Univ, Coll Med, Dept Pathol, Washington, DC 20060 USA.
   [Schwartz, Russell] Carnegie Mellon Univ, Pittsburgh, PA 15213 USA.
   [Nickerson, Michael L.] NCI, Ctr Canc Res, Frederick, MD 21701 USA.
C3 Howard University; Howard University; Children's National Health System;
   Howard University; Carnegie Mellon University; National Institutes of
   Health (NIH) - USA; NIH National Cancer Institute (NCI)
RP Ashktorab, H (corresponding author), Howard Univ, Coll Med, Canc Res Ctr, 2041 Georgia Ave NW, Washington, DC 20060 USA.
EM hashktorab@howard.edu
RI Ashktorab, hassan/AAJ-2908-2020; Schwartz, Russell/A-1998-2016; Varma,
   Sudhir/N-8763-2014
OI Schwartz, Russell/0000-0002-4970-2252; Varma, Sudhir/0000-0002-4096-4782
FU National Institute on Minority Health and Health Disparities of the
   National Institutes of Health [G12MD007597]
FX This project was supported (in part) by the National Institute on
   Minority Health and Health Disparities of the National Institutes of
   Health under Award Number G12MD007597.
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NR 48
TC 30
Z9 33
U1 0
U2 16
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
EI 1097-0142
J9 CANCER-AM CANCER SOC
JI Cancer
PD JAN 1
PY 2015
VL 121
IS 1
BP 34
EP 42
DI 10.1002/cncr.28922
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AW8CF
UT WOS:000346487500009
PM 25250560
OA Bronze, Green Accepted
DA 2025-01-04
ER

PT J
AU Boisteau, E
   Lespagnol, A
   De Tayrac, M
   Corre, S
   Perrot, A
   Rioux-Leclercq, N
   Martin-Lannerée, S
   Artru, P
   Chalabreysse, P
   Poureau, PG
   Doucet, L
   Coupez, D
   Bennouna, J
   Bossard, C
   Coriat, R
   Beuvon, F
   Bauguion, L
   Leclair, F
   Chautard, R
   Lecomte, T
   Guyetant, S
   Desgrippes, R
   Grasset, D
   Lhostis, H
   Bouhier-Leporrier, K
   Bibeau, F
   Edeline, J
   Galibert, MD
   Lièvre, A
AF Boisteau, Emeric
   Lespagnol, Alexandra
   De Tayrac, Marie
   Corre, Sebastien
   Perrot, Anthony
   Rioux-Leclercq, Nathalie
   Martin-Lanneree, Severine
   Artru, Pascal
   Chalabreysse, Philippe
   Poureau, Pierre-Guillaume
   Doucet, Laurent
   Coupez, Dahna
   Bennouna, Jaafar
   Bossard, Celine
   Coriat, Romain
   Beuvon, Frederic
   Bauguion, Lucile
   Leclair, Francois
   Chautard, Romain
   Lecomte, Thierry
   Guyetant, Serge
   Desgrippes, Romain
   Grasset, Denis
   Lhostis, Helene
   Bouhier-Leporrier, Karine
   Bibeau, Frederic
   Edeline, Julien
   Galibert, Marie-Dominique
   Lievre, Astrid
TI MiR-31-3p do not predict anti-EGFR efficacy in first-line therapy of<i>
   RAS</i> wild-type metastatic right-sided colon cancer
SO CLINICS AND RESEARCH IN HEPATOLOGY AND GASTROENTEROLOGY
LA English
DT Article
DE Colorectal cancer; Metastasis; Biomarker; miR-31-3p; anti-EGFR mAb;
   Bevacizumab
ID COLORECTAL-CANCER; PLUS BEVACIZUMAB; INITIAL THERAPY; CETUXIMAB;
   SURVIVAL; KRAS; IRINOTECAN; MUTATIONS; FLUOROURACIL; CHEMOTHERAPY
AB Background: Low miR-31-3p expression was identified as predictive of anti-EGFR efficacy in RASwt mCRC. Primary tumor side was also proposed as a predictive factor of anti-EGFR benefit. This retrospective multicentric study evaluated the predictive role of miR-31-3p in right-sided RAS- wt mCRC patients treated with first-line CT+anti-EGFR or CT+bevacizumab (Beva).Methods: Seventy-two right-sided RAS-wt mCRC patients treated in first-line with CT+anti-EGFR (n = 43) or Beva (n = 29) were included. Overall survival (OS), progression-free survival (PFS) and response rate (RR) were analyzed and stratified according to tumor miR-31-3p expression level and targeted therapy (TT).Results: BRAFV600E mutation was more frequent in high vs low miR-31-3p expressers (60.6% vs 15.4%, P < 0.001). PFS was significantly longer with CT+Beva than with CT+anti-EGFR (13 vs 7 months; P = 0.024). Among low miR-31-3p expressers, PFS, OS and RR were not significantly different between the two groups, while in high miR-31-3p expressers, only PFS was longer in the CT+Beva group (11 vs 6 months; P = 0.03). In patients treated with CT+anti-EGFR, low miR-31-3p expressers had a significantly longer OS (20 vs 13 months; P = 0.02) than high miR-31-3p expressers. ORR was not significantly different between the two groups of treatment, in both low and high miR-31-3p expressers. MiR-31-3p expression status was statistically correlated between primary tumors and corresponding metastases.Conclusion: In this study, miR-31-3p couldn't identify a subgroup of patients with right-sided RAS-wt mCRC who might benefit from anti-EGFR and suggest that Beva is the TT of choice in first-line treatment of these patients.(c) 2022 Elsevier Masson SAS. All rights reserved.
C1 [Boisteau, Emeric; Lievre, Astrid] Rennes Univ Hosp, Univ Hosp Pontchaillou, Dept Gastroenterol, 2 Rue Henri Le Guilloux, F-35033 Rennes 09, France.
   [Lespagnol, Alexandra; De Tayrac, Marie; Perrot, Anthony; Galibert, Marie-Dominique] Rennes Univ Hosp, Dept Somat Genet Canc, Dept Mol Genet & Genom, 2 Rue Henri Le Guilloux, F-35033 Rennes 09, France.
   [De Tayrac, Marie; Corre, Sebastien; Galibert, Marie-Dominique] Univ Rennes, CNRS, IGDR Inst Genet & Dev Rennes, UMR 6290, F-35000 Rennes, France.
   [Rioux-Leclercq, Nathalie; Edeline, Julien] Univ Rennes 1, Rennes, France.
   [Rioux-Leclercq, Nathalie] Rennes Univ Hosp, Dept Pathol Anat & Cytol, Rennes, France.
   [Martin-Lanneree, Severine] IntegraGen SA, 5 Rue Henri Desbrueres, Evry, France.
   [Artru, Pascal] Private Hosp Jean Mermoz, Digest Oncol, Lyon, France.
   [Chalabreysse, Philippe] Cabinet Pathol CYPATH, Philippe Chalabreysse, 201 Route Genas, F-69100 Villeurbanne, France.
   [Poureau, Pierre-Guillaume] Univ Hosp, Dept Oncol, Brest, France.
   [Doucet, Laurent] CHRU Brest, Serv Anat & Cytol Pathol, Hop Morvan, Brest, France.
   [Coupez, Dahna; Bennouna, Jaafar] Ctr Hosp Univ Nantes, Inst Malad Appareil Digestif, Digest Oncol, Nantes, France.
   [Bossard, Celine] CHU Nantes, Serv Anat & Cytol Pathol, Nantes, France.
   [Bossard, Celine] Univ Nantes, INSERM CRCINA, F-44000 Nantes, France.
   [Coriat, Romain] Univ Paris, APHP Ctr, Gastroenterol & Digest Oncol Unit, Paris, France.
   [Beuvon, Frederic] Hop Cochin, AP HP, Dept Pathol, Ctr Univ Paris, Paris, France.
   [Bauguion, Lucile] Ctr Hosp Vendee, Dept Gastroenterol, La Roche Sur Yon, France.
   [Leclair, Francois] CHD Vendee, Serv Anat & Cytol Pathol, La Roche Sur Yon, France.
   [Chautard, Romain; Lecomte, Thierry] CHRU Tours, Dept Hepatogastroenterol & Digest Oncol, Tours, France.
   [Lecomte, Thierry] Univ Tours, EA GICC 7501, Tours, France.
   [Guyetant, Serge] CHRU Tours, Hop Trousseau, Serv Anat Pathol, Tours, France.
   [Guyetant, Serge] Univ Tours, INRAE, ISP, F-37000 Tours, France.
   [Desgrippes, Romain] Ctr Hosp St Malo, HepatoGastro Enterol, Cancerol Digest, St Malo, France.
   [Grasset, Denis] Ctr Hosp Bretagne Atlantique, Serv Gastroenterol, 20 Blvd Guillaudot, F-56017 Vannes, France.
   [Lhostis, Helene] Ctr Hosp Bretagne Atlantique, Dept Anat & Cytopathol, Vannes, France.
   [Bouhier-Leporrier, Karine] CHU Caen, Serv HepatoGastroEnterol, Caen, France.
   [Bibeau, Frederic] Univ Caen, Serv Anat & Cytol Pathol, CHU Caen, Normandie, France.
   [Edeline, Julien] Eugene Marquis Anticanc Ctr, Dept Med Oncol, Rennes, France.
   [Lievre, Astrid] Rennes 1 Univ, INSERM U1242 Chem Oncogenesis Stress Signaling, Rennes, France.
C3 CHU Rennes; CHU Rennes; Universite de Rennes; Centre National de la
   Recherche Scientifique (CNRS); CNRS - National Institute for Biology
   (INSB); Universite de Rennes; Universite de Rennes; CHU Rennes; CHU
   Brest; CHU Brest; Universite de Bretagne Occidentale; Nantes Universite;
   CHU de Nantes; Nantes Universite; CHU de Nantes; Nantes Universite;
   Institut National de la Sante et de la Recherche Medicale (Inserm);
   Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Cochin - APHP; CHD Vendee; CHD Vendee; CHU Tours;
   Universite de Tours; CHU Tours; Universite de Tours; INRAE; Universite
   de Caen Normandie; CHU de Caen NORMANDIE; CHU de Caen NORMANDIE;
   Universite de Caen Normandie; UNICANCER; Centre Eugene Marquis;
   Universite de Rennes; Universite de Rennes; Institut National de la
   Sante et de la Recherche Medicale (Inserm)
RP Lièvre, A (corresponding author), Rennes Univ Hosp, Univ Hosp Pontchaillou, Dept Gastroenterol, 2 Rue Henri Le Guilloux, F-35033 Rennes 09, France.; Galibert, MD (corresponding author), Rennes Univ Hosp, Dept Somat Genet Canc, Dept Mol Genet & Genom, 2 Rue Henri Le Guilloux, F-35033 Rennes 09, France.
EM mgaliber@univ-rennes1.fr; astrid.lievre@chu-rennes.fr
RI Bennouna, Jaafar/JPA-1723-2023; Edeline, Julien/F-6852-2013; CORRE,
   Sebastien/B-7069-2018
OI BOISTEAU, Emeric/0000-0003-1831-6145; Lespagnol,
   Alexandra/0000-0001-9411-0515; Artru, Pascal/0000-0002-9777-0866; CORRE,
   Sebastien/0000-0003-1532-5660
FU Rennes University Hospital; centre dEtude des Maladies Digestives de
   Rennes (CEMDR)
FX This research received no external funding. We thank the Rennes
   University Hospital and the centre dEtude des Maladies Digestives de
   Rennes (CEMDR) for their financial support. Anthony Perrot was
   financially supported by the Rennes University Hospital.
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NR 35
TC 2
Z9 2
U1 0
U2 3
PU ELSEVIER MASSON, CORP OFF
PI PARIS
PA 65 CAMILLE DESMOULINS CS50083 ISSY-LES-MOULINEAUX, 92442 PARIS, FRANCE
SN 2210-7401
EI 2210-741X
J9 CLIN RES HEPATOL GAS
JI Clin. Res. Hepatol. Gastroenterol.
PD MAY
PY 2022
VL 46
IS 5
AR 101888
DI 10.1016/j.clinre.2022.101888
EA APR 2022
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 1I5AZ
UT WOS:000797242700007
PM 35189426
OA Green Submitted, Bronze
DA 2025-01-04
ER

PT J
AU Ghorbanzadeh, F
   Jafari-Gharabaghlou, D
   Dashti, MR
   Hashemi, M
   Zarghami, N
AF Ghorbanzadeh, Fatemeh
   Jafari-Gharabaghlou, Davoud
   Dashti, Mohammad Reza
   Hashemi, Mehrdad
   Zarghami, Nosratollah
TI Advanced nano-therapeutic delivery of metformin: potential anti-cancer
   effect against human colon cancer cells through inhibition of GPR75
   expression
SO MEDICAL ONCOLOGY
LA English
DT Article
DE Metformin; Nanoparticle; Colorectal cancer; Niosome; GPR75; Caco2
ID MOLECULAR TARGET THERAPY; TELOMERASE ACTIVITY; PLGA-PEG; PROLIFERATION;
   APOPTOSIS; TISSUE
AB The high incidence rate coupled with significant mortality makes colorectal cancer one of the most prevalent and devastating cancers worldwide. Research is currently underway to explore new forms of treatment that could potentially maximize treatment outcomes while minimizing the side effects associated with conventional chemotherapy. Metformin, a natural biguanide drug, has anti-cancer properties that can inhibit the growth and proliferation of cancer cells. However, due to its short half-life and low bioavailability, the efficacy of Metf as an anti-cancer agent is limited. The purpose of this research is to assess the potency of PEGylated niosomes as a nano-delivery system for Metf, with the aim of increasing its anti-cancer effects on CaCo2 colorectal cancer cells through the effect on the expression of genes, including GPR75, hTERT, Bax, Bcl2, and Cyclin D1. Metf-loaded niosomal NPs (N-Metf) were synthesized using the thin-film hydration method and then characterized using SEM, FTIR, AFM, and DLS techniques. The release pattern of the drug from the nanoparticles (NPS) was determined using the dialysis membrane method. Furthermore, the cytotoxic effect of the metformin-loaded PEGylated niosome on the CaCo2 cell line was evaluated by the MTT test. Additionally, an apoptosis assay was conducted to assess the effect of free Metf and Metf-loaded NPS on the programmed death of the CaCo2 cells, and the impact on the cell cycle was studied through a cell cycle test. Finally, the expression levels of hTERT, Cyclin D1, BCL2, GPR75, and BAX genes were assessed in the presence of free Metf and Metf-loaded NPs by RT-PCR. Characterization experiments showed successful loading of metformin into PEGylated niosomes. The results of cytotoxicity evaluation showed that Metf-NPs had more cytotoxicity than free Metf in a dose-dependent manner. Furthermore, nuclear fragmentation and the percentage of apoptotic cells induced by Metf-NPs were significantly higher than those induced by free Metf. Additionally, Metf-NPs were found to induce more cell cycle arrest at the sub-G1 checkpoint than free Metf did. Compared with Metf-treated cells, the mRNA expression levels of GPR75, Cyclin D1, and hTERT were significantly changed in cells treated with Metf-NPs. Ultimately, it is hypothesized the nano-encapsulation of Metf into PEGylated niosomal NPs could be a worthwhile drug delivery system to enhance its effectiveness in treating colorectal cancer cells.
C1 [Ghorbanzadeh, Fatemeh; Hashemi, Mehrdad] Islamic Azad Univ, Fac Adv Sci & Technol, Dept Genet, Tehran Med Sci, Tehran, Iran.
   [Ghorbanzadeh, Fatemeh; Jafari-Gharabaghlou, Davoud; Dashti, Mohammad Reza] Tabriz Univ Med Sci, Drug Appl Res Ctr, Tabriz, Iran.
   [Dashti, Mohammad Reza] Tabriz Univ Med Sci, Fac Med, Dept Clin Biochem & Lab Med, Tabriz, Iran.
   [Zarghami, Nosratollah] Istanbul Aydin Univ, Fac Med, Dept Med Biochem, Istanbul, Turkiye.
C3 Islamic Azad University; Tabriz University of Medical Science; Tabriz
   University of Medical Science; Istanbul Aydin University
RP Zarghami, N (corresponding author), Istanbul Aydin Univ, Fac Med, Dept Med Biochem, Istanbul, Turkiye.
EM zarghamin@gmail.com
RI Zarghami, Nosratollah/A-7821-2017; Hashemi, Mehrdad/JHT-4661-2023
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NR 50
TC 6
Z9 6
U1 4
U2 13
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1357-0560
EI 1559-131X
J9 MED ONCOL
JI Med. Oncol.
PD JUL 29
PY 2023
VL 40
IS 9
AR 255
DI 10.1007/s12032-023-02120-8
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA N4MQ7
UT WOS:001036776800002
PM 37515667
DA 2025-01-04
ER

PT J
AU Cheng, SF
   Qian, FY
   Huang, Q
   Wei, LR
   Fug, YW
   Du, YZ
AF Cheng, Shaofei
   Qian, Fengying
   Huang, Qin
   Wei, Lirong
   Fug, Yawen
   Du, Yuzhen
TI HOXA4, down-regulated in lung cancer, inhibits the growth, motility and
   invasion of lung cancer cells
SO CELL DEATH & DISEASE
LA English
DT Article
ID GLYCOGEN-SYNTHASE KINASE-3-BETA; MOLECULAR TARGETED THERAPY; RETINOIC
   ACID; HOX-1.4 GENE; CYCLIN D1; EXPRESSION; WNT;
   GLYCOGEN-SYNTHASE-KINASE-3-BETA; EGFR; OVEREXPRESSION
AB The involvement of HOXA4 in colorectal cancer and epithelial ovarian cancer has been reported. Although it has been reported that the Hoxa4 gene is involved in the patterning of the mouse lung during embryonic development, little is known about the biological functions of HOXA4 in lung cancer. In the current study, HOXA4 expression was down regulated in lung cancer tissues when compared with non-cancerous tissues. HOXA4 expression was associated with tumor size, TNM stage, lymph node metastasis and prognosis. Bioinformatics analysis revealed that HOXA4 expression was negatively correlated with cell cycle, metastasis, and the Wnt signaling pathway. Moreover, HOXA4 overexpression in lung cancer cell lines suppressed cell proliferation, migration, and invasion. HOXA4 decreased the protein expression levels of beta-catenin, Cyclin D1, c-Myc and Survivin, indicating the inhibition of Wnt signaling. HOXA4 significantly increased the protein and mRNA levels of glycogen synthase kinase-3 beta (GSK3 beta) by promoting its transcription. Furthermore, inhibition of GSK3 beta by LiCI abolished the suppression of cell growth, migration, and invasion mediated by HOXA4. Overexpression of HOXA4 in xenograft tumors also decreased tumor growth and Wnt signaling. Collectively, these data suggest that HOXA4 is a potential diagnostic and prognostic marker in lung cancer, and its overexpression could inhibit lung cancer progression in part by promoting GSK3 beta transcription.
C1 [Cheng, Shaofei] Shanghai Jiao Tong Univ, Affiliated Peoples Hosp 6, Dept Thorac Cardiovasc Surg, Shanghai, Peoples R China.
   [Qian, Fengying; Wei, Lirong; Fug, Yawen; Du, Yuzhen] Shanghai Jiao Tong Univ, Affiliated Peoples Hosp 6, Dept Lab Med, Shanghai, Peoples R China.
   [Huang, Qin] Shanghai Jiao Tong Univ, Affiliated Peoples Hosp 6, Dept Pathol, Shanghai, Peoples R China.
C3 Shanghai Jiao Tong University; Shanghai Jiao Tong University; Shanghai
   Jiao Tong University
RP Du, YZ (corresponding author), Shanghai Jiao Tong Univ, Affiliated Peoples Hosp 6, Dept Lab Med, Shanghai, Peoples R China.
EM sd_duyz@sumhs.edu.cn
FU Shanghai Pudong New Area Science and Technology Development Fund
   [PKJ2014-Y06]
FX This study was supported by the Shanghai Pudong New Area Science and
   Technology Development Fund (PKJ2014-Y06).
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NR 43
TC 31
Z9 34
U1 0
U2 7
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD APR 27
PY 2018
VL 9
AR 465
DI 10.1038/s41419-018-0497-x
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA GF2QE
UT WOS:000431784000002
PM 29700285
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ghazvinian, Z
   Abdolahi, S
   Tokhanbigli, S
   Tarzemani, S
   Piccin, A
   Zali, MR
   Verdi, J
   Baghaei, K
AF Ghazvinian, Zeinab
   Abdolahi, Shahrokh
   Tokhanbigli, Samaneh
   Tarzemani, Shadi
   Piccin, Andrea
   Reza Zali, Mohammad
   Verdi, Javad
   Baghaei, Kaveh
TI Contribution of natural killer cells in innate immunity against
   colorectal cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE natural killer cell; colorectal cancer; CAR-NK cell; check point
   inhibitor; cancer vaccine; cancer immune-cell therapy; adoptive cell
   immunotherapy
ID TUMOR-INFILTRATING LYMPHOCYTES; NK CELLS; T-CELLS; MICROSATELLITE
   INSTABILITY; INTRATUMORAL INJECTION; ANTITUMOR-ACTIVITY; PROSTAGLANDIN
   E-2; ADOPTIVE TRANSFER; INTERFERON-GAMMA; DENDRITIC CELLS
AB Natural killer cells are members of the innate immune system and promote cytotoxic activity against tumor or infected cells independently from MHC recognition. NK cells are modulated by the expression of activator/inhibitory receptors. The ratio of this activator/inhibitory receptors is responsible for the cytotoxic activity of NK cells toward the target cells. Owing to the potent anti-tumor properties of NK cells, they are considered as interesting approach in tumor treatment. Colorectal cancer (CRC) is the second most common cause of death in the world and the incidence is about 2 million new cases per year. Metastatic CRC is accompanied by a poor prognosis with less than three years of overall survival. Chemotherapy and surgery are the most adopted treatments. Besides, targeted therapy and immune checkpoint blockade are novel approach to CRC treatment. In these patients, circulating NK cells are a prognostic marker. The main target of CRC immune cell therapy is to improve the tumor cell's recognition and elimination by immune cells. Adaptive NK cell therapy is the milestone to achieve the purpose. Allogeneic NK cell therapy has been widely investigated within clinical trials. In this review, we focus on the NK related approaches including CAR NK cells, cell-based vaccines, monoclonal antibodies and immunomodulatory drugs against CRC tumoral cells.
C1 [Ghazvinian, Zeinab; Verdi, Javad] Univ Tehran Med Sci, Sch Adv Technol Med, Dept Appl Cell Sci, Tehran, Iran.
   [Abdolahi, Shahrokh; Tokhanbigli, Samaneh; Tarzemani, Shadi; Reza Zali, Mohammad; Baghaei, Kaveh] Shahid Beheshti Univ Med Sci, Res Inst Gastroenterol & Liver Dis, Basic & Mol Epidemiol Gastrointestinal Disorders R, Tehran, Iran.
   [Piccin, Andrea] Northern Ireland Blood Transfus Serv, Belfast, North Ireland.
   [Piccin, Andrea] Med Univ Innsbruck, Dept Internal Med 5, Innsbruck, Austria.
   [Piccin, Andrea] Univ Trento, Dept Ind Engn, Trento, Italy.
C3 Tehran University of Medical Sciences; Shahid Beheshti University
   Medical Sciences; Medical University of Innsbruck; University of Trento
RP Baghaei, K (corresponding author), Shahid Beheshti Univ Med Sci, Res Inst Gastroenterol & Liver Dis, Basic & Mol Epidemiol Gastrointestinal Disorders R, Tehran, Iran.
EM kavehbaghai@gmail.com
RI Piccin, Andrea/L-1632-2018
OI Piccin, Andrea/0000-0002-2645-8496
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NR 232
TC 9
Z9 10
U1 1
U2 8
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD JAN 4
PY 2023
VL 12
AR 1077053
DI 10.3389/fonc.2022.1077053
PG 22
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 7Y3WV
UT WOS:000914814700001
PM 36686835
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ashouri, K
   Wong, A
   Mittal, P
   Torres-Gonzalez, L
   Lo, JH
   Soni, S
   Algaze, S
   Khoukaz, T
   Zhang, W
   Yang, Y
   Millstein, J
   Lenz, HJ
   Battaglin, F
AF Ashouri, Karam
   Wong, Alexandra
   Mittal, Pooja
   Torres-Gonzalez, Lesly
   Lo, Jae Ho
   Soni, Shivani
   Algaze, Sandra
   Khoukaz, Taline
   Zhang, Wu
   Yang, Yan
   Millstein, Joshua
   Lenz, Heinz-Josef
   Battaglin, Francesca
TI Exploring Predictive and Prognostic Biomarkers in Colorectal Cancer: A
   Comprehensive Review
SO CANCERS
LA English
DT Review
DE colorectal cancer; gene expression profiling; molecular targeted
   therapy; tumor biomarkers
ID RAS WILD-TYPE; EGFR MONOCLONAL-ANTIBODIES; CHEMOKINE RECEPTOR CXCR4;
   IMMUNE CHECKPOINT INHIBITORS; OPEN-LABEL; MICROSATELLITE INSTABILITY;
   ACQUIRED-RESISTANCE; BRAF MUTATION; MOLECULAR PROFILES; PD-L1 EXPRESSION
AB Simple Summary Colorectal cancer is a major health concern globally, and finding ways to improve treatment outcomes is crucial. This review explores the role of biomarkers-biological indicators that can predict how a patient will respond to treatment or indicate the likely course of the disease-in managing colorectal cancer. By examining both well-established and emerging biomarkers, we hope to provide a clearer understanding of how these markers can guide personalized treatment plans. The findings from this research could help doctors make more informed decisions, ultimately improving patient care and outcomes in colorectal cancer.Abstract Colorectal cancer (CRC) remains the second leading cause of cancer-related mortality worldwide. While immune checkpoint inhibitors have significantly improved patient outcomes, their effectiveness is mostly limited to tumors with microsatellite instability (MSI-H/dMMR) or an increased tumor mutational burden, which comprise 10% of cases. Advancing personalized medicine in CRC hinges on identifying predictive biomarkers to guide treatment decisions. This comprehensive review examines established tissue markers such as KRAS and HER2, highlighting their roles in resistance to anti-EGFR agents and discussing advances in targeted therapies for these markers. Additionally, this review summarizes encouraging data on promising therapeutic targets and highlights the clinical utility of liquid biopsies. By synthesizing current evidence and identifying knowledge gaps, this review provides clinicians and researchers with a contemporary understanding of the biomarker landscape in CRC. Finally, the review examines future directions and challenges in translating promising biomarkers into clinical practice, with the goal of enhancing personalized medicine approaches for colorectal cancer patients.
C1 [Ashouri, Karam; Wong, Alexandra; Mittal, Pooja; Torres-Gonzalez, Lesly; Lo, Jae Ho; Soni, Shivani; Algaze, Sandra; Khoukaz, Taline; Zhang, Wu; Yang, Yan; Lenz, Heinz-Josef; Battaglin, Francesca] Univ Southern Calif, Keck Sch Med, Norris Comprehens Canc Ctr, Div Med Oncol, Los Angeles, CA 90089 USA.
   [Millstein, Joshua] Univ Southern Calif, Norris Comprehens Canc Ctr, Keck Sch Med, Dept Populat & Publ Hlth Sci, Los Angeles, CA 90089 USA.
C3 University of Southern California; University of Southern California
RP Lenz, HJ; Battaglin, F (corresponding author), Univ Southern Calif, Keck Sch Med, Norris Comprehens Canc Ctr, Div Med Oncol, Los Angeles, CA 90089 USA.
EM karam.ashouri@med.usc.edu; alexandra.wong@med.usc.edu; lenz@med.usc.edu;
   fbattagl@usc.edu
RI Battaglin, Francesca/C-2746-2017
OI Battaglin, Francesca/0000-0002-9869-0163; Ashouri,
   Karam/0009-0000-1825-1033
FU National Cancer Institute [P30CA014089]; Gloria Borges WunderGlo
   Foundation; Dhont Family Foundation; Victoria and Philip Wilson Research
   Fund; San Pedro Peninsula Cancer Guild; Ming Hsieh Research award;
   Daniel Butler Research Fund
FX This study was partly supported by the National Cancer Institute (grant
   number P30CA014089) [to H.-J.L.], the Gloria Borges WunderGlo
   Foundation, Dhont Family Foundation, Victoria and Philip Wilson Research
   Fund, San Pedro Peninsula Cancer Guild, Ming Hsieh Research award, and
   Daniel Butler Research Fund. The content is solely the responsibility of
   the authors and does not necessarily represent the official views of the
   National Institutes of Health.
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NR 191
TC 1
Z9 1
U1 3
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD AUG
PY 2024
VL 16
IS 16
AR 2796
DI 10.3390/cancers16162796
PG 25
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA E8V4C
UT WOS:001305718300001
PM 39199569
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ostwal, V
   Kapoor, A
   Engineer, R
   Saklani, A
   desouza, A
   Patil, P
   Arya, S
   Ankathi, SK
   Chopra, S
   Patil, M
   Jain, S
   Ramaswamy, A
AF Ostwal, Vikas
   Kapoor, Akhil
   Engineer, Reena
   Saklani, Avanish
   desouza, Ashwin
   Patil, Prachi
   Arya, Supreeta
   Ankathi, Suman Kumar
   Chopra, Supriya
   Patil, Mangesh
   Jain, Shanu
   Ramaswamy, Anant
TI Systemic chemotherapy and short-course radiation in metastatic rectal
   cancers: A feasible paradigm in unresectable and potentially resectable
   cancers
SO SOUTH ASIAN JOURNAL OF CANCER
LA English
DT Article
DE Chemotherapy; metastatectomy; metastatic rectal cancers; resectability;
   short-course radiotherapy
ID SHORT-COURSE RADIOTHERAPY; IV COLORECTAL-CANCER; TERTIARY CARE CENTER;
   LIVER METASTASES; PHASE-II; 1ST-LINE CHEMOTHERAPY; PERFORMANCE STATUS;
   RANDOMIZED-TRIAL; BEVACIZUMAB; OXALIPLATIN
AB Background: The optimal use and sequencing of short-course radiotherapy (SCRT) in metastatic rectal cancers (mRCs) are not well established. Materials and Methods: We retrospectively reviewed the records of mRC patients receiving SCRT followed by palliative chemotherapy between January 1, 2013, and December 31. 2016, in Tata Memorial Hospital. Patients were classified as having "potentially resectable" disease (local and metastatic) or "unresectable" disease at baseline based on prespecified criteria. Results: A total of 105 consecutive patients were available for analysis.The median age of patients was 48 years (range: 16-62 years), and 57.1% were male patients. Signet ring histology was seen in 13.3% of patients.The most common site of metastases was liver limited (29.5%), nonloco-regional nodes (12.4%), and lung limited metastases (9.5%). Chemotherapeutic regimens administered were capecitabine-oxaliplatin (70.5%), modified 5 fluorouracil (5 FU)-leucovorin-irinotecan-oxaliplatin (10.5%), and modified 5 FU-leucovorin-irinotecan (8.6%). Targeted therapy accompanying chemotherapy was administered in 27.6% of patients.About 42.1% of patients with potentially resectable disease and 1 1.1% with the unresectable disease at baseline underwent curative-intent resection of the primary and address of metastatic sites. With a median follow-up 18.2 months, median overall survival (OS) was 15.7 months (95% confidence interval: 10.42-20.99). Patients classified as potentially resectable had a median OS of 32.62 months while patients initially classified as unresectable had a median OS of 13.04 months (P = 0.016).The presence of signet ring morphology predicted for inferior mOS (P = 0.021). Conclusions: SCRT followed by systemic therapy in mRC is a feasible, efficacious paradigm for maximizing palliation, and achieving objective responses.The classification of patients based on resectability was predictive of actual resection rates as well as outcomes. Signet ring mRC show inferior outcomes in this cohort of patients.
C1 [Ostwal, Vikas; Kapoor, Akhil; Ramaswamy, Anant] Tata Mem Hosp, Dept Med Oncol, Mumbai, Maharashtra, India.
   [Engineer, Reena; Chopra, Supriya; Patil, Mangesh; Jain, Shanu] Tata Mem Hosp, Dept Radiat Oncol, Mumbai, Maharashtra, India.
   [Saklani, Avanish; desouza, Ashwin] Tata Mem Hosp, Dept Surg Oncol, Mumbai, Maharashtra, India.
   [Patil, Prachi] Tata Mem Hosp, Dept Med Gastroenterol, Mumbai, Maharashtra, India.
   [Arya, Supreeta; Ankathi, Suman Kumar] Tata Mem Hosp, Dept Radiol, Mumbai, Maharashtra, India.
C3 Tata Memorial Centre (TMC); Tata Memorial Hospital; Tata Memorial Centre
   (TMC); Tata Memorial Hospital; Tata Memorial Centre (TMC); Tata Memorial
   Hospital; Tata Memorial Centre (TMC); Tata Memorial Hospital; Tata
   Memorial Centre (TMC); Tata Memorial Hospital
RP Ramaswamy, A (corresponding author), Tata Mem Hosp, Dept Med Oncol, Mumbai, Maharashtra, India.
EM anantr13@gmail.com
RI Kapoor, Akhil/H-4224-2019; Ganorkar, Saurabh/M-5961-2013
OI Saklani, Avanish/0000-0003-4498-7612
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NR 45
TC 2
Z9 2
U1 0
U2 1
PU WOLTERS KLUWER MEDKNOW PUBLICATIONS
PI MUMBAI
PA WOLTERS KLUWER INDIA PVT LTD , A-202, 2ND FLR, QUBE, C T S  NO 1498A-2
   VILLAGE MAROL, ANDHERI EAST, MUMBAI, 400059, INDIA
SN 2278-330X
EI 2278-4306
J9 SOUTH ASIAN J CANCER
JI South Asian J. Cancer
PD APR-JUN
PY 2019
VL 8
IS 2
BP 92
EP +
DI 10.4103/sajc.sajc_174_18
PG 7
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA HU3CZ
UT WOS:000465150500006
PM 31069186
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ciepiela, I
   Szczepaniak, M
   Ciepiela, P
   Hincza-Nowak, K
   Kopczynski, J
   Macek, P
   Kubicka, K
   Chrapek, M
   Tyka, M
   Gózdz, S
   Kowalik, A
AF Ciepiela, Izabela
   Szczepaniak, Magdalena
   Ciepiela, Przemyslaw
   Hincza-Nowak, Kinga
   Kopczynski, Janusz
   Macek, Pawel
   Kubicka, Kamila
   Chrapek, Magdalena
   Tyka, Magdalena
   Gozdz, Stanislaw
   Kowalik, Artur
TI Tumor location matters, next generation sequencing mutation profiling of
   left-sided, rectal, and right-sided colorectal tumors in 552 patients
SO SCIENTIFIC REPORTS
LA English
DT Article
ID CANCER; COLON; HER2; ANTIBODIES; RESISTANCE; BIOMARKER; GENE
AB Despite the introduction of new molecular classifications, advanced colorectal cancer (CRC) is treated with chemotherapy supplemented with anti-EGFR and anti-VEGF targeted therapy. In this study, 552 CRC cases with different primary tumor locations (250 left side, 190 rectum, and 112 right side) were retrospectively analyzed by next generation sequencing for mutations in 50 genes. The most frequently mutated genes were TP53 in left-sided tumors compared to right-sided tumors and BRAF in right-sided tumors compared to left-sided tumors. Mutations in KRAS, NRAS, and BRAF were not detected in 45% of patients with left-sided tumors and in 28.6% of patients with right-sided tumors. Liver metastases were more common in patients with left-sided tumors. Tumors on the right side were larger at diagnosis and had a higher grade (G3) than tumors on the left. Rectal tumors exhibit distinctive biological characteristics when compared to left-sided tumors, including a higher absence rate of KRAS, NRAS, and BRAF mutations (47.4% in rectal versus 42.8% in left-sided tumors). These rectal tumors are also unique in their primary metastasis site, which is predominantly the lungs, and they have varying mutation rates, particularly in genes such as BRAF, FBXW7, and TP53, that distinguish them from tumors found in other locations. Primary tumor location has implications for the potential treatment of CRC with anti-EGFR therapy.
C1 [Ciepiela, Izabela] Holy Cross Canc Ctr, Radiotherapy Dept, PL-25734 Kielce, Poland.
   [Szczepaniak, Magdalena; Hincza-Nowak, Kinga; Kubicka, Kamila; Tyka, Magdalena; Kowalik, Artur] Holy Cross Canc Ctr, Dept Mol Diagnost, PL-25734 Kielce, Poland.
   [Ciepiela, Przemyslaw] Holy Cross Canc Ctr, Surg Oncol Dept, PL-25734 Kielce, Poland.
   [Hincza-Nowak, Kinga] Holy Cross Canc Ctr, Endocrinol Clin, PL-25734 Kielce, Poland.
   [Kopczynski, Janusz] Holy Cross Canc Ctr, Surg Pathol, PL-25734 Kielce, Poland.
   [Macek, Pawel; Gozdz, Stanislaw] Jan Kochanowski Univ, Coll Med, PL-25319 Kielce, Poland.
   [Macek, Pawel] Holy Cross Canc Ctr, Dept Epidemiol & Canc Control, PL-25734 Kielce, Poland.
   [Chrapek, Magdalena] Jan Kochanowski Univ, Fac Nat Sci, Dept Math, PL-25406 Kielce, Poland.
   [Gozdz, Stanislaw] Holy Cross Canc Ctr, Clin Oncol Clin, PL-25734 Kielce, Poland.
   [Kowalik, Artur] Jan Kochanowski Univ, Inst Biol, Div Med Biol, PL-25406 Kielce, Poland.
C3 Jan Kochanowski University; Jan Kochanowski University; Jan Kochanowski
   University
RP Kowalik, A (corresponding author), Holy Cross Canc Ctr, Dept Mol Diagnost, PL-25734 Kielce, Poland.; Kowalik, A (corresponding author), Jan Kochanowski Univ, Inst Biol, Div Med Biol, PL-25406 Kielce, Poland.
EM Artur.Kowalik@onkol.kielce.pl
RI Kowalik, Artur/AAB-5690-2020
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NR 60
TC 2
Z9 2
U1 0
U2 1
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD FEB 26
PY 2024
VL 14
IS 1
AR 4619
DI 10.1038/s41598-024-55139-w
PG 14
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA KB2G1
UT WOS:001177429500035
PM 38409377
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Choi, BJ
   Lee, D
   Park, JH
   Hong, TH
   Kim, OH
   Lee, SC
   Kim, KH
   Choi, HJ
   Kim, SJ
AF Choi, Byung-Jo
   Lee, Dosang
   Park, Jung Hyun
   Hong, Tae Ho
   Kim, Ok-Hee
   Lee, Sang Chul
   Kim, Kee-Hwan
   Choi, Ho Joong
   Kim, Say-June
TI Innovative Therapeutic Delivery of Metastasis-Associated in Colon Cancer
   1-Suppressing miRNA Using High Transmembrane 4 L6 Family Member
   5-Targeting Exosomes in Colorectal Cancer Mouse Models
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE colorectal cancer; exosome; MACC1; microRNA; targeted therapy; TM4SF5
   protein
ID EXTRACELLULAR VESICLES; MACC1; APOPTOSIS
AB Elevated metastasis-associated in colon cancer 1 (MACC1) expression in colorectal cancer patients, and high transmembrane 4 L6 family member 5 (TM4SF5) protein expressed on various solid tumors' surface, are linked to aggressive cancer behavior and progression. In this study, adipose-derived stem cells (ASCs) were engineered to produce exosomes (Ex) that target the TM4SF5 protein on tumors. Moreover, MACC1-targeting microRNA was encapsulated within the Ex, resulting in TM4SF5-targeting Ex (MACC1-suppressing miRNA; miR-143). The anticancer effects of these Ex were investigated in vitro using the human colorectal cell line HCT116 and in vivo using colorectal cancer mouse xenograft models. In the in vivo assessment, administration of TM4SF5-targeting Ex[miR-143], referred to as tEx[miR-143] herein, resulted in the smallest tumor size, the lowest tumor growth rate, and the lightest excised tumors compared to other treatments (p < 0.05). It also led to the decreased expression of MACC-1 and anti-apoptotic markers MCL-1 and Bcl-xL while inducing the highest expression of pro-apoptotic markers BAX and BIM. These results were consistent with in vitro findings, where t Ex[miR-143] demonstrated the highest inhibition of HCT116 cell migration and invasion. These findings highlight the potential of tEx[miR-143] as an effective therapeutic strategy for colorectal cancer, demonstrating promising results in both targetability and anti-tumor effects in vitro and in vivo, warranting further investigation in clinical settings.
C1 [Choi, Byung-Jo; Lee, Sang Chul] Catholic Univ Korea, Daejeon St Marys Hosp, Coll Med, Dept Surg, Daejeon 34943, South Korea.
   [Choi, Byung-Jo; Lee, Dosang; Park, Jung Hyun; Hong, Tae Ho; Kim, Ok-Hee; Kim, Kee-Hwan; Kim, Say-June] Catholic Univ Korea, Coll Med, Catholic Cent Lab Surg, Seoul 06591, South Korea.
   [Lee, Dosang; Hong, Tae Ho; Choi, Ho Joong; Kim, Say-June] Catholic Univ Korea, Seoul St Marys Hosp, Coll Med, Dept Surg, 222 Banpo Daero, Seoul 06591, South Korea.
   [Park, Jung Hyun] Catholic Univ Korea, Eunpyeong St Marys Hosp, Coll Med, Dept Surg, Seoul 03312, South Korea.
   [Kim, Ok-Hee; Kim, Say-June] Surginex Co Ltd, Translat Res Team, Seoul 06591, South Korea.
   [Kim, Kee-Hwan] Catholic Univ Korea, Uijeongbu St Marys Hosp, Coll Med, Dept Surg, Uijongbu 11765, Gyeonggi, South Korea.
C3 Catholic University of Korea; Catholic University of Korea; Seoul St.
   Mary's Hospital; Catholic University of Korea; Catholic University of
   Korea; Catholic University of Korea
RP Kim, SJ (corresponding author), Catholic Univ Korea, Coll Med, Catholic Cent Lab Surg, Seoul 06591, South Korea.; Kim, SJ (corresponding author), Catholic Univ Korea, Seoul St Marys Hosp, Coll Med, Dept Surg, 222 Banpo Daero, Seoul 06591, South Korea.; Kim, SJ (corresponding author), Surginex Co Ltd, Translat Res Team, Seoul 06591, South Korea.
EM bottlebird@catholic.ac.kr; dosangs@catholic.ac.kr;
   angle49@catholic.ac.kr; gshth@catholic.ac.kr; ok6201@hanmail.net;
   zambo9@catholic.ac.kr; keehwan@catholic.ac.kr; hopej0126@catholic.ac.kr;
   sayjunekim@catholic.ac.kr
FU National Research Foundation of Korea (NRF) [NRF-2020R1G1A1099947];
   National Research Foundation of Korea (NRF) - Korea government (MSIT)
FX This work was supported by the National Research Foundation of Korea
   (NRF) grant funded by the Korea government (MSIT) (No.
   NRF-2020R1G1A1099947).
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NR 37
TC 0
Z9 0
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD SEP
PY 2024
VL 25
IS 17
AR 9232
DI 10.3390/ijms25179232
PG 19
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA F9G9K
UT WOS:001312827200001
PM 39273182
OA gold
DA 2025-01-04
ER

PT J
AU Ahmed, S
   Strand, S
   Weinmann-Menke, J
   Urbansky, L
   Galle, PR
   Neumann, H
AF Ahmed, Shakil
   Strand, Susanne
   Weinmann-Menke, Julia
   Urbansky, Lana
   Galle, Peter R.
   Neumann, Helmut
TI Molecular endoscopic imaging in cancer
SO DIGESTIVE ENDOSCOPY
LA English
DT Review
DE antibody labeling; confocal endomicroscopy; endoscopy; ex-vivo study;
   molecular imaging
ID CONFOCAL LASER ENDOMICROSCOPY; GROWTH-FACTOR RECEPTOR; GASTRIC-CANCER;
   COLONIC DYSPLASIA; COLORECTAL-CANCER; VIVO; NEOPLASIA; ADENOMAS;
   COLONOSCOPY; PREVALENCE
AB Cancer is one of the major causes of death in both the USA and Europe. Molecular imaging is a novel field that is revolutionizing cancer management. It is based on the molecular signature of cells in order to study the human body both in normal and diseased conditions. The emergence of molecular imaging has been driven by the difficulties associated with cancer detection, particularly early-stage premalignant lesions which are often unnoticed as a result of minimal or no structural changes. Endoscopic surveillance is the standard method for early-stage cancer detection. In addition to recent major advancements in endoscopic instruments, significant progress has been achieved in the exploration of highly specific molecular probes and the combination of both will permit significant improvement of patient care. In this review, we provide an outline of the current status of endoscopic imaging and focus on recent applications of molecular imaging in gastrointestinal, hepatic and other cancers in the context of detection, targeted therapy and personalized medicine. As new imaging agents have the potential to broadly expand our cancer diagnostic capability, we will also present an overview of the main types of optical molecular probes with their pros and cons. We conclude by discussing the challenges and future prospects of the field.
C1 [Ahmed, Shakil; Strand, Susanne; Weinmann-Menke, Julia; Urbansky, Lana; Galle, Peter R.; Neumann, Helmut] Univ Hosp Mainz, Dept Interdisciplinary Endoscopy, Med Clin & Polyclin 1, Mainz, Germany.
C3 University Hospital Mainz
RP Neumann, H (corresponding author), Univ Hosp Mainz, Dept Interdisciplinary Endoscopy, Med Clin & Polyclin 1, Mainz, Germany.
EM Helmut.Neumann@unimedizin-mainz.de
RI Weinmann-Menke, Julia/X-7847-2019; Galle, Peter/ABE-2872-2021
OI Galle, Peter Robert/0000-0001-8294-0992; Weinmann-Menke,
   Julia/0000-0001-7344-8381
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NR 72
TC 12
Z9 13
U1 0
U2 14
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0915-5635
EI 1443-1661
J9 DIGEST ENDOSC
JI Dig. Endosc.
PD NOV
PY 2018
VL 30
IS 6
BP 719
EP 729
DI 10.1111/den.13199
PG 11
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA GZ9OL
UT WOS:000449829700001
PM 29846982
OA hybrid
DA 2025-01-04
ER

PT J
AU Jiang, JY
   Chen, X
   Liu, H
   Shao, J
   Xie, RH
   Gu, P
   Duan, CH
AF Jiang, Junyi
   Chen, Xu
   Liu, Hao
   Shao, Jing
   Xie, Ruihui
   Gu, Peng
   Duan, Chaohui
TI Polypyrimidine Tract-Binding Protein 1 promotes proliferation, migration
   and invasion in clear-cell renal cell carcinoma by regulating
   alternative splicing of PKM
SO AMERICAN JOURNAL OF CANCER RESEARCH
LA English
DT Article
DE PTBP1; renal cell carcinoma; proliferation; metastasis; PKM2
ID PYRUVATE-KINASE M2; COLORECTAL-CANCER CELLS; LUNG-CANCER; TARGETED
   THERAPY; DOWN-REGULATION; BLADDER-CANCER; BREAST-CANCER; UP-REGULATION;
   RNA; METASTASIS
AB Polypyrimidine Tract-Binding Protein 1 (PTBP1) is an essential RNA-binding protein that regulates diverse biological events through regulating alternative splice of mRNA. PTBP1 induces cancer-promoting splice variants and is related to tumorigenesis in several cancers. However, both the expression patterns and biological mechanisms of PTBP1 in clear-cell renal cell carcinoma (ccRCC) are unclear. We investigated PTBP1 expression in 533 ccRCC patients from TCGA and 30 ccRCC patients by immunohistochemistry, and found that PTBP1 expression levels were significantly increased in ccRCC tissues and that high PTBP1 expression was closely correlated with advanced tumor stage, AJCC stage and poor prognosis. Cell biological assays with siRNA-mediated knockdown and lentivirus vector-mediated over-expression demonstrated that PTBP1 promoted proliferation, migration and invasion in ccRCC cells in vitro. Furthermore, PTBP1 increased the transformation from pyruvate kinase muscle 1 (PKM1) to PKM2. Knockdown of PKM2 mainly abolished PTBP1-induced proliferation, migration and invasion in ccRCC cells in vitro. In conclusion, our study indicates that PTBP1 plays a tumorigenic role in ccRCC by mediating PKM2 alternative splicing and it may be a potential prognostic marker and a promising target for treatment of ccRCC.
C1 [Jiang, Junyi; Duan, Chaohui] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Lab Med, Guangzhou, Guangdong, Peoples R China.
   [Chen, Xu; Liu, Hao; Xie, Ruihui; Gu, Peng] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Urol, Guangzhou, Guangdong, Peoples R China.
   [Jiang, Junyi; Chen, Xu; Liu, Hao; Shao, Jing; Xie, Ruihui; Gu, Peng; Duan, Chaohui] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Guangdong Prov Key Lab Malignant Tumor Epigenet &, Guangzhou, Guangdong, Peoples R China.
   [Shao, Jing] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Med Res Ctr, Guangzhou, Guangdong, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen University;
   Sun Yat Sen University
RP Duan, CH (corresponding author), Sun Yat Sen Mem Hosp, Dept Lab Med, 107th Yanjiangxi Rd, Guangzhou, Guangdong, Peoples R China.; Chen, X (corresponding author), Sun Yat Sen Mem Hosp, Dept Urol, 107th Yanjiangxi Rd, Guangzhou, Guangdong, Peoples R China.
EM Joshua_18chen@163.com; 1725012289@qq.com
RI Liu, Hao/M-1010-2019; Chen, Xu/ISS-8928-2023; jiang, jun/GWC-9329-2022;
   Gu, Peng/GPW-7040-2022
OI Chen, Xu/0000-0002-8425-036X
FU National Natural Science Foundation of China [81572514, 81472384];
   Guangdong Province Natural Scientific Foundation [2014A030313070]; Sun
   Yat-sen Initiative Program for Scientific Research [YXQH201708]; Key
   Laboratory of Malignant Tumor Molecular Mechanism and Translational
   Medicine of Guangzhou Bureau of Science and Information Technology
   [[2013]163]; Key Laboratory of Malignant Tumor Gene Regulation and
   Target Therapy of Guangdong Higher Education Institutes [KLB09001];
   Guangdong Science and Technology Department [2015B050501004]
FX This study was funded by the National Natural Science Foundation of
   China (Grant No. 81572514, 81472384), Guangdong Province Natural
   Scientific Foundation (Grant No. 2014A030313070), and Sun Yat-sen
   Initiative Program for Scientific Research (for Xu Chen, YXQH201708).
   This work was supported by Grant [2013]163 from Key Laboratory of
   Malignant Tumor Molecular Mechanism and Translational Medicine of
   Guangzhou Bureau of Science and Information Technology; Grant KLB09001
   from the Key Laboratory of Malignant Tumor Gene Regulation and Target
   Therapy of Guangdong Higher Education Institutes. Grant from Guangdong
   Science and Technology Department (2015B050501004).
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NR 52
TC 37
Z9 40
U1 0
U2 14
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 2156-6976
J9 AM J CANCER RES
JI Am. J. Cancer Res.
PY 2017
VL 7
IS 2
BP 245
EP +
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EO6WW
UT WOS:000396834200006
PM 28337374
DA 2025-01-04
ER

PT J
AU Voutsadakis, IA
AF Voutsadakis, Ioannis A.
TI The Landscape of PIK3CA Mutations in Colorectal Cancer
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE Bowel; Catalytic subunit; PI3K kinase; Targeted therapies; Molecular
   lesions
ID PATHWAY; PTEN; INACTIVATION; RESISTANCE; OUTCOMES; IMPACT; TUMORS; KRAS
AB PIK3CA gene mutations are common in colorectal cancers. This article analyzes the landscape of these mutations based on published genomic studies. Cancers with PIK3CA mutations have concomitant mutations in other genes of cancer-associated pathways in higher frequencies than unmutated colorectal cancer. Tumor mutation burden is higher in these cancers. These observations have implications for the development of targeted therapies.
   Background: Colorectal cancer is one of the most common malignancies in both men and women. Despite progress in the treatment of the disease, metastatic colorectal cancer remains lethal with a median survival slightly surpassing 2 years and commonly for some cases a more aggressive course. New therapies are urgently needed based on a better understanding of the molecular pathogenesis of the disease. Methods: The focus of this investigation is the PIK3CA gene, encoding the alpha catalytic subunit of the enzyme phosphatidylinositol-3 kinase (PI3K). Publicly available data from 3 extensive published series of colorectal carcinomas were analyzed to define the molecular landscape of colorectal adenocarcinomas with and without mutations of PIK3CA. An analysis for discovery of associations with alterations in other critical genes and pathways involved in colorectal cancer was performed. The total mutation burden (TMB) and copy number alteration burden of colorectal cancers with and without mutations of PIK3CA, as well as prognostic implications of alterations of the gene for survival, were examined. Results: Mutations in PIK3CA are observed in 20% to 25% of colorectal cancers. PIK3CA represents one of the most frequently mutated oncogenes in these cancers. Mutations in PIK3CA are associated with higher rates of mutations in other genes of important cancer-associated pathways such as the tyrosine kinase receptors/K-Ras/BRAF/MAPK and the Wnt/beta-catenin pathway. In addition, PIK3CA mutated colorectal cancers display a higher TMB than nonmutated cancers. Conclusion: Frequent mutations of PIK3CA gene in colorectal carcinomas may represent an opportunity for targeted therapy combination development inhibiting both the PI3K kinase itself and associated pathway defects. Increased TMB may additionally confer immunotherapy sensitivity, which could be augmented by other targeted therapies. (c) 2021 Elsevier Inc. All rights reserved.
C1 [Voutsadakis, Ioannis A.] Sault Area Hosp, Algoma Dist Canc Program, 750 Great Northern Rd, Sault Ste Marie, ON P6B 0A8, Canada.
   [Voutsadakis, Ioannis A.] Northern Ontario Sch Med, Div Clin Sci, Sect Internal Med, Sudbury, ON, Canada.
C3 NOSM University
RP Voutsadakis, IA (corresponding author), Sault Area Hosp, Algoma Dist Canc Program, 750 Great Northern Rd, Sault Ste Marie, ON P6B 0A8, Canada.
EM ivoutsadakis@yahoo.com
RI Voutsadakis, Ioannis/AAU-7224-2020
OI Voutsadakis, Ioannis/0000-0002-9301-5951
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NR 47
TC 35
Z9 36
U1 1
U2 12
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1533-0028
EI 1938-0674
J9 CLIN COLORECTAL CANC
JI Clin. Colorectal Canc.
PD SEP
PY 2021
VL 20
IS 3
BP 201
EP 215
DI 10.1016/j.clcc.2021.02.003
EA SEP 2021
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UK9ZM
UT WOS:000692321400011
PM 33744168
DA 2025-01-04
ER

PT J
AU Xuan, TT
   Wang, ZM
   Meng, SB
   Li, JX
   Li, JS
   Cao, FL
   Qu, LL
AF Xuan, Tiantian
   Wang, Zhanmei
   Meng, Sibo
   Li, Jiaxin
   Li, Jisheng
   Cao, Fangli
   Qu, Linli
TI Efficacy and Safety of Maintenance Therapy Using Cetuximab in Patients
   with Metastatic Colorectal Cancer: Retrospective Study
SO CANCER MANAGEMENT AND RESEARCH
LA English
DT Article
DE colorectal cancer; maintenance therapy; cetuximab; RAS and RAF
   wild-type; targeted therapy
ID EARLY TUMOR SHRINKAGE; PLUS BEVACIZUMAB; 1ST-LINE TREATMENT;
   CHEMOTHERAPY PLUS; LIVER METASTASES; OPEN-LABEL; IMPACT; RAS
AB Purpose: Cetuximab (CET) combined with chemotherapy significantly improved the survival in RAS and RAF wild-type metastatic colorectal cancer (mCRC) patients, while clinical evidence was lacking on the use of maintenance therapy (MT). The study aimed to explore the role of maintenance therapy following Cetuximab + chemotherapy and the optimal Cetuximab-based maintenance therapy regimen. Patients and Methods: We retrospectively reviewed data on the efficacy and safety of CET-based MT in patients with mCRC who achieved disease control after induction therapy. Results: Eighty-one patients with mCRC who achieved disease control after CET + chemotherapy induction were enrolled. Overall median progression-free survival (PFS) was 10.5 (95% CI = 8.8-12.2) months and median maintenance/observation PFS (mnPFS) was 6.0 (95% CI = 5.0-7.0) months. Among these 81 patients, 61 patients were prescribed MT (CET alone for 21 patients and CET + chemotherapy for 40 patients). Median PFS and mnPFS in the MT group were significantly longer than those for the non-MT group. Different MT regimens did not affect PFS and mnPFS significantly. Univariate and multivariate analysis demonstrated MT, complete response/partial response during induction therapy, and absence of peritoneal metastasis to be positively associated with longer PFS and mnPFS. Treatment-related adverse events (AEs) were tolerable during MT, and AE-related deaths were not observed. Conclusion: MT with CET or CET + chemotherapy was an appropriate option following initial induction chemotherapy for patients with RAS and RAF wild-type mCRC. This strategy endowed survival benefits and a tolerable safety profile.
C1 [Xuan, Tiantian; Wang, Zhanmei; Meng, Sibo; Li, Jiaxin; Cao, Fangli; Qu, Linli] Shandong Univ, Qilu Hosp Qingdao, Cheeloo Coll Med, Dept Med Oncol, Qingdao, Shandong, Peoples R China.
   [Li, Jisheng] Shandong Univ, Qilu Hosp, Cheeloo Coll Med, Dept Med Oncol, Jinan, Shandong, Peoples R China.
   [Cao, Fangli; Qu, Linli] Shandong Univ, Qilu Hosp Qingdao, Cheeloo Coll Med, Dept Med Oncol, 758 Hefei Rd, Qingdao 266035, Shandong, Peoples R China.
C3 Shandong University; Shandong University; Shandong University
RP Cao, FL; Qu, LL (corresponding author), Shandong Univ, Qilu Hosp Qingdao, Cheeloo Coll Med, Dept Med Oncol, 758 Hefei Rd, Qingdao 266035, Shandong, Peoples R China.
EM caofangliqilu@163.com; qulinli2021@163.com
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NR 30
TC 1
Z9 1
U1 3
U2 3
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1179-1322
J9 CANCER MANAG RES
JI Cancer Manag. Res.
PY 2024
VL 16
BP 185
EP 197
DI 10.2147/CMAR.S443666
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LT3N5
UT WOS:001189014600001
PM 38525371
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wadood, A
   Ajmal, A
   Rehman, AU
AF Wadood, Abdul
   Ajmal, Amar
   Rehman, Ashfaq Ur
TI Strategies for Targeting KRAS: A Challenging Drug Target
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Review
DE KRAS oncogene; KRAS signalling; KRAS structure; targeted therapy; KRAS4B
   isoform; drug target
ID RAS; INHIBITOR; BIND
AB In the developed world, cancer is the most common cause of death. Among the 36 human genes of the RAS family, KRAS, NRAS, and HRAS play a prominent role in human cancer. KRAS belongs to the Ras superfamily of proteins and is a small GTPase signal transduction protein. Among the RAS isoform, KRAS is the dominant mutant that induces approximately 86% of the RAS mutations. The most frequently mutated KRAS isoform is KRAS4B. About 90% of pancreatic cancer, 30-40% of colon cancer, and 15 to 20% of lung cancers are caused by mutations KRAS4B isoform. Liver cancer, bladder cancer, breast cancer, and myeloid leukaemia are also caused by mutations in KRAS but are rare. The FDA has recently approved sotorasib for the treatement of KRASG12C-mutated advanced non-small cell lung cancer (NSCLC) patients. However, no FDA-approved drugs are available for other KRAS-driven cancer. As the KRAS proteins lack a druggable pocket accessible to the chemical inhibitors, the cancer-causing mutant proteins are almost identical to their essential wild-type counterparts. Therefore, they are considered undruggable. The new insights into the structure and function of RAS have changed this understanding and encouraged the development of many drug candidates. This review provides information about the different strategies for targeting KRAS, a challenging drug target that might be valuable for the scientific community.
C1 [Wadood, Abdul; Ajmal, Amar] Abdul Wali Khan Univ Mardan, Dept Biochem, Mardan 23200, KP, Pakistan.
   [Rehman, Ashfaq Ur] Univ Calif Irvine, Dept Mol Biol & Biochem, Irvine, CA 92697 USA.
C3 University of California System; University of California Irvine
RP Wadood, A (corresponding author), Abdul Wali Khan Univ Mardan, Dept Biochem, Mardan 23200, KP, Pakistan.
EM awadood@awkum.edu.pk
RI Wadood, Abdul/ABG-2789-2021; Rehman, Ashfaq ur/AFU-9778-2022
OI Rehman, Ashfaq ur/0000-0002-7261-3645
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   EMIRATES
SN 1381-6128
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WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 4I8LC
UT WOS:000850825000004
PM 35524675
DA 2025-01-04
ER

PT J
AU Sartore-Bianchi, A
   Trusolino, L
   Martino, C
   Bencardino, K
   Lonardi, S
   Bergamo, F
   Zagonel, V
   Leone, F
   Depetris, I
   Martinelli, E
   Troiani, T
   Ciardiello, F
   Racca, P
   Bertotti, A
   Siravegna, G
   Torri, V
   Amatu, A
   Ghezzi, S
   Marrapese, G
   Palmeri, L
   Valtorta, E
   Cassingena, A
   Lauricella, C
   Vanzulli, A
   Regge, D
   Veronese, S
   Comoglio, PM
   Bardelli, A
   Marsoni, S
   Siena, S
AF Sartore-Bianchi, Andrea
   Trusolino, Livio
   Martino, Cosimo
   Bencardino, Katia
   Lonardi, Sara
   Bergamo, Francesca
   Zagonel, Vittorina
   Leone, Francesco
   Depetris, Ilaria
   Martinelli, Erika
   Troiani, Teresa
   Ciardiello, Fortunato
   Racca, Patrizia
   Bertotti, Andrea
   Siravegna, Giulia
   Torri, Valter
   Amatu, Alessio
   Ghezzi, Silvia
   Marrapese, Giovanna
   Palmeri, Laura
   Valtorta, Emanuele
   Cassingena, Andrea
   Lauricella, Calogero
   Vanzulli, Angelo
   Regge, Daniele
   Veronese, Silvio
   Comoglio, Paolo M.
   Bardelli, Alberto
   Marsoni, Silvia
   Siena, Salvatore
TI Dual-targeted therapy with trastuzumab and lapatinib in
   treatment-refractory, <i>KRAS</i> codon 12/13 wild-type, HER2-positive
   metastatic colorectal cancer (HERACLES): a proof-of-concept,
   multicentre, open-label, phase 2 trial
SO LANCET ONCOLOGY
LA English
DT Article
ID GENE COPY NUMBER; RECTAL-CANCER; EGFR; CHEMOTHERAPY; COMBINATION;
   BIOMARKERS; RATIONALE; PATIENT; COLON
AB Background We previously found that dual HER2 blockade with trastuzumab and lapatinib led to inhibition of tumour growth in patient-derived xenografts of HER2-amplified metastatic colorectal cancer. In this study, we aimed to assess the antitumour activity of trastuzumab and lapatinib in patients with HER2-positive colorectal cancer.
   Methods HERACLES was a proof-of-concept, multicentre, open-label, phase 2 trial done at four Italian academic cancer centres. We enrolled adult patients with KRAS exon 2 (codons 12 and 13) wild-type and HER2-positive metastatic colorectal cancer refractory to standard of care (including cetuximab or panitumumab), an Eastern Cooperative Oncology Group performance status of 0 or 1, and at least one measurable lesion. We defined HER2 positivity in tumour samples by use of immunohistochemistry and fluorescence in-situ hybridisation in accordance with our previously validated colorectal cancer-specific diagnostic criteria. Eligible patients received intravenous trastuzumab at 4 mg/kg loading dose followed by 2 mg/kg once per week, and oral lapatinib at 1000 mg per day until evidence of disease progression. The primary endpoint was the proportion of patients achieving an objective response (defined as complete response or partial response), which was assessed by independent central review in the intention-to-treat population. This trial is registered with EudraCT, number 2012-002128-33.
   Findings Between Aug 27, 2012, and May 15, 2015, we screened 914 patients with KRAS exon 2 (codons 12 and 13) wild-type metastatic colorectal cancer and identified 48 (5%) patients with HER2-positive tumours, although two died before enrolment. Of these patients, 27 were eligible for the trial. All were evaluable for response. At the time of data cutoff on Oct 15, 2015, with a median follow-up of 94 weeks (IQR 51-127), eight (30%, 95% CI 14-50) of 27 patients had achieved an objective response, with one patient (4%, 95% CI -3 to 11) achieving a complete response, and seven (26%, 95% CI 9-43) achieving partial responses; 12 (44%, 95% CI 25-63) patients had stable disease. Six (22%) of 27 patients had grade 3 adverse events, which consisted of fatigue in four patients, skin rash in one patient, and increased bilirubin concentration in one patient. No grade 4 or 5 adverse events were reported. We detected no drug-related serious adverse events.
   Interpretation The combination of trastuzumab and lapatinib is active and well tolerated in treatment-refractory patients with HER2-positive metastatic colorectal cancer.
C1 [Sartore-Bianchi, Andrea; Bencardino, Katia; Amatu, Alessio; Ghezzi, Silvia; Marrapese, Giovanna; Palmeri, Laura; Valtorta, Emanuele; Cassingena, Andrea; Lauricella, Calogero; Vanzulli, Angelo; Veronese, Silvio; Siena, Salvatore] Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, Milan, Italy.
   [Trusolino, Livio; Martino, Cosimo; Leone, Francesco; Bertotti, Andrea; Siravegna, Giulia; Regge, Daniele; Comoglio, Paolo M.; Bardelli, Alberto; Marsoni, Silvia] Fdn Piemonte Oncol IRCCS, Ist Candiolo, I-10060 Candiolo, Italy.
   [Lonardi, Sara; Bergamo, Francesca; Zagonel, Vittorina] Ist Oncol Veneto IRCCS, Oncol Med 1, Padua, Italy.
   [Martinelli, Erika; Troiani, Teresa; Ciardiello, Fortunato] Univ Naples 2, Naples, Italy.
   [Racca, Patrizia] Azienda Osped Univ Citta Salute & Sci, Turin, Italy.
   [Torri, Valter] Ist Mario Negri IRCCS, Milan, Italy.
   [Trusolino, Livio; Leone, Francesco; Depetris, Ilaria; Bertotti, Andrea; Siravegna, Giulia; Regge, Daniele; Comoglio, Paolo M.; Bardelli, Alberto] Univ Turin, Dipartimento Oncol, Turin, Italy.
   [Siena, Salvatore] Univ Milan, Dipartimento Oncol & Ematooncol, Milan, Italy.
C3 IRCCS Fondazione del Piemonte per l'Oncologia; IRCCS Istituto Oncologico
   Veneto (IOV); Universita della Campania Vanvitelli; A.O.U. Citta della
   Salute e della Scienza di Torino; University of Turin; University of
   Milan
RP Marsoni, S (corresponding author), Fdn Piemonte Oncol IRCCS, Ist Candiolo, I-10060 Candiolo, Italy.
EM silvia.marsoni@ircc.it
RI Sartore-Bianchi, Andrea/AAB-9848-2019; Bergamo, Francesca/AAB-9010-2019;
   SIENA, SALVATORE/AAC-5806-2019; Trusolino, Livio/A-3896-2011; Torri,
   Valter/H-7550-2015; Comoglio, Paolo/G-6323-2011; Leone,
   Francesco/AAB-2355-2022; Vanzulli, Angelo/X-4175-2019; Regge,
   Daniele/AAC-6816-2022; Siravegna, Giulia/Z-2826-2019; Cassingena,
   Andrea/AGD-7137-2022; Lonardi, Sara/F-4228-2014; LEONE,
   Francesco/R-3248-2016; BARDELLI, Alberto/J-9721-2018; zagonel,
   vittorina/F-4226-2014; Bergamo, Francesca/G-3134-2014
OI Torri, Valter/0000-0001-9541-9354; Lonardi, Sara/0000-0002-7593-8138;
   Trusolino, Livio/0000-0002-6379-3365; Marsoni,
   Silvia/0000-0002-5361-7122; Depetris, Ilaria/0000-0001-6748-4992; LEONE,
   Francesco/0000-0001-5422-9706; Siravegna, Giulia/0000-0002-7132-6484;
   Cassingena, Andrea/0000-0003-4116-3992; Amatu,
   Alessio/0000-0001-5396-3378; Vanzulli, Angelo/0000-0002-2452-3370;
   Regge, Daniele/0000-0001-8267-5279; Comoglio, Paolo/0000-0002-7056-5328;
   Martino, Cosimo/0000-0002-7286-9755; BARDELLI,
   Alberto/0000-0003-1647-5070; Bertotti, Andrea/0000-0001-8196-7608;
   VALTORTA, EMANUELE/0000-0002-5087-6233; Veronese, Silvio
   Marco/0000-0002-5280-3740; Sartore-Bianchi, Andrea/0000-0003-0780-0409;
   zagonel, vittorina/0000-0002-0829-2525; SIENA,
   SALVATORE/0000-0002-2681-2846; Bergamo, Francesca/0000-0002-8795-4653
FU AIRC via Special Program Molecular Clinical Oncology 5 x 1000 [9970];
   Terapia Molecolare Tumori by Fondazione Oncologia Niguarda Onlus
FX This study was funded by AIRC via 2010 Special Program Molecular
   Clinical Oncology 5 x 1000 (project 9970). The study was also partly
   supported by grant Terapia Molecolare Tumori by Fondazione Oncologia
   Niguarda Onlus (to AS-B and SS). We also acknowledge a contribution from
   F Hoffmann-La Roche. We thank the patients and their families, all
   caregivers, and the referring oncologists; G Aprile, A Ardizzoni, S
   Artale, A Cubillo, A Falcone, B Frau, C Garufi, C Graiff, R Labianca, F
   Loupakis, S Mosconi, F Pietrantonio, C Pinto, G Tonini, E Villa, and M G
   Zampino; L Gianni for discussing drug doses for the study design; M
   Gambacorta for his contribution to the development of the HERACLES
   diagnostic criteria; A Bartosek and S Colombini for data management; F
   Astegiano and G Cappello for technical help with the radiological
   reviews; and B Mussolin for plasma sample processing.
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TC 727
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U2 68
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
EI 1474-5488
J9 LANCET ONCOL
JI Lancet Oncol.
PD JUN
PY 2016
VL 17
IS 6
BP 738
EP 746
DI 10.1016/S1470-2045(16)00150-9
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DN4VX
UT WOS:000377066400058
PM 27108243
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Arora, S
   Scott, AM
   Janes, PW
AF Arora, Sakshi
   Scott, Andrew M.
   Janes, Peter W.
TI Eph Receptors in Cancer
SO BIOMEDICINES
LA English
DT Review
DE Eph receptor; ephrin; receptor tyrosine kinase; cancer biology; targeted
   therapy
ID TRIPLE-NEGATIVE BREAST; CELL LUNG-CANCER; TYROSINE KINASE;
   COLORECTAL-CANCER; THERAPEUTIC TARGET; INITIATING CELLS;
   PROSTATE-CANCER; EPHRINB LIGANDS; SMALL MOLECULES; PDZ PROTEINS
AB Eph receptor tyrosine kinases play critical functions during development, in the formation of tissue and organ borders, and the vascular and neural systems. Uniquely among tyrosine kinases, their activities are controlled by binding to membrane-bound ligands, called ephrins. Ephs and ephrins generally have a low expression in adults, functioning mainly in tissue homeostasis and plasticity, but are often overexpressed in cancers, where they are especially associated with undifferentiated or progenitor cells, and with tumour development, vasculature, and invasion. Mutations in Eph receptors also occur in various tumour types and are suspected to promote tumourigenesis. Ephs and ephrins have the capacity to operate as both tumour promoters and tumour suppressors, depending on the circumstances. They have been demonstrated to impact tumour cell proliferation, migration, and invasion in vitro, as well as tumour development, angiogenesis, and metastases in vivo, making them potential therapeutic targets. However, successful development of therapies will require detailed understanding of the opposing roles of Ephs in various cancers. In this review, we discuss the variations in Eph expression and functions in a variety of malignancies. We also describe the multiple strategies that are currently available to target them in tumours, including preclinical and clinical development.
C1 [Arora, Sakshi; Scott, Andrew M.; Janes, Peter W.] La Trobe Univ, Olivia Newton John Canc Res Inst, Sch Canc Med, Heidelberg, Vic 3084, Australia.
C3 La Trobe University; Olivia Newton-John Cancer Research Institute
RP Janes, PW (corresponding author), La Trobe Univ, Olivia Newton John Canc Res Inst, Sch Canc Med, Heidelberg, Vic 3084, Australia.
EM peter.janes@onjcri.org.au
OI Janes, Peter/0000-0002-9039-1097; Arora, Sakshi/0000-0002-1296-9447
FU Australian National Health and Medical Research Council [1183532,
   1183533, 1183534, 1183535, 1183536, 1183537]; Victorian Government
   Operational Infrastructure
FX S.A. is a recipient of a La Trobe Graduate Research Scholarship (LTGRS)
   and a La Trobe University Full-Fee Research Scholarship (LTUFFRS).
   P.W.J. and A.M.S. are funded by the Australian National Health and
   Medical Research Council (Ideas grant 1183532 to P.W.J., Investigator
   grant 1177837 to A.M.S.). The Olivia Newton-John Cancer Research
   Institute acknowledges the support of the Victorian Government
   Operational Infrastructure Support Program.
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NR 137
TC 18
Z9 20
U1 2
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD FEB
PY 2023
VL 11
IS 2
AR 315
DI 10.3390/biomedicines11020315
PG 24
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental;
   Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine;
   Pharmacology & Pharmacy
GA 9H6IX
UT WOS:000938935500001
PM 36830852
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Moradi-Kalbolandi, S
   Hosseinzade, A
   Salehi, M
   Merikhian, P
   Farahmand, L
AF Moradi-Kalbolandi, Shima
   Hosseinzade, Aysooda
   Salehi, Malihe
   Merikhian, Parnaz
   Farahmand, Leila
TI Monoclonal antibody-based therapeutics, targeting the epidermal growth
   factor receptor family: from herceptin to Pan HER
SO JOURNAL OF PHARMACY AND PHARMACOLOGY
LA English
DT Review
DE anti-EGFR family monoclonal antibody; anti-EGFR mAb resistance;
   epidermal growth factor receptors; targeted therapy
ID SQUAMOUS-CELL CARCINOMA; METASTATIC BREAST-CANCER; PHASE-II TRIAL;
   WILD-TYPE KRAS; EGFR ANTIBODY; COLORECTAL-CANCER; LUNG-CANCER;
   OPEN-LABEL; ACQUIRED-RESISTANCE; IN-VITRO
AB ObjectivesMonoclonal antibody-based of cancer therapy has been considered as one of the most successful therapeutic strategies for both haematologic malignancies and solid tumours in the last two decades. Epidermal growth factor receptor (EGFR) family signalling pathways play a key role in the regulation of cell proliferation, survival and differentiation. Hence, anti-EGFR family mAbs is one of the most promising approaches in cancer therapy.
   Key findingsHere, recent advances in anti-EGFR mAb including approved or successfully tested in preclinical and clinical studies have been reviewed. Although we focus on monoclonal antibodies against the EGF receptor, but the mechanisms underlying the effects of EGFR-specific mAb in cancer therapy, to some extend the resistance to existing anti-EGFR therapies and some therapeutic strategies to overcome resistance such as combination of mAbs on different pathways are briefly discussed as well.
   SummaryThe EGFR family receptors, is considered as an attractive target for mAb development to inhibit their consecutive activities in tumour growth and resistance. However, due to resistance mechanisms, the combination therapies may become a good candidate for targeting EGFR family receptors.
C1 [Moradi-Kalbolandi, Shima; Hosseinzade, Aysooda; Salehi, Malihe; Merikhian, Parnaz; Farahmand, Leila] ACECR, Motamed Canc Inst, Breast Canc Res Ctr, Recombinant Prot Dept, Tehran, Iran.
C3 Academic Center for Education, Culture & Research (ACECR)
RP Farahmand, L (corresponding author), Motamed Breast Canc Res Ctr, Recombinant Prot Dept, Vanak Squar, Tehran 1517964311, Iran.
EM laylafarahmand@gmail.com
RI Farahmand, Leila/Y-3671-2019; Hosseinzadeh, Aysooda/ABD-4905-2021
OI Moradi-Kalbolandi, Shima/0000-0002-0488-0506; Merikhian,
   Parnaz/0000-0001-7482-836X
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NR 137
TC 30
Z9 36
U1 1
U2 21
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3573
EI 2042-7158
J9 J PHARM PHARMACOL
JI J. Pharm. Pharmacol.
PD JUL
PY 2018
VL 70
IS 7
BP 841
EP 854
DI 10.1111/jphp.12911
PG 14
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA GI6VZ
UT WOS:000434642600001
PM 29574771
OA hybrid
DA 2025-01-04
ER

PT J
AU Azeez, RA
   Al-Jowari, SAK
   Mahmood, HJ
AF Azeez, Rasha Abbas
   Al-Jowari, Suha Abdul-Khaliq
   Mahmood, Hayder Jamal
TI Study the Gene Expression of <i>PIK3CA</i> in Tissue and Blood Samples
   of Iraqi Patients with Colorectal Cancer
SO JOURNAL OF CONTEMPORARY MEDICAL SCIENCES
LA English
DT Article
DE PIKCA3; gene expression; qRT-PCR; colorectal neoplasms
ID BIOMARKERS; MUTATIONS
AB Objectives: The primary objective of this investigation is to explore the correlation between gene expression of PIKCA3 and colorectal cancer in both tissue and blood samples, while also performing a comparative analysis between these sample types.
   Methods: This research involved the collection of blood and tissue samples. The study was conducted at the Gastroenterology Hospital within the Medical City Department in Baghdad, Iraq, spanning from December 2021 to December 2022. A total of 80 volunteers, encompassing both genders and aged between 24 and 77, participated in the study. The real time qRT-PCR analysis method was employed to assess the expression of PIKCA3 genes within patient and control groups.
   Results: The findings indicate significant distinctions in Ct PIK3CA between blood and tissue samples across all study groups. Moreover, PIK3CA expression displayed a notable association with CRC patients, showing higher expression levels compared to the other groups. This disparity was particularly pronounced when comparing tissue and blood samples. Statistical analysis, specifically Receiver Operating Characteristic (ROC) Curve Analysis, affirmed the excellent predictive capacity of the AUC (Area Under the Curve) value. The study established that PIK3CA gene expression in tissue outperformed that in blood, demonstrating a considerably elevated gene expression in tissue (P < 0.001). Notably, the fold increase in gene expression within CRC patients was significantly higher compared to the group of healthy participants, with values of 23.630 in blood samples and 124.810 in tissue samples, respectively. The present study underscores the prevalence of PIK3CA gene mutations in colorectal carcinomas.
   Conclusion: The frequent occurrence of PIK3CA gene mutations in colorectal carcinomas may hold promise for the development of targeted therapy combinations. These could involve inhibiting both the PI3K kinase itself and addressing associated pathway anomalies.
C1 [Azeez, Rasha Abbas] Univ Baghdad, Coll Dens, Dept Basic Sci, Baghdad, Iraq.
   [Al-Jowari, Suha Abdul-Khaliq] Univ Baghdad, Coll Sci, Dept Biol, Baghdad, Iraq.
   [Mahmood, Hayder Jamal] Minist Hlth, Endoscopy Dept, Gastroenterol & Hepatol Hosp, Med City Dept, Baghdad, Iraq.
C3 University of Baghdad; University of Baghdad; Ministry of Health Iraq
RP Azeez, RA (corresponding author), Univ Baghdad, Coll Dens, Dept Basic Sci, Baghdad, Iraq.
EM rasha.abbas@codental.uobaghdad.edu
RI Al-Jowari, Suha/Y-1773-2019
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TC 0
Z9 0
U1 0
U2 0
PU NABA AL-HAYAT FOUNDATION MEDICAL SCIENCES & HEALTH CARE
PI NAJAF
PA PO BOX 494, NAJAF, 00000, IRAQ
SN 2413-0516
J9 J CONTEMP MED SCI
JI J. Contemp. Med. Sci.
PD JUL-AUG
PY 2023
VL 9
IS 4
BP 280
EP 285
PG 6
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA GF3F8
UT WOS:001151204700009
DA 2025-01-04
ER

PT J
AU Ma, SY
   Kim, JH
   Chen, W
   Li, L
   Lee, J
   Xue, JL
   Liu, YX
   Chen, G
   Tang, B
   Tao, W
   Kim, JS
AF Ma, Siyue
   Kim, Ji Hyeon
   Chen, Wei
   Li, Lu
   Lee, Jieun
   Xue, Junlian
   Liu, Yuxia
   Chen, Guang
   Tang, Bo
   Tao, Wei
   Kim, Jong Seung
TI Cancer Cell-Specific Fluorescent Prodrug Delivery Platforms
SO ADVANCED SCIENCE
LA English
DT Review
DE cancer specific targeting; drug delivery system; fluorescent prodrug;
   nanoparticles; tumor therapy
ID REVERSE TAMOXIFEN RESISTANCE; HEPATOCELLULAR-CARCINOMA; DRUG-DELIVERY;
   LUNG-CANCER; TRANSFERRIN RECEPTOR; TARGETED THERAPY; PHOTODYNAMIC
   THERAPY; CAMPTOTHECIN PRODRUG; POLYMERIC PRODRUG; ACID
AB Targeting cancer cells with high specificity is one of the most essential yet challenging goals of tumor therapy. Because different surface receptors, transporters, and integrins are overexpressed specifically on tumor cells, using these tumor cell-specific properties to improve drug targeting efficacy holds particular promise. Targeted fluorescent prodrugs not only improve intracellular accumulation and bioavailability but also report their own localization and activation through real-time changes in fluorescence. In this review, efforts are highlighted to develop innovative targeted fluorescent prodrugs that efficiently accumulate in tumor cells in different organs, including lung cancer, liver cancer, cervical cancer, breast cancer, glioma, and colorectal cancer. The latest progress and advances in chemical design and synthetic considerations in fluorescence prodrug conjugates and how their therapeutic efficacy and fluorescence can be activated by tumor-specific stimuli are reviewed. Additionally, novel perspectives are provided on strategies behind engineered nanoparticle platforms self-assembled from targeted fluorescence prodrugs, and how fluorescence readouts can be used to monitor the position and action of the nanoparticle-mediated delivery of therapeutic agents in preclinical models. Finally, future opportunities for fluorescent prodrug-based strategies and solutions to the challenges of accelerating clinical translation for the treatment of organ-specific tumors are proposed.
C1 [Ma, Siyue; Li, Lu; Xue, Junlian; Liu, Yuxia; Chen, Guang] Shaanxi Univ Sci & Technol, Youth Innovat Team Shaanxi Univ, Coll Chem & Chem Engn, Shaanxi Key Lab Chem Addit Ind, Xian 710021, Peoples R China.
   [Ma, Siyue] Hainan Med Univ, Coll Emergency & Trauma, Key Lab Emergency & Trauma, Minist Educ, Haikou 571199, Peoples R China.
   [Kim, Ji Hyeon; Lee, Jieun; Kim, Jong Seung] Korea Univ, Dept Chem, Seoul 02841, South Korea.
   [Kim, Ji Hyeon; Lee, Jieun; Kim, Jong Seung] Harvard Med Sch, Ctr Nanomed, Boston, MA 02115 USA.
   [Kim, Ji Hyeon; Chen, Wei; Lee, Jieun; Tao, Wei; Kim, Jong Seung] Harvard Med Sch, Brigham & Womens Hosp, Dept Anesthesiol, Coll Chem, Boston, MA 02115 USA.
   [Chen, Guang; Tang, Bo] Shandong Normal Univ, Collaborat Innovat Ctr Functionalized Probes Chem, Inst Biomed Sci, Coll Chem,Chem Engn & Mat Sci,Key Lab Mol & Nano P, Jinan 250014, Peoples R China.
C3 Shaanxi University of Science & Technology; Hainan Medical University;
   Korea University; Harvard University; Harvard Medical School; Harvard
   University; Brigham & Women's Hospital; Harvard Medical School; Shandong
   Normal University
RP Chen, G (corresponding author), Shaanxi Univ Sci & Technol, Youth Innovat Team Shaanxi Univ, Coll Chem & Chem Engn, Shaanxi Key Lab Chem Addit Ind, Xian 710021, Peoples R China.; Kim, JS (corresponding author), Korea Univ, Dept Chem, Seoul 02841, South Korea.; Tao, W; Kim, JS (corresponding author), Harvard Med Sch, Brigham & Womens Hosp, Dept Anesthesiol, Coll Chem, Boston, MA 02115 USA.; Chen, G; Tang, B (corresponding author), Shandong Normal Univ, Collaborat Innovat Ctr Functionalized Probes Chem, Inst Biomed Sci, Coll Chem,Chem Engn & Mat Sci,Key Lab Mol & Nano P, Jinan 250014, Peoples R China.
EM chenandguang@163.com; tangb@sdnu.edu.cn; wtao@bwh.harvard.edu;
   jongskim@korea.ac.kr
RI Kim, Jong Seung/N-4504-2015; Kim, Ji Hyeon/GWU-9811-2022; Tao,
   Wei/AAE-7955-2020
OI , Ji Hyeon/0000-0002-3107-6548; Chen, Guang/0000-0002-0454-1686
FU National Science Foundation of China; Natural Science Basic Research
   Program of Shaanxi; Long-term Project of high-level talents innovation
   in Shaanxi Province; High-end project of National Foreign Expert
   Program; fellowship of China Postdoctoral Science Foundation; Key
   Laboratory of Emergency and Trauma (Hainan Medical University) Ministry
   of Education; Special Scientific Research Project of Education
   Department of Shaanxi Provincial Government [22174090]; Young Talent
   Fund of Xi'an Association for Science and Technology [2022JM-089];
   National Research Foundation of Korea (NRF) - Ministry of Science and
   ICT (CRI); Ministry of Education [G2021041002L]; US METAvivor Early
   Career Investigator Award [2022M711994]; Harvard Medical School/Brigham
   and Women's Hospital Department Basic Scientist Grant [KLET-202010];
   Gillian Reny Stepping Strong Center for Trauma Innovation Breakthrough
   Innovator Award [21JK0545]; Center for Nanomedicine Research Fund
   [095920211319]; Nanotechnology Foundation [2018R1A3B1052702]; Farokhzad
   Family Distinguished Chair Foundation [2019H1A2A1074096]; Khoury
   Innovation Award [2018A020560]; American Heart Association (AHA)
   Collaborative Sciences Award [2420 BPA075];  [113548];  [2019A014810]; 
   [2022A002721];  [018129];  [2020A003219];  [2018A004190]
FX S.M., J.H.K., and W.C. contributed equally to this work. This work was
   supported by the National Science Foundation of China (No. 22174090, G.
   C.); the Natural Science Basic Research Program of Shaanxi (No.
   2022JM-089, Y. L.); Long-term Project of high-level talents innovation
   in Shaanxi Province (G.C.); the High-end project of National Foreign
   Expert Program (No. G2021041002L, G. C.); the fellowship of China
   Postdoctoral Science Foundation (No. 2022M711994, S. M.); Key Laboratory
   of Emergency and Trauma (Hainan Medical University) Ministry of
   Education (Grant No. KLET-202010, S. M.); Special Scientific Research
   Project of Education Department of Shaanxi Provincial Government (No.
   21JK0545, S. M.); Young Talent Fund of Xi'an Association for Science and
   Technology (No. 095920211319, S. M.); National Research Foundation of
   Korea (NRF) funded by the Ministry of Science and ICT (CRI Project No.
   2018R1A3B1052702, J.S.K.) and by the Ministry of Education (No.
   2019H1A2A1074096, J.H.K.). This work was also supported by the US
   METAvivor Early Career Investigator Award (No. 2018A020560, W.T.),
   Harvard Medical School/Brigham and Women's Hospital Department Basic
   Scientist Grant (No. 2420 BPA075, W.T.), Gillian Reny Stepping Strong
   Center for Trauma Innovation Breakthrough Innovator Award (No. 113548,
   W.T.), Center for Nanomedicine Research Fund (No. 2019A014810, W.T.),
   Nanotechnology Foundation (No. 2022A002721, W.T.), and Farokhzad Family
   Distinguished Chair Foundation (No. 018129, W.T.). W.T. is also a
   recipient of the Khoury Innovation Award (No. 2020A003219), and American
   Heart Association (AHA) Collaborative Sciences Award (No. 2018A004190).
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NR 174
TC 22
Z9 22
U1 30
U2 153
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2198-3844
J9 ADV SCI
JI Adv. Sci.
PD JUN
PY 2023
VL 10
IS 16
DI 10.1002/advs.202207768
EA APR 2023
PG 18
WC Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials
   Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA H8VX2
UT WOS:000964002500001
PM 37026629
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Landmesser, ME
   Raup-Konsavage, WM
   Lehman, HL
   Stairs, DB
AF Landmesser, Mary E.
   Raup-Konsavage, Wesley M.
   Lehman, Heather L.
   Stairs, Douglas B.
TI Loss of p120ctn causes EGFR-targeted therapy resistance and failure
SO PLOS ONE
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; CELL LUNG-CANCER; TYROSINE KINASE INHIBITORS;
   E-CADHERIN; PROGNOSTIC VALUE; P120-CATENIN EXPRESSION;
   ACQUIRED-RESISTANCE; REDUCED EXPRESSION; COLORECTAL-CANCER; POOR
   SURVIVAL
AB Epidermal growth factor receptor (EGFR) plays a vital role in cell division and survival signaling pathways. EGFR is activated in nearly every cancer type, and its high expression in tumors is correlated with poor patient outcome. Altogether, EGFR is a prime candidate as a therapeutic target. While targeted EGFR therapy is initially effective in 75% of patients, a majority of patients relapse within the first year due to poorly understood mechanisms of resistance. p120-catenin (p120ctn) has recently been implicated as a biomarker for EGFR therapy. In previous studies, we demonstrated that p120ctn is a tumor suppressor and its loss is capable of inducing cancer. Furthermore, p120ctn down-regulation synergizes with EGFR overexpression to cause a highly invasive cell phenotype. The purpose of this present study was to investigate whether p120ctn down-regulation induced EGFR therapeutic resistance. Using human esophageal keratinocytes, we have found that EGFR-targeting compounds are toxic to cells overexpressing EGFR. Interestingly, these therapies do not cause toxicity in cells with EGFR overexpression and decreased p120ctn expression. These data suggest that decreased p120ctn causes resistance to EGFR therapy. We believe these findings are of utmost importance, as there is an unmet need to discover mechanisms of EGFR resistance.
C1 [Landmesser, Mary E.; Stairs, Douglas B.] Penn State Univ, Coll Med, Dept Pathol, Hershey, PA 17033 USA.
   [Raup-Konsavage, Wesley M.] Penn State Univ, Dept Pharmacol, Coll Med, Hershey, PA USA.
   [Lehman, Heather L.] Millersville Univ Pennsylvania, Dept Biol, Millersville, PA USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE);
   Pennsylvania State University; Penn State Health; Pennsylvania
   Commonwealth System of Higher Education (PCSHE); Pennsylvania State
   University; Penn State Health; Pennsylvania State System of Higher
   Education (PASSHE); Millersville University of Pennsylvania
RP Stairs, DB (corresponding author), Penn State Univ, Coll Med, Dept Pathol, Hershey, PA 17033 USA.
EM dbs18@psu.edu
RI Raup-Konsavage, Wesley/ABB-1910-2020
OI Raup-Konsavage, Wesley/0000-0001-9413-9852; Stairs,
   Douglas/0000-0002-4875-6582
FU American Cancer Society [RSG-16-219-01-TBG]; Department of Pathology
   Researcher-Initiated Grant; ET Program Development Award from the Penn
   State Cancer Institute; Penn State Cancer Institute; Highmark Community
   Health Reinvestment Grant
FX This research was supported by a Research Scholar Grant,
   RSG-16-219-01-TBG, from the American Cancer Society, a Department of
   Pathology Researcher-Initiated Grant, as well as an ET Program
   Development Award and a Program Project Development Award, both from the
   Penn State Cancer Institute and Highmark Community Health Reinvestment
   Grant (all to DBS). The funders had no role in study design, data
   collection and analysis, decision to publish, or preparation of the
   manuscript.
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NR 52
TC 4
Z9 4
U1 0
U2 0
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD OCT 28
PY 2020
VL 15
IS 10
AR e0241299
DI 10.1371/journal.pone.0241299
PG 14
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA OP8XL
UT WOS:000588374000037
PM 33112928
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Moehler, M
   Thomaidis, T
   Zeifri, C
   Barhoom, T
   Marquardt, J
   Ploch, P
   Schattenberg, J
   Maderer, A
   Schimanski, CC
   Weinmann, A
   Woerns, MA
   Kranich, AL
   Warnecke, JM
   Galle, PR
AF Moehler, Markus
   Thomaidis, Thomas
   Zeifri, Chourouk
   Barhoom, Tareq
   Marquardt, Jens
   Ploch, Philippe
   Schattenberg, Joern
   Maderer, Annett
   Schimanski, Carl Christoph
   Weinmann, Arndt
   Woerns, Marcus Alexander
   Kranich, Anne L.
   Warnecke, Jens M.
   Galle, Peter Robert
TI Inclusion of targeted therapies in the standard of care for metastatic
   colorectal cancer patients in a German cancer center: the more the
   better?!
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Article
DE Targeted treatment; VEGF; EGFR; Palliative treatment; Colorectal cancer
ID PHASE-III TRIAL; INFUSIONAL FLUOROURACIL; IRINOTECAN FOLFIRI; 1ST-LINE
   TREATMENT; PLUS IRINOTECAN; OXALIPLATIN; LEUCOVORIN; BEVACIZUMAB;
   CETUXIMAB; CHEMOTHERAPY
AB Purpose Significant prolongation of overall survival (OS) has been reached in metastatic colorectal cancer (mCRC) treatment within the last 5-10 years. Our study was conducted in order to evaluate and compare OS of different standard of care treatment options in a university-based outpatient clinic.
   Methods One hundred and three mCRC patients were identified by retrospective analysis and treated according to available guidelines. OS was analyzed according to the different combinations of first-and second-line treatments.
   Results mCRC patients revealed an mOS of 34.4 months. Patients receiving anti-vascular endothelial growth factor (VEGF) blockade in at least one treatment line showed a significantly longer survival time (p = 0.0056) versus patients without any bevacizumab. No OS differences were detected comparing the different first-and second-line chemotherapy (CTX) strategies in the unselected population. However, wild-type (wt) Kras patients treated with anti-epidermal growth factor receptor (EGFR) therapy plus CTX in first-line therapy showed significantly longer OS compared to those receiving only additional VEGF inhibition or no targeted therapy (p = 0.0056; mOS 46.8 vs. 20.4 months, respectively). wt Kras patients profited in trend (p = 0.076) from CTX combinations of first-line anti-EGFR followed by second-line anti-VEGF compared to first-line anti-VEGF followed by second-line anti-EGFR (mOS 46.8 vs. 19.2 months, respectively).
   Conclusions Our results indicate successful allocation of the current mCRC treatment according to the Kras status. Differences in OS of wt Kras patients indicated the further need for randomized trials to define the potential benefit of sequential therapy with EGFR inhibition in first-line therapy followed by VEGFR inhibition vice versa.
C1 [Moehler, Markus; Thomaidis, Thomas; Zeifri, Chourouk; Barhoom, Tareq; Marquardt, Jens; Ploch, Philippe; Schattenberg, Joern; Maderer, Annett; Weinmann, Arndt; Woerns, Marcus Alexander; Galle, Peter Robert] Johannes Gutenberg Univ Mainz, Dept Med 1, D-55131 Mainz, Germany.
   [Schimanski, Carl Christoph] Marienhospital, Med Clin, Darmstadt, Germany.
   [Kranich, Anne L.; Warnecke, Jens M.] GSO mbH, Hamburg, Germany.
C3 Johannes Gutenberg University of Mainz; St. Marien Hospital
RP Moehler, M (corresponding author), Johannes Gutenberg Univ Mainz, Dept Med 1, Langenbeckstr 1, D-55131 Mainz, Germany.
EM moehler@mail.uni-mainz.de; Thomas.thomaidis@unimedizin-mainz.de;
   marokko.z@hotmail.de; tbarhoum83@hotmail.com;
   jens.marquardt@unimedizin-mainz.de; Philippe.ploch@unimedizin-mainz.de;
   Joern.schattenberg@unimedizin-mainz.de;
   Annett.Maderer@unimedizin-mainz.de;
   c.schimanski@marienhospital-darmstadt.de;
   Arndt.weinmann@unimedizin-mainz.de;
   marcus-alexander.woerns@unimedizin-mainz.de; kranich@gso-hamburg.com;
   warnecke@gso-hamburg.com; peter.galle@unimedizin-mainz.de
RI Schattenberg, Jörn/C-1301-2013; Lerch, Markus/E-2206-2016; Galle,
   Peter/ABE-2872-2021; Weinmann, Arndt/X-7935-2019
OI Galle, Peter Robert/0000-0001-8294-0992; Schattenberg, Jorn
   M./0000-0002-4224-4703; Maderer, Annett/0000-0001-9891-5046; ,
   Markus/0000-0003-2490-9131; Marquardt, Jens/0000-0002-8314-2682
FU Merck Serono
FX M Moehler received honoraria for presentations in satellite symposia by
   Merck and Roche. The rest of the authors have no competing interests to
   declare. Medical writing by GSOmbH (ALK and JMW) was supported by an
   unrestricted grant of Merck Serono. However, ALK and JMW did not prepare
   the first draft and did not contribute to critical revisions,
   interpretation of results, or any critical intellectual impact.
CR [Anonymous], EUR CANC C 2013
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NR 29
TC 10
Z9 10
U1 1
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0171-5216
EI 1432-1335
J9 J CANCER RES CLIN
JI J. Cancer Res. Clin. Oncol.
PD MAR
PY 2015
VL 141
IS 3
BP 515
EP 522
DI 10.1007/s00432-014-1829-6
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CB1FZ
UT WOS:000349373800013
PM 25230900
DA 2025-01-04
ER

PT J
AU Qin, SK
   Xu, RH
   Shen, L
   Xu, JM
   Bai, YX
   Yang, L
   Deng, YH
   Chen, ZD
   Zhong, HJ
   Pan, HM
   Guo, WJ
   Shu, YQ
   Yuan, Y
   Zhou, JF
   Xu, N
   Liu, TS
   Ma, D
   Wu, CP
   Cheng, Y
   Chen, DH
   Li, W
   Sun, SY
   Yu, Z
   Cao, PG
   Chen, HH
   Wang, JJ
   Wang, SB
   Wang, HB
   Wang, N
   Zhang, B
   Zhang, Q
   Su, WG
   Guo, XJ
   Li, J
AF Qin, Shukui
   Xu, Rui-Hua
   Shen, Lin
   Xu, Jianming
   Bai, Yuxian
   Yang, Lei
   Deng, Yanhong
   Chen, Zhen-dong
   Zhong, Haijun
   Pan, Hongming
   Guo, Weijian
   Shu, Yongqian
   Yuan, Ying
   Zhou, Jianfeng
   Xu, Nong
   Liu, Tianshu
   Ma, Dong
   Wu, Changping
   Cheng, Ying
   Chen, Donghui
   Li, Wei
   Sun, Sanyuan
   Yu, Zhuang
   Cao, Peiguo
   Chen, Haihui
   Wang, Jiejun
   Wang, Shubin
   Wang, Hongbing
   Wang, Ning
   Zhang, Bin
   Zhang, Qiang
   Su, Weiguo
   Guo, Xiaojun
   Li, Jin
TI Subgroup Analysis by Liver Metastasis in the FRESCO Trial Comparing
   Fruquintinib versus Placebo Plus Best Supportive Care in Chinese
   Patients with Metastatic Colorectal Cancer
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE colorectal cancer; FRESCO trial; fruquintinib; liver metastasis
ID ANTI-EGFR; CHEMOTHERAPY
AB Objective: The aim of the present subgroup analysis of the FRESCO trial is to determine the efficacy and hepatotoxicity of fruquintinib in Chinese patients with metastatic CRC with liver metastasis (CRLM) who were receiving third-line or posterior-line therapy.
   Methods: Overall survival (OS) and progression-free survival (PFS) were evaluated by Kaplan-Meier method. Hazard ratio (HR) was estimated through Cox proportional hazards model. Hepatotoxicity was coded using the standardized MedDRA queries of hepatic failure, fibrosis, cirrhosis, and other liver injury-related conditions and graded using the Common Terminology Criteria Adverse Events grades. The efficacy of fruquintinib in patients with CRLM was evaluated in various subgroups.
   Results: A total of 287 (69.0%) patients with metastatic CRC had liver metastasis (LM, fruquintinib: 185 and placebo: 102). Median OS in patients with CRLM was significantly prolonged with fruquintinib compared with placebo (8.61 months vs 5.98 months; HR=0.59, 95% CI, 0.45-0.77, P<0.001). In patients with CRLM, the incremental median PFS for patients in the fruquintinib-treated group was significantly higher than in the placebo group (median PFS: 3.71 vs.1.84 months; HR=0.22, 95% CI: 0.17-0.30; P<0.001). Compared with placebo, significant improvements in OS were observed with fruquintinib in LM patients regardless of lung metastasis, prior target therapy, and K-RAS status. In patients with CRLM, treatment-emergent hepatotoxicities of any grade occurred in 7 (3.8%) patients in the fruquintinib group vs 2 (2.0%) in the placebo group.
   Conclusion: Fruquintinib demonstrated a statistically significant increase in OS and PFS as compared with placebo in Chinese patients with CRLM. The hepatotoxicity of fruquintinib was less reported, and comparable with placebo in patients with CRLM.
C1 [Qin, Shukui] Jinling Hosp, Canc Ctr, Nanjing, Peoples R China.
   [Xu, Rui-Hua] Sun Yat Sen Univ, Dept Med Oncol, State Key Lab Oncol South China, Canc Ctr, Guangzhou, Peoples R China.
   [Shen, Lin] Peking Univ, Dept Gastrointestinal Oncol, Key Lab Carcinogenesis & Translat Res, Minist Educ,Canc Hosp & Inst, Beijing, Peoples R China.
   [Xu, Jianming] Chinese Peoples Liberat Army Gen Hosp, Dept Med Oncol, Med Ctr 5, Beijing, Peoples R China.
   [Bai, Yuxian] Harbin Med Univ, Dept Med Oncol, Canc Hosp, Harbin, Peoples R China.
   [Yang, Lei] Nantong Canc Hosp, Dept Med Oncol, Nantong, Peoples R China.
   [Deng, Yanhong] Sun Yat Sen Univ, Dept Med Oncol, Affiliated Hosp 6, Guangzhou, Peoples R China.
   [Chen, Zhen-dong] Anhui Med Univ, Dept Med Oncol, Hosp 2, Hefei, Peoples R China.
   [Zhong, Haijun] Zhejiang Canc Hosp, Dept Med Oncol, Hangzhou, Peoples R China.
   [Pan, Hongming] Zhejiang Univ, Sir Run Run Shaw Hosp, Coll Med, Dept Med Oncol, Hangzhou, Peoples R China.
   [Guo, Weijian] Fudan Univ, Shanghai Med Coll, Dept Med Oncol, Shanghai Canc Ctr, Shanghai, Peoples R China.
   [Shu, Yongqian] Jiangsu Prov Hosp, Dept Med Oncol, Nanjing, Peoples R China.
   [Yuan, Ying] Zhejiang Univ, Dept Med Oncol, Affiliated Hosp 2, Sch Med, Hangzhou, Peoples R China.
   [Zhou, Jianfeng] Peking Union Med Coll Hosp, Dept Med Oncol, Beijing, Peoples R China.
   [Xu, Nong] Zhejiang Univ, Dept Med Oncol, Affiliated Hosp 1, Coll Med, Hangzhou, Peoples R China.
   [Liu, Tianshu] Fudan Univ, Shanghai Med Coll, Dept Med Oncol, Zhongshan Hosp, Shanghai, Peoples R China.
   [Ma, Dong] Guangdong Prov Peoples Hosp, Dept Med Oncol, Guangzhou, Peoples R China.
   [Wu, Changping] First Peoples Hosp Changzhou, Dept Med Oncol, Changzhou, Peoples R China.
   [Cheng, Ying] Jilin Prov Canc Hosp, Dept Med Oncol, Changchun, Peoples R China.
   [Chen, Donghui] Shanghai Jiao Tong Univ, Dept Med Oncol, Peoples Hosp 1, Shanghai, Peoples R China.
   [Li, Wei] First Hosp Jilin Univ, Dept Med Oncol, Changchun, Peoples R China.
   [Sun, Sanyuan] Xuzhou Cent Hosp, Dept Med Oncol, Xuzhou, Jiangsu, Peoples R China.
   [Yu, Zhuang] Qingdao Univ, Dept Med Oncol, Affiliated Hosp, Med Coll, Qingdao, Peoples R China.
   [Cao, Peiguo] Cent South Univ, Dept Med Oncol, Xiangya Hosp 3, Changsha, Peoples R China.
   [Chen, Haihui] Liuzhou Workers Hosp, Dept Med Oncol, Liuzhou, Peoples R China.
   [Wang, Jiejun] Second Mil Med Univ, Shanghai Changzheng Hosp, Dept Med Oncol, Shanghai, Peoples R China.
   [Wang, Shubin] Beijing Univ, Shenzhen Hosp, Dept Med Oncol, Shenzhen, Peoples R China.
   [Wang, Hongbing] Xuzhou Med Coll, Dept Med Oncol, Affiliated Hosp, Xuzhou, Jiangsu, Peoples R China.
   [Wang, Ning; Zhang, Bin; Zhang, Qiang] Eli Lilly & Co, Shanghai, Peoples R China.
   [Su, Weiguo; Guo, Xiaojun] Hutchison MediPharma Ltd, Shanghai, Peoples R China.
   [Li, Jin] Tongji Univ, Dept Med Oncol, Shanghai East Hosp, Shanghai, Peoples R China.
C3 State Key Lab Oncology South China; Sun Yat Sen University; Peking
   University; Chinese People's Liberation Army General Hospital; Fifth
   Medical Center of Chinese PLA General Hospital; Harbin Medical
   University; Sun Yat Sen University; Anhui Medical University; Zhejiang
   Cancer Hospital; Zhejiang University; Fudan University; Nanjing Medical
   University; Zhejiang University; Chinese Academy of Medical Sciences -
   Peking Union Medical College; Peking Union Medical College Hospital;
   Zhejiang University; Fudan University; Guangdong Academy of Medical
   Sciences & Guangdong General Hospital; Shanghai Jiao Tong University;
   Jilin University; Qingdao University; Central South University; Naval
   Medical University; Peking University; Xuzhou Medical University; Eli
   Lilly; Tongji University
RP Li, J (corresponding author), Tongji Univ, Dept Med Oncol, Shanghai East Hosp, Shanghai, Peoples R China.
EM lijin@csco.org.cn
RI Zhang, Qiang/HDN-0452-2022; xu, rui/GRX-5734-2022; Shu,
   Yongqian/ABD-5698-2021; Shen, Lin/JPX-7656-2023; Chen,
   Dong-Hui/C-6618-2018; Liu, Tianshu/H-6879-2019; Xu,
   Jianming/KWU-3367-2024; Xu, Rui-Hua/AAW-4766-2021
OI QIN, SHU-KUI/0000-0003-2289-1521; Cao, Peiguo/0000-0002-8828-9755; Xu,
   Rui-Hua/0000-0001-9771-8534
FU Eli Lilly and Company (Indianapolis, IN, USA); Hutchison MediPharma
   (Shanghai, China); Eli Lilly and Company
FX The FRESCO trial was co-funded by Eli Lilly and Company (Indianapolis,
   IN, USA) and Hutchison MediPharma (Shanghai, China) . The role of the
   funding source includes study design, data acquisition, analysis and
   interpretation of data, and the decision to submit the article for
   publication. All authors had full access to all of the data in this
   study and take complete responsibility for the integrity of the data and
   accuracy of the data analysis. Medical writing assistance support for
   this publication was funded by Eli Lilly and Company.
CR Aparicio J, 2005, CLIN COLORECTAL CANC, V5, P263, DOI 10.3816/CCC.2005.n.037
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NR 23
TC 2
Z9 2
U1 0
U2 5
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6930
J9 ONCOTARGETS THER
JI OncoTargets Ther.
PY 2021
VL 14
BP 4439
EP 4450
DI 10.2147/OTT.S307273
PG 12
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA TY4HE
UT WOS:000683744300005
PM 34408440
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Xu, L
   Liu, Y
   Xia, YB
   Huang, XX
   Hu, KF
AF Xu, Li
   Liu, Yi
   Xia, Yabin
   Huang, Xiaoxu
   Hu, Kaifeng
TI High expression of HDAC6 correlates with poor prognosis in colon cancer
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
LA English
DT Article
DE HDAC6; colon cancer; tissue microarray; immunohistochemistry; prognosis;
   targeted therapy
ID HISTONE DEACETYLASE INHIBITORS; ANTICANCER AGENTS; IDENTIFICATION;
   ANGIOGENESIS; CARCINOMA
AB Objectives: To elaborate the correlation between the expression of HDAC6 and tumor progression as well as prognosis in colon cancer patients. Methods: We chose a tissue microarray containing 90 colon cancer specimens with more than 5 years follow-up information. The expression level of HDAC6 was investigated by immunohistochemistry using a specific antibody. The experimental data, as well as relationship between HDAC6 expression and clinical pathological parameters were statistically analyzed by SPSS software. Results: HDAC6, expressed specifically in the cytoplasm, was obviously higher in colon cancer tissues than para-carcinoma tissues (P = 0.000). The expression of HDAC6 was negatively correlated with tumor size in colon cancer significantly (r = -0.213, P = 0.048). Survival analysis showed patients with HDAC6 over-expression had worse prognosis (18.2% vs 47.0%, P = 0.013) and HDAC6 was an independent prognostic factor (P = 0.033). Survival analysis of groups based on the tumor size indicated that patients with HDAC6 over-expression had worse prognosis among colon cancer groups bearing tumor diameter <= 5.5 cm (18.8% vs 51.4%, P = 0.006). However, there was no obvious correlation among groups bearing tumor diameter >5.5 cm patients (P = 0.532). In addition, the correlation analysis between HDAC6 and mismatch repair gene family showed that there was a negative correlation between HDAC6 expression and MSH2 expression (r = -0.205, P = 0.060). Conclusions: HDAC6 may specifically shorten the survival time of the colon patients bearing smaller-size tumor through promoting cell growth and proliferation; on the contrary, it had no effect on patients developing bigger-size tumor for the accomplishment of tumor cell growth and proliferation. At the same time, we also speculate that HDAC6 may promote colon cancer progression by inhibiting the gene repair function of patients.
C1 [Xu, Li; Liu, Yi] Anhui Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Hefei 230022, Peoples R China.
   [Xu, Li; Xia, Yabin; Huang, Xiaoxu; Hu, Kaifeng] Wannan Med Coll, Affiliated Hosp 1, Dept Gastrointestinal Surg, Wuhu 241000, Peoples R China.
C3 Anhui Medical University; Wannan Medical College
RP Xu, L; Liu, Y (corresponding author), Anhui Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Hefei 230001, Peoples R China.
EM xl829@sina.com; yiliu@medmail.com.cn
RI xu, li/D-5310-2009
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NR 15
TC 3
Z9 4
U1 0
U2 2
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1936-2625
J9 INT J CLIN EXP PATHO
JI Int. J. Clin. Exp. Pathol.
PY 2016
VL 9
IS 4
BP 4505
EP 4512
PG 8
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA DO2HZ
UT WOS:000377601900026
DA 2025-01-04
ER

PT J
AU Lund, CM
   Vistisen, KK
   Dehlendorff, C
   Ronholt, F
   Johansen, JS
   Nielsen, DL
AF Lund, Cecilia M.
   Vistisen, Kirsten K.
   Dehlendorff, Christian
   Ronholt, Finn
   Johansen, Julia S.
   Nielsen, Dorte L.
TI Age-dependent differences in first-line chemotherapy in patients with
   metastatic colorectal cancer: the DISCO study
SO ACTA ONCOLOGICA
LA English
DT Article
ID III COLON-CANCER; ELDERLY-PATIENTS; OLDER PATIENTS;
   INTERNATIONAL-SOCIETY; ADJUVANT THERAPY; CLINICAL-TRIALS; POOLED
   ANALYSIS; OPEN-LABEL; STAGE-II; SURVIVAL
AB Objectives: First-line chemotherapy for metastatic colorectal cancer (mCRC) is effective and feasible in selected older patients. We investigated age-dependent differences in treatment and outcomes in patients with mCRC in clinical practice. Material and methods: A retrospective study of 654 patients with mCRC referred to first-line chemotherapy in 2008-2014. Patients were divided into two age groups: 50-69 and >= 70 (older patients). Binary outcomes were analyzed by logistic regression. Progression-free survival (PFS) and overall survival (OS) were analyzed by Cox proportional hazards regression, CRC-specific and other-cause mortality with Fine and Gray proportional hazard model for the sub-distribution of a competing risk. Results: After adjusting for performance status (PS) and comorbidity, older patients were more likely to receive monotherapy (adjusted odds ratio (aOR) = 9.00, 95% confidence interval (CI) 4.52-17.91), lower doses, and no additional targeted therapy (aOR = 1.89, 95% CI 1.28-2.78) than younger patients. Yet, older patients experienced more toxicity and hospitalizations (aOR = 1.53, 95% CI 1.08-2.17). Among those treated, older patients had shorter PFS (hazard ratio (HR) = 1.32, 95% CI 1.11-1.57), but after adjusting for PS and comorbidity, PFS was similar. No significant difference was found in CRC mortality (HR = 1.15, 95% CI 0.95-1.40) between age groups. Poor PS was associated with shorter OS and PFS and higher CRC mortality. Conclusions: In the DISCO study, older patients with mCRC received less aggressive first-line chemotherapy. Yet, they experienced more toxicity. Younger and older patients had similar CRC mortality. Shorter PFS and higher CRC mortality were observed in patients with poor PS.
C1 [Lund, Cecilia M.; Ronholt, Finn; Johansen, Julia S.] Copenhagen Univ Hosp, Herlev & Gentofte Hosp, Herlev, Denmark.
   [Lund, Cecilia M.; Vistisen, Kirsten K.; Johansen, Julia S.; Nielsen, Dorte L.] Copenhagen Univ Hosp, Herlev & Gentofte Hosp, Dept Oncol, Herlev, Denmark.
   [Dehlendorff, Christian] Danish Canc Soc, Danish Canc Soc Res Ctr, Dept Stat & Pharmacoepidemiol, Copenhagen, Denmark.
   [Johansen, Julia S.; Nielsen, Dorte L.] Univ Copenhagen, Fac Hlth & Med Sci, Dept Clin Med, Copenhagen, Denmark.
C3 University of Copenhagen; University of Copenhagen; Danish Cancer
   Society; University of Copenhagen
RP Lund, CM (corresponding author), Herlev & Gentofte Hosp, Dept Med, O106,Herlev Ringvej 75, DK-2730 Herlev, Denmark.
EM Cecilia.margareta.lund.01@regionh.dk
RI Lund, Cecilia/GVT-9357-2022; Dehlendorff, Christian/AAG-9421-2019
OI Dehlendorff, Christian/0000-0001-6161-4565; Nielsen, Dorte
   Lisbet/0000-0002-8766-8729; Lund, Cecilia/0000-0002-9894-029X
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NR 36
TC 20
Z9 20
U1 0
U2 2
PU Medical Journal Sweden AB
PI Uppsala
PA Kungsngsvgen 27St, Uppsala, SWEDEN
SN 0284-186X
EI 1651-226X
J9 ACTA ONCOL
JI Acta Oncol.
PD NOV 2
PY 2018
VL 57
IS 11
BP 1445
EP 1454
DI 10.1080/0284186X.2018.1531299
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HC2ER
UT WOS:000451615600004
PM 30375911
OA Bronze
DA 2025-01-04
ER

PT J
AU Azad, NS
   Gray, RJ
   Overman, MJ
   Schoenfeld, JD
   Mitchell, EP
   Zwiebel, JA
   Sharon, E
   Streicher, H
   Li, SL
   McShane, LM
   Rubinstein, L
   Patton, DR
   Williams, PM
   Coffey, B
   Hamilton, SR
   Bahary, N
   Suga, JM
   Hatoum, H
   Abrams, JS
   Conley, BA
   Arteaga, CL
   Harris, L
   O'Dwyer, PJ
   Chen, AP
   Flaherty, KT
AF Azad, Nilofer S.
   Gray, Robert J.
   Overman, Michael J.
   Schoenfeld, Jonathan D.
   Mitchell, Edith P.
   Zwiebel, James A.
   Sharon, Elad
   Streicher, Howard
   Li, Shuli
   McShane, Lisa M.
   Rubinstein, Larry
   Patton, David R.
   Williams, P. Mickey
   Coffey, Brent
   Hamilton, Stanley R.
   Bahary, Nathan
   Suga, J. Marie
   Hatoum, Hassan
   Abrams, Jeffrey S.
   Conley, Barbara A.
   Arteaga, Carlos L.
   Harris, Lyndsay
   O'Dwyer, Peter J.
   Chen, Alice P.
   Flaherty, Keith T.
TI Nivolumab Is Effective in Mismatch Repair-Deficient Noncolorectal
   Cancers: Results From Arm Z1D-A Subprotocol of the NCI-MATCH (EAY131)
   Study
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID MICROSATELLITE INSTABILITY STATUS; TUMOR MUTATIONAL BURDEN; SOLID
   TUMORS; IMMUNOHISTOCHEMISTRY; VALIDATION; CRITERIA; UTILITY; RISK
AB PURPOSE The National Cancer Institute Molecular Analysis for Therapy Choice (NCI-MATCH) trial, the largest national precision oncology study to date (> 1,100 sites) of patients with relapsed or refractory malignancies, assigned patients to targeted therapy in parallel phase II studies based on tumor molecular alterations. The anti-programmed death receptor 1 inhibitor nivolumab previously showed activity in mismatch repair (MMR)-deficient colon cancer. We hypothesized that nivolumab would have activity in patients with MMR-deficient, noncolorectal tumors.
   PATIENTS AND METHODS Eligible patients with relapsed or refractory tumors, good end-organ function, and Eastern Cooperative Oncology Group performance status of <= 1 underwent tumor biopsy for centralized screening of molecular alterations. MMR deficiency was defined by complete loss of nuclear expression of MLH1 or MSH2 MMR gene products by immunohistochemistry (IHC). Patients with MMR-deficient colorectal cancer were excluded. Nivolumab, 3 mg/kg every 2 weeks (28-day cycles) and 480 mg every 4 weeks after cycle 4, was administered intravenously. Disease reassessment was performed every 2 cycles. The primary end point was RECIST 1.1 objective response rate (ORR).
   RESULTS Two percent of 4,902 screened patients had an MMR-deficient cancer by IHC. Forty-two evaluable patients were enrolled, with a median age of 60 years and a median of 3 prior therapies. The most common histologies were endometrioid endometrial adenocarcinoma (n = 13), prostate adenocarcinoma (n = 5), and uterine carcinosarcoma (n = 4). ORR was 36% (15 of 42 patients). An additional 21% of patients had stable disease. The estimated 6-, 12-, and 18-month progression-free survival rates were 51.3% (90% CI, 38.2% to 64.5%), 46.2% (90% CI, 33.1% to 59.3%), and 31.4% (90% CI, 18.7% to 44.2%), respectively. Median overall survival was 17.3 months. Toxicity was predominantly low grade.
   CONCLUSION A variety of refractory cancers (2.0% of those screened) had MMR deficiency as defined in NCI-MATCH. Nivolumab has promising activity in MMR-deficient noncolorectal cancers of a wide variety of histopathologic types. (C) 2019 by American Society of Clinical Oncology
C1 [Azad, Nilofer S.] Johns Hopkins Univ, Baltimore, MD USA.
   [Gray, Robert J.; Li, Shuli] Dana Farber Canc Inst, Boston, MA 02115 USA.
   [Overman, Michael J.; Hamilton, Stanley R.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
   [Schoenfeld, Jonathan D.] Brigham & Womens Canc Ctr, Boston, MA USA.
   [Mitchell, Edith P.] Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
   [Zwiebel, James A.; Sharon, Elad; Streicher, Howard; McShane, Lisa M.; Rubinstein, Larry; Patton, David R.; Abrams, Jeffrey S.; Conley, Barbara A.; Harris, Lyndsay; Chen, Alice P.] NCI, Bethesda, MD 20892 USA.
   [Williams, P. Mickey; Coffey, Brent] Frederick Natl Lab Canc Res, Frederick, MD USA.
   [Bahary, Nathan] Univ Pittsburgh, Pittsburgh, PA USA.
   [Suga, J. Marie] Kaiser Permanente Vallejo Med Ctr, San Diego, CA USA.
   [Hatoum, Hassan] Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK USA.
   [Arteaga, Carlos L.] Univ Texas Southwestern Med Ctr Dallas, Dallas, TX 75390 USA.
   [O'Dwyer, Peter J.] Univ Penn, Philadelphia, PA 19104 USA.
   [Flaherty, Keith T.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
C3 Johns Hopkins University; Harvard University; Dana-Farber Cancer
   Institute; University of Texas System; UTMD Anderson Cancer Center;
   Harvard University; Brigham & Women's Hospital; Jefferson University;
   National Institutes of Health (NIH) - USA; NIH National Cancer Institute
   (NCI); National Institutes of Health (NIH) - USA; NIH National Cancer
   Institute (NCI); Frederick National Laboratory for Cancer Research;
   Pennsylvania Commonwealth System of Higher Education (PCSHE); University
   of Pittsburgh; University of Oklahoma System; University of Oklahoma
   Health Sciences Center; University of Texas System; University of Texas
   Southwestern Medical Center Dallas; University of Pennsylvania; Harvard
   University; Massachusetts General Hospital
RP Azad, NS (corresponding author), Johns Hopkins Med Sidney Kimmel Comprehens Canc C, 1650 Orleans St,Room 4M10, Baltimore, MD 20815 USA.
EM nilo@jhmi.edu
RI McShane, Lisa/GXM-8870-2022; Chen, Alice/AAG-9400-2020; gray,
   robert/HJB-2567-2022; Hatoum, hassan/KVB-6841-2024
OI Patton, David R/0000-0003-3855-0166; Rubinstein,
   Lawrence/0000-0002-9720-9737
FU National Cancer Institute of the National Institutes of Health
   [CA180820, CA180794, CA180802, CA180858, CA180867, CA180844, CA180798,
   CA189821, CA180868, CA180870]
FX Supported by the National Cancer Institute of the National Institutes of
   Health by Grants No. CA180820, CA180794, CA180802, CA180858, CA180867,
   CA180844, CA180798, CA189821, CA180868, and CA180870.
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NR 30
TC 113
Z9 130
U1 1
U2 11
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
EI 1527-7755
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD JAN 20
PY 2020
VL 38
IS 3
BP 214
EP +
DI 10.1200/JCO.19.00818
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KD9QY
UT WOS:000508197300006
PM 31765263
OA Green Published
DA 2025-01-04
ER

PT J
AU Bueno, MLP
   Saad, STO
   Roversi, FM
AF Bueno, Maura Lima Pereira
   Saad, Sara Teresinha Olalla
   Roversi, Fernanda Marconi
TI WNT5A in tumor development and progression: A comprehensive review
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE WNT5A; Tumor suppressor; Oncogene; Tumor microenvironment; Prognostic
   factor; Target therapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; POTENTIAL THERAPEUTIC TARGET; CANCER
   CELL-MIGRATION; SIGNALING PATHWAY; COLON-CANCER; PANCREATIC-CANCER;
   PROMOTER METHYLATION; CARCINOMA-CELLS; STEM-CELLS; LOW-GRADE
AB The investigation of tumor microenvironment (TME) is essential to better characterize the complex cellular crosstalk and to identify important immunological phenotypes and biomarkers. The niche is a crucial contributor to neoplasm initiation, maintenance and progression. Therefore, a deeper analysis of tumor surroundings could improve cancer diagnosis, prognosis and assertive treatment. Thus, the WNT family exerts a critical action in tumorigenesis of different types of neoplasms due to dysregulations in the TME. WNT5A, an evolutionary WNT member, is involved in several cellular and physiopathological processes, in addition to tissue homeostasis. The WNT5A protein exerts paradoxical effects while acting as both an oncogene or tumor suppressor by regulating several non-canonical signaling pathways, and consequently interfering in cell growth, cytoskeletal remodeling, migration and invasiveness. This review focuses on a thorough characterization of the role of WNT5A in neoplastic transformation and progression, which may help to understand the prognostic potentiality of WNT5A and its features as a therapeutic target in several cancers. Additionally, we herein summarized novel findings on the mechanisms by which WNT5A might favor tumorigenesis or suppression of cancer progression and discussed the recently developed treatment strategies using WNT5A as a protagonist.
C1 [Bueno, Maura Lima Pereira; Saad, Sara Teresinha Olalla; Roversi, Fernanda Marconi] Univ Estadual Campinas, Hematol & Transfus Med Ctr, UNICAMP, Hemoctr, Campinas, SP, Brazil.
   [Bueno, Maura Lima Pereira; Roversi, Fernanda Marconi] Univ Estadual Campinas, Hematol & Transfus Med Ctr, Rua Carlos Chagas, 480, Barao Geraldo, BR-13083878 Campinas, SP, Brazil.
C3 Universidade Estadual de Campinas; Universidade Estadual de Campinas
RP Bueno, MLP; Roversi, FM (corresponding author), Univ Estadual Campinas, Hematol & Transfus Med Ctr, Rua Carlos Chagas, 480, Barao Geraldo, BR-13083878 Campinas, SP, Brazil.
EM mauralimabueno@gmail.com; fermr@unicamp.br
RI Saad, Sara/IXN-6799-2023; Roversi, Fernanda/M-7819-2018
OI Bueno, Maura/0000-0003-2979-5145
FU FAPESP [2017/21801-2, 2019/25247-5, 2021/05320-0]; CNPq [303405/2018-0]
FX The authors would like to thank Raquel S Foglio (Hematology and
   Hemotherapy Center, University of Campinas, Sao Paulo, Brazil) for the
   English revision. The authors thank FAPESP (Grants 2017/21801-2,
   2019/25247-5 and 2021/05320-0) and CNPq (Grants 303405/2018-0.
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   Zoico E, 2016, ONCOTARGET, V7, P20223, DOI 10.18632/oncotarget.7936
NR 100
TC 17
Z9 18
U1 0
U2 13
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD NOV
PY 2022
VL 155
AR 113599
DI 10.1016/j.biopha.2022.113599
EA OCT 2022
PG 18
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 6D5XU
UT WOS:000882763900012
PM 36089446
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Sandberg, TP
   Sweere, I
   van Pelt, GW
   Putter, H
   Vermeulen, L
   Kuppen, PJ
   Tollenaar, RAEM
   Mesker, WE
AF Sandberg, Tessa P.
   Sweere, Iris
   van Pelt, Gabi W.
   Putter, Hein
   Vermeulen, Louis
   Kuppen, Peter J.
   Tollenaar, Rob A. E. M.
   Mesker, Wilma E.
TI Prognostic value of low CDX2 expression in colorectal cancers with a
   high stromal content - a short report
SO CELLULAR ONCOLOGY
LA English
DT Article
DE Colorectal cancer; CDX2 expression; Tumour-stroma ratio; Prognosis
ID COLON-CANCER; DOWN-REGULATION; TUMOR-STROMA; STAGE-II; CARCINOMA;
   SURVIVAL; SUBTYPES; RATIO
AB PurposeLack of expression of the intestinal transcription factor CDX2 in colorectal cancer (CRC) identifies patients with a poor prognosis. This biomarker has previously been suggested to be prognostic in CRCs with a high stromal content based on mRNA expression data. We investigated the prognostic value of CDX2 expression in microsatellite stable CRC stratified by stromal content using microscopy-based techniques.Methods and resultsThe study included a cohort of 236 patients with stage I-IV CRC. We assessed by microscopy the tumour-stroma ratio (TSR) and the immunohistochemical CDX2 intensity. We found that patients of the stroma-high group had a worse prognosis compared to those of the stroma-low group [disease-free survival in a multivariate analysis (DFSmultivariate) HR 1.52 (95% CI 1.05-2.21)]. In our cohort, low CDX2 expression (14.6%) showed prognostic value for DFSmultivariate [HR 1.93 (95% CI 1.16-3.23)]. Interestingly, when stratifying the cohort by TSR, no prognostic difference was observed related to CDX2 expression in stroma-low tumours. However, CDX2 expression was found to be prognostic within the stroma-high group [DFSmultivariate HR 3.02 (95% CI 1.49-6.13)]. The p value for interaction between TSR and CDX2 status was borderline significant in DFS (p=0.071).ConclusionsThe present study confirms a poor outcome of patients with stroma-high tumours. Low CDX2 expression in tumours with a high stromal content identified patients with a particularly poor prognosis. The present study did not reveal a clear difference in TSR associated with CDX2 status and survival. This method, solely based on microscopy, identifies patients who have a high risk of relapse and a poor outcome, and who may benefit from targeted therapy.
C1 [Sandberg, Tessa P.; van Pelt, Gabi W.; Kuppen, Peter J.; Tollenaar, Rob A. E. M.; Mesker, Wilma E.] Leiden Univ, Med Ctr, Dept Surg, Albinusdreef 2, NL-2333 ZA Leiden, Netherlands.
   [Sandberg, Tessa P.; Sweere, Iris] Leiden Univ, Med Ctr, Dept Pathol, Leiden, Netherlands.
   [Putter, Hein] Leiden Univ, Med Ctr, Dept Med Stat, Leiden, Netherlands.
   [Vermeulen, Louis] Acad Med Ctr, Ctr Expt & Mol Med CEMM, Lab Expt Oncol & Radiobiol LEXOR, Amsterdam, Netherlands.
   [Vermeulen, Louis] Canc Ctr Amsterdam, Amsterdam, Netherlands.
C3 Leiden University - Excl LUMC; Leiden University; Leiden University
   Medical Center (LUMC); Leiden University; Leiden University Medical
   Center (LUMC); Leiden University - Excl LUMC; Leiden University; Leiden
   University Medical Center (LUMC); Leiden University - Excl LUMC;
   University of Amsterdam; Academic Medical Center Amsterdam; University
   of Amsterdam; Vrije Universiteit Amsterdam
RP Sandberg, TP (corresponding author), Leiden Univ, Med Ctr, Dept Surg, Albinusdreef 2, NL-2333 ZA Leiden, Netherlands.; Sandberg, TP (corresponding author), Leiden Univ, Med Ctr, Dept Pathol, Leiden, Netherlands.
EM t.p.sandberg@lumc.nl
RI Vermeulen, Louis/B-7488-2008; Putter, Hein/C-2244-2018
OI Sandberg, Tessa/0000-0001-5037-798X; Putter, Hein/0000-0001-5395-1422
FU LUMC through the BWplus grant
FX The authors thank the LUMC for financial support of T.P.S through the
   BWplus grant.
CR Baba Y, 2009, CLIN CANCER RES, V15, P4665, DOI 10.1158/1078-0432.CCR-09-0401
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   Brabletz T, 2004, CANCER RES, V64, P6973, DOI 10.1158/0008-5472.CAN-04-1132
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   de Kruijf EM, 2011, BREAST CANCER RES TR, V125, P687, DOI 10.1007/s10549-010-0855-6
   Goossens-Beumer IJ, 2014, BRIT J CANCER, V110, P2935, DOI 10.1038/bjc.2014.226
   Huijbers A, 2013, ANN ONCOL, V24, P179, DOI 10.1093/annonc/mds246
   Lugli A, 2008, MODERN PATHOL, V21, P1403, DOI 10.1038/modpathol.2008.117
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   Mesker WE, 2007, CELL ONCOL, V29, P387
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NR 18
TC 3
Z9 3
U1 0
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 2211-3428
EI 2211-3436
J9 CELL ONCOL
JI Cell. Oncol.
PD JUN
PY 2019
VL 42
IS 3
BP 397
EP 403
DI 10.1007/s13402-019-00436-0
PG 7
WC Oncology; Cell Biology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology; Pathology
GA IA1XB
UT WOS:000469354700012
PM 30847807
OA hybrid
DA 2025-01-04
ER

PT J
AU Phelip, JM
   Tougeron, D
   Léonard, D
   Benhaim, L
   Desolneux, G
   Dupré, A
   Michel, P
   Penna, C
   Tournigand, C
   Louvet, C
   Christou, N
   Chevallier, P
   Dohan, A
   Rousseaux, B
   Bouché, O
AF Phelip, Jean Marc
   Tougeron, David
   Leonard, David
   Benhaim, Leonor
   Desolneux, Gregoire
   Dupre, Aurelien
   Michel, Pierre
   Penna, Christophe
   Tournigand, Christophe
   Louvet, Christophe
   Christou, Nikki
   Chevallier, Patrick
   Dohan, Anthony
   Rousseaux, Benoist
   Bouche, Olivier
TI Metastatic colorectal cancer (mCRC): French intergroup clinical practice
   guidelines for diagnosis, treatments and follow-up (SNFGE, FFCD, GERCOR,
   UNICANCER, SFCD, SFED, SFRO, SFR)
SO DIGESTIVE AND LIVER DISEASE
LA English
DT Review
DE Chemotherapy; Colorectal cancer; French clinical practice guidelines;
   Metastatic hepatic metastases surgery; Targeted therapy; Therapeutic
   strategy
ID PHASE-III TRIAL; OXALIPLATIN-BASED CHEMOTHERAPY; BEVACIZUMAB PLUS
   CAPECITABINE; RESECTABLE LIVER METASTASES; 1ST-LINE TREATMENT;
   COMBINATION CHEMOTHERAPY; HEPATIC METASTASES; SURVIVAL BENEFIT;
   RADIOFREQUENCY ABLATION; INFUSIONAL FLUOROURACIL
AB Introduction: This document is a summary of the French intergroup guidelines regarding the management of metastatic colorectal cancer (mCRC) published in January 2019, and available on the French Society of Gastroenterology website (SNFGE) (www.tncd.org).
   Methods: This collaborative work was realized by all French medical and surgical societies involved in the management of mCRC. Recommendations are graded in three categories (A, B and C), according to the level of evidence found in the literature, up until December 2018.
   Results: The management of metastatic colorectal cancer has become complex because of increasing available medical, radiological and surgical treatments alone or in combination. The therapeutic strategy should be defined before the first-line treatment, mostly depending on the presentation of the disease (resectability of the metastases, symptomatic and/or threatening disease), of the patient's condition (ECOG PS, comorbidities), and tumor biology (RAS, BRAF, MSI). The sequence of targeted therapies also seems to have an impact on the outcome (angiogenesis inhibition beyond progression). Surgical resection of metastases was the only curative intent treatment to date, joined recently by percutaneous tumor ablation tools (radiofrequency, microwave). Localized therapies such as hepatic intra-arterial infusion, radioembolization and hyperthermic intraperitoneal chemotherapy, also have seen their indications specified (liver-dominant disease and resectable peritoneal carcinomatosis). New treatments have been developed in heavily pretreated patients, increasing overall survival and preserving quality of life (regorafenib and trifluridine/tipiracil). Finally, immune checkpoint inhibitors have demonstrated high efficacy in MSI mCRC.
   Conclusion: French guidelines for mCRC management are put together to help offer the best personalized therapeutic strategy in daily clinical practice, as the mCRC therapeutic landscape is complexifying. These recommendations are permanently being reviewed and updated. Each individual case must be discussed within a multidisciplinary team (MDT). (C) 2019 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
C1 [Phelip, Jean Marc] Univ Hosp St Etienne, Dept Gastroenterol & Digest Oncol, St Etienne, France.
   [Tougeron, David] Univ Hosp Poitiers, Dept Gastroenterol, Poitiers, France.
   [Leonard, David] Clin Loire, Dept Surg Oncol, Saumur, France.
   [Benhaim, Leonor] UNICANCER, Dept Surg Oncol, GustaveRoussy Canc Ctr, Villejuif, France.
   [Desolneux, Gregoire] UNICANCER, Bergonie Inst, Dept Surg Oncol, Bordeaux, France.
   [Dupre, Aurelien] UNICANCER, Dept Surg Oncol, Leon Berard Canc Ctr, Lyon, France.
   [Dupre, Aurelien; Michel, Pierre] Univ Hosp Rouen, Dept Gastroenterol & Digest Oncol, Rouen, France.
   [Penna, Christophe] Bicetres Hosp, AP HP, Dept Surg Oncol, Paris, France.
   [Tournigand, Christophe] Henri Mondor Univ Hosp, AP HP, Dept Gastroenterol & Digest Oncol, Creteil, France.
   [Louvet, Christophe] IMM, Dept Med Oncol, Paris, France.
   [Christou, Nikki] Univ Hosp Limoges, Dept Digest Endocrine & Gen Surg, Limoges, France.
   [Chevallier, Patrick] Archet Univ Hosp, Dept Radiol, Nice, France.
   [Dohan, Anthony] Cochin Unvers Hosp, AP HP, Dept Abdominal & Intervent Radiol, Paris, France.
   [Rousseaux, Benoist] Henri Mondor Hosp, AP HP, Dept Med Oncol, Creteil, France.
   [Rousseaux, Benoist] Mem Sloan Kettering Canc Ctr, Solid Tumor Dept, 1275 York Ave, New York, NY 10021 USA.
   [Bouche, Olivier] Univ Hosp Reims, Dept Digest Oncol, Reims, France.
C3 CHU de St Etienne; CHU Poitiers; Universite de Poitiers; UNICANCER;
   UNICANCER; Institut Bergonie; UNICANCER; Centre Leon Berard; Universite
   de Rouen Normandie; CHU de Rouen; Assistance Publique Hopitaux Paris
   (APHP); Hopital Universitaire Bicetre - APHP; Assistance Publique
   Hopitaux Paris (APHP); Universite Paris-Est-Creteil-Val-de-Marne (UPEC);
   Hopital Universitaire Henri-Mondor - APHP; Universite Paris Cite;
   Institute Mutualiste Montsouris; CHU Limoges; CHU Nice; Assistance
   Publique Hopitaux Paris (APHP); Universite Paris Cite; Hopital
   Universitaire Cochin - APHP; Assistance Publique Hopitaux Paris (APHP);
   Universite Paris-Est-Creteil-Val-de-Marne (UPEC); Hopital Universitaire
   Henri-Mondor - APHP; Memorial Sloan Kettering Cancer Center; Universite
   de Reims Champagne-Ardenne; CHU de Reims
RP Phelip, JM (corresponding author), Univ Jean Monnet, Univ Hosp St Etienne, Dept Gastroenterol & Digest Oncol, F-42055 St Etienne, France.
EM j.marc.phelip@chu-st-etienne.fr
RI chevallier, patrick/AAF-2427-2021; CHRISTOU, Niki/Y-7427-2019; Rousseau,
   Benoit/K-5651-2017; tougeron, david/ABF-3217-2020; dupré,
   aurélien/J-4027-2019
OI CHRISTOU, Niki/0000-0003-2125-0503; Rousseau,
   Benoit/0000-0002-1594-4827; dupre, aurelien/0000-0002-5216-538X;
   tougeron, david/0000-0002-8065-9635
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NR 77
TC 83
Z9 84
U1 0
U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1590-8658
EI 1878-3562
J9 DIGEST LIVER DIS
JI Dig. Liver Dis.
PD OCT
PY 2019
VL 51
IS 10
BP 1357
EP 1363
DI 10.1016/j.dld.2019.05.035
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA JA1RI
UT WOS:000487594200001
PM 31320305
OA Green Published
DA 2025-01-04
ER

PT J
AU Nemecek, R
   Berkovcova, J
   Radova, L
   Kazda, T
   Mlcochova, J
   Vychytilova-Faltejskova, P
   Slaby, O
   Svoboda, M
AF Nemecek, Radim
   Berkovcova, Jitka
   Radova, Lenka
   Kazda, Tomas
   Mlcochova, Jitka
   Vychytilova-Faltejskova, Petra
   Slaby, Ondrej
   Svoboda, Marek
TI Mutational analysis of primary and metastatic colorectal cancer samples
   underlying the resistance to cetuximab-based therapy
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE colorectal cancer; cetuximab; resistance to anti-EGFR therapy;
   next-generation sequencing; FBXW7; KRAS
ID GROWTH-FACTOR RECEPTOR; WILD-TYPE KRAS; MONOCLONAL-ANTIBODIES; RAS
   MUTATIONS; EGFR; BENEFIT; PANITUMUMAB; BRAF; METAANALYSIS; BEVACIZUMAB
AB Purpose: Although several molecular markers predicting resistance to cetuximab-or panitumumab-based therapy of metastatic colorectal cancer were described, mutations in RAS proto-oncogenes remain the only predictors being used in daily clinical practice. However, 35%-45% of wild-type RAS patients still do not respond to this anti-epidermal growth factor receptor (anti-EGFR) monoclonal antibody-based therapy, and therefore the definition of other predictors forms an important clinical need. The aim of the present retrospective single-institutional study was to evaluate potential genes responsible for resistance to anti-EGFR therapy in relation to mutational analysis of primary versus metastatic lesions.
   Patients and methods: Twenty-four paired primary and corresponding metastatic tissue samples from eight nonresponding and four responding metastatic colorectal cancer patients treated with cetuximab-based therapy were sequenced using a next-generation sequencing panel of 26 genes involved in EGFR signaling pathway and colorectal carcinogenesis.
   Results: Mutational status of primary tumors and metastatic lesions was highly concordant in TP53, APC, CTNNB1, KRAS, PIK3CA, PTEN, and FBXW7 genes. Metastatic samples harbor significantly more mutations than primary tumors. Potentially negative predictive value of FBXW7 mutations in relationship to anti-EGFR treatment outcomes was confirmed. Finally, new occurrences of activating KRAS mutations were identified in a group of patients initially determined as wild-type RAS by routinely used qPCR-based RAS mutational tests. All newly detected activating KRAS mutations most likely led to cetuximab treatment failure.
   Conclusion: The results of the present study suggest a need of careful consideration of previously published results of anti-EGFR-targeted therapy with regard to potentially inaccurate diagnostic tools used in the past. Based on our findings, we recommend more extensive use of next-generation sequencing testing in daily clinical practice, as it brings a significant added value in terms of validity of the diagnostic procedure.
C1 [Nemecek, Radim; Vychytilova-Faltejskova, Petra; Slaby, Ondrej; Svoboda, Marek] Masaryk Univ, Masaryk Mem Canc Inst, Dept Comprehens Canc Care, Zluty Kopec 7, Brno 65653, Czech Republic.
   [Berkovcova, Jitka] Masaryk Mem Canc Inst, Dept Oncol & Expt Pathol, Brno, Czech Republic.
   [Radova, Lenka; Mlcochova, Jitka; Vychytilova-Faltejskova, Petra; Slaby, Ondrej] Masaryk Univ, Cent European Inst Technol, Brno, Czech Republic.
   [Kazda, Tomas] Masaryk Univ, Masaryk Mem Canc Inst, Dept Radiat Oncol, Brno, Czech Republic.
C3 Masaryk University Brno; Masaryk Memorial Cancer Institute; Masaryk
   Memorial Cancer Institute; Masaryk University Brno; Masaryk University
   Brno; Masaryk Memorial Cancer Institute
RP Svoboda, M (corresponding author), Masaryk Univ, Masaryk Mem Canc Inst, Dept Comprehens Canc Care, Zluty Kopec 7, Brno 65653, Czech Republic.
EM msvoboda@mou.cz
RI Svoboda, Marek/GNW-6742-2022; Slaby, Ondrej/E-1082-2012; Radova,
   Lenka/I-1182-2014; Kazda, Tomas/AAQ-1740-2020; Vychytilova,
   Petra/E-2805-2012
OI Vychytilova, Petra/0000-0003-0063-2078; Svoboda,
   Marek/0000-0003-4455-0461; Radova, Lenka/0000-0001-8103-148X
FU MH CZ - DRO (MMCI) [00209805]; Czech Ministry of Health [IGA NT/13860 -
   4/2012]; project CEITEC - Ministry of Education, Youth and Sports of the
   Czech Republic [LQ1601]
FX This work was supported by MH CZ - DRO (MMCI, 00209805), grant IGA
   NT/13860 - 4/2012 of the Czech Ministry of Health, and by the project
   CEITEC 2020 (LQ1601) supported by the Ministry of Education, Youth and
   Sports of the Czech Republic. We are grateful to Pavel Fabian,
   participating investigator, for assistance with sample preparation.
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NR 41
TC 13
Z9 14
U1 0
U2 5
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6930
J9 ONCOTARGETS THER
JI OncoTargets Ther.
PY 2016
VL 9
BP 4695
EP 4703
DI 10.2147/OTT.S102891
PG 9
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA DS2AS
UT WOS:000380519700001
PM 27555788
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Ebrahimzadeh, S
   Ahangari, H
   Soleimanian, A
   Hosseini, K
   Ebrahimi, V
   Ghasemnejad, T
   Soofiyani, SR
   Tarhriz, V
   Eyvazi, S
AF Ebrahimzadeh, Sara
   Ahangari, Hossein
   Soleimanian, Alireza
   Hosseini, Kamran
   Ebrahimi, Vida
   Ghasemnejad, Tohid
   Soofiyani, Saiedeh Razi
   Tarhriz, Vahideh
   Eyvazi, Shirin
TI Colorectal cancer treatment using bacteria: focus on molecular
   mechanisms
SO BMC MICROBIOLOGY
LA English
DT Review
DE Colorectal cancer; Biotherapeutical toxins; Bacteriocins; Bacterial
   peptides
ID MICROBIOTA TRANSPLANTATION; SALMONELLA-TYPHIMURIUM; FECAL MICROBIOTA;
   TUMOR; INFECTION; ANTIBACTERIAL; DELIVERY; ANTIGEN; AZURIN; CELLS
AB Background Colorectal cancer which is related to genetic and environmental risk factors, is among the most prevalent life-threatening cancers. Although several pathogenic bacteria are associated with colorectal cancer etiology, some others are considered as highly selective therapeutic agents in colorectal cancer. Nowadays, researchers are concentrating on bacteriotherapy as a novel effective therapeutic method with fewer or no side effects to pay the way of cancer therapy. The introduction of advanced and successful strategies in bacterial colorectal cancer therapy could be useful to identify new promising treatment strategies for colorectal cancer patients. Main text In this article, we scrutinized the beneficial effects of bacterial therapy in colorectal cancer amelioration focusing on different strategies to use a complete bacterial cell or bacterial-related biotherapeutics including toxins, bacteriocins, and other bacterial peptides and proteins. In addition, the utilization of bacteria as carriers for gene delivery or other known active ingredients in colorectal cancer therapy are reviewed and ultimately, the molecular mechanisms targeted by the bacterial treatment in the colorectal cancer tumors are detailed. Conclusions Application of the bacterial instrument in cancer treatment is on its way through becoming a promising method of colorectal cancer targeted therapy with numerous successful studies and may someday be a practical strategy for cancer treatment, particularly colorectal cancer.
C1 [Ebrahimzadeh, Sara] Tabriz Univ Med Sci, Dept Pharmaceut Biotechnol, Fac Pharm, Tabriz, Iran.
   [Ahangari, Hossein] Tabriz Univ Med Sci, Fac Nutr & Food Sci, Dept Food Sci & Technol, Tabriz, Iran.
   [Soleimanian, Alireza] Univ Tabriz, Dept Biol, Fac Nat Sci, Tabriz, Iran.
   [Hosseini, Kamran; Ghasemnejad, Tohid; Tarhriz, Vahideh] Tabriz Univ Med Sci, Biomed Inst, Mol Med Res Ctr, Tabriz, Iran.
   [Ebrahimi, Vida] Shahid Beheshti Univ Med Sci, Sch Pharm, Dept Pharmaceut Biotechnol, Tehran, Iran.
   [Soofiyani, Saiedeh Razi] Tabriz Univ Med Sci, Clin Res Dev Unit, Sina Educ Res & Treatment Ctr, Tabriz, Iran.
   [Eyvazi, Shirin] Islamic Azad Univ, Tabriz Branch, Dept Biol, Tabriz, Iran.
   [Eyvazi, Shirin] Islamic Azad Univ, Tabriz Branch, Biotechnol Res Ctr, Tabriz, Iran.
C3 Tabriz University of Medical Science; Tabriz University of Medical
   Science; University of Tabriz; Tabriz University of Medical Science;
   Shahid Beheshti University Medical Sciences; Tabriz University of
   Medical Science; Islamic Azad University; Islamic Azad University
RP Tarhriz, V (corresponding author), Tabriz Univ Med Sci, Biomed Inst, Mol Med Res Ctr, Tabriz, Iran.; Eyvazi, S (corresponding author), Islamic Azad Univ, Tabriz Branch, Dept Biol, Tabriz, Iran.
EM t.tarhriz@yahoo.com; Shirin_Biotech@yahoo.com
RI Ghasemnejad, Tohid/AAD-6968-2021; Ebrahimi, Vida/JFJ-1495-2023; Eyvazi,
   Shirin/AAO-3828-2021; Soofiyani, Saiedeh/AAA-1029-2020
OI Tarhriz, Vahideh/0000-0002-3018-9313
FU Tabriz University of Medical Sciences of Iran [66901]
FX This work was supported by Tabriz University of Medical Sciences of Iran
   [Grant number 66901]. The funders had no role in study design, data
   collection and analysis, decision to publish, or preparation of the
   manuscript.
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NR 93
TC 24
Z9 25
U1 2
U2 46
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2180
J9 BMC MICROBIOL
JI BMC Microbiol.
PD JUL 19
PY 2021
VL 21
IS 1
AR 218
DI 10.1186/s12866-021-02274-3
PG 12
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA TM8RM
UT WOS:000675813100002
PM 34281519
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Overman, MJ
   Morris, V
   Kee, B
   Fogelman, D
   Xiao, L
   Eng, C
   Dasari, A
   Shroff, R
   Mazard, T
   Shaw, K
   Vilar, E
   Raghav, K
   Shureiqi, I
   Liang, L
   Mills, GB
   Wolff, RA
   Hamilton, S
   Meric-Bernstam, F
   Abbruzzese, J
   Morris, J
   Maru, D
   Kopetz, S
AF Overman, M. J.
   Morris, V.
   Kee, B.
   Fogelman, D.
   Xiao, L.
   Eng, C.
   Dasari, A.
   Shroff, R.
   Mazard, T.
   Shaw, K.
   Vilar, E.
   Raghav, K.
   Shureiqi, I.
   Liang, L.
   Mills, G. B.
   Wolff, R. A.
   Hamilton, S.
   Meric-Bernstam, F.
   Abbruzzese, J.
   Morris, J.
   Maru, D.
   Kopetz, S.
TI Utility of a molecular prescreening program in advanced colorectal
   cancer for enrollment on biomarker-selected clinical
   trials<SUP>aEuro</SUP>
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE prescreening; molecular; colorectal cancer; targeted; screening
ID TARGETED THERAPY; TRIAL; MULTICENTER; PATIENT
AB Background: Incorporation of multiple enrichment biomarkers into prospective clinical trials is an active area of investigation, but the factors that determine clinical trial enrollment following a molecular prescreening program have not been assessed.
   Patients with 5-fluorouracil-refractory metastatic colorectal cancer at the MD Anderson Cancer Center were offered screening in the Assessment of Targeted Therapies Against Colorectal Cancer (ATTACC) program to identify eligibility for companion phase I or II clinical trials with a therapy targeted to an aberration detected in the patient, based on testing by immunohistochemistry, targeted gene sequencing panels, and CpG island methylation phenotype assays.
   Between August 2010 and December 2013, 484 patients were enrolled, 458 (95%) had a biomarker result, and 157 (32%) were enrolled on a clinical trial (92 on biomarker-selected and 65 on nonbiomarker selected). Of the 458 patients with a biomarker result, enrollment on biomarker-selected clinical trials was ninefold higher for predefined ATTACC-companion clinical trials as opposed to nonpredefined biomarker-selected clinical trials, 17.9% versus 2%, P < 0.001. Factors that correlated positively with trial enrollment in multivariate analysis were higher performance status, older age, lack of standard of care therapy, established patient at MD Anderson, and the presence of an eligible biomarker for an ATTACC-companion study. Early molecular screening did result in a higher rate of patients with remaining standard of care therapy enrolling on ATTACC-companion clinical trials, 45.1%, in contrast to nonpredefined clinical trials, 22.7%; odds ratio 3.1, P = 0.002.
   Though early molecular prescreening for predefined clinical trials resulted in an increase rate of trial enrollment of nonrefractory patients, the majority of patients enrolled on clinical trials were refractory to standard of care therapy. Within molecular prescreening programs, tailoring screening for preidentified and open clinical trials, temporally linking screening to treatment and optimizing both patient and physician engagement are efforts likely to improve enrollment on biomarker-selected clinical trials.
   The study NCT number is NCT01196130.
C1 [Overman, M. J.; Morris, V.; Kee, B.; Fogelman, D.; Eng, C.; Dasari, A.; Shroff, R.; Mazard, T.; Vilar, E.; Raghav, K.; Shureiqi, I.; Wolff, R. A.; Kopetz, S.] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, 1515 Holcombe Blvd,Unit 426, Houston, TX 77030 USA.
   [Xiao, L.; Liang, L.; Morris, J.] Univ Texas MD Anderson Canc Ctr, Dept Biostat, Houston, TX 77030 USA.
   [Shaw, K.; Mills, G. B.; Meric-Bernstam, F.] Univ Texas MD Anderson Canc Ctr, Sheikh Khalifa Nahyan Ben Zayed Inst Personalized, Houston, TX 77030 USA.
   [Mills, G. B.] Univ Texas MD Anderson Canc Ctr, Dept Syst Biol, Houston, TX 77030 USA.
   [Hamilton, S.; Maru, D.] Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA.
   [Vilar, E.] Univ Texas MD Anderson Canc Ctr, Dept Clin Canc Prevent, Houston, TX 77030 USA.
   [Abbruzzese, J.] Duke Univ, Med Ctr, Dept Med, Div Med Oncol, Durham, NC 27706 USA.
   [Meric-Bernstam, F.] Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapeut, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; University of
   Texas System; UTMD Anderson Cancer Center; University of Texas System;
   UTMD Anderson Cancer Center; University of Texas System; UTMD Anderson
   Cancer Center; University of Texas System; UTMD Anderson Cancer Center;
   University of Texas System; UTMD Anderson Cancer Center; Duke
   University; University of Texas System; UTMD Anderson Cancer Center
RP Overman, MJ (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, 1515 Holcombe Blvd,Unit 426, Houston, TX 77030 USA.
EM moverman@mdanderson.org
RI Vilar, Eduardo/AAE-8127-2020; Shroff, Rachna/AAR-5802-2020; MAZARD,
   Thibault/ABH-6334-2020; Morris, Van/KIE-0809-2024; Kopetz,
   Scott/AAC-1387-2019; Mills, Gordon/L-5416-2014; Meric-Bernstam,
   Funda/JRZ-1866-2023; Shureiqi, imad/T-6214-2019
OI Shureiqi, Imad/0000-0003-2019-938X; Kopetz, Scott/0000-0001-9647-3416;
   Eng, Cathy/0000-0003-2335-0612; Vilar, Eduardo/0000-0001-6404-3761
FU Sheikh Khalifa Al Nahyan Ben Zayed Institute for Personalized Cancer
   Therapy; Cancer Prevention Research Institute of Texas; MD Anderson
   Cancer Center [P30 CA016672]
FX This work was supported in part by the Sheikh Khalifa Al Nahyan Ben
   Zayed Institute for Personalized Cancer Therapy, Cancer Prevention
   Research Institute of Texas, and the MD Anderson Cancer Center Support
   grant (P30 CA016672).
CR André F, 2014, LANCET ONCOL, V15, P267, DOI 10.1016/S1470-2045(13)70611-9
   Andre F, 2011, J CLIN ONCOL, V29, P1236, DOI 10.1200/JCO.2010.31.6877
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NR 11
TC 22
Z9 25
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
EI 1569-8041
J9 ANN ONCOL
JI Ann. Oncol.
PD JUN
PY 2016
VL 27
IS 6
BP 1068
EP 1074
DI 10.1093/annonc/mdw073
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DN9VD
UT WOS:000377427900016
PM 27045102
OA Bronze, Green Published
DA 2025-01-04
ER

PT J
AU Yamashiro, Y
   Saito, T
   Hayashi, T
   Murakami, T
   Yanai, Y
   Tsuyama, S
   Suehara, Y
   Takamochi, K
   Yao, T
AF Yamashiro, Yuya
   Saito, Tsuyoshi
   Hayashi, Takuo
   Murakami, Takashi
   Yanai, Yuka
   Tsuyama, Sho
   Suehara, Yoshiyuki
   Takamochi, Kazuya
   Yao, Takashi
TI Molecular and clinicopathological features of colorectal adenocarcinoma
   with enteroblastic differentiation
SO HISTOPATHOLOGY
LA English
DT Article
DE adenocarcinoma with enteroblastic differentiation; alpha-fetoprotein;
   colorectal adenocarcinoma; glypican-3; next-generation sequencing;
   spalt-like transcription factor 4
ID CLEAR-CELL ADENOCARCINOMA; HER2 SCORING SYSTEM; MICROSATELLITE
   INSTABILITY; GASTRIC ADENOCARCINOMA; CANCER; CARCINOMA; PROGNOSIS;
   VARIANT; EXPRESSION; MUTATION
AB Background Colorectal adenocarcinoma with enteroblastic differentiation (CAED) is a rare subtype of colorectal malignancy with expression of enteroblastic markers (glypican 3, SALL4, AFP); however, the clinicopathological and epidemiological features are not fully elucidated. Aims The aims of this study were to elucidate and establish the molecular and clinicopathological characteristics of CAED. Materials and Methods In addition to three cases recently diagnosed as CAED, colorectal carcinoma (CRC) with expression of enteroblastic markers were selected by using immunohistochemistry (IHC) on tissue microarrays of 988 advanced CRC. We employed next-generation sequencing (NGS) and Sanger sequencing for the detection of genetic alterations. IHC for p53 and HER2, HER2-FISH and MSI status was also investigated. Survival analyses for clinicopathological parameters were performed using Kaplan-Meier methods. Results Thirty-nine cases (4.0%) were positive for at least one enteroblastic marker. Histological evaluation of the total of 42 cases revealed that 10 contained tumour cells with clear cytoplasm. Enteroblastic marker-positive cases had aggressive behaviour and poor prognosis. NGS revealedTP53as the most frequently mutated gene. The rate of HER2-positive cases and MSI-H cases was 9.5% (four of 42) and 12.2% (five of 41), respectively. Among these 42 cases, there were no molecular and clinicopathological differences according to the presence of tumour cells with clear cytoplasm. Conclusions Enteroblastic marker-positive CRC could be grouped together as CAED regardless of clear cell cytoplasm. Using this definition, the frequency of CAED is 4.0% and has a poorer prognosis than that for conventional CRCs. HER2 targeted therapy would be a meaningful treatment for CAED, and CAEDs contain both MSI-H and MSI-stable CRCs, although the MSS phenotype is dominant.
C1 [Yamashiro, Yuya; Saito, Tsuyoshi; Hayashi, Takuo; Yanai, Yuka; Tsuyama, Sho; Yao, Takashi] Juntendo Univ, Sch Med, Dept Human Pathol, Tokyo, Japan.
   [Saito, Tsuyoshi; Suehara, Yoshiyuki] Juntendo Univ, Intractable Dis Res Ctr, Grad Sch Med, Tokyo, Japan.
   [Murakami, Takashi] Juntendo Univ, Dept Gastroenterol, Sch Med, Tokyo, Japan.
   [Suehara, Yoshiyuki] Juntendo Univ, Dept Orthopaed Surg, Sch Med, Tokyo, Japan.
   [Takamochi, Kazuya] Juntendo Univ, Dept Gen Thorac Surg, Sch Med, Tokyo, Japan.
C3 Juntendo University; Juntendo University; Juntendo University; Juntendo
   University; Juntendo University
RP Saito, T (corresponding author), Juntendo Univ, Sch Med, Dept Human Pathol, Bunkyo Ku, 2-1-1 Hongo, Tokyo, Japan.
EM tysaitou@juntendo.ac.jp
RI Murakami, Takashi/AAS-9039-2020
OI Saito, Tsuyoshi/0000-0001-9690-8440; HAYASHI, TAKUO/0000-0002-8544-9370
FU Leading Advanced Projects for Medical Innovation (LEAP) from Japan
   Agency for Medical Research and Development; Ministry of Education,
   Science, Sports and Culture, Tokyo, Japan [17K08730, 17K08740];
   Grants-in-Aid for Scientific Research [17K08730, 17K08740] Funding
   Source: KAKEN
FX This study was supported in part by a grant, Leading Advanced Projects
   for Medical Innovation (LEAP), from Japan Agency for Medical Research
   and Development, and by a Grant-in-Aid for General Scientific Research
   from the Ministry of Education, Science, Sports and Culture (no.
   17K08730 to T. Saito, no. 17K08740 to T. Yao), Tokyo, Japan.
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NR 36
TC 18
Z9 20
U1 0
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0309-0167
EI 1365-2559
J9 HISTOPATHOLOGY
JI Histopathology
PD SEP
PY 2020
VL 77
IS 3
BP 492
EP 502
DI 10.1111/his.14158
EA JUL 2020
PG 11
WC Cell Biology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Pathology
GA NM9FN
UT WOS:000544375600001
PM 32438490
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Vuonga, T
   Garant, A
   Vendrely, V
   Martin, AG
   Devic, S
AF Vuonga, T.
   Garant, A.
   Vendrely, V.
   Martin, A. -G.
   Devic, S.
TI Clinical applications of high dose rate endorectal brachytherapy for
   patients with rectal cancer
SO CANCER RADIOTHERAPIE
LA English
DT Review
DE Rectal brachytherapy; Non-operative management of rectal&nbsp; cancer;
   Targeted therapy for rectal cancer
ID EXTERNAL-BEAM RADIOTHERAPY; TOTAL MESORECTAL EXCISION; PREOPERATIVE
   RADIOTHERAPY; IRRADIATED PATIENTS; FOLLOW-UP
AB With the establishment of total mesorectal excision for the treatment of rectal cancer, local recurrence rates have significantly decreased. The addition of preoperative external beam irradiation further reduces this risk to less than 6%. As the local treatment becomes successful and more widely used, the associated treatment-related toxicity is becoming clinically important. If 4 to 6% of the patients are to benefit from neo-adjuvant therapy before total mesorectal excision, the acute and the long-term toxicity burden must be reasonable. With the introduction of better-quality imaging for tumour visualization and treatment planning, a new-targeted radiation treatment was introduced with high dose rate endorectal brachytherapy. The treatment concept was tested in phase I and II studies first in the preoperative setting, then as a boost after external beam radiation therapy as a dose escalation study to achieve higher tumour local control in a radical treatment setting with no surgery. High dose rate endorectal brachytherapy is safe and effective in achieving high tumour regression rate and was well tolerated. It is presently explored in a phase III dose escalation study in the non-operative management of patients with operable rectal cancer. (c) 2022 Societe franc, aise de radiotherapie oncologique (SFRO). Published by Elsevier Masson SAS. All rights reserved.
C1 [Vuonga, T.; Devic, S.] McGill Univ, Jewish Gen Hosp, Radiat Oncol Dept, Montreal, PQ H3T 1E2, Canada.
   [Garant, A.] UT Southwestern Med Ctr, Dept Radiat Oncol, Dallas, TX USA.
   [Vendrely, V.] CHU Bordeaux, Dept Radiat Oncol, F-33000 Bordeaux, France.
   [Vendrely, V.] Univ Bordeaux, Inserm, UMR1312, BoRdeaux Inst onCol BRIC, F-33000 Bordeaux, France.
   [Martin, A. -G.] Univ Laval, CHU Quebec, Serv Radiooncol, Quebec City, PQ, Canada.
C3 McGill University; University of Texas System; University of Texas
   Southwestern Medical Center Dallas; Universite de Bordeaux; CHU
   Bordeaux; Universite de Bordeaux; Institut National de la Sante et de la
   Recherche Medicale (Inserm); Laval University
RP Vuonga, T (corresponding author), McGill Univ, Jewish Gen Hosp, Radiat Oncol Dept, Montreal, PQ H3T 1E2, Canada.
EM te.vuong.med@ssss.gouv.qc.ca
CR Appelt A, 2020, RADIOTHER ONCOL, V152, pS76
   Appelt AL, 2015, LANCET ONCOL, V16, P919, DOI 10.1016/S1470-2045(15)00120-5
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NR 20
TC 2
Z9 2
U1 0
U2 2
PU ELSEVIER
PI BRIDGEWATER
PA 685 ROUTE 202-206, BRIDGEWATER, NJ 08807 USA
SN 1278-3218
EI 1769-6658
J9 CANCER RADIOTHER
JI Cancer Radiother.
PD OCT
PY 2022
VL 26
IS 6-7
SI SI
BP 879
EP 883
DI 10.1016/j.canrad.2022.07.001
EA SEP 2022
PG 5
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 6I4DZ
UT WOS:000886078900022
PM 36031497
DA 2025-01-04
ER

PT J
AU Bencsikova, B
   Budinska, E
   Selingerova, I
   Pilatova, K
   Fedorova, L
   Greplova, K
   Nenutil, R
   Valik, D
   Obermannova, R
   Sheard, MA
   Zdrazilova-Dubska, L
AF Bencsikova, Beatrix
   Budinska, Eva
   Selingerova, Iveta
   Pilatova, Katerina
   Fedorova, Lenka
   Greplova, Kristina
   Nenutil, Rudolf
   Valik, Dalibor
   Obermannova, Radka
   Sheard, Michael A.
   Zdrazilova-Dubska, Lenka
TI Circulating T cell subsets are associated with clinical outcome of
   anti-VEGF-based 1st-line treatment of metastatic colorectal cancer
   patients: a prospective study with focus on primary tumor sidedness
SO BMC CANCER
LA English
DT Article
DE Metastatic colorectal cancer; T cell subsets; Regulatory T cells;
   Antitumor immune response; Anti-VEGF; Primary colorectal carcinoma
   sidedness
ID CONSENSUS MOLECULAR SUBTYPES; PROGNOSTIC-FACTOR; KRAS MUTATION;
   COLON-CANCER; BEVACIZUMAB; CD8(+); CLASSIFICATION; RESPONSES; SURVIVAL;
   IMPACT
AB BackgroundIn a prospective study with long-term follow-up, we analyzed circulating T cell subsets in patients with metastatic colorectal cancer (mCRC) in the context of primary tumor sidedness, KRAS status, and clinical outcome. Our primary goal was to investigate whether baseline levels of circulating T cell subsets serve as a potential biomarker of clinical outcome of mCRC patients treated with an anti-VEGF-based regimen.MethodsThe study group consisted of 36 patients with colorectal adenocarcinoma who started first-line chemotherapy with bevacizumab for metastatic disease. We quantified T cell subsets including Tregs and CD8(+) T cells in the peripheral blood prior to therapy initiation. Clinical outcome was evaluated as progression-free survival (PFS), overall survival (OS), and objective response rate (ORR).Results1) mCRC patients with KRAS wt tumors had higher proportions of circulating CD8(+) cytotoxic T cells among all T cells but also higher measures of T regulatory (Treg) cells such as absolute count and a higher proportion of Tregs in the CD4(+) subset. 2) A low proportion of circulating Tregs among CD4(+) cells, and a high CD8:Treg ratio at initiation of VEGF-targeting therapy, were associated with favorable clinical outcome. 3) In a subset of patients with primarily right-sided mCRC, superior PFS and OS were observed when the CD8:Treg ratio was high.ConclusionsThe baseline level of circulating immune cells predicts clinical outcome of 1st-line treatment with the anti-VEGF angio/immunomodulatory agent bevacizumab. Circulating immune biomarkers, namely the CD8:Treg ratio, identified patients in the right-sided mCRC subgroup with favorable outcome following treatment with 1st-line anti-VEGF treatment.
C1 [Bencsikova, Beatrix; Obermannova, Radka] Masaryk Mem Canc Inst, Dept Comprehens Canc Care, Brno, Czech Republic.
   [Bencsikova, Beatrix; Budinska, Eva; Selingerova, Iveta; Pilatova, Katerina; Greplova, Kristina; Nenutil, Rudolf; Valik, Dalibor; Obermannova, Radka; Sheard, Michael A.; Zdrazilova-Dubska, Lenka] Masaryk Mem Canc Inst, Reg Ctr Appl Mol Oncol, Brno, Czech Republic.
   [Selingerova, Iveta; Pilatova, Katerina; Fedorova, Lenka; Greplova, Kristina; Valik, Dalibor; Zdrazilova-Dubska, Lenka] Masaryk Mem Canc Inst, Dept Lab Med, Brno, Czech Republic.
   [Nenutil, Rudolf] Masaryk Mem Canc Inst, Dept Oncol & Expt Pathol, Brno, Czech Republic.
C3 Masaryk Memorial Cancer Institute; Masaryk Memorial Cancer Institute;
   Masaryk Memorial Cancer Institute; Masaryk Memorial Cancer Institute
RP Zdrazilova-Dubska, L (corresponding author), Masaryk Mem Canc Inst, Reg Ctr Appl Mol Oncol, Brno, Czech Republic.; Zdrazilova-Dubska, L (corresponding author), Masaryk Mem Canc Inst, Dept Lab Med, Brno, Czech Republic.
EM dubska@mou.cz
RI Selingerova, Iveta/AAF-6396-2019; Sheard, Michael/J-1374-2019; Budinska,
   Eva/F-2698-2011
OI Selingerova, Iveta/0000-0003-3713-3504; Gescheidtova,
   Lenka/0000-0002-3786-2400; Budinska, Eva/0000-0002-9004-9187; Sheard,
   Michael/0000-0002-4960-7650; Nenutil, Rudolf/0000-0003-0068-9760
FU Czech Ministry of Health [AZV 16-31966A, DRO 00209805]; Czech Ministry
   of Education, Youth and Sports [LO1413, LM2015089]
FX The work was supported by the Czech Ministry of Health for projects AZV
   16-31966A (data interpretation) and DRO 00209805 (design of the study,
   writing the manuscript) and the Czech Ministry of Education, Youth and
   Sports for projects LO1413 (sample and data analysis, writing the
   manuscript) and LM2015089 (sample collection).
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NR 41
TC 16
Z9 18
U1 0
U2 12
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD JUL 15
PY 2019
VL 19
AR 687
DI 10.1186/s12885-019-5909-5
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IJ2CU
UT WOS:000475706700010
PM 31307428
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Turano, M
   Cammarota, F
   Duraturo, F
   Izzo, P
   De Rosa, M
AF Turano, Mimmo
   Cammarota, Francesca
   Duraturo, Francesca
   Izzo, Paola
   De Rosa, Marina
TI A Potential Role of IL-6/IL-6R in the Development and Management of
   Colon Cancer
SO MEMBRANES
LA English
DT Review
DE IL-6 signaling; membrane IL-6 receptor; soluble IL-6 receptor;
   colorectal cancer; polyposis syndromes; IL-6-targeting therapy;
   nutraceutical IL-6 inhibition
ID ANTI-INTERLEUKIN-6 MONOCLONAL-ANTIBODY; SOLUBLE INTERLEUKIN-6 RECEPTOR;
   C-REACTIVE PROTEIN; COLORECTAL-CANCER; INTESTINAL INFLAMMATION;
   PROGNOSTIC-SIGNIFICANCE; SERUM INTERLEUKIN-6; SIGNAL TRANSDUCER; DIETARY
   PATTERNS; LKB1 DEFICIENCY
AB Colorectal cancer (CRC) is the third most frequent cancer worldwide and the second greatest cause of cancer deaths. About 75% of all CRCs are sporadic cancers and arise following somatic mutations, while about 10% are hereditary cancers caused by germline mutations in specific genes. Several factors, such as growth factors, cytokines, and genetic or epigenetic alterations in specific oncogenes or tumor-suppressor genes, play a role during the adenoma-carcinoma sequence. Recent studies have reported an increase in interleukin-6 (IL-6) and soluble interleukin-6 receptor (sIL-6R) levels in the sera of patients affected by colon cancer that correlate with the tumor size, suggesting a potential role for IL-6 in colon cancer progression. IL-6 is a pleiotropic cytokine showing both pro- and anti-inflammatory roles. Two different types of IL-6 signaling are known. Classic IL-6 signaling involves the binding of IL-6 to its membrane receptor on the surfaces of target cells; alternatively, IL-6 binds to sIL-6R in a process called IL-6 trans-signaling. The activation of IL-6 trans-signaling by metalloproteinases has been described during colon cancer progression and metastasis, involving a shift from membrane-bound interleukin-6 receptor (IL-6R) expression on the tumor cell surface toward the release of soluble IL-6R. In this review, we aim to shed light on the role of IL-6 signaling pathway alterations in sporadic colorectal cancer and the development of familial polyposis syndrome. Furthermore, we evaluate the possible roles of IL-6 and IL-6R as biomarkers useful in disease follow-up and as potential targets for therapy, such as monoclonal antibodies against IL-6 or IL-6R, or a food-based approach against IL-6.
C1 [Turano, Mimmo] Univ Naples Federico II, Dept Biol, I-80126 Naples, Italy.
   [Cammarota, Francesca; Duraturo, Francesca; Izzo, Paola; De Rosa, Marina] Univ Naples Federico II, Dept Mol Med & Med Biotechnol, I-80131 Naples, Italy.
   [Cammarota, Francesca; Duraturo, Francesca; Izzo, Paola; De Rosa, Marina] Ceinge Biotecnol Avanzate, I-80131 Naples, Italy.
C3 University of Naples Federico II; University of Naples Federico II;
   CEINGE Biotecnologie Avanzate
RP De Rosa, M (corresponding author), Univ Naples Federico II, Dept Mol Med & Med Biotechnol, I-80131 Naples, Italy.; De Rosa, M (corresponding author), Ceinge Biotecnol Avanzate, I-80131 Naples, Italy.
EM mimmo.turano@unina.it; cammarota@ceinge.unina.it;
   francesca.duraturo@unina.it; paola.izzo@unina.it; marina.derosa@unina.it
RI Turano, Mimmo/AAC-3147-2022; Duraturo, Francesca/AAB-9722-2022; De Rosa,
   Marina/IVV-5745-2023
OI Duraturo, Francesca/0000-0002-0787-6182; Izzo,
   Paola/0000-0003-1549-0615; De Rosa, Marina/0000-0002-4752-5678; TURANO,
   Mimmo/0000-0002-4934-0562
FU Department of Biology, University of Naples Federico II
FX The APC was funded by the Department of Biology, University of Naples
   Federico II.
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NR 103
TC 25
Z9 29
U1 2
U2 42
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0375
J9 MEMBRANES-BASEL
JI Membranes
PD MAY
PY 2021
VL 11
IS 5
AR 312
DI 10.3390/membranes11050312
PG 13
WC Biochemistry & Molecular Biology; Chemistry, Physical; Engineering,
   Chemical; Materials Science, Multidisciplinary; Polymer Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry; Engineering; Materials
   Science; Polymer Science
GA SH7FN
UT WOS:000654299700001
PM 33923292
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Inamoto, S
   Itatani, Y
   Yamamoto, T
   Minamiguchi, S
   Hirai, H
   Iwamoto, M
   Hasegawa, S
   Taketo, MM
   Sakai, Y
   Kawada, K
AF Inamoto, Susumu
   Itatani, Yoshiro
   Yamamoto, Takamasa
   Minamiguchi, Sachiko
   Hirai, Hideyo
   Iwamoto, Masayoshi
   Hasegawa, Suguru
   Taketo, Makoto Mark
   Sakai, Yoshiharu
   Kawada, Kenji
TI Loss of SMAD4 Promotes Colorectal Cancer Progression by Accumulation of
   Myeloid-Derived Suppressor Cells through the CCL15-CCR1 Chemokine Axis
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID COLON-CANCER; LIVER METASTASIS; TGF-BETA; MICROENVIRONMENT;
   TUMORIGENESIS; ACTIVATION; IMMUNE; TUMORS
AB Purpose: We previously reported that loss of SMAD4 promotes chemokine CCL15 expression to recruit CCR1(+) myeloid cells via the CCL15-CCR1 axis, which facilitates metastasis of colorectal cancer to the liver. The purposes of this study were to investigate whether essentially the same mechanism works in tumor invasion of the primary colorectal cancer and to evaluate the clinical importance of CCL15 expression and CCR1(+) cell accumulation.
   Experimental Design: Using human colorectal cancer cell lines with reduced expression of SMAD4 or CCL15, we investigated tumor growth activities in vivo. We used immunohistochemistry (IHC) to investigate expression of SMAD4, CCL15, and CCR1 with 333 clinical specimens of primary colorectal cancer. We next characterized the CCR1(+) cells using double immunofluorescence staining with several specific cell-type markers. Finally, we determined the serum CCL15 levels in 132 colorectal cancer patients.
   Results: In an orthotopic xenograft model, CCL15 secreted from SMAD4-deficient colorectal cancer cells recruited CCR1(+) cells, resulting in aggressive tumor growth. IHC indicated that loss of SMAD4 was significantly associated with CCL15 expression, and that CCL15-positive primary colorectal cancers recruited approximately 2.2 times more numbers of CCR1(+) cells at their invasion front than CCL15-negative colorectal cancers. Importantly, these CCR1(+) cells were of the myeloid-derived suppressor cell (MDSC) phenotype (CD11b(+), CD33(+), and HLA-DR+). Most CCR1(+) cells showed the granulocytic-MDSC phenotype (CD15(+)), whereas some showed the monocytic-MDSC phenotype (CD14(+)). Serum CCL15 levels in colorectal cancer patients were significantly higher than in controls.
   Conclusions: Blocking the recruitment of CCR1(+) MDSCs may represent a novel molecular-targeted therapy, and serum CCL15 concentration can be a novel biomarker for colorectal cancer. (C)2015 AACR.
C1 [Inamoto, Susumu; Itatani, Yoshiro; Yamamoto, Takamasa; Iwamoto, Masayoshi; Hasegawa, Suguru; Taketo, Makoto Mark; Sakai, Yoshiharu; Kawada, Kenji] Kyoto Univ, Dept Surg, Grad Sch Med, Kyoto, Japan.
   [Itatani, Yoshiro; Taketo, Makoto Mark] Kyoto Univ, Grad Sch Med, Dept Pharmacol, Kyoto, Japan.
   [Minamiguchi, Sachiko] Kyoto Univ, Grad Sch Med, Dept Diagnost Pathol, Kyoto, Japan.
   [Hirai, Hideyo] Kyoto Univ, Grad Sch Med, Dept Transfus Med & Cell Therapy, Kyoto, Japan.
C3 Kyoto University; Kyoto University; Kyoto University; Kyoto University
RP Kawada, K (corresponding author), Kyoto Univ, Grad Sch Med, Dept Surg, Sakyo Ku, 54 Shogoin Kawara Cho, Kyoto 6068507, Japan.
EM kkawada@kuhp.kyoto-u.ac.jp
OI Inamoto, Susumu/0009-0007-5138-8630
FU Ministry of Education, Culture, Sports, Science and Technology of Japan;
   Japan Research Foundation for Clinical Pharmacology; research program of
   the Project for Development of Innovative Research on Cancer
   Therapeutics (P-Direct), Ministry of Education, Culture, Sports, Science
   and Technology of Japan; Grants-in-Aid for Scientific Research
   [25253022] Funding Source: KAKEN
FX This work was supported by grants from the Ministry of Education,
   Culture, Sports, Science and Technology of Japan, and from Japan
   Research Foundation for Clinical Pharmacology (to K. Kawada), and also
   performed as a research program of the Project for Development of
   Innovative Research on Cancer Therapeutics (P-Direct), Ministry of
   Education, Culture, Sports, Science and Technology of Japan (to M. M.
   Taketo and H. Hirai).
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U1 1
U2 29
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD JAN 15
PY 2016
VL 22
IS 2
BP 492
EP 501
DI 10.1158/1078-0432.CCR-15-0726
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DC2VP
UT WOS:000369076500025
PM 26341919
OA Green Submitted, Bronze
DA 2025-01-04
ER

PT J
AU Johnson, B
   Morris, V
   Wang, XM
   Dasari, A
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   Shen, JP
   Lee, MS
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   Drusbosky, LM
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   Kopetz, S
AF Johnson, Benny
   Morris, Van
   Wang, Xuemei
   Dasari, Arvind
   Raghav, Kanwal
   Shen, John Paul
   Lee, Michael S.
   Huey, Ryan
   Parseghian, Christine
   Willis, Jason
   Wolff, Robert
   Drusbosky, Leylah M.
   Overman, Michael J.
   Kopetz, Scott
TI Comprehensive Landscape of BRAF Variant Classes, Clonalities, and
   Co-Mutations in Metastatic Colorectal Cancer Using ctDNA Profiling
SO CANCERS
LA English
DT Article
DE atypical BRAF; metastatic colorectal cancer; BRAF mutation; KRAS
   mutation; NRAS mutation
ID NIVOLUMAB
AB Simple Summary Patients with atypical (nonV600) BRAF mutations represent a unique category of metastatic colorectal cancer patients. In the past, these patients were considered to be similar to those with the more common BRAFV600E mutation. However, additional investigation confirmed patients with atypical BRAF mutations have a distinct molecular make up, clinical course, and treatment response to both chemotherapy and targeted therapy, compared to those of patients with BRAFV600E mutations. Here, we report the key characteristics of patients with atypical BRAF mutations identified from a large circulating tumor DNA database and a real-world clinical cohort, highlighting important differences, such as the presence of additional mutations and related survival outcomes. These findings support the need for dedicated research efforts to understand the intricacies of atypical BRAF mutations in colon cancer and promote the discovery of new therapies for these patients.Abstract Although V600E accounts for the majority of the BRAF mutations in metastatic colorectal cancer (mCRC), non-V600 BRAF variants have been shown in recent years to represent a distinct molecular subtype. This study provides a comprehensive profile of BRAF variants in mCRC using a large genomic database of circulating tumor DNA (ctDNA) and analyzing clinical outcomes in a cohort of patients with atypical (non-V600) BRAF variants (aBRAF; class II, class III, unclassified). Overall, 1733 out of 14,742 mCRC patients in the ctDNA cohort had at least one BRAF variant. Patients with atypical BRAF variants tended to be younger and male. In contrast to BRAFV600E, BRAF class II and III variants and their co-occurrence with KRAS/NRAS mutations were increased at baseline and especially with those patients predicted to have prior anti-EGFR exposure. Our clinical cohort included 38 patients with atypical BRAF mCRC treated at a large academic referral center. While there were no survival differences between atypical BRAF classes, concurrent RAS mutations or liver involvement was associated with poorer prognosis. Notably, patients younger than 50 years of age had extremely poor survival. In these patients, the high-frequency KRAS/NRAS co-mutation and its correlation with poorer prognosis underlines the urgent need for novel therapeutic strategies. This study represents one of the most comprehensive characterizations to date of atypical BRAF variants, utilizing both ctDNA and clinical cohorts.
C1 [Johnson, Benny; Morris, Van; Dasari, Arvind; Raghav, Kanwal; Shen, John Paul; Lee, Michael S.; Huey, Ryan; Parseghian, Christine; Willis, Jason; Wolff, Robert; Overman, Michael J.; Kopetz, Scott] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Div Canc Med, Houston, TX 77030 USA.
   [Wang, Xuemei] Univ Texas MD Anderson Canc Ctr, Dept Biostat, Houston, TX 77030 USA.
   [Drusbosky, Leylah M.] Guardant Hlth, Redwood City, CA 94063 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; University of
   Texas System; UTMD Anderson Cancer Center; Guardant Health, Inc.
RP Johnson, B (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Div Canc Med, Houston, TX 77030 USA.
EM benjohnson2010@gmail.com
RI Lam, Michael/KWU-4480-2024
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NR 31
TC 0
Z9 0
U1 0
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD FEB
PY 2024
VL 16
IS 4
AR 737
DI 10.3390/cancers16040737
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JH0Z4
UT WOS:001172169300001
PM 38398128
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Man, RJ
   Zhang, YL
   Jiang, AQ
   Zhu, HL
AF Man, Ruo-Jun
   Zhang, Ya-Liang
   Jiang, Ai-Qin
   Zhu, Hai-Liang
TI A patent review of RAF kinase inhibitors (2010-2018)
SO EXPERT OPINION ON THERAPEUTIC PATENTS
LA English
DT Review
DE RAF kinase inhibitors; chemical structure; anti-tumor; classification
ID ACQUIRED-RESISTANCE; ANTITUMOR-ACTIVITY; COLORECTAL-CANCER; BRAF
   INHIBITOR; MAPK PATHWAY; MEK INHIBITOR; MELANOMA; VEMURAFENIB;
   MUTATIONS; THERAPY
AB Introduction: RAF kinase inhibitors block and regulate RAS/RAF/MEK/ERK signaling, which is a key to tumor treatment. At present, although RAF kinase inhibitors have good efficacy, there are few such drugs with low toxicity, and thus, it is urgent to find novel RAF kinase inhibitors associated with higher activity and fewer adverse reactions. This review highlights the anti-tumor effects of several published RAF kinase inhibitors and might be helpful in providing new ideas for the development of novel drug candidates in the future. Areas covered: This article covers the pertinent literature published on RAF kinase inhibitors from 2010 to 2018, as well as the potential use of these compounds as therapeutics for cancer. Expert opinion: To date, many RAF kinase inhibitors with different structures have been studied, many of which have prominent inhibitory activities toward RAF kinase. Further, the specificity of these drugs offers hope for the targeted therapy of tumors. Although RAF kinase inhibition has achieved promising results for the treatment of many cancers, overcoming limitations associated with drug resistance and safety comprises a new direction for the optimization and improvement of RAF kinase inhibitors.
C1 [Man, Ruo-Jun; Zhang, Ya-Liang; Jiang, Ai-Qin; Zhu, Hai-Liang] Nanjing Univ, State Key Lab Pharmaceut Biotechnol, 163 Xianlin Rd, Nanjing 210023, Jiangsu, Peoples R China.
   [Man, Ruo-Jun] Guangxi Univ Nationalities, Coll Chem & Chem Engn, Nanning, Peoples R China.
C3 Nanjing University; Guangxi Minzu University
RP Zhu, HL (corresponding author), Nanjing Univ, State Key Lab Pharmaceut Biotechnol, 163 Xianlin Rd, Nanjing 210023, Jiangsu, Peoples R China.
EM zhuhl@nju.edu.cn
RI Zhang, Yaliang/AAM-1684-2021
OI Zhang, Yaliang/0000-0002-1352-0676
FU Guangxi University for Nationalities [2018KJQD13]; Guangxi Minority
   Preparatory Education Base Research Project [2017B002]; Guangxi
   Biological Polysaccharide Separation, Purification and Modification
   Research Platform [GKZY18076005]
FX This work was supported by Guangxi University for Nationalities Research
   Funded Project (no. 2018KJQD13), Guangxi Minority Preparatory Education
   Base Research Project (no. 2017B002) and Guangxi Biological
   Polysaccharide Separation, Purification and Modification Research
   Platform (GKZY18076005).
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NR 130
TC 15
Z9 16
U1 0
U2 22
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1354-3776
EI 1744-7674
J9 EXPERT OPIN THER PAT
JI Expert Opin. Ther. Patents
PD SEP 2
PY 2019
VL 29
IS 9
BP 675
EP 688
DI 10.1080/13543776.2019.1651842
EA AUG 2019
PG 14
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA IS0AL
UT WOS:000480210500001
PM 31370713
DA 2025-01-04
ER

PT J
AU Jun, SY
   Kim, M
   Gu, MJ
   Bae, YK
   Chang, HK
   Jung, ES
   Jang, KT
   Kim, J
   Yu, E
   Eom, DW
   Hong, SM
AF Jun, Sun-Young
   Kim, Misung
   Gu, Mi Jin
   Bae, Young Kyung
   Chang, Hee-Kyung
   Jung, Eun Sun
   Jang, Kee-Taek
   Kim, Jihun
   Yu, Eunsil
   Eom, Dae Woon
   Hong, Seung-Mo
TI Clinicopathologic and prognostic associations of <i>KRAS</i> and
   <i>BRAF</i> mutations in small intestinal adenocarcinoma
SO MODERN PATHOLOGY
LA English
DT Article
ID SMALL-BOWEL ADENOCARCINOMA; KIRSTEN RAS MUTATIONS; COLORECTAL-CANCER;
   GENETIC ALTERATIONS; KI-RAS; CHEMOTHERAPY; EXPRESSION; CETUXIMAB; P53
AB Activating KRAS and/or BRAF mutations have been identified as predictors of resistance to anti-epidermal growth factor receptor (EGFR) chemotherapy in colorectal cancer. But the status of KRAS and BRAF mutations and their clinicopathologic and prognostic significance has not been extensively evaluated in small intestinal adenocarcinomas. In this work, the KRAS and BRAF genes in 190 surgically resected small intestinal adenocarcinoma cases were sequenced and their association with various clinicopathologic variables, including survival of the patients, was analyzed. KRAS or BRAF mutations were observed in 63 (33%) cases. Sixty-one cases had KRAS mutations and 2 had BRAF mutations and the two types of mutation were mutually exclusive. The majority of KRAS mutations were G>A transition (43/61 cases, 71%) or p.G12D (31/61 cases, 51%). The patients with mutant KRAS tended to have higher pT classifications (P=0.034) and more frequent pancreatic invasion (P=0.020) than those with wild-type KRAS. Multivariate logistic regression analysis showed that certain mutated KRAS subtypes (G>A transitions and G12D mutations) were significantly correlated with higher pT classification (P=0.015 and 0.004, respectively) than wild-type KRAS and other KRAS mutations. The patients with KRAS or BRAF mutation had a tendency to shorter overall survival than those with wild-type KRAS and BRAF (P=0.148), but subgroup analysis demonstrated the patients with KRAS mutations showed worse survival (median, 46.0 months; P=0.046) than those with wild-type KRAS (85.4 months) in lower pT classification (pT1pT3) group. In summary, KRAS and, infrequently, BRAF mutations are observed in a subset of small intestinal adenocarcinomas, and are associated with higher pT classification and more frequent pancreatic invasion. KRAS mutation is a poor prognostic predictor in patients with lower pT classification tumors. Anti-EGFR targeted therapy could be applied to about two-thirds of small intestinal adenocarcinoma patients, namely those with wildtype KRAS and BRAF if they have metastatic disease, similar to colorectal cancer patients.
C1 [Jun, Sun-Young] Catholic Univ Korea, Incheon St Marys Hosp, Dept Pathol, Inchon, South Korea.
   [Kim, Misung] Univ Ulsan, Coll Med, Ulsan Univ Hosp, Dept Pathol, Ulsan 680749, South Korea.
   [Gu, Mi Jin; Bae, Young Kyung] Yeungnam Univ, Coll Med, Dept Pathol, Daegu, South Korea.
   [Chang, Hee-Kyung] Kosin Univ, Coll Med, Dept Pathol, Busan, South Korea.
   [Jung, Eun Sun] Catholic Univ Korea, Coll Med, Dept Pathol, Seoul, South Korea.
   [Jang, Kee-Taek] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pathol, Seoul, South Korea.
   [Kim, Jihun; Yu, Eunsil; Hong, Seung-Mo] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Pathol, 88,Olymp Ro 43 Gil, Seoul 138736, South Korea.
   [Eom, Dae Woon] Univ Ulsan, Coll Med, Gangneung Asan Hosp, Dept Pathol, Kangnung, South Korea.
C3 Catholic University of Korea; University of Ulsan; Ulsan University
   Hospital; Yeungnam University; Catholic University of Korea;
   Sungkyunkwan University (SKKU); Samsung Medical Center; University of
   Ulsan; Asan Medical Center; University of Ulsan
RP Hong, SM (corresponding author), Univ Ulsan, Coll Med, Asan Med Ctr, Dept Pathol, 88,Olymp Ro 43 Gil, Seoul 138736, South Korea.; Eom, DW (corresponding author), Univ Ulsan, Coll Med, Gangneung Asan Hosp, Dept Pathol, 415 Bangdong Ri, Kangnung 210711, Gangwon Do, South Korea.
EM edwjyh@gnah.co.kr; smhong28@gmail.com
RI Eun, Jung Woo/ABB-5127-2020; Yu, Ed/P-1871-2019
OI Hong, Seung-Mo/0000-0002-8888-6007; Jun, Sun-Young/0000-0002-3007-2094
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NR 34
TC 29
Z9 30
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0893-3952
EI 1530-0285
J9 MODERN PATHOL
JI Mod. Pathol.
PD APR
PY 2016
VL 29
IS 4
BP 402
EP 415
DI 10.1038/modpathol.2016.40
PG 14
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA DI0AP
UT WOS:000373157500008
PM 26892442
OA Bronze
DA 2025-01-04
ER

PT J
AU Siemiaszko, G
   Niemirowicz-Laskowska, K
   Markiewicz, KH
   Misztalewska-Turkowicz, I
   Dudz, E
   Milewska, S
   Misiak, P
   Kurowska, I
   Sadowska, A
   Car, H
   Wilczewska, AZ
AF Siemiaszko, Gabriela
   Niemirowicz-Laskowska, Katarzyna
   Markiewicz, Karolina H.
   Misztalewska-Turkowicz, Iwona
   Dudz, Ewelina
   Milewska, Sylwia
   Misiak, Pawel
   Kurowska, Izabela
   Sadowska, Anna
   Car, Halina
   Wilczewska, Agnieszka Z.
TI Synergistic effect of folate-conjugated polymers and 5-fluorouracil in
   the treatment of colon cancer
SO CANCER NANOTECHNOLOGY
LA English
DT Article
DE Folic acid; Colon cancer; 5-Fluorouracil; Drug delivery system; Targeted
   therapy; RAFT; MADIX polymerization; Polymeric micelles;
   Thermoresponsive polymer
ID TARGETED DRUG-DELIVERY; 2-HYDROXYETHYL ACRYLATE; COPOLYMERS; RECEPTOR;
   POLYMERIZATION; NANOPARTICLES; MECHANISMS; MICELLES; BEHAVIOR; BLOCK
AB Background In recent years, targeted drug delivery strategies have received special attention from the scientific world due to advantages such as more effective therapy and reduction of side effects. The principle of operation is delayed excretion from the bloodstream of the drug delivery system compared to the drug itself, as well as facilitated penetration into diseased cells thanks to the use of ligands recognized by appropriate receptors. Particularly interesting drug carriers are amphiphilic copolymers that form nano-sized micelles with a drug, which can release the drug at a specific place in the body under the influence of appropriate stimuli. Results We describe the synthesis of the diblock polymer, poly(2-hydroxyethyl acrylate)-b-poly(N-vinylcaprolactam) using RAFT/MADIX (Reversible Addition-Fragmentation chain Transfer/MAcromolecular Design by Interchange of Xanthate) controlled polymerization affording polymers with good dispersity according to SEC (Size-Exclusion Chromatography). Some post-modifications of the polymer with folic acid were then performed as evidenced by NMR (Nuclear Magnetic Resonance), UV-Vis (UltraViolet-Visible) and FT-IR (Fourier-Transform Infrared) spectroscopy, and TGA (ThermoGravimetric Analysis). The formation of stable micellar systems from polymers with and without the drug, 5-fluorouracil, was confirmed by DLS (Dynamic Light Scattering) and zeta potential measurements, and TEM (Transmission Eelectron Microscopy) imaging. Finally, the cloud point of the polymers was investigated, which turned out to be close to the temperature of the human body. Most importantly, these micellar systems have been explored as a drug delivery system against colon cancer, showing increased cytotoxicity compared to the drug alone. This effect was achieved due to the easier cellular uptake by the interaction of folic acid and its receptors on the surface of cancer cells. Conclusions The presented results constitute a solid foundation for the implementation of a nano-sized drug delivery system containing folic acid for practical use in the treatment of drug-resistant cancer, as well as more effective therapy with fewer side effects.
C1 [Siemiaszko, Gabriela; Markiewicz, Karolina H.; Misztalewska-Turkowicz, Iwona; Dudz, Ewelina; Misiak, Pawel; Kurowska, Izabela; Wilczewska, Agnieszka Z.] Univ Bialystok, Fac Chem, Ciolkowskiego 1K, PL-15245 Bialystok, Poland.
   [Niemirowicz-Laskowska, Katarzyna; Milewska, Sylwia; Sadowska, Anna; Car, Halina] Med Univ Bialystok, Dept Expt Pharmacol, Szpitalna 37, PL-15361 Bialystok, Poland.
   [Milewska, Sylwia] Med Univ Bialystok, Doctoral Sch, Kilinskiego 1, PL-15089 Bialystok, Poland.
   [Kurowska, Izabela] Univ Bialystok, Doctoral Sch Exact & Nat Sci, Ciolkowskiego 1K, PL-15245 Bialystok, Poland.
C3 University of Bialystok; Medical University of Bialystok; Medical
   University of Bialystok; University of Bialystok
RP Siemiaszko, G; Wilczewska, AZ (corresponding author), Univ Bialystok, Fac Chem, Ciolkowskiego 1K, PL-15245 Bialystok, Poland.; Niemirowicz-Laskowska, K (corresponding author), Med Univ Bialystok, Dept Expt Pharmacol, Szpitalna 37, PL-15361 Bialystok, Poland.
EM gsiemiaszko@gmail.com; katarzyna.niemirowicz@umb.edu.pl;
   agawilcz@uwb.edu.pl
RI Niemirowicz, Katarzyna/T-5011-2018; Misztalewska-Turkowicz,
   Iwona/ABF-9723-2020; WILCZEWSKA, AGNIESZKA/J-4423-2013; Sadowska,
   Anna/S-1907-2018; Misiak, Pawel/KHD-2894-2024
OI Siemiaszko, Gabriela/0000-0002-3246-6986; Misiak,
   Pawel/0000-0002-6882-3519; Kurowska, Izabela/0000-0001-7728-1339;
   Markiewicz, Karolina Halina/0000-0002-4857-0489; Misztalewska-Turkowicz,
   Iwona/0000-0001-6191-6053
FU National Science Centre, Poland [NCN/2016/21/B/ST5/01365]; EU
   [POPW.01.03.00-20-034/09-00, POPW.01.03.00-20-004/11]
FX This work was financially supported by the National Science Centre,
   Poland, grant no. NCN/2016/21/B/ST5/01365 (AZW). Analyses were performed
   in the Centre of Synthesis and Analysis BioNanoTechno of the University
   of Bialystok. The equipment in the Centre was funded by the EU as a part
   of the Operational Program Development of Eastern Poland 2007-2013,
   projects: POPW.01.03.00-20-034/09-00 and POPW.01.03.00-20-004/11.
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NR 61
TC 11
Z9 11
U1 1
U2 16
PU SPRINGER WIEN
PI Vienna
PA Prinz-Eugen-Strasse 8-10, A-1040 Vienna, AUSTRIA
SN 1868-6958
EI 1868-6966
J9 CANCER NANOTECHNOL
JI Cancer Nanotechnol.
PD DEC
PY 2021
VL 12
IS 1
AR 31
DI 10.1186/s12645-021-00104-9
PG 24
WC Oncology; Nanoscience & Nanotechnology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Science & Technology - Other Topics
GA XA1JG
UT WOS:000720411900001
OA gold
DA 2025-01-04
ER

PT J
AU Wahoski, CC
   Singh, B
AF Wahoski, Claudia C.
   Singh, Bhuminder
TI The Roles of RAC1 and RAC1B in Colorectal Cancer and Their Potential
   Contribution to Cetuximab Resistance
SO CANCERS
LA English
DT Review
DE colorectal cancer; cetuximab; drug resistance; RAC1; RAC1B
ID EPIDERMAL-GROWTH-FACTOR; TUMOR-RELATED RAC1B; ANTI-EGFR THERAPY;
   EPITHELIAL-MESENCHYMAL TRANSITION; CONSENSUS MOLECULAR SUBTYPES;
   SIGNAL-REGULATED KINASE; FACTOR RECEPTOR; SPLICE VARIANT;
   MONOCLONAL-ANTIBODY; RHO GTPASES
AB Simple Summary Cetuximab is a treatment widely used to treat advanced, metastatic colorectal cancer (CRC), and it works by blocking epidermal growth factor receptor signaling. Unfortunately, patients inevitably develop resistance to cetuximab. The most common resistance mechanisms are well established, but there are still patients that become resistant to cetuximab due to unknown mechanisms. The small guanosine triphosphatases (GTPases) RAC1 and RAC1B have been shown to contribute to CRC progression, but their role in cetuximab resistance is unclear. This review highlights the known cetuximab resistance mechanisms and summarizes how RAC1 and RAC1B could contribute to these resistance mechanisms to propose RAC1 and RAC1B as additional therapeutic targets that could increase the efficacy of cetuximab.Abstract Colorectal cancer (CRC) is one of the most diagnosed cancers and a leading contributor to cancer-related deaths in the United States. Clinically, standard treatment regimens include surgery, radiation, and chemotherapy; however, there has been increasing development and clinical use of targeted therapies for CRC. Unfortunately, many patients develop resistance to these treatments. Cetuximab, the first targeted therapy approved to treat advanced CRC, is a monoclonal antibody that targets the epidermal growth factor receptor and inhibits downstream pathway activation to restrict tumor cell growth and proliferation. CRC resistance to cetuximab has been well studied, and common resistance mechanisms include constitutive signal transduction through downstream protein mutations and promotion of the epithelial-to-mesenchymal transition. While the most common resistance mechanisms are known, a proportion of patients develop resistance through unknown mechanisms. One protein predicted to contribute to therapy resistance is RAC1, a small GTPase that is involved in cytoskeleton rearrangement, cell migration, motility, and proliferation. RAC1 has also been shown to be overexpressed in CRC. Despite evidence that RAC1 and its alternative splice isoform RAC1B play important roles in CRC and the pathways known to contribute to cetuximab resistance, there is a need to directly study the relationship between RAC1 and RAC1B and cetuximab resistance. This review highlights the recent studies investigating RAC1 and RAC1B in the context of CRC and suggests that these proteins could play a role in resistance to cetuximab.
C1 [Wahoski, Claudia C.] Vanderbilt Univ, Program Canc Biol, Nashville, TN 37232 USA.
   [Wahoski, Claudia C.; Singh, Bhuminder] Vanderbilt Univ, Med Ctr, Dept Med, Nashville, TN 37232 USA.
C3 Vanderbilt University; Vanderbilt University
RP Singh, B (corresponding author), Vanderbilt Univ, Med Ctr, Dept Med, Nashville, TN 37232 USA.
EM bhuminder.singh@vumc.org
RI Singh, Bhuminder/ADR-5679-2022; Singh, Bhuminder/J-3727-2014
OI Singh, Bhuminder/0000-0003-1357-2158
FU NCI [R01CA248505]; American Cancer Society [RSG-20-130-01-DDC]; CDMRP
   [W81XWH-21-1-0694]
FX The authors acknowledge funding support to the Singh laboratory by NCI
   R01CA248505, American Cancer Society-Research Scholar Grant
   RSG-20-130-01-DDC, and CDMRP W81XWH-21-1-0694.
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NR 178
TC 2
Z9 2
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUL
PY 2024
VL 16
IS 13
AR 2472
DI 10.3390/cancers16132472
PG 25
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YQ0C8
UT WOS:001269822300001
PM 39001533
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Jesinghaus, M
   Pfarr, N
   Endris, V
   Kloor, M
   Volckmar, AL
   Brandt, R
   Herpel, E
   Muckenhuber, A
   Lasitschka, F
   Schirmacher, P
   Penzel, R
   Weichert, W
   Stenzinger, A
AF Jesinghaus, Moritz
   Pfarr, Nicole
   Endris, Volker
   Kloor, Matthias
   Volckmar, Anna-Lena
   Brandt, Regine
   Herpel, Esther
   Muckenhuber, Alexander
   Lasitschka, Felix
   Schirmacher, Peter
   Penzel, Roland
   Weichert, Wilko
   Stenzinger, Albrecht
TI Genotyping of colorectal cancer for cancer precision medicine: Results
   from the IPH Center for Molecular Pathology
SO GENES CHROMOSOMES & CANCER
LA English
DT Article
ID MICROSATELLITE INSTABILITY; COLON-CANCER; TARGETED THERAPY;
   CLINICAL-TRIALS; RAS MUTATIONS; PIK3CA; TUMORS; EGFR; PD-1;
   TUMORIGENESIS
AB Cancer precision medicine has opened up new avenues for the treatment of colorectal cancer (CRC). To fully realize its potential, high-throughput sequencing platforms that allow genotyping beyond KRAS need to be implemented and require performance assessment. We comprehensively analyzed first-year data of 202 consecutive formalin-fixed paraffin embedded (FFPE) CRC samples for which prospective genotyping at our institution was requested. Deep targeted genotyping was done using a semiconductor-based sequencing platform and a self-designed panel of 30 CRC-related genes. Additionally, microsatellite status (MS) was determined. Ninety-seven percent of tumor samples were suitable for sequencing and in 88% MS could be assessed. The minimal drop-out rates of 6 and 25 cases, respectively were due to too low amounts or heavy degradation of DNA. Of 557 nonsynonymous mutations, 90 (16%) have not been described in COSMIC at the time of data query. Forty-three cases (22%) had double- or triple mutations affecting a single gene. Sixty-four percent had genetic alterations influencing oncological therapy. Eight percent of patients (MSI phenotype: 6%; mutated POLE: 2%) were potentially eligible for treatment with immune checkpoint inhibitors. Of 56% of KRASwt CRC that potentially qualified for anti-EGFR treatment, 30% presented with mutations in BRAF/NRAS. Mutated PIK3CA was detected in 21%. In conclusion, we here present real-life routine diagnostics data that not only demonstrate the robustness and feasibility of deep targeted sequencing and MS-analysis of FFPE CRC samples but also contribute to the understanding of CRC genetics. Most importantly, in more than half of the patients our approach enabled the selection of the best treatment currently available. (c) 2016 Wiley Periodicals, Inc.
C1 [Jesinghaus, Moritz; Pfarr, Nicole; Endris, Volker; Volckmar, Anna-Lena; Brandt, Regine; Herpel, Esther; Lasitschka, Felix; Schirmacher, Peter; Penzel, Roland; Weichert, Wilko; Stenzinger, Albrecht] Univ Heidelberg Hosp, Inst Pathol, D-69120 Heidelberg, Germany.
   [Jesinghaus, Moritz; Pfarr, Nicole; Muckenhuber, Alexander; Weichert, Wilko] Tech Univ Munich, Inst Pathol, D-81675 Munich, Germany.
   [Kloor, Matthias] Univ Heidelberg Hosp, Inst Pathol, Appl Tumor Biol, D-69120 Heidelberg, Germany.
   [Herpel, Esther] Natl Ctr Tumor Dis NCT, NCT Tissue Bank, Heidelberg, Germany.
   [Weichert, Wilko; Stenzinger, Albrecht] Natl Ctr Tumor Dis NCT, Heidelberg, Germany.
   [Stenzinger, Albrecht] Natl Ctr Tumor Dis NCT, HSO, Heidelberg, Germany.
C3 Ruprecht Karls University Heidelberg; Technical University of Munich;
   Ruprecht Karls University Heidelberg; Helmholtz Association; German
   Cancer Research Center (DKFZ); Ruprecht Karls University Heidelberg;
   Helmholtz Association; German Cancer Research Center (DKFZ); Ruprecht
   Karls University Heidelberg; Helmholtz Association; German Cancer
   Research Center (DKFZ); Ruprecht Karls University Heidelberg
RP Stenzinger, A (corresponding author), Natl Ctr Tumor Dis NCT, HSO, Heidelberg, Germany.; Stenzinger, A (corresponding author), Neuenheimer Feld 224, D-69120 Heidelberg, Germany.
EM albrecht.stenzinger@med.uni-heidelberg.de
RI Volckmar, Anna-Lena/ABE-3676-2021
FU German Cancer Consortium (DKTK); NCT-Heidelberg School of Oncology,
   Heidelberg, Germany
FX Supported by: German Cancer Consortium (DKTK; to W.W.) and
   NCT-Heidelberg School of Oncology, Heidelberg, Germany (to A.S.).
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NR 66
TC 32
Z9 33
U1 0
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1045-2257
EI 1098-2264
J9 GENE CHROMOSOME CANC
JI Gene Chromosomes Cancer
PD JUN
PY 2016
VL 55
IS 6
BP 505
EP 521
DI 10.1002/gcc.22352
PG 17
WC Oncology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Genetics & Heredity
GA DK1VS
UT WOS:000374703700002
PM 26917275
DA 2025-01-04
ER

PT J
AU Hossain, MS
   Karuniawati, H
   Jairoun, AA
   Urbi, Z
   Ooi, DJ
   John, A
   Lim, YC
   Kibria, KMK
   Mohiuddin, AKM
   Ming, LC
   Goh, KW
   Hadi, MA
AF Hossain, Md Sanower
   Karuniawati, Hidayah
   Jairoun, Ammar Abdulrahman
   Urbi, Zannat
   Ooi, Der Jiun
   John, Akbar
   Lim, Ya Chee
   Kibria, K. M. Kaderi
   Mohiuddin, A. K. M.
   Ming, Long Chiau
   Goh, Khang Wen
   Hadi, Muhammad Abdul
TI Colorectal Cancer: A Review of Carcinogenesis, Global Epidemiology,
   Current Challenges, Risk Factors, Preventive and Treatment Strategies
SO CANCERS
LA English
DT Article
DE anus cancer; colon cancer; drug resistance; prevalence; rectum cancer
ID SERUM 25-HYDROXYVITAMIN D; DRUG-DELIVERY SYSTEM; COLON-CANCER;
   PHYSICAL-ACTIVITY; VITAMIN-D; DENDRITIC CELLS; DOSE-RESPONSE;
   ALCOHOL-CONSUMPTION; GENETIC ALTERATIONS; NATURAL-HISTORY
AB Simple Summary The high lethality of colorectal cancer (CRC) is anticipated to continue in the following decades. Early-stage CRC is entirely treatable with surgery and adjuvant therapy (chemotherapy/radiotherapy). However, recurrence is common, and cancer drug resistance increases the chances of treatment failure. At the same time, there are many risk factors leading to high prevalence among both genders. Despite significant improvements in treating other cancers, CRC management is not yet at a satisfactory level. In this comprehensive review, we discussed the development of CRC and its associated risk factors, preventive and treatment strategies and proposed some recommendations. Furthermore, besides chemotherapy and targeted therapy, we discussed natural products as therapeutics for CRC. Colorectal cancer (CRC) is the second most deadly cancer. Global incidence and mortality are likely to be increased in the coming decades. Although the deaths associated with CRC are very high in high-income countries, the incidence and fatalities related to CRC are growing in developing countries too. CRC detected early is entirely curable by surgery and subsequent medications. However, the recurrence rate is high, and cancer drug resistance increases the treatment failure rate. Access to early diagnosis and treatment of CRC for survival is somewhat possible in developed countries. However, these facilities are rarely available in developing countries. Highlighting the current status of CRC, its development, risk factors, and management is crucial in creating public awareness. Therefore, in this review, we have comprehensively discussed the current global epidemiology, drug resistance, challenges, risk factors, and preventive and treatment strategies of CRC. Additionally, there is a brief discussion on the CRC development pathways and recommendations for preventing and treating CRC.
C1 [Hossain, Md Sanower] Int Islamic Univ Malaysia, Dept Biomed Sci, Kulliyyah Allied Hlth Sci, Kuantan 25200, Pahang, Malaysia.
   [Hossain, Md Sanower] Sristy Coll Tangail, Fac Sci, Tangail 1900, Bangladesh.
   [Karuniawati, Hidayah; Jairoun, Ammar Abdulrahman] Univ Sains Malaysia, Sch Pharmaceut Sci, Discipline Social & Adm Pharm, Gelugor 11800, Pulau Pinang, Malaysia.
   [Karuniawati, Hidayah] Univ Muhammadiyah Surakarta, Fac Pharm, Dept Pharmacol & Clin Pharm, Surakarta 57102, Indonesia.
   [Jairoun, Ammar Abdulrahman] Dubai Municipal, Hlth & Safety Dept, Dubai 67, U Arab Emirates.
   [Urbi, Zannat] Univ Malaysia Pahang, Fac Ind Sci & Technol, Dept Ind Biotechnol, Kuantan 26300, Pahang, Malaysia.
   [Ooi, Der Jiun] MAHSA Univ, Fac Dent, Dept Oral Biol & Biomed Sci, Jenjarom 42610, Selangor, Malaysia.
   [John, Akbar] Int Islamic Univ Malaysia, Inst Oceanog & Maritime Studies INOCEM, Kulliyyah Sci, Kuantan 25200, Pahang, Malaysia.
   [Lim, Ya Chee; Ming, Long Chiau] Univ Brunei Darussalam, PAP Rashidah Saadatul Bolkiah Inst Hlth Sci, BE-1410 Gadong, Brunei.
   [Kibria, K. M. Kaderi; Mohiuddin, A. K. M.] Mawlana Bhashani Sci & Technol Univ, Dept Biotechnol & Genet Engn, Tangail 1902, Bangladesh.
   [Goh, Khang Wen] INTI Int Univ, Fac Data Sci & Informat Technol, Nilai 71800, Negeri Sembilan, Malaysia.
   [Hadi, Muhammad Abdul] Qatar Univ, Coll Pharm, QU Hlth, Doha 2713, Qatar.
C3 International Islamic University Malaysia; Universiti Sains Malaysia;
   Universitas Muhammadiyah Surakarta; Universiti Malaysia Pahang Al-Sultan
   Abdullah (UMPSA); Mahsa University; International Islamic University
   Malaysia; University Brunei Darussalam; Mawlana Bhashani Science &
   Technology University; INTI International University; Qatar University
RP Hossain, MS (corresponding author), Int Islamic Univ Malaysia, Dept Biomed Sci, Kulliyyah Allied Hlth Sci, Kuantan 25200, Pahang, Malaysia.; Hossain, MS (corresponding author), Sristy Coll Tangail, Fac Sci, Tangail 1900, Bangladesh.; Ming, LC (corresponding author), Univ Brunei Darussalam, PAP Rashidah Saadatul Bolkiah Inst Hlth Sci, BE-1410 Gadong, Brunei.
EM mshossainbge@gmail.com; hk170@ums.ac.id; aajairoun@dm.gov.ae;
   urbi.zannat@gmail.com; djooi@mahsa.edu.my; akbarjohn@iium.edu.my;
   yachee.lim@ubd.edu.bn; km_kibria@mbstu.ac.bd; mohiuddin@mbstu.ac.bd;
   long.ming@ubd.edu.bn; khangwen.goh@newinti.edu.my; mabdulhadi@qu.edu.qa
RI Karuniawati, Hidayah/AAU-2450-2020; Chee, Lim/AAF-7541-2020; Ooi, Der
   Jiun/N-3801-2014; Hadi, Muhammad/AAL-7439-2020; Ming, Long
   Chiau/J-5210-2015; Karuniawati, Hidayah/Y-8467-2018; Kibria, K. M.
   Kaderi/K-2999-2019; Hossain, Md. Sanower/H-7341-2014
OI Hadi, Muhammad Abdul/0000-0003-0108-7833; Ming, Long
   Chiau/0000-0002-6971-1383; Karuniawati, Hidayah/0000-0003-2776-250X;
   /0000-0001-8111-6926; Kibria, K. M. Kaderi/0000-0002-8741-2918; Hossain,
   Md. Sanower/0000-0001-5686-2943
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NR 158
TC 346
Z9 360
U1 39
U2 273
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD APR
PY 2022
VL 14
IS 7
AR 1732
DI 10.3390/cancers14071732
PG 25
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 0K0OX
UT WOS:000780497900001
PM 35406504
OA Green Published, gold
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Yu, YJ
   Kolat, D
   Kaluzinska-Kolat, Z
   Liang, Z
   Peng, BQ
   Zhu, YF
   Liu, K
   Mei, JX
   Yu, G
   Zhang, WH
   Chen, XL
   Yang, K
   Hu, JK
   Zhao, LY
AF Yu, Yi-Jin
   Kolat, Damian
   Kaluzinska-Kolat, Zaneta
   Liang, Zhu
   Peng, Bo-Qiang
   Zhu, Yun-Feng
   Liu, Kai
   Mei, Jia-Xin
   Yu, Gang
   Zhang, Wei-Han
   Chen, Xiao-Long
   Yang, Kun
   Hu, Jian-Kun
   Zhao, Lin-Yong
TI The AP-2 Family of Transcription Factors-Still Undervalued Regulators in
   Gastroenterological Disorders
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE AP-2; TFAP2; transcription factors; gastroenterological disorders;
   gastric cancer; colorectal cancer
ID CANCER CELLS; CLONING; RISK; CHEMORESISTANCE; AP-2-ALPHA; EXPRESSION;
   GROWTH; GENES; CYCLE; DKK4
AB Activating enhancer-binding protein 2 (AP-2) is a family of transcription factors (TFs) that play crucial roles in regulating embryonic and oncogenic development. In addition to splice isoforms, five major family members encoded by the TFAP2A/B/C/D/E genes have been identified in humans, i.e., AP-2 alpha/beta/gamma/delta/epsilon. In general, the first three TFs have been studied more thoroughly than AP-2 delta or AP-2 epsilon. Currently, there is a relatively limited body of literature focusing on the AP-2 family in the context of gastroenterological research, and a comprehensive overview of the existing knowledge and recommendations for further research directions is lacking. Herein, we have collected available gastroenterological data on AP-2 TFs, discussed the latest medical applications of each family member, and proposed potential future directions. Research on AP-2 in gastrointestinal tumors has predominantly been focused on the two best-described family members, AP-2 alpha and AP-2 gamma. Surprisingly, research in the past decade has highlighted the importance of AP-2 epsilon in the drug resistance of gastric cancer (GC) and colorectal cancer (CRC). While numerous questions about gastroenterological disorders await elucidation, the available data undoubtedly open avenues for anti-cancer targeted therapy and overcoming chemotherapy resistance. In addition to gastrointestinal cancers, AP-2 family members (primarily AP-2 beta and marginally AP-2 gamma) have been associated with other health issues such as obesity, type 2 diabetes, liver dysfunction, and pseudo-obstruction. On the other hand, AP-2 delta has been poorly investigated in gastroenterological disorders, necessitating further research to delineate its role. In conclusion, despite the limited attention given to AP-2 in gastroenterology research, pivotal functions of these transcription factors have started to emerge and warrant further exploration in the future.
C1 [Yu, Yi-Jin; Peng, Bo-Qiang; Zhu, Yun-Feng; Liu, Kai; Mei, Jia-Xin; Yu, Gang; Zhang, Wei-Han; Chen, Xiao-Long; Yang, Kun; Hu, Jian-Kun; Zhao, Lin-Yong] Sichuan Univ, West China Hosp, Dept Gen Surg, Chengdu 610041, Peoples R China.
   [Yu, Yi-Jin; Peng, Bo-Qiang; Zhu, Yun-Feng; Liu, Kai; Mei, Jia-Xin; Yu, Gang; Zhang, Wei-Han; Chen, Xiao-Long; Yang, Kun; Hu, Jian-Kun; Zhao, Lin-Yong] Sichuan Univ, West China Hosp, Collaborat Innovat Ctr Biotherapy, Lab Gastr Canc ,State Key Lab Biotherapy, Chengdu 610041, Peoples R China.
   [Yu, Yi-Jin; Peng, Bo-Qiang; Zhu, Yun-Feng; Liu, Kai; Mei, Jia-Xin; Yu, Gang; Zhang, Wei-Han; Chen, Xiao-Long; Yang, Kun; Hu, Jian-Kun; Zhao, Lin-Yong] Sichuan Univ, West China Hosp, Canc Ctr, Chengdu 610041, Peoples R China.
   [Yu, Yi-Jin; Peng, Bo-Qiang; Zhu, Yun-Feng; Liu, Kai; Mei, Jia-Xin; Yu, Gang; Zhang, Wei-Han; Chen, Xiao-Long; Yang, Kun; Hu, Jian-Kun; Zhao, Lin-Yong] Sichuan Univ, West China Hosp, Gastr Canc Ctr, Chengdu 610041, Peoples R China.
   [Kolat, Damian; Kaluzinska-Kolat, Zaneta] Med Univ Lodz, Dept Funct Genom, PL-90752 Lodz, Lodzkie, Poland.
   [Kolat, Damian; Kaluzinska-Kolat, Zaneta] Med Univ Lodz, Dept Biomed & Expt Surg, PL-90136 Lodz, Lodzkie, Poland.
   [Liang, Zhu] Univ Oxford, Target Discovery Inst, Ctr Med Discovery, Nuffield Dept Med, Oxford OX1 2JD, England.
   [Liang, Zhu] Univ Oxford, CAMS Oxford Inst COI, Chinese Acad Med Sci CAMS, Nuffield Dept Med, Oxford OX1 2JD, England.
C3 Sichuan University; Sichuan University; Sichuan University; Sichuan
   University; Medical University Lodz; Medical University Lodz; University
   of Oxford; University of Oxford
RP Zhao, LY (corresponding author), Sichuan Univ, West China Hosp, Dept Gen Surg, Chengdu 610041, Peoples R China.; Zhao, LY (corresponding author), Sichuan Univ, West China Hosp, Collaborat Innovat Ctr Biotherapy, Lab Gastr Canc ,State Key Lab Biotherapy, Chengdu 610041, Peoples R China.; Zhao, LY (corresponding author), Sichuan Univ, West China Hosp, Canc Ctr, Chengdu 610041, Peoples R China.; Zhao, LY (corresponding author), Sichuan Univ, West China Hosp, Gastr Canc Ctr, Chengdu 610041, Peoples R China.
EM yuyijin0314@163.com; damian.kolat@stud.umed.lodz.pl;
   153795352@scu.edu.cn
RI liu, li/HGC-0900-2022; Hu, Jiankun/D-9856-2012; Kolat,
   Damian/W-6134-2019; Kaluzinska-Kolat, Zaneta/W-6078-2019
OI Kolat, Damian/0000-0002-1086-3796; Yu, Yijin/0009-0002-9983-7910;
   Kaluzinska-Kolat, Zaneta/0000-0002-2335-3293
FU National Natural Science Foundation of China [82102998]
FX This review is supported by the National Natural Science Foundation of
   China, No. 82102998, to Lin-Yong Zhao.
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NR 49
TC 0
Z9 0
U1 3
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD SEP
PY 2024
VL 25
IS 17
AR 9138
DI 10.3390/ijms25179138
PG 11
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA F6T2E
UT WOS:001311114600001
PM 39273087
OA gold
DA 2025-01-04
ER

PT J
AU Bui, TM
   Butin-Israeli, V
   Wiesolek, HL
   Zhou, M
   Rehring, JF
   Wiesmüller, L
   Wu, JD
   Yang, GY
   Hanauer, SB
   Sebag, JA
   Sumagin, R
AF Bui, Triet M.
   Butin-Israeli, Veronika
   Wiesolek, Hannah L.
   Zhou, Meredith
   Rehring, Jake F.
   Wiesmueller, Lisa
   Wu, Jennifer D.
   Yang, Guang-Yu
   Hanauer, Stephen B.
   Sebag, Julien A.
   Sumagin, Ronen
TI Neutrophils Alter DNA Repair Landscape to Impact Survival and Shape
   Distinct Therapeutic Phenotypes of Colorectal Cancer
SO GASTROENTEROLOGY
LA English
DT Article
DE Colon Cancer; Ku70; MicroRNA; Rad51; DSB
ID DAMAGE; INSTABILITY; INHIBITOR; OLAPARIB; PROTEIN; CHOICE; CELLS; PK
AB BACKGROUND & AIMS: Tumor-infiltrating neutrophils (polymorphonuclear neutrophils [PMNs]) are a prominent feature of colorectal cancer (CRC), where they can promote cytotoxicity or exacerbate disease outcomes. We recently showed that in acute colon injury, PMNs can increase DNA double-strand break (DSB) burden and promote genomic instability via microRNA-dependent inhibition of homologous recombination (HR) repair. In this study, we aimed to establish whether in inflamed colon, neutrophils shape the DSB-repair responses to impact CRC progression and sensitivity/resistance to DNA-repair targeted therapy. METHODS: Human sporadic CRC biopsies, The Cancer Genome Atlas gene expression analyses, tumor xenografts, and murine CRC models, as well as small-molecule inhibition of key DSB-repair factors were leveraged to investigate changes in the DSB-repair landscape and identify unique CRC responses with/without tumor infiltration by PMNs. RESULTS: We reveal that neutrophils exert a functional dualism in cancer cells, driving temporal modulation of the DNA damage landscape and resolution of DSBs. PMNs were found to promote HR deficiency in low-grade CRC by miR-155-dependent downregulation of RAD51, thus attenuating tumor growth. However, neutrophil-mediated genotoxicity due to accumulation of DSBs led to the induction of non-homologous end-joining (NHEJ), allowing for survival and growth of advanced CRC. Our findings identified a PMN-induced HR-deficient CRC phenotype, featuring low RAD51 and low Ku70 levels, rendering it susceptible to synthetic lethality induced by clinically approved PARP1 inhibitor Olaparib. We further identified a distinct PMN-induced HR-deficient CRC phenotype, featuring high Ku70 and heightened NHEJ, which can be therapeutically targeted by specific inhibition of NHEJ. CONCLUSIONS: Our work delineates 2 mechanism-based translatable therapeutic interventions in sporadic CRC.
C1 [Bui, Triet M.; Wiesolek, Hannah L.; Zhou, Meredith; Rehring, Jake F.; Yang, Guang-Yu; Sumagin, Ronen] Northwestern Univ, Dept Pathol, Feinberg Sch Med, 300 East Super St, Chicago, IL 60611 USA.
   [Butin-Israeli, Veronika; Wu, Jennifer D.] Northwestern Univ, Dept Urol & Microbiol Immunol, Feinberg Sch Med, Chicago, IL 60611 USA.
   [Wiesmueller, Lisa] Ulm Univ, Dept Obstet & Gynecol, Ulm, Germany.
   [Hanauer, Stephen B.] Northwestern Mem Hosp, Dept Med Gastroenterol & Hepatol, Chicago, IL 60611 USA.
   [Sebag, Julien A.] Univ Iowa, Dept Mol Physiol & Biophys, Iowa City, IA USA.
C3 Northwestern University; Feinberg School of Medicine; Northwestern
   University; Feinberg School of Medicine; Ulm University; Northwestern
   Memorial Hospital; University of Iowa
RP Sumagin, R (corresponding author), Northwestern Univ, Dept Pathol, Feinberg Sch Med, 300 East Super St, Chicago, IL 60611 USA.
EM roan.sumagin@normwb.tem.edu
RI Israeli, Veronika/ITU-2544-2023; sebag, julien/AAU-2142-2020; Wu,
   Jennifer/GRX-1831-2022
OI Sumagin, Ronen/0000-0002-5689-1100; Rehring, Jacob/0000-0003-4927-0880;
   Bui, Triet Minh/0000-0002-1092-9820
FU Digestive Health Foundation; American Cancer Society Research Scholar
   Award; Crohn's & Colitis Foundation Senior Research Award; Department of
   Defense's Congressionally Directed Medical Research Program Horizon
   Award; German Research Foundation (DFG) Grant Project B3 in Research
   Training Group GRK [2254]
FX This work was supported by grants from the Digestive Health Foundation,
   American Cancer Society Research Scholar Award, and Crohn's & Colitis
   Foundation Senior Research Award to Ronen Sumagin, and the Department of
   Defense's Congressionally Directed Medical Research Program Horizon
   Award to Triet M. Bui. Lisa Wiesmuller was supported by the German
   Research Foundation (DFG) Grant Project B3 in Research Training Group
   GRK 2254 "Heterogeneity and evolution in solid tumors (HEIST)."
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NR 38
TC 23
Z9 25
U1 1
U2 5
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
EI 1528-0012
J9 GASTROENTEROLOGY
JI Gastroenterology
PD JUL
PY 2021
VL 161
IS 1
BP 225
EP +
DI 10.1053/j.gastro.2021.03.027
EA JUN 2021
PG 29
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA SY0NP
UT WOS:000665592300037
PM 33753103
DA 2025-01-04
ER

PT J
AU Babajanyan, S
   Pollack, M
   Castelo, S
   Kavati, A
   Bekaii-Saab, TS
AF Babajanyan, Svetlana
   Pollack, Megan
   Castelo, Sarah
   Kavati, Abhishek
   Bekaii-Saab, Tanios S.
TI Sequenced treatment after regorafenib and survival in metastatic
   colorectal cancer: a qualitative clinical review
SO COLORECTAL CANCER
LA English
DT Review
DE maximize; mCRC; metastatic colorectal cancer; refractory; regorafenib;
   targeted agents; treatment sequence
ID TRIFLURIDINE/TIPIRACIL; EFFICACY; SAFETY; CHEMOTHERAPY; TAS-102;
   RECHALLENGE
AB There is limited evidence-based guidance regarding treatment sequencing and outcomes following regorafenib in patients with refractory metastatic colorectal cancer (mCRC). A targeted literature review was conducted to identify studies with clinical outcomes associated with regorafenib therapy and subsequent treatment following regorafenib therapy. The median overall survival range of the nine studies with sequenced-based survival data was 2.1-19.3 months for regorafenib prior to subsequent therapy in refractory mCRC. Safety outcomes in patients treated with regorafenib prior to other therapies in mCRC were generally comparable to reported adverse events in clinical trials for subsequent agents. Data from this review demonstrate a potential correlation between survival and the use of regorafenib prior to subsequent chemotherapy or targeted therapy in patients with refractory mCRC.
   Plain language summary There is limited information regarding the best order of medications for the treatment of patients with metastatic colorectal cancer (mCRC). Multiple scientific studies were read to find results associated with regorafenib treatment and other medications that may follow regorafenib treatment in mCRC. In these studies, patients lived between 2.1 and 19.3 months when using regorafenib before other medications. Patients treated with regorafenib before other medications had the same side effects as if they were only treated with the other medications. Using regorafenib before other medications may be useful in patients with mCRC.
C1 [Babajanyan, Svetlana; Kavati, Abhishek] Bayer Healthcare Pharmaceut Inc, 100 Bayer Blvd, Whippany, NJ 07981 USA.
   [Pollack, Megan; Castelo, Sarah] Xcenda LLC, 5025 Plano Pkwy, Carrollton, TX 75010 USA.
   [Bekaii-Saab, Tanios S.] Mayo Clin, Canc Ctr, 5881 E Mayo Blvd, Phoenix, AZ 85054 USA.
C3 Bayer AG; Bayer Healthcare Pharmaceuticals; Mayo Clinic; Mayo Clinic
   Phoenix
RP Pollack, M (corresponding author), Xcenda LLC, 5025 Plano Pkwy, Carrollton, TX 75010 USA.
EM megan.pollack@xcenda.com
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NR 56
TC 0
Z9 0
U1 0
U2 3
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1758-194X
EI 1758-1958
J9 COLORECTAL CANCER
JI Colorectal Cancer
PD MAR
PY 2021
VL 10
IS 1
AR CRC37
DI 10.2217/crc-2022-0006
PG 12
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA 4D8IL
UT WOS:000847383000001
DA 2025-01-04
ER

PT J
AU Ma, J
   Jiang, Y
   Zhou, CP
   Wang, DT
   Zhao, CX
   Zhang, YM
AF Ma, Jun
   Jiang, Ye
   Zhou, Chaoping
   Wang, Datian
   Zhao, Chunxia
   Zhang, Yaming
TI Case report: Rupture of an ileus tube in a patient with recurrent rectal
   cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE rectal cancer; recurrence or metastasis; intestinal obstruction; ileus
   tube; complication
ID SMALL-BOWEL; DECOMPRESSION; OBSTRUCTION
AB The insertion of an ileus tube is an important treatment for intestinal obstruction. According to previous reports, jejunal intussusception has been reported as a complication associated with ileus tube placement. However, rupture of the weighted tip of an ileus tube has not been reported before. Herein, we report a 55-year-old Chinese woman who underwent radical proctectomy (DIXON) for rectal cancer and developed pelvic recurrence and lung metastasis 65 months after surgery, accompanied by symptoms of acute intestinal obstruction. An ileus tube was inserted before the operation (extensive total hysterectomy, bilateral adnexal resection, rectal Hartman operation, partial enterectomy, and intestinal adhesion lysis). Rupture of the ileus tube occurred after the operation and was treated with paraffin oil and enteral nutrition, and the metal beads and spring were eliminated through the colostomy. During the follow-up, the patient received targeted therapy plus immunotherapy, which was successful: the quality of life of the patient was excellent, and no obvious abnormal symptoms were found. Endoscopy-assisted ileus tube insertion should be performed under intravenous anesthesia, and a knot should be tied at the tip of the ileus tube before insertion so that the ileus tube can be inserted easily by grasping the thread with biopsy forceps(the "thread-knotting" method). With the above methods, the procedure of ileus tube insertion could be improved to reduce the incidence of tube-related rupture.
C1 [Ma, Jun; Zhou, Chaoping; Wang, Datian; Zhao, Chunxia; Zhang, Yaming] Anqing Municipal Hosp, Dept Gen Surg, Anqing, Peoples R China.
   [Jiang, Ye] Anqing Municipal Hosp, Dept Gastroenterol, Anqing, Peoples R China.
RP Zhang, YM (corresponding author), Anqing Municipal Hosp, Dept Gen Surg, Anqing, Peoples R China.
EM zhangyaming2014@163.com
RI Zhao, Chunxia/KBB-4190-2024
FU Research Projects Foundation at Universities of Anhui Province
   [2023AH050577]
FX The author(s) declare financial support was received for the research,
   authorship, and/or publication of this article. This work was supported
   by grants from Research Projects Foundation at Universities of Anhui
   Province (2023AH050577).
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NR 14
TC 0
Z9 0
U1 1
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD DEC 15
PY 2023
VL 13
AR 1270728
DI 10.3389/fonc.2023.1270728
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DP7U7
UT WOS:001133334700001
PM 38162506
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhao, XH
   Chang, CC
   Chuang, TL
   Lin, CW
AF Zhao, Xihong
   Chang, Chia-Chen
   Chuang, Tsung-Liang
   Lin, Chii-Wann
TI Detection of KRAS mutations of colorectal cancer with
   peptide-nucleic-acid-mediated real-time PCR clamping
SO BIOTECHNOLOGY & BIOTECHNOLOGICAL EQUIPMENT
LA English
DT Article
DE KRAS; mutation; peptide nucleic acid (PNA); colorectal cancer
ID SURFACE-PLASMON RESONANCE; FACTOR RECEPTOR MUTATIONS; RAPID DETECTION;
   LUNG-CANCER; TARGETED THERAPY; RAS MUTATIONS; AMPLIFICATION; SAMPLES;
   PATHOLOGISTS; BIOMARKERS
AB Colorectal cancer (CRC) is the third most common cancer in the world and its disease-specific mortality is estimated to be approximately 33% in the developed world. KRAS mutations have been shown to predict response to anti-EGFR (epidermal growth factor receptor) targeted monoclonal antibody therapy. Therefore, KRAS mutation testing of metastatic CRC patients is mandatory in the clinical setting to aid in the choice of appropriate therapy. Currently, the most common strategy for KRAS mutation detection consists of conventional polymerase chain reaction (PCR) and direct sequencing. However, it is a time-consuming and complicated procedure, not suitable for routine clinical test. The objective of this study is to develop and evaluate a highly sensitive and rapid method using peptide nucleic acid (PNA) oligomers mediated real-time PCR clamping for detection of KRAS mutations. The PNA-mediated PCR clamping assay can real-time detect a mutation in a sample containing 1% of the mutant allele in a mixture of wild-type genomic DNA, which also enables the accurate and rapid detection of all KRAS codon 12 and 13 mutations in a single reaction. The total assay time is short as it requires only 1.5hours after the samples preparation. Thus, the present method offers a potential alternative to be applied in clinical samples of CRC for detection of DNA carrying KRAS mutations.
C1 [Zhao, Xihong] Wuhan Inst Technol, Sch Chem Engn & Pharm, Hubei Key Lab Novel Reactor & Green Chem Technol, Key Lab Green Chem Proc,Minist Educ, Wuhan, Peoples R China.
   [Zhao, Xihong; Chang, Chia-Chen; Chuang, Tsung-Liang; Lin, Chii-Wann] Natl Taiwan Univ, Inst Biomed Engn, Taipei, Taiwan.
C3 Wuhan Institute of Technology; National Taiwan University
RP Lin, CW (corresponding author), Natl Taiwan Univ, Inst Biomed Engn, Taipei, Taiwan.
EM cwlinx@ntu.edu.tw
RI , xihong/F-8869-2015; Chang, Chia-Chen/D-1600-2011
OI , xihong/0000-0003-1491-7808; Chang, Chia-Chen/0000-0001-5466-4724
FU Taiwan National Science Council [NSC102-2218-E-002-014-MY3]; Center for
   Emerging Material and Advanced Devices of National Taiwan University;
   National Natural Science Foundation of China [31501582]
FX This work was supported by the Taiwan National Science Council [grant
   number NSC102-2218-E-002-014-MY3]; the Center for Emerging Material and
   Advanced Devices of National Taiwan University, and in part by grants
   from the National Natural Science Foundation of China [grant number
   31501582].
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NR 30
TC 3
Z9 3
U1 1
U2 30
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1310-2818
EI 1314-3530
J9 BIOTECHNOL BIOTEC EQ
JI Biotechnol. Biotechnol. Equip.
PD DEC
PY 2016
VL 30
IS 6
BP 1155
EP 1162
DI 10.1080/13102818.2016.1228479
PG 8
WC Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology
GA EB5TR
UT WOS:000387443800015
OA gold
DA 2025-01-04
ER

PT J
AU Sinicrope, FA
   Okamoto, K
   Kasi, PM
   Kawakami, H
AF Sinicrope, Frank A.
   Okamoto, Koichi
   Kasi, Pashtoon M.
   Kawakami, Hisato
TI Molecular Biomarkers in the Personalized Treatment of Colorectal Cancer
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Predictive Markers; Prognostic Markers; Colorectal Cancer; Molecular
   Subtypes; RAS; BRAF; MSI; DNA Mismatch Repair; Immunotherapy; Targeted
   Therapy; Biologics; Anti-EGFR; Anti-VEGF
ID III COLON-CANCER; ISLAND METHYLATOR PHENOTYPE; MISMATCH REPAIR STATUS;
   MICROSATELLITE-INSTABILITY; STAGE-II; ADJUVANT CHEMOTHERAPY; 1ST-LINE
   TREATMENT; BRAF MUTATION; PROGNOSTIC VALUE; PLUS IRINOTECAN
AB Colorectal cancer (CRC) is a disease in which pathogenesis is influenced by genetic and epigenetic events that occur with tumor initiation and progression. Large variation exists in individual patient prognosis and response to chemotherapy, caused by molecular heterogeneity. Certain biomarkers have been identified that can predict clinical outcome beyond tumor staging, and inform treatment selection. Molecular testing is routinely performed in clinical practice for the selection of patients for targeted biological agents or immunotherapy, and is advocated for prognostic stratification. Estimating prognosis can avoid undertreatment or overtreatment and also guide the intensity of patient followup. Classifiers of CRC have been developed that integrate genetic and/or epigenetic features. The mutational status of KRAS and BRAF(V600E) oncogenes combined with analysis of the DNA mismatch repair system with/without the CpG island methylator phenotype (CIMP) has been shown to identify colon cancer subtypes with distinct clinical features and prognoses. Gene expression profiling has also been used to subtype CRCs and can overcome the limitations of single/limited gene testing. A recent effort identified 4 consensus molecular subtypes of biological relevance that were associated with different patient outcomes. Efforts to validate and refine these subtypes to include additional genomic features are ongoing. The focus of this article is to highlight molecular markers that can inform clinical decision-making in patients with CRC.
C1 [Sinicrope, Frank A.; Okamoto, Koichi; Kawakami, Hisato] Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN 55905 USA.
   [Sinicrope, Frank A.; Okamoto, Koichi; Kawakami, Hisato] Mayo Canc Ctr, Rochester, MN USA.
   [Sinicrope, Frank A.; Kasi, Pashtoon M.] Mayo Clin, Div Med Oncol, Rochester, MN 55905 USA.
   [Sinicrope, Frank A.; Kasi, Pashtoon M.] Mayo Canc Ctr, Rochester, MN USA.
C3 Mayo Clinic; Mayo Clinic; Mayo Clinic; Mayo Clinic
RP Sinicrope, FA (corresponding author), Mayo Clin, 200 First St SW, Rochester, MN 55905 USA.
EM sinicrope.frank@mayo.edu
RI Kasi, Pashtoon/M-2569-2019; Kawakami, Hisato/L-6845-2019
OI Kasi, Pashtoon Murtaza/0000-0002-5169-7085; Kawakami,
   Hisato/0000-0002-3280-4850
FU NCI NIH HHS [K05 CA142885] Funding Source: Medline
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NR 58
TC 95
Z9 101
U1 0
U2 29
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD MAY
PY 2016
VL 14
IS 5
BP 651
EP 658
DI 10.1016/j.cgh.2016.02.008
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DK6WS
UT WOS:000375067000008
PM 26872400
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Takayoshi, K
   Kusaba, H
   Uenomachi, M
   Mitsugi, K
   Makiyama, C
   Makiyama, A
   Uchino, K
   Shirakawa, T
   Shibata, Y
   Shinohara, Y
   Inadomi, K
   Tsuchihashi, K
   Arita, S
   Ariyama, H
   Esaki, T
   Akashi, K
   Baba, E
AF Takayoshi, Kotoe
   Kusaba, Hitoshi
   Uenomachi, Masato
   Mitsugi, Kenji
   Makiyama, Chinatsu
   Makiyama, Akitaka
   Uchino, Keita
   Shirakawa, Tsuyoshi
   Shibata, Yoshihiro
   Shinohara, Yudai
   Inadomi, Kyoko
   Tsuchihashi, Kenji
   Arita, Shuji
   Ariyama, Hiroshi
   Esaki, Taito
   Akashi, Koichi
   Baba, Eishi
TI Suggestion of added value by bevacizumab to chemotherapy in patients
   with unresectable or recurrent small bowel cancer
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE Advanced small bowel adenocarcinoma; Chemotherapy; Molecular targeting
   therapy; Bevacizumab
ID METASTATIC COLORECTAL-CANCER; RANDOMIZED PHASE-III; 1ST-LINE THERAPY;
   LYNCH-SYNDROME; ADVANCED ADENOCARCINOMA; PROGNOSTIC-FACTORS;
   GASTRIC-CANCER; DOUBLE-BLIND; OXALIPLATIN; CAPECITABINE
AB Purpose Standard therapy for advanced small bowel adenocarcinoma (SBA) has not yet been established. The present study assessed the efficacy and safety of chemotherapy (CT) in association with molecular targeting approaches for SBA.
   Methods The histories of 33 advanced SBA patients from six different institutions in Japan, who received CT from 2008 to 2016, were retrospectively examined for background, clinical course and outcome.
   Results Median patient age was 65 years (range 39-83). Primary tumor was located in the duodenum in 21 patients (67%), the ampulla of Vater in three patients (9%), the jejunum in seven patients (21%) and the ileum in one patient (3%). Histologically, well-to-moderately and poorly differentiated adenocarcinoma were identified in 20 (61%) and nine (27%) patients, respectively. Thirteen patients received a single CT regimen, seven patients received two types of CT regimen, and 13 patients received three or more CT regimens. As first-line CT, modified FOLFOX6, capecitabine plus oxaliplatin, and S-1 plus cisplatin were employed in 13, 1, and 4 patients, respectively. The response rate (RR) and median progression-free survival (PFS) were 25% and 6.0 months, respectively. Median overall survival (OS) was 13.0 months. Nine out of the 33 patients received bevacizumab-containing CT and three received cetuximab-containing CT. Median OS of bevacizumab-containing CT patients was 21.9 months. No unexpected serious adverse events were observed.
   Conclusions The analysis indicates that combination CT for advanced SBA is associated with modest efficacy and safety, and bevacizumab-containing CT may contribute to favorable outcome in these patients.
C1 [Takayoshi, Kotoe; Kusaba, Hitoshi; Inadomi, Kyoko; Tsuchihashi, Kenji; Ariyama, Hiroshi; Akashi, Koichi] Kyushu Univ, Grad Sch Med Sci, Dept Med & Biosyst Sci, Higashi Ku, 3-1-1 Maidashi, Fukuoka 8128582, Japan.
   [Takayoshi, Kotoe; Shinohara, Yudai; Esaki, Taito] Natl Hosp Org Kyushu Canc Ctr, Dept Gastrointestinal & Med Oncol, Minami Ku, 3-1-1 Notame, Fukuoka 8111395, Japan.
   [Uenomachi, Masato; Mitsugi, Kenji] Hamanomachi Hosp, Dept Oncol, Chuou Ku, 3-3-1 Nagahama, Fukuoka 8108539, Japan.
   [Makiyama, Chinatsu; Makiyama, Akitaka] Japan Community Healthcare Org Kyushu Hosp, Dept Hematol & Oncol, Yahatanishi Ku, 1-8-1 Kishinoura, Kitakyushu, Fukuoka 8068501, Japan.
   [Uchino, Keita] Natl Hosp Org Kyushu Med Ctr, Dept Med Oncol, Clin Res Inst, Chuou Ku, 1-8-1 Jigyouhama, Fukuoka 8100065, Japan.
   [Shirakawa, Tsuyoshi] Miyazaki Prefectural Miyazaki Hosp, Dept Oncol, 5-30 Kita Takamatsucho, Miyazaki 8808510, Japan.
   [Shibata, Yoshihiro] Fukuoka Wajiro Hosp, Dept Med Oncol, Higashi Ku, 2-2-75 Wajirooka, Fukuoka 8110213, Japan.
   [Arita, Shuji; Baba, Eishi] Kyushu Univ, Dept Comprehens Clin Oncol, Fac Med Sci, Higashi Ku, 3-1-1 Maidashi, Fukuoka 8128582, Japan.
C3 Kyushu University; Kyushu Cancer Center; Kyushu University
RP Baba, E (corresponding author), Kyushu Univ, Dept Comprehens Clin Oncol, Fac Med Sci, Higashi Ku, 3-1-1 Maidashi, Fukuoka 8128582, Japan.
EM e-baba@c-oncology.med.kyushu-u.ac.jp
RI Ariyama, Hiroshi/HZL-0608-2023; Makiyama, Akitaka/AAU-7256-2020
OI Yamaguchi, Kyoko/0000-0002-5458-5345
FU Chugai; Merck Serono; Yakult
FX Baba E. has received research Grants from Chugai and Merck Serono.
   Akashi K. has received research Grants from Chugai, Yakult and Merck
   Serono and an honorarium from Chugai. Esaki T. has received a research
   Grant from Merck Serono and honoraria from Chugai and Merck Serono.
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NR 38
TC 19
Z9 19
U1 0
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
EI 1432-0843
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD AUG
PY 2017
VL 80
IS 2
BP 333
EP 342
DI 10.1007/s00280-017-3371-0
PG 10
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA FC1ZZ
UT WOS:000406638200011
PM 28653251
DA 2025-01-04
ER

PT J
AU Li, ZH
   Fei, X
   Pan, Z
   Liang, YH
   Yang, QC
   Cheng, DD
AF Li, Zhaohui
   Fei, Xiang
   Pan, Zhen
   Liang, Yonghui
   Yang, Qingcheng
   Cheng, Dongdong
TI Mometasone furoate inhibits tumor progression and promotes apoptosis
   through activation of the AMPK/mTOR signaling pathway in osteosarcoma
SO JOURNAL OF BONE ONCOLOGY
LA English
DT Article
DE Apoptosis; Osteosarcoma; Mometasone furoate; AMPK; Targeted therapy
ID COLON-CANCER; EFFICACY; ARREST
AB Osteosarcoma is the most common primary malignant bone tumor in adolescents. While treatments for osteosarcoma have improved, the overall survival has not changed for three decades, and thus, new targets for therapeutic development are needed. Recently, glucocorticoids have been reported to have antitumor effects. Mometasone furoate (MF), a synthetic glucocorticoid, is of great value in clinical application, but there are few reports on its antitumor effect. Here, we verified the effect of MF on osteosarcoma in vitro and in vivo. In vitro, cell proliferation, cell cycle progression, apoptosis and cell metastasis were detected using Cell Counting Kit-8 (CCK8), colony formation, flow cytometry, wound-healing and transwell assays, respectively. In vivo, we generated a xenograft mouse model. To examine the potential role of the AMPK pathway, an AMPK-specific inhibitor (dorsomorphin) was used. The expression levels of factors related to the cell cycle, apoptosis and activation of the AMPK/mTOR pathway were assessed by immunohistochemistry and Western blotting. MF inhibited proliferation and metastasis and induced S phase arrest and apoptosis in osteosarcoma cells in a dose-dependent manner. In vivo, MF effectively inhibited osteosarcoma cell growth and pulmonary metastasis; however, it had no negative effect on the internal organs. Additionally, MF could activate the AMPK/mTOR pathway in osteosarcoma. Dorsomorphin significantly attenuated MF-induced antitumor activities. In summary, MF can inhibit osteosarcoma proliferation and metastasis and promote osteosarcoma cell apoptosis through the AMPK/mTOR signaling pathway in vitro and in vivo, which can provide a new rationale for subsequent academic and clinical research on osteosarcoma treatment.
C1 [Li, Zhaohui; Fei, Xiang; Liang, Yonghui; Yang, Qingcheng; Cheng, Dongdong] Shanghai Jiao Tong Univ, Dept Orthoped, Shanghai Sixth Peoples Hosp Affiliated, Sch Med, Shanghai 200233, Peoples R China.
   [Pan, Zhen] Shanghai Jiao Tong Univ, Dept Orthoped, Tong Ren Hosp Affiliated, Sch Med, Shanghai 200233, Peoples R China.
C3 Shanghai Jiao Tong University; Shanghai Jiao Tong University
RP Yang, QC; Cheng, DD (corresponding author), Shanghai Jiao Tong Univ, Dept Orthoped, Shanghai Sixth Peoples Hosp Affiliated, Sch Med, Shanghai 200233, Peoples R China.
EM tjyqc@163.com; 1988noodle@163.com
RI Fei, Xiang/Z-1378-2019
OI Fei, Xiang/0009-0004-3773-550X
FX The authors declare that they have no known competing financial
   interests or personal relationships that could have appeared to
   influence the work reported in this paper.
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NR 30
TC 0
Z9 0
U1 3
U2 3
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2212-1374
J9 J BONE ONCOL
JI J. Bone Oncol.
PD AUG
PY 2024
VL 47
AR 100618
DI 10.1016/j.jbo.2024.100618
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA XU2A0
UT WOS:001264113100001
PM 39050186
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Tao, L
   Zhou, Y
   Luo, Y
   Qiu, JH
   Xiao, YZ
   Zou, J
   Zhang, Y
   Liu, XC
   Yang, XY
   Gou, K
   Xu, J
   Guan, XQ
   Cen, XB
   Zhao, YL
AF Tao, Lei
   Zhou, Yue
   Luo, Yuan
   Qiu, Jiahao
   Xiao, Yuzhou
   Zou, Jiao
   Zhang, Yu
   Liu, Xingchen
   Yang, Xinyu
   Gou, Kun
   Xu, Jing
   Guan, Xinqi
   Cen, Xiaobo
   Zhao, Yinglan
TI Epigenetic regulation in cancer therapy: From mechanisms to clinical
   advances
SO MEDCOMM-ONCOLOGY
LA English
DT Review
DE cancer therapy; DNA methylation; histone modifications; epigenetic
   drugs; epigenetic regulation
ID EPITHELIAL-MESENCHYMAL TRANSITION; 1ST-IN-HUMAN PHASE-I; CELL
   LUNG-CANCER; TUMOR-SUPPRESSOR; PROSTATE-CANCER; COLORECTAL-CANCER;
   PROMOTER HYPERMETHYLATION; PANCREATIC-CANCER; ANDROGEN RECEPTOR;
   POOR-PROGNOSIS
AB Epigenetic regulation refers to the alteration of gene expression independent of changes in DNA sequence. It involves chemical modifications such as DNA methylation, histone methylation, and histone acetylation, which are regulated by a coordinated interplay of various regulators to ensure precise spatial and temporal regulation of gene expression. Epigenetic aberrations are commonly observed in cancer and are considered as hallmarks of cancer. In recent years, small molecules targeting specific epigenetic regulators have been developed and are demonstrating promising therapeutic potential in preclinical and clinical trials for cancer treatment. In this review, we summarize the essential regulatory mechanisms and dysfunctions of epigenetic regulators involved in DNA methylation, histone methylation, and histone acetylation during tumor development and progression. Moreover, we discuss the current advances and challenges in cancer epigenetic therapy that target these mechanisms in both hematologic malignancies and solid tumors. Finally, we discuss the potential of combining epigenetic drugs with other therapies, including chemotherapy, radiotherapy, targeted therapy, and immunotherapy, as a promising approach for cancer treatment. Overall, we aim to enhance the understanding of epigenetic regulation in cancer therapy and explore targeted therapeutic strategies based on these mechanisms, to ultimately advance cancer therapy and improve patient prognosis.
   Epigenetic regulation involves chemical modifications including DNA methylation, histone methylation, and histone acetylation, which are governed by a coordinated interplay of various regulators. In cancer, epigenetic aberrations are commonly observed and considered as a hallmark of cancer. Small molecules have been developed to target specific epigenetic regulators and reverse the epigenetic reprogramming occurring in cancer. image
C1 [Tao, Lei; Zhou, Yue; Luo, Yuan; Qiu, Jiahao; Xiao, Yuzhou; Zou, Jiao; Liu, Xingchen; Gou, Kun; Xu, Jing; Guan, Xinqi; Cen, Xiaobo; Zhao, Yinglan] Sichuan Univ, West China Hosp, Canc Ctr, Dept Biotherapy, Chengdu 610041, Peoples R China.
   [Tao, Lei; Zhou, Yue; Luo, Yuan; Qiu, Jiahao; Xiao, Yuzhou; Zou, Jiao; Liu, Xingchen; Gou, Kun; Xu, Jing; Guan, Xinqi; Cen, Xiaobo; Zhao, Yinglan] Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Chengdu 610041, Peoples R China.
   [Qiu, Jiahao; Cen, Xiaobo] Sichuan Univ, West China Hosp, Natl Chengdu Ctr Safety Evaluat Drugs, Chengdu, Peoples R China.
   [Zhang, Yu; Yang, Xinyu] Sichuan Univ, West China Sch Pharm, Dept Pharmacol, Chengdu, Peoples R China.
   [Zhang, Yu] Tibet Univ, Dept Med, Lhasa, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University; Sichuan
   University; Tibet University
RP Zhao, YL (corresponding author), Sichuan Univ, West China Hosp, Canc Ctr, Dept Biotherapy, Chengdu 610041, Peoples R China.; Zhao, YL (corresponding author), Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Chengdu 610041, Peoples R China.
EM zhaoyinglan@scu.edu.cn
RI Yang, Xinyu/KIL-0555-2024
FU Natural Science Foundation of Sichuan Province [2022NSFSC0053]; The
   1.3.5 Project for Disciplines of Excellence, West China Hospital,
   Sichuan University [ZYGD23011]
FX Natural Science Foundation of Sichuan Province, Grant/Award Number:
   2022NSFSC0053; National Natural Science Foundation of China, Grant/Award
   Number: 882272716; 1 center dot 3 center dot 5 Project for Disciplines
   of Excellence, West China Hospital, Sichuan University, Grant/Award
   Number: ZYGD23011
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NR 494
TC 7
Z9 7
U1 8
U2 8
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2769-6448
J9 MEDCOMM-ONCOL
JI MedComm-Oncol.
PD MAR
PY 2024
VL 3
IS 1
AR e59
DI 10.1002/mog2.59
PG 53
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA I1X9S
UT WOS:001328267400003
OA gold
DA 2025-01-04
ER

PT J
AU Cavalieri, S
   Serafini, MS
   Carenzo, A
   Canevari, S
   Lenoci, D
   Pistore, F
   Miceli, R
   Vecchio, S
   Ferrari, D
   Moro, C
   Sponghini, A
   Caldara, A
   Rocca, MC
   Secondino, S
   Moretti, G
   Denaro, N
   Caponigro, F
   Vaccher, E
   Rinaldi, G
   Ferraù, F
   Bossi, P
   Licitra, L
   De Cecco, L
AF Cavalieri, Stefano
   Serafini, Mara Serena
   Carenzo, Andrea
   Canevari, Silvana
   Lenoci, Deborah
   Pistore, Federico
   Miceli, Rosalba
   Vecchio, Stefania
   Ferrari, Daris
   Moro, Cecilia
   Sponghini, Andrea
   Caldara, Alessia
   Rocca, Maria Cossu
   Secondino, Simona
   Moretti, Gabriella
   Denaro, Nerina
   Caponigro, Francesco
   Vaccher, Emanuela
   Rinaldi, Gaetana
   Ferrau, Francesco
   Bossi, Paolo
   Licitra, Lisa
   De Cecco, Loris
TI An Inflammatory Signature to Predict the Clinical Benefit of First-Line
   Cetuximab Plus Platinum-Based Chemotherapy in Recurrent/Metastatic Head
   and Neck Cancer
SO CELLS
LA English
DT Article
DE HNSCC; targeted therapy; cetuximab; gene-expression; immune biomarkers;
   inflammatory signature
ID SQUAMOUS-CELL CARCINOMA; COLORECTAL-CANCER; PROGNOSTIC ROLE;
   NATURAL-KILLER; OPEN-LABEL; EXPRESSION; RECURRENT; THERAPY;
   PEMBROLIZUMAB; SURVIVAL
AB Epidermal growth factor receptor (EGFR) pathway has been shown to play a crucial role in several inflammatory conditions and host immune-inflammation status is related to tumor prognosis. This study aims to evaluate the prognostic significance of a four-gene inflammatory signature in recurrent/metastatic (R/M) head and neck squamous cell carcinoma (HNSCC) patients treated with the EGFR inhibitor cetuximab plus chemotherapy. The inflammatory signature was assessed on 123 R/M HNSCC patients, enrolled in the multicenter trial B490 receiving first-line cetuximab plus platinum-based chemotherapy. The primary endpoint of the study was progression free survival (PFS), while secondary endpoints were overall survival (OS) and objective response rate (ORR). The patient population was subdivided into 3 groups according to the signature score groups. The four-genes-signature proved a significant prognostic value, resulting in a median PFS of 9.2 months in patients with high vs. 6.2 months for intermediate vs. 3.9 months for low values (p = 0.0016). The same findings were confirmed for OS, with median time of 18.4, 13.4, and 7.5 months for high, intermediate, and low values of the score, respectively (p = 0.0001). When ORR was considered, the signature was significantly higher in responders than in non-responders (p = 0.0092), reaching an area under the curve (AUC) of 0.65 (95% CI: 0.55-0.75). Our findings highlight the role of inflammation in the response to cetuximab and chemotherapy in R/M-HNSCC and may have translational implications for improving treatment selection.
C1 [Cavalieri, Stefano; Pistore, Federico; Bossi, Paolo; Licitra, Lisa] Fdn IRCCS Ist Ricovero & Cura Carattere Sci, Head & Neck Med Oncol Dept, Ist Nazl Tumori, I-20133 Milan, Italy.
   [Cavalieri, Stefano; Licitra, Lisa] Univ Milan, Dept Oncol & Hematooncol, I-20122 Milan, Italy.
   [Serafini, Mara Serena; Carenzo, Andrea; Lenoci, Deborah; De Cecco, Loris] Fdn IRCCS Ist Nazl Tumori, Dept Res, Mol Mech Unit, I-20133 Milan, Italy.
   [Canevari, Silvana] Fdn IRCCS Ist Nazl Tumori, I-20133 Milan, Italy.
   [Miceli, Rosalba] Fdn IRCCS Ist Nazl Tumori, Clin Epidemiol & Trial Org, I-20133 Milan, Italy.
   [Vecchio, Stefania] IRCCS Osped Policlin San Martino, Med Oncol, I-16132 Genoa, Italy.
   [Ferrari, Daris] Osped Santi Paolo & Carlo, Med Oncol, I-20142 Milan, Italy.
   [Moro, Cecilia] Azienda Osped Papa Giovanni XXIII, Med Oncol, I-24127 Bergamo, Italy.
   [Sponghini, Andrea] AO Univ Maggiore Carita, Med Oncol, I-28100 Novara, Italy.
   [Caldara, Alessia] Osped Santa Chiara, Med Oncol, I-38122 Trento, Italy.
   [Rocca, Maria Cossu] European Inst Oncol IRCCS, Div Urogenital & Head & Neck Med Oncol, I-20133 Milan, Italy.
   [Secondino, Simona] Fdn IRCCS Policlin San Matteo, Med Oncol, I-27100 Pavia, Italy.
   [Moretti, Gabriella] Azienda USL IRCCS Reggio Emilia, I-42122 Reggio Emilia, Italy.
   [Denaro, Nerina] St Croce & Carle Univ Teaching Hosp, Med Oncol, I-12045 Cuneo, Italy.
   [Denaro, Nerina] ARCO Fdn, I-12045 Cuneo, Italy.
   [Caponigro, Francesco] Ist Nazl Tumori IRCCS Fdn Pascale, Med Oncol, I-80131 Naples, Italy.
   [Vaccher, Emanuela] Ctr Riferimento Oncol Aviano CRO IRCCS, Med Oncol & Immune Related Tumours, I-33081 Aviano, Italy.
   [Rinaldi, Gaetana] AOU Policlin Paolo Giaccone, Med Oncol, I-90127 Palermo, Italy.
   [Ferrau, Francesco] Osped San Vincenzo, Med Oncol, I-98039 Taormina, Italy.
C3 Fondazione IRCCS Istituto Nazionale Tumori Milan; University of Milan;
   Fondazione IRCCS Istituto Nazionale Tumori Milan; Fondazione IRCCS
   Istituto Nazionale Tumori Milan; Fondazione IRCCS Istituto Nazionale
   Tumori Milan; ASST Papa Giovanni XXIII; Azienda Ospedaliera Maggiore
   della Carita di Novara; University of Eastern Piedmont Amedeo Avogadro;
   Santa Chiara Hospital; IRCCS European Institute of Oncology (IEO); IRCCS
   Fondazione San Matteo; IRCCS Fondazione Pascale; University of Palermo;
   Policlinico Paolo Giaccone
RP Cavalieri, S (corresponding author), Fdn IRCCS Ist Ricovero & Cura Carattere Sci, Head & Neck Med Oncol Dept, Ist Nazl Tumori, I-20133 Milan, Italy.; Cavalieri, S (corresponding author), Univ Milan, Dept Oncol & Hematooncol, I-20122 Milan, Italy.; De Cecco, L (corresponding author), Fdn IRCCS Ist Nazl Tumori, Dept Res, Mol Mech Unit, I-20133 Milan, Italy.
EM stefano.cavalieri@istitutotumori.mi.it;
   loris.dececco@istitutotumori.mi.it
RI Vaccher, Emanuela/AAC-9372-2020; Cavalieri, Stefano/AAB-3879-2019;
   Licitra, Lisa/C-6271-2017; Serafini, Mara/AAH-3079-2021; Miceli,
   Rosalba/C-1215-2017; Bossi, Paolo/IAR-1470-2023; Bernardi,
   Simona/AAO-9572-2020; Moretti, Gabriella/AAC-2780-2020; denaro,
   nerina/HDM-0764-2022; Carenzo, Andrea/AAC-2004-2020; de cecco,
   loris/K-7036-2016; Bossi, Paolo/D-1807-2017
OI Canevari, Silvana/0000-0002-2963-3587; de cecco,
   loris/0000-0002-7066-473X; Carenzo, Andrea/0000-0001-6804-9984; denaro,
   nerina/0000-0002-8605-4290; Serafini, Mara Serena/0000-0001-9192-9170;
   Bossi, Paolo/0000-0003-0135-0224; Cossu Rocca,
   maria/0000-0002-5780-3774; Ferrari, Daris/0000-0002-1941-7549; Lenoci,
   Deborah/0000-0002-5958-8035; Cavalieri, Stefano/0000-0003-1294-6859;
   Pistore, Federico/0000-0002-3254-9247
FU Bristol Myers Squibb (Princeton, NJ, USA) [OT123-388]; AIRC [IG 23573,
   14750]; FRRB (Fondazione Regionale per la Ricerca Biomedica) project
   Supporting Personalized Treatment Decisions in Head and Neck Cancer
   through Big Data-SuPerTreat
FX This study was supported by Bristol Myers Squibb (Princeton, NJ, USA)
   grant to Lisa Licitra (OT123-388), AIRC funding (IG 23573 Loris De Cecco
   and 14750 to Silvana Canevari) and FRRB (Fondazione Regionale per la
   Ricerca Biomedica) project Supporting Personalized Treatment Decisions
   in Head and Neck Cancer through Big Data-SuPerTreat, under the frame of
   EraPerMed JTC2019. The funders had no role in the design and conduct of
   the study.
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NR 32
TC 0
Z9 0
U1 0
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD OCT
PY 2022
VL 11
IS 19
AR 3176
DI 10.3390/cells11193176
PG 11
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 5G0CS
UT WOS:000866676700001
PM 36231138
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Tracz-Gaszewska, Z
   Dobrzyn, P
AF Tracz-Gaszewska, Zuzanna
   Dobrzyn, Pawel
TI Stearoyl-CoA Desaturase 1 as a Therapeutic Target for the Treatment of
   Cancer
SO CANCERS
LA English
DT Review
DE lipid metabolism; stearoyl-CoA desaturase 1 (SCD1); monounsaturated
   fatty acids; SCD1 inhibitors; targeted therapy
ID COENZYME-A DESATURASE; FATTY-ACID SYNTHESIS; DE-NOVO LIPOGENESIS;
   BREAST-CANCER; HEPATOCELLULAR-CARCINOMA; INSULIN-RESISTANCE;
   COLORECTAL-CANCER; LIPID-METABOLISM; DIFFERENTIAL EXPRESSION;
   MESENCHYMAL TRANSITION
AB A distinctive feature of cancer cells of various origins involves alterations of the composition of lipids, with significant enrichment in monounsaturated fatty acids. These molecules, in addition to being structural components of newly formed cell membranes of intensely proliferating cancer cells, support tumorigenic signaling. An increase in the expression of stearoyl-CoA desaturase 1 (SCD1), the enzyme that converts saturated fatty acids to 9-monounsaturated fatty acids, has been observed in a wide range of cancer cells, and this increase is correlated with cancer aggressiveness and poor outcomes for patients. Studies have demonstrated the involvement of SCD1 in the promotion of cancer cell proliferation, migration, metastasis, and tumor growth. Many studies have reported a role for this lipogenic factor in maintaining the characteristics of cancer stem cells (i.e., the population of cells that contributes to cancer progression and resistance to chemotherapy). Importantly, both the products of SCD1 activity and its direct impact on tumorigenic pathways have been demonstrated. Based on these findings, SCD1 appears to be a significant player in the development of malignant disease and may be a promising target for anticancer therapy. Numerous chemical compounds that exert inhibitory effects on SCD1 have been developed and preclinically tested. The present review summarizes our current knowledge of the ways in which SCD1 contributes to the progression of cancer and discusses opportunities and challenges of using SCD1 inhibitors for the treatment of cancer.
C1 [Tracz-Gaszewska, Zuzanna; Dobrzyn, Pawel] Polish Acad Sci, Nencki Inst Expt Biol, Lab Mol Med Biochem, PL-02093 Warsaw, Poland.
C3 Polish Academy of Sciences; Nencki Institute of Experimental Biology of
   the Polish Academy of Sciences
RP Dobrzyn, P (corresponding author), Polish Acad Sci, Nencki Inst Expt Biol, Lab Mol Med Biochem, PL-02093 Warsaw, Poland.
EM p.dobrzyn@nencki.gov.pl
RI ; Dobrzyn, Pawel/R-4076-2016
OI Tracz-Gaszewska, Zuzanna/0000-0003-1340-6379; Dobrzyn,
   Pawel/0000-0002-2433-1897
FU National Science Center, Poland [UMO-2016/22/E/NZ4/00650,
   UMO-2014/13/B/NZ4/00199]
FX This research was funded by National Science Center, Poland, grant
   numbers UMO-2016/22/E/NZ4/00650 and UMO-2014/13/B/NZ4/00199.
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NR 186
TC 169
Z9 183
U1 5
U2 48
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUN 26
PY 2019
VL 11
IS 7
AR 948
DI 10.3390/cancers11070948
PG 25
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IO4AV
UT WOS:000479322800059
PM 31284458
OA gold, Green Published, Green Submitted
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Schrijver, WAME
   van Diest, PJ
   Moelans, CB
AF Schrijver, Willemijne A. M. E.
   van Diest, Paul J.
   Moelans, Cathy B.
CA Dutch Distant Breast Canc Metastas
TI Unravelling site-specific breast cancer metastasis: a microRNA
   expression profiling study
SO ONCOTARGET
LA English
DT Article
DE microRNA; breast cancer; metastasis; expression profiling;
   site-specificity
ID DIFFERENTIAL EXPRESSION; RECEPTOR CONVERSION; CELL-PROLIFERATION;
   COLORECTAL-CANCER; PROGNOSTIC VALUE; POTENTIAL ROLE; INVASION; TISSUE;
   IDENTIFICATION; MIGRATION
AB Distant metastasis is still the main cause of death from breast cancer. MicroRNAs (miRs) are important regulators of many physiological and pathological processes, including metastasis. Molecular breast cancer subtypes are known to show a site-specific pattern of metastases formation. In this study, we set out to determine the underlying molecular mechanisms of site-specific breast cancer metastasis by microRNA expression profiling.
   To identify a miR signature for metastatic breast carcinoma that could predict metastatic localization, we compared global miR expression in 23 primary breast cancer specimens with their corresponding multiple distant metastases to ovary (n = 9), skin (n = 12), lung (n = 10), brain (n = 4) and gastrointestinal tract (n = 10) by miRCURY microRNA expression arrays. For validation, we performed quantitative real-time (qRT) PCR on the discovery cohort and on an independent validation cohort of 29 primary breast cancer specimens and their matched metastases.
   miR expression was highly patient specific and miR signatures in the primary tumor were largely retained in the metastases, with the exception of several differentially expressed, location specific miRs. Validation with qPCR demonstrated that hsa-miR-106b-5p was predictive for the development of lung metastases. In time, the second metastasis often showed a miR upregulation compared to the first metastasis.
   This study discovered a metastatic site-specific miR and found miR expression to be highly patient specific. This may lead to novel biomarkers predicting site of distant metastases, and to adjuvant, personalized targeted therapy strategies that could prevent such metastases from becoming clinically manifest.
C1 [Schrijver, Willemijne A. M. E.; van Diest, Paul J.; Moelans, Cathy B.] Univ Med Ctr Utrecht, Dept Pathol, Utrecht, Netherlands.
C3 Utrecht University; Utrecht University Medical Center
RP van Diest, PJ (corresponding author), Univ Med Ctr Utrecht, Dept Pathol, Utrecht, Netherlands.
EM p.j.vandiest@umcutrecht.nl
FU Dutch Cancer Society grant [UU 2011-5195]; Philips Consumer Lifestyle; A
   Sister's Hope research grant
FX This work was supported by Dutch Cancer Society grant UU 2011-5195,
   Philips Consumer Lifestyle and an A Sister's Hope research grant.
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NR 41
TC 20
Z9 22
U1 0
U2 9
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD JAN 10
PY 2017
VL 8
IS 2
BP 3111
EP 3123
DI 10.18632/oncotarget.13623
PG 13
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EH1EL
UT WOS:000391506300102
PM 27902972
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Jedeszko, C
   Paez-Ribes, M
   Di Desidero, T
   Man, S
   Lee, CR
   Xu, P
   Bjarnason, GA
   Bocci, G
   Kerbel, RS
AF Jedeszko, Christopher
   Paez-Ribes, Marta
   Di Desidero, Teresa
   Man, Shan
   Lee, Christina R.
   Xu, Ping
   Bjarnason, Georg A.
   Bocci, Guido
   Kerbel, Robert S.
TI Postsurgical adjuvant or metastatic renal cell carcinoma therapy models
   reveal potent antitumor activity of metronomic oral topotecan with
   pazopanib
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Article
ID TYROSINE KINASE INHIBITORS; ADVANCED OVARIAN-CANCER; BREAST-CANCER;
   COLORECTAL-CANCER; PRECLINICAL MODEL; TARGETED THERAPY; MOUSE MODELS;
   TUMOR-CELLS; SOLID TUMOR; NUDE-MICE
AB Renal cell carcinoma (RCC), normally considered an intrinsically chemotherapy-resistant cancer, is currently treated with targeted biologic therapies, including antiangiogenic tyrosine kinase inhibitors (TKIs), such as pazopanib. The efficacy of these agents is limited by both intrinsic and acquired resistance. Death is almost always due to advanced metastatic disease, a treatment circumstance seldom modeled in preclinical (mouse) drug testing. Similarly, therapy results using postsurgical adjuvant therapy models of microscopic disease have not been reported. Using in vivo selection and transfection of established human RCC cell lines (786-0 and SN12-PM6), we derived clonal luciferaseexpressing variants capable of spontaneous metastasis from an orthotopic primary tumor to organs typical of clinical RCC, including bone, lungs, and brain. The bioluminescence and consistent metastatic spread of von Hippel-Lindau- wild type SN12-PM6-1 cells allowed for the establishment of perioperative therapy models of RCC. We report that the combination of daily low-dose metronomic topotecan with pazopanib has highly potent antiprimary tumor as well as both postsurgical adjuvant and metastatic therapy efficacy despite lack of an antimetastatic effect of pazopanib monotherapy. The combination therapy resulted in sustained metastatic tumor cell dormancy, but tumor progression occurred upon treatment cessation. We also obtained evidence for a direct effect of pazopanib on RCC cells, resulting in increased intracellular concentration of topotecan. Our results suggest that this type of treatment combination should be considered for clinical evaluation in early-or late-stage metastatic disease, even for tumors seemingly intrinsically "resistant" to antiangiogenic TKIs or chemotherapy.
C1 [Jedeszko, Christopher; Paez-Ribes, Marta; Man, Shan; Lee, Christina R.; Xu, Ping; Kerbel, Robert S.] Sunnybrook Res Inst, Biol Sci Platform, Toronto, ON M4N 3M5, Canada.
   [Di Desidero, Teresa; Bocci, Guido] Univ Pisa, Dipartimento Med Clin & Sperimentale, Div Farmacol, I-56126 Pisa, Italy.
   [Bjarnason, Georg A.] Sunnybrook Odette Canc Ctr, Toronto, ON M4N 3M5, Canada.
   [Kerbel, Robert S.] Univ Toronto, Dept Med Biophys, Toronto, ON M5S 2J7, Canada.
C3 University of Toronto; Sunnybrook Health Science Center; Sunnybrook
   Research Institute; University of Pisa; University of Toronto;
   Sunnybrook Research Institute; Sunnybrook Health Science Center;
   University of Toronto
RP Kerbel, RS (corresponding author), Sunnybrook Res Inst, Biol Sci Platform, Toronto, ON M4N 3M5, Canada.
EM robert.kerbel@sri.utoronto.ca
RI Bocci, Guido/AAC-7515-2022; Bjarnason, Georg/L-6032-2019; Bjarnason,
   Georg Arnold/Q-5302-2016
OI Bjarnason, Georg Arnold/0000-0001-6903-5357; Di Desidero,
   Teresa/0000-0002-5487-071X; Bocci, Guido/0000-0001-7120-9141
FU Ontario Institute for Cancer Research; Canadian Institutes for Health
   Research; Israel Cancer Research Foundation; Italian Association for
   Cancer Research; Beatriu de Pinos fellowship (Generalitat de Catalunya);
   Research Fellowship for Abroad FIRC (Italian Foundation for Cancer
   Research); SIF (Italian Society of Pharmacology) Award; GSK
FX This work was supported by grants from the Ontario Institute for Cancer
   Research, the Canadian Institutes for Health Research, the Israel Cancer
   Research Foundation, through a donation made by R. and M. Buckstein to
   R.S.K.; a sponsored research agreement from GSK to R.S.K.; and a grant
   from the Italian Association for Cancer Research to G.B. R.S.K. is a
   Canada Research Chair in Tumor Biology, Angiogenesis and Antiangiogenic
   Therapy. M.P.-R. is a recipient of a Beatriu de Pinos fellowship
   (Generalitat de Catalunya), and T.D.D. is a recipient of a Research
   Fellowship for Abroad 2011 FIRC (Italian Foundation for Cancer Research)
   and the 2013 SIF (Italian Society of Pharmacology) Award.
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NR 51
TC 45
Z9 47
U1 0
U2 22
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1946-6234
EI 1946-6242
J9 SCI TRANSL MED
JI Sci. Transl. Med.
PD APR 8
PY 2015
VL 7
IS 282
AR 282ra50
DI 10.1126/scitranslmed.3010722
PG 12
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA CF4QK
UT WOS:000352535200007
PM 25855496
DA 2025-01-04
ER

PT J
AU Elaidy, NF
   Elwan, A
   Hegazy, MW
   Atwa, HA
AF Elaidy, Noha F.
   Elwan, Amira
   Hegazy, Mohamed Wahba
   Atwa, Hanaa A.
TI Prognostic Significance of Notch-4, SATB-2, and Glutaminase-1 in
   Colorectal Adenocarcinoma
SO MIDDLE EAST JOURNAL OF CANCER
LA English
DT Article
DE Colorectal neoplasms; Immunohistochemistry; Prognosis
ID CANCER; EXPRESSION; MARKER; PROGRESSION; METABOLISM; TRANSITION; CELLS
AB Background: Neurogenic locus notch homology 4 (Notch-4) is crucial in maintaining stem cells. Special AT-rich sequence-binding protein 2 (SATB-2) is a transcription factor that binds to the nuclear matrix and serves various functions, including brain development. Glutaminase-1 (GLS-1) plays a pivotal role in cancer cell metabolism, growth, and proliferation. This study aims to assess the expression of these markers in colorectal cancer, establishing correlations with clinicopathological characteristics and patient survival.Method: In this retrospective study, we retrieved and analyzed 68 formalin-fixed, paraffin-embedded blocks of primary colorectal adenocarcinoma, not otherwise specified cases, and adjacent normal mucosa. Notch-4, SATB-2 and GLS-1 expressions were analyzed using immunohistochemistry at the Zagazig School of Medicine, Egypt.Results: High expressions of Notch-4 and GLS-1 and low expression of SATB-2 were observed in colonic adenocarcinoma but not in adjacent non-neoplastic mucosa (P < 0.001). High expressions of Notch-4 and GLS-1, along with low expression of SATB-2, were associated with a higher tumor grade, advanced stage (P < 0.001), lymphovascular invasion, lymph node metastasis, and poor disease-free survival and overall survival rates (P < 0.001). Conclusion: High expression of Notch-4 and GLS-1 is correlated with a poor prognosis in colorectal cancer, while high expression of SATB-2 is associated with a favorable prognosis for colorectal carcinoma. These markers can aid in predicting tumor prognosis and guiding targeted therapy for colorectal carcinoma.
C1 [Elaidy, Noha F.; Atwa, Hanaa A.] Zagazig Univ, Med Coll, Pathol Dept, Zagazig, Egypt.
   [Elwan, Amira; Hegazy, Mohamed Wahba] Zagazig Univ, Med Coll, Dept Clin Oncol & Nucl Med, Zagazig, Egypt.
C3 Egyptian Knowledge Bank (EKB); Zagazig University; Egyptian Knowledge
   Bank (EKB); Zagazig University
RP Hegazy, MW (corresponding author), Zagazig Univ, Med Coll, Dept Clin Oncol & Nucl Med, Zagazig, Egypt.
EM F1501625@gmail.com
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NR 30
TC 0
Z9 0
U1 1
U2 1
PU SHIRAZ UNIV MEDICAL SCIENCES
PI SHIRAZ
PA NEMAZEE HOSPITAL, SHIRAZ, 71934, IRAN
SN 2008-6709
EI 2008-6687
J9 MIDDLE EAST J CANCER
JI Middle East J. Cancer
PD JAN
PY 2022
VL 15
IS 1
BP 15
EP 24
DI 10.30476/mejc.2023.97207.1852
PG 10
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA DU4F5
UT WOS:001134573600003
DA 2025-01-04
ER

PT J
AU Sun, SN
   Meng, L
   Xing, XF
   Li, NN
   Song, Q
   Qiao, DB
   Qu, LK
   Liu, CY
   An, G
   Li, ZW
   Shou, CC
   Lian, SY
AF Sun, Shuning
   Meng, Lin
   Xing, Xiaofang
   Li, Ningning
   Song, Qian
   Qiao, Dongbo
   Qu, Like
   Liu, Caiyun
   An, Guo
   Li, Zhongwu
   Shou, Chenchao
   Lian, Shenyi
TI Anti-PRL-3 Monoclonal Antibody inhibits the Growth and Metastasis of
   colorectal adenocarcinoma
SO JOURNAL OF CANCER
LA English
DT Article
DE PRL-3; monoclonal antibody; colon cancer; metastasis
ID PHOSPHATASE; OVEREXPRESSION; EXPRESSION; PROTEIN; PATHWAY; CANCER
AB Background: Colon cancer is the one of leading causes of cancer-related death. Chemotherapy, radiotherapy and immunotherapy will be the mainstream in inoperable advanced cancer in clinics. Precision treatment is still lack in colon cancer.Materials and Methods: We developed a series of mAbs targeting PRL-3 through different types of immunogens. The binding domains of mAbs were identified through the ELISA and Western blotting experiments. The antitumor activity of mAbs was verified by cell proliferation, migration and invasion experiments. Xenograft subcutaneous and metastatic models and patient derived Xenograft (PDX) model were established.Results: mAb 12G12 targeting 77-120AA exhibited inhibition in migration and invasion experiments. 12G12 inhibited the migration of multiple types of cancer cells, including colon cancer, gastric cancer, esophagus cancer, liver cancer, lung cancer and pancreatic cancer cells. 12G12 decreased the tumor growth and metastasis in Xenograft subcutaneous and metastatic tumor model, respectively. The antitumor activity of mAb 12G12 was also confirmed in PDX model of gastric cancer. PRL-3 interacted with Golgi protein TMED10. Knockdown of TMED10 expression attenuated the cell migration triggered by purified GST-PRL-3 protein.Conclusion: Our results confirmed the antitumor activity of mAb 12G12 in colorectal adenocarcinoma and provided a new potential targeted therapy of colon cancer.
C1 [Sun, Shuning; Meng, Lin; Qu, Like; Liu, Caiyun; Li, Zhongwu; Shou, Chenchao] Peking Univ Canc Hosp & Inst, Key Lab Carcinogenesis & Translat Res, Dept Biochem & Mol Biol, Minist Educ Beijing, Beijing, Peoples R China.
   [Xing, Xiaofang; Lian, Shenyi] Peking Univ Canc Hosp & Inst, Minist Educ Beijing, Dept Gastrointestinal Canc Translat Res, Key Lab Carcinogenesis & Translat Res, Beijing, Peoples R China.
   [Li, Ningning; Qiao, Dongbo; Li, Zhongwu; Lian, Shenyi] Peking Univ Canc Hosp & Inst, Dept Pathol, Key Lab Carcinogenesis & Translat Res, Minist Educ Beijing, Beijing, Peoples R China.
   [Song, Qian] Chinese Acad Sci, Zhejiang Canc Hosp, Hangzhou Inst Med HIM, Hangzhou, Zhejiang, Peoples R China.
   [An, Guo] Peking Univ Canc Hosp & Inst, Dept Lab Anim, Minist Educ Beijing, Key Lab Carcinogenesis & Translat Res, Beijing, Peoples R China.
C3 Peking University; Chinese Academy of Sciences; Hangzhou Institute of
   Medicine, CAS; Zhejiang Cancer Hospital
RP Li, ZW; Shou, CC (corresponding author), Peking Univ Canc Hosp & Inst, Key Lab Carcinogenesis & Translat Res, Dept Biochem & Mol Biol, Minist Educ Beijing, Beijing, Peoples R China.; Li, ZW; Lian, SY (corresponding author), Peking Univ Canc Hosp & Inst, Dept Pathol, Key Lab Carcinogenesis & Translat Res, Minist Educ Beijing, Beijing, Peoples R China.
EM zhwuli@hotmail.com; cshou@vip.sina.com; liansy2007@bjmu.edu.cn
FU Natural Science Foundation of China [81872309]; Beijing Hospitals
   Authority Youth Programme [QML20191109]; Zhejiang Provincial Natural
   Science Foundation of China [LQ21H200001]
FX <B>Funding</B> This research was supported by Natural Science Foundation
   of China [grant number 81872309] , Beijing Hospitals Authority Youth
   Programme [grant number QML20191109] and Zhejiang Provincial Natural
   Science Foundation of China [grant number LQ21H200001] .
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NR 29
TC 1
Z9 2
U1 2
U2 3
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1837-9664
J9 J CANCER
JI J. Cancer
PY 2023
VL 14
IS 13
BP 2585
EP 2595
DI 10.7150/jca.81702
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AD9Y8
UT WOS:001116654800002
PM 37670977
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Mesti, T
   Boshkoska, BM
   Kos, M
   Tekavcic, M
   Ocvirk, J
AF Mesti, Tanja
   Boshkoska, Biljana Mileva
   Kos, Mitja
   Tekavcic, Metka
   Ocvirk, Janja
TI The cost of systemic therapy for metastatic colorectal carcinoma in
   Slovenia: discrepancy analysis between cost and reimbursement
SO RADIOLOGY AND ONCOLOGY
LA English
DT Article
DE cost of treatment; metastatic colorectal cancer; cost of targeted
   therapy; monitoring costs
ID CANCER; CARE
AB Background. The aim of the study was to estimate the direct medical costs of metastatic colorectal cancer (mCRC) treated at the Institute of Oncology Ljubljana and to question the healthcare payment system in Slovenia.
   Methods. Using an internal patient database, the costs of mCRC patients were estimated in 2009 by examining (1) mCRC direct medical related costs, and (2) the cost difference between payment received by Slovenian health insurance and actual mCRC costs. Costs were analysed in the treatment phase of the disease by assessing the direct medical costs of hospital treatment with systemic therapy together with hospital treatment of side effects, without assessing radiotherapy or surgical treatment. Follow-up costs, indirect medical costs, and nonmedical costs were not included.
   Results. A total of 209 mCRC patients met all eligibility criteria. The direct medical costs of mCRC hospitalization with systemic therapy in Slovenia for 2009 were estimated as the cost of medications (cost of systemic therapy + cost of drugs for premedication) + labor cost (the cost of carrying out systemic treatment) + cost of lab tests + cost of imaging tests + KRAS testing cost + cost of hospital treatment due to side effects of mCRC treatment, and amounted to (sic)3,914,697. The difference between the cost paid by health insurance and actual costs, estimated as direct medical costs of hospitalization of mCRC patients treated with systemic therapy at the Institute of Oncology Ljubljana in 2009, was (sic) 1,900,757.80.
   Conclusions. The costs paid to the Institute of Oncology Ljubljana by health insurance for treating mCRC with systemic therapy do not match the actual cost of treatment. In fact, the difference between the payment and the actual cost estimated as direct medical costs of hospitalization of mCRC patients treated with systemic therapy at the Institute of Oncology Ljubljana in 2009 was (sic)1,900,757.80. The model Australian Refined Diagnosis Related Groups (AR-DRG) for cost assessment in oncology being currently used is probably one of the reasons for the discrepancy between pay-outs and actual costs. We propose new method for more precise cost assessment in oncology.
C1 [Mesti, Tanja; Ocvirk, Janja] Inst Oncol Ljubljana, Dept Med Oncol, Ljubljana, Slovenia.
   [Boshkoska, Biljana Mileva] Fac Informat Studies, Novo Mesto, Slovenia.
   [Kos, Mitja] Univ Ljubljana, Fac Pharm, Ljubljana, Slovenia.
   [Tekavcic, Metka] Univ Ljubljana, Fac Econ, Ljubljana, Slovenia.
C3 Institute of Oncology - Slovenia; University of Ljubljana; University of
   Ljubljana
RP Mesti, T (corresponding author), Inst Oncol Ljubljana, Zaloska 2, Ljubljana, Slovenia.
EM tmesti@onko-i.si
RI Mileva Boshkoska, Biljana/N-6298-2015; Kos, Mitja/C-7440-2019
OI Mileva Boshkoska, Biljana/0000-0002-1137-9795; Kos,
   Mitja/0000-0002-6801-6450
FU Creative Core 'Simulations' project - European Union, The European
   Regional Development Fund [FISNM-3330-13-500033]
FX The work of the second author is supported by Creative Core
   FISNM-3330-13-500033 'Simulations' project funded by the European Union,
   The European Regional Development Fund.
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NR 21
TC 3
Z9 3
U1 1
U2 9
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1318-2099
EI 1581-3207
J9 RADIOL ONCOL
JI Radiol. Oncol.
PD JUN
PY 2015
VL 49
IS 2
BP 200
EP 208
DI 10.2478/raon-2014-0046
PG 9
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA CE5DU
UT WOS:000351851500014
PM 26029033
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Heinemann, V
   Stintzing, S
   Modest, DP
   Giessen-Jung, C
   Michl, M
   Mansmann, UR
AF Heinemann, Volker
   Stintzing, Sebastian
   Modest, Dominik P.
   Giessen-Jung, Clemens
   Michl, Marlies
   Mansmann, Ulrich R.
TI Early tumour shrinkage (ETS) and depth of response (DpR) in the
   treatment of patients with metastatic colorectal cancer (mCRC)
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Review
DE Metastatic colorectal cancer; Early tumour shrinkage; Chemotherapy;
   Targeted therapy; Cetuximab; Depth of response
ID 1ST-LINE TREATMENT; PLUS IRINOTECAN; PHASE-III; CETUXIMAB; BEVACIZUMAB;
   LEUCOVORIN; SURVIVAL; FLUOROURACIL; CHEMOTHERAPY; COMBINATION
AB Background: Response evaluation criteria in solid tumours (RECIST) are used to define degrees of response to anti-tumour agents. In retrospective analyses, early tumour shrinkage (ETS) has been investigated as an alternative early-on-treatment predictor of treatment efficacy with regard to progression-free and overall survival. While cut-off based analysis of ETS facilitates the categorisation of patients into responders and non-responders after a defined period of treatment, depth of response (DpR) serves as a continuous measure, which defines the nadir of tumour response.
   Methods: A systematic literature search for 'early tumour shrinkage' or 'tumour size decrease' in 'metastatic colorectal cancer' reported from January 2000 to July 2014 was performed. The present review summarises available data concerning ETS and DpR and evaluates their potential as predictive markers for the clinical management of patients with metastatic colorectal cancer (mCRC).
   Results: A total of 10 clinical trials investigated the role of ETS as a marker of clinical outcome in patients with mCRC. In addition, DpR was investigated using the efficacy data from three of these trials. Available data show that ETS differentiates patients with high sensitivity to treatment and more favourable prognosis from a heterogeneous group of patients classified Aas non-ETS patients. ETS is an early indicator of the potentially achievable response. In contrast, DpR estimates the nadir of tumour response as a continuous measure, which may affect the subsequent disease history, thus translating into superior survival.
   Conclusions: The concepts of ETS and DpR offer potential as clinical end-points to aid the clinical decision making process and thus further optimise mCRC patient management in the era of tailored therapy approaches. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Heinemann, Volker; Stintzing, Sebastian; Modest, Dominik P.; Giessen-Jung, Clemens; Michl, Marlies] Univ Munich, Klinikum Grosshadern, Dept Med Oncol, D-81377 Munich, Germany.
   [Heinemann, Volker] Univ Munich, Klinikum Grosshadern, Ctr Comprehens Canc, D-81377 Munich, Germany.
   [Mansmann, Ulrich R.] Univ Munich, Inst Med Informat Biometry & Epidemiol, D-81377 Munich, Germany.
C3 University of Munich; University of Munich; University of Munich
RP Stintzing, S (corresponding author), Univ Munich, Dept Hematol & Oncol, Marchioninistr 15, D-81377 Munich, Germany.
EM sebastian.stintzing@med.uni-muenchen.de;
   dominik.modest@med.uni-muenchen.de;
   clemens.giessen-jung@med.uni-muenchen.de;
   marlies.michl@med.uni-muenchen.de; mansmann@ibe.uni-muenchen.de
RI Modest, Dominik Paul/AAW-9756-2021; Michl, Marlies/M-7969-2019;
   Stintzing, Sebastian/I-4538-2016
OI Stintzing, Sebastian/0000-0002-3297-5801
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NR 48
TC 142
Z9 148
U1 0
U2 6
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 0959-8049
EI 1879-0852
J9 EUR J CANCER
JI Eur. J. Cancer
PD SEP
PY 2015
VL 51
IS 14
BP 1927
EP 1936
DI 10.1016/j.ejca.2015.06.116
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CP7PW
UT WOS:000360081300010
PM 26188850
DA 2025-01-04
ER

PT J
AU Gao, J
   Lan, JQ
   Liao, HY
   Yang, F
   Qiu, P
   Jin, F
   Wang, SB
   Shen, L
   Chao, TF
   Zhang, C
   Zhu, Y
AF Gao, Jing
   Lan, Jianqiang
   Liao, Haiyan
   Yang, Fang
   Qiu, Pei
   Jin, Feng
   Wang, Shubin
   Shen, Lin
   Chao, Tengfei
   Zhang, Cheng
   Zhu, Yu
TI Promising preclinical patient-derived organoid (PDO) and xenograft (PDX)
   models in upper gastrointestinal cancers: progress and challenges
SO BMC CANCER
LA English
DT Review
DE Upper gastrointestinal cancer; Organoid; PDX; Personalized therapy
ID SQUAMOUS-CELL CARCINOMA; GASTRIC-CANCER; MOUSE MODELS; ESOPHAGEAL;
   REVEAL; LINES; ERA; HETEROGENEITY; EXPRESSION; CULTURES
AB Gastrointestinal (GI) cancers (gastric cancer, oesophageal cancer, liver cancer, colorectal cancer, etc.) are the most common cancers with the highest morbidity and mortality in the world. The therapy for most GI cancers is difficult and is associated with a poor prognosis. In China, upper GI cancers, mainly gastric cancer (GC) and oesophageal cancer (EC), are very common due to Chinese people's characteristics, and more than half of patients are diagnosed with distant metastatic or locally advanced disease. Compared to other solid cancers, such as lung cancer and breast cancer, personalized therapies, especially targeted therapy and immunotherapy, in GC and EC are relatively lacking, leading to poor prognosis. For a long time, most studies were carried out by using in vitro cancer cell lines or in vivo cell line-derived xenograft models, which are unable to reproduce the characteristics of tumours derived from patients, leading to the possible misguidance of subsequent clinical validation. The patient-derived models represented by patient-derived organoid (PDO) and xenograft (PDX) models, known for their high preservation of patient tumour features, have emerged as a very popular platform that has been widely used in numerous studies, especially in the research and development of antitumour drugs and personalized medicine. Herein, based on some of the available published literature, we review the research and application status of PDO and PDX models in GC and EC, as well as detail their future challenges and prospects, to promote their use in basic and translational studies or personalized therapy.
C1 [Gao, Jing; Liao, Haiyan; Yang, Fang; Jin, Feng; Wang, Shubin] Peking Univ Shenzhen Hosp, Shenzhen Peking Univ Hong Kong Univ Sci & Technol, Shenzhen Key Lab Gastrointestinal Canc Translat Re, Dept Oncol,Canc Inst, Shenzhen 518000, Peoples R China.
   [Lan, Jianqiang; Qiu, Pei; Zhu, Yu] Guangdong Res Ctr Organoid Engn & Technol, 11 Kaiyuan Ave, Guangzhou, Peoples R China.
   [Shen, Lin; Zhang, Cheng] Peking Univ Canc Hosp & Inst, Dept Gastrointestinal Oncol, Key Lab Carcinogenesis & Translat Res, Minist Educ Beijing, 52 Fucheng Rd, Beijing, Peoples R China.
   [Chao, Tengfei] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Oncol, 1095 Jiefang Ave, Wuhan, Peoples R China.
C3 Peking University; Hong Kong University of Science & Technology;
   Huazhong University of Science & Technology
RP Zhu, Y (corresponding author), Guangdong Res Ctr Organoid Engn & Technol, 11 Kaiyuan Ave, Guangzhou, Peoples R China.; Zhang, C (corresponding author), Peking Univ Canc Hosp & Inst, Dept Gastrointestinal Oncol, Key Lab Carcinogenesis & Translat Res, Minist Educ Beijing, 52 Fucheng Rd, Beijing, Peoples R China.; Chao, TF (corresponding author), Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Oncol, 1095 Jiefang Ave, Wuhan, Peoples R China.
EM turnface@126.com; qenya@163.com; zhuyu@accibio.com
RI Shen, Lin/JPX-7656-2023
OI Liao, Haiyan/0000-0002-4424-7334
FU National Natural Science Foundation of China
FX Not applicable.
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NR 84
TC 5
Z9 5
U1 7
U2 15
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD DEC 7
PY 2023
VL 23
IS 1
AR 1205
DI 10.1186/s12885-023-11434-9
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AE7F2
UT WOS:001116845500005
PM 38062430
OA gold
DA 2025-01-04
ER

PT J
AU Du, XJ
   Yang, BW
   An, QL
   Assaraf, YG
   Cao, X
   Xia, JL
AF Du, Xiaojing
   Yang, Biwei
   An, Quanlin
   Assaraf, Yehuda G.
   Cao, Xin
   Xia, Jinglin
TI Acquired resistance to third-generation EGFR-TKIs and emerging
   next-generation EGFR inhibitors
SO INNOVATION
LA English
DT Review
DE Cancer; targeted therapy; EGFR inhibitors; drug resistance; mutations;
   chemoresistance mechanisms; surmounting chemoresistance
ID GROWTH-FACTOR RECEPTOR; CELL LUNG-CANCER; PHASE-II TRIAL; METASTATIC
   COLORECTAL-CANCER; TYROSINE KINASE INHIBITORS; 1ST-LINE TREATMENT;
   PROTEIN OVEREXPRESSION; CLINICAL-SIGNIFICANCE; GENE AMPLIFICATION;
   OPEN-LABEL
AB The discovery that mutations in the EGFR gene are detected in up to 50% of lung adenocarcinoma patients, along with the development of highly efficacious epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), has revolutionized the treatment of this frequently occurring lung malignancy. Indeed, the clinical success of these TKIs constitutes a critical milestone in targeted cancer therapy. Three generations of EGFR-TKIs are currently approved for the treatment of EGFR mutation-positive non-small cell lung cancer (NSCLC). The first-generation TKIs include erlotinib, gefitinib, lapatinib, and icotinib; the second-generation ErbB family blockers include afatinib, neratinib, and dacomitinib; whereas osimertinib, approved by the FDA on 2015, is a third-generation TKI targeting EGFR harboring specific mutations. Compared with the first- and second-generation TKIs, third-generation EGFR inhibitors display a significant advantage in terms of patient survival. For example, the median overall survival in NSCLC patients receiving osimertinib reached 38.6 months. Unfortunately, however, like other targeted therapies, new EGFR mutations, as well as additional drug-resistance mechanisms emerge rapidly after treatment, posing formidable obstacles to cancer therapeutics aimed at surmounting this chemoresistance. In this review, we summarize the molecular mechanisms underlying resistance to third-generation EGFR inhibitors and the ongoing efforts to address and overcome this chemoresistance. We also discuss the current status of fourth-generation EGFR inhibitors, which are of great value in overcoming resistance to EGFR inhibitors that appear to have greater therapeutic benefits in the clinic.
C1 [Du, Xiaojing; Yang, Biwei; An, Quanlin; Cao, Xin; Xia, Jinglin] Fudan Univ, Zhongshan Hosp, Inst Clin Sci, Shanghai 200032, Peoples R China.
   [Du, Xiaojing; Yang, Biwei; Xia, Jinglin] Fudan Univ, Zhongshan Hosp, Liver Canc Inst, Shanghai 200032, Peoples R China.
   [Du, Xiaojing; Xia, Jinglin] Fudan Univ, Minhang Hosp, Inst Fudan Minhang Acad Hlth Syst, Shanghai 201199, Peoples R China.
   [Assaraf, Yehuda G.] Technion Israel Inst Technol, Dept Biol, Fred Wyszkowski Canc Res Lab, IL-3200000 Haifa, Israel.
   [Xia, Jinglin] Wenzhou Med Univ, Affiliated Hosp 1, Wenzhou 325000, Peoples R China.
C3 Fudan University; Fudan University; Fudan University; Technion Israel
   Institute of Technology; Wenzhou Medical University
RP Cao, X; Xia, JL (corresponding author), Fudan Univ, Zhongshan Hosp, Inst Clin Sci, Shanghai 200032, Peoples R China.; Xia, JL (corresponding author), Fudan Univ, Zhongshan Hosp, Liver Canc Inst, Shanghai 200032, Peoples R China.; Xia, JL (corresponding author), Fudan Univ, Minhang Hosp, Inst Fudan Minhang Acad Hlth Syst, Shanghai 201199, Peoples R China.; Assaraf, YG (corresponding author), Technion Israel Inst Technol, Dept Biol, Fred Wyszkowski Canc Res Lab, IL-3200000 Haifa, Israel.; Xia, JL (corresponding author), Wenzhou Med Univ, Affiliated Hosp 1, Wenzhou 325000, Peoples R China.
EM assaraf@technion.ac.il; caox@fudan.edu.cn; xiajinglin@fudan.edu.cn
RI Cao, Xin/L-7110-2019; Assaraf, Yehuda G/JPA-0451-2023; Cao,
   Xin/V-6015-2017
OI Du, Xiaojing/0000-0001-8228-5086; Xia, Jinglin/0000-0001-9443-7075; Cao,
   Xin/0000-0003-1722-023X
FU Natural Science Foundation of Shanghai [20ZR1410400]; Extraordinary 2025
   Elite Project of Fudan University; National Natural Science Foundation
   of China [81772590, 81572395]; Open Funding of Key Laboratory of
   Diagnosis and Treatment of Severe Hepato-pancreatic Diseases of Zhejiang
   Province [2018E10008]; CAS Interdisciplinary Innovation Team
   [JCTD-2019-07]
FX The study was supported by the Natural Science Foundation of Shanghai
   (No. 20ZR1410400), the Extraordinary 2025 Elite Project of Fudan
   University, the National Natural Science Foundation of China (No.
   81772590 and 81572395), the Open Funding of Key Laboratory of Diagnosis
   and Treatment of Severe Hepato-pancreatic Diseases of Zhejiang Province
   (No. 2018E10008), and the CAS Interdisciplinary Innovation
   TeamJCTD-2019-07. All figures showing EGFR kinase structure and binding
   modes were generated using PyMol 2.4.1 (www.pymol.org).
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NR 196
TC 87
Z9 90
U1 3
U2 51
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
SN 2666-6758
J9 INNOVATION-AMSTERDAM
JI Innovation-Amsterdam
PD MAY 28
PY 2021
VL 2
IS 2
AR 100103
DI 10.1016/j.xinn.2021.100103
EA APR 2021
PG 18
WC Multidisciplinary Sciences
WE Emerging Sources Citation Index (ESCI)
SC Science & Technology - Other Topics
GA YN4OA
UT WOS:000747238500007
PM 34557754
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Ren, CX
   Wang, HC
   Li, JC
   Li, S
AF Ren Chongxi
   Wang Hongchen
   Li Jiangchun
   Li Sheng
TI Continuum of care strategy in metastatic colorectal cancer: a review
SO COLORECTAL CANCER
LA English
DT Review
DE continuum of care strategy; individualized treatment; maintenance and/or
   intermittent therapy; metastatic colorectal cancer
ID PHASE-III TRIAL; BEVACIZUMAB PLUS CAPECITABINE; 1ST-LINE TREATMENT;
   OPEN-LABEL; MAINTENANCE THERAPY; NON-INFERIORITY; CHEMOTHERAPY;
   FLUOROURACIL; INTERMITTENT; OXALIPLATIN
AB Treatment of human metastatic colorectal cancer (mCRC) has changed remarkably in the past two decades. The use of novel therapies and more complex treatment strategies have contributed to progressively increase the median life expectancy of patients up to approximately 30months. Although traditional cytotoxic chemotherapy and newer targeted therapy are now available for use in treating patients with mCRC, the optimal treatment strategy remains unknown. In recent years, there has been a treatment paradigm shift for mCRC patients with the emergence of the concept of continuum of care' as the optimal palliative therapy strategy. It is based on the concept whereby patients are exposed throughout the course of their disease to different active drugs; the therapy is personalized according to the need for rapid response, the burden of disease and molecular subtype status, such as RAS, BRAF, MMR and HER2. Drugs are often reintroduced if they demonstrated activity in a previous line of therapy, and most importantly, maintenance chemotherapy and/or intermittent therapy are considered. This review details available data for the use of the continuum of care strategy in mCRC, in which the strategy has provided significant clinical benefit in clinical studies. As our understanding advances, optimal treatment strategy for the patients with mCRC should still be individualized.
C1 [Ren Chongxi; Wang Hongchen; Li Jiangchun; Li Sheng] Hebei Med Univ, Dept Oncol, Cangzhou Clin Coll Integrated Tradit Chinese & We, Cangzhou 061000, Peoples R China.
C3 Hebei Medical University
RP Ren, CX (corresponding author), Hebei Med Univ, Dept Oncol, Cangzhou Clin Coll Integrated Tradit Chinese & We, Cangzhou 061000, Peoples R China.
EM rcxvip@outlook.com
RI Ren, Chongxi/AGS-4631-2022; jing, wang/KCZ-2144-2024
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NR 60
TC 0
Z9 0
U1 0
U2 3
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1758-194X
EI 1758-1958
J9 COLORECTAL CANCER
JI Colorectal Cancer
PD DEC
PY 2017
VL 6
IS 3
BP 95
EP 103
DI 10.2217/crc-2017-0009
PG 9
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA FQ7ND
UT WOS:000418548500004
DA 2025-01-04
ER

PT J
AU Kim, JE
   Kim, KK
   Kim, SY
   Lee, J
   Park, SH
   Park, JO
   Park, YS
   Lim, HY
   Kang, WK
   Kim, ST
AF Kim, J. E.
   Kim, K. K.
   Kim, S. Y.
   Lee, J.
   Park, S. H.
   Park, J. O.
   Park, Y. S.
   Lim, H. Y.
   Kang, W. K.
   Kim, S. T.
TI MAP2K1 Mutation in Colorectal Cancer Patients: Therapeutic Challenge
   Using Patient-Derived Tumor Cell Lines
SO JOURNAL OF CANCER
LA English
DT Article
DE MAP2K1 mutation; MEK inhibitor; RAF inhibitor
ID CETUXIMAB PLUS IRINOTECAN; PHASE-III TRIAL; 1ST-LINE TREATMENT;
   MOLECULAR CHARACTERIZATION; ACQUIRED-RESISTANCE; THYROID CARCINOMAS;
   TARGETED THERAPY; EGFR BLOCKADE; BRAF MUTATION; FLUOROURACIL
AB BACKGROUND: The MAP2K1 K57T mutation is known to be a potential mechanism of primary and secondary resistance to EGFR inhibitors in metastatic colorectal cancer (CRC) and has also been reported to promote resistance to BRAF and MEK inhibitors. It is important to overcome therapeutic resistance to EGFR inhibitors to improve the treatment outcomes of metastatic CRC.
   METHODS: We established patient-derived tumor cells (PDCs) from metastatic lesions that newly appeared during treatment with a BRAF inhibitor (LGX-818) plus an EGFR inhibitor (cetuximab) in a patient with BRAF-mutant CRC. To investigate therapeutic options to overcome acquired resistance due to MAP2K1 mutation in BRAF-mutant CRC, we performed cell viability assays using the PDCs.
   RESULTS: We tested whether the PDCs were resistant to an EGFR inhibitor (cetuximab) and a BRAF inhibitor (sorafenib) as these cells were established at the time of resistance to the EGFR plus BRAF inhibitors. Moreover, the anti-tumor effect of AZD6244 (MEK inhibitor) was evaluated because PDCs harbored a MAP2K1 mutation at the time of resistance to the EGFR plus BRAF inhibitors. MTT proliferation assays showed that monotherapy with cetuximab, sorafenib, or AZD6244 did not suppress cell viability. We next tested viability of the PDCs to combination treatment with cetuximab plus AZD6244 and sorafenib plus AZD6244. Proliferation of PDCs was significantly inhibited by sorafenib and AZD6244, but not by cetuximab plus AZD6244. Investigation of the combined effect of sorafenib and AZD6244 using the calculated combination index (CI) showed synergistic effects of sorafenib and AZD6244 in combination therapy applied to PDCs with the MAP2K1 K57T mutation.
   CONCLUSION: Our results suggest that combination treatment with BRAF and MEK inhibitors might be a novel treatment strategy for MAP2K1 K57T-mutant CRC. This finding will be helpful to guide treatment of patients with CRC that is resistant to EGFR inhibitors.
C1 [Kim, J. E.; Kim, S. Y.; Lee, J.; Park, S. H.; Park, J. O.; Park, Y. S.; Lim, H. Y.; Kang, W. K.; Kim, S. T.] Sungkyunkwan Univ, Samsung Med Ctr, Sch Med, Dept Med,Div Hematol Oncol, 81 Irwon Ro, Seoul 06351, South Korea.
   [Kim, K. K.] Sungkyunkwan Univ, Sch Med, Samsung Biomed Res Inst, Inst Basic Sci,Dept Mol Cell Biol, Suwon 440746, South Korea.
C3 Sungkyunkwan University (SKKU); Samsung Medical Center; Sungkyunkwan
   University (SKKU); Institute for Basic Science - Korea (IBS)
RP Kim, ST (corresponding author), Sungkyunkwan Univ, Samsung Med Ctr, Sch Med, Dept Med,Div Hematol Oncol, 81 Irwon Ro, Seoul 06351, South Korea.
EM seungtae1.kim@samsung.com
RI Park, Junsu/IQU-2241-2023; Park, Jihye/AAC-1333-2022; Park, Se
   Hoon/GMX-1199-2022; Lee, Jee/C-9646-2011; Kim, Kyunga/LCL-2839-2024;
   Kim, Sung/G-4114-2014; kim, st/O-5928-2014; Kim, Kyeong/ABH-1988-2020;
   Lim, Ho Yeong/KBA-8868-2024; Kim, Sun Young/O-4847-2018
OI Kim, Sun Young/0000-0002-1180-0367
FU Korean Health Technology R&D Project, Ministry of Health & Welfare,
   Republic of Korea [HI14C3418, HI16C1990]; Samsung Medical Center
   [GF01140111, SMX1170421]
FX This work was supported by a grant from the Korean Health Technology R&D
   Project, Ministry of Health & Welfare, Republic of Korea (HI14C3418,
   HI16C1990). Support was also provided by grants (GF01140111) and
   (SMX1170421) of Samsung Medical Center.
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NR 35
TC 7
Z9 7
U1 1
U2 7
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1837-9664
J9 J CANCER
JI J. Cancer
PY 2017
VL 8
IS 12
BP 2263
EP 2268
DI 10.7150/jca.19582
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FC6GQ
UT WOS:000406938800013
PM 28819429
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Kang, WB
   Zheng, Q
   Lei, J
   Chen, CY
   Yu, CJ
AF Kang, Weibiao
   Zheng, Qiang
   Lei, Jun
   Chen, Changyu
   Yu, Changjun
TI Prognostic Value of Long Noncoding RNAs in Patients with
   Gastrointestinal Cancer: A Systematic Review and Meta-Analysis
SO DISEASE MARKERS
LA English
DT Review
ID SQUAMOUS-CELL CARCINOMA; PREDICTS POOR-PROGNOSIS; UP-REGULATED
   EXPRESSION; EPITHELIAL-MESENCHYMAL TRANSITION; PROMOTES TUMOR-GROWTH;
   COLORECTAL-CANCER; GASTRIC-CANCER; ABERRANT EXPRESSION; CHEMOTHERAPY
   RESISTANCE; UNFAVORABLE PROGNOSIS
AB Gastrointestinal cancers (GICs) are a huge threat to human health, which mainly include esophageal, gastric, and colorectal cancers. The purpose of this study was to clarify the prognostic value of long noncoding RNAs (lncRNAs) in GICs. A total of 111 articles were included, and 13103 patients (3123 with esophageal cancer, 4972 with gastric cancer, and 5008 with colorectal cancer) were enrolled in this study. The pooled hazard ratio (HR) values and corresponding 95% confidence interval (95% CI) of overall survival (OS) related to different lncRNA expressions in esophageal, gastric, colorectal, and gastrointestinal cancer patients were 1.92 (1.70-2.16), 1.96 (1.77-2.16), 2.10 (1.87-2.36), and 2.00 (1.87-2.13), respectively. We have identified 74 lncRNAs which were associated closely with poor prognosis of GIC patients, including 58 significantly upregulated lncRNA expression and 16 significantly downregulated lncRNA expression. In addition, 47 of the included studies revealed relative mechanisms and 12 of them investigated the correlation between lncRNAs and microRNAs. Taken together, this meta-analysis supports that specific lncRNAs are significantly related to the prognosis of GIC patients and may serve as novel markers for predicting the prognosis of GIC patients. Furthermore, lncRNAs may have a promising contribution to lncRNA-based targeted therapy and clinical decision-making in the future.
C1 [Kang, Weibiao; Zheng, Qiang; Yu, Changjun] Anhui Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Dept Gen Surg, Hefei, Anhui, Peoples R China.
   [Lei, Jun] Luan Peoples Hosp, Dept Gen Surg, Luan, Peoples R China.
   [Chen, Changyu] Anhui Tradit Med Univ, Affiliated Hosp 1, Dept Gen Surg, Hefei, Anhui, Peoples R China.
C3 Anhui Medical University
RP Yu, CJ (corresponding author), Anhui Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Dept Gen Surg, Hefei, Anhui, Peoples R China.
EM yuchangjun1206@163.com
OI Yu, Changjun/0000-0001-5950-4666
FU Natural Science Research Projects at Higher Institutions in Anhui
   Province [KJ2018ZD017]
FX The authors thank all authors of the included studies. This work was
   supported by the Natural Science Research Projects at Higher
   Institutions in Anhui Province (KJ2018ZD017).
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NR 123
TC 15
Z9 16
U1 0
U2 3
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 0278-0240
EI 1875-8630
J9 DIS MARKERS
JI Dis. Markers
PY 2018
VL 2018
AR 5340894
DI 10.1155/2018/5340894
PG 15
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine; Pathology
GA HS5JN
UT WOS:000463907700001
PM 30598708
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Yu, Y
   Ying, JM
   Zhang, W
   Li, WH
   Sun, YK
   Yang, L
   Cui, CX
   Zeng, YX
   Zhou, AP
AF Yu, Yue
   Ying, Jianming
   Zhang, Wen
   Li, Weihua
   Sun, Yongkun
   Yang, Lin
   Cui, Chengxu
   Zeng, Yixin
   Zhou, Aiping
TI Outcome of chemotherapy with or without targeted agents in metastatic
   colorectal cancer patients with deficient DNA mismatch repair: A single
   center, cohort study
SO ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
DE chemotherapy; deficient DNA mismatch repair; metastatic colorectal
   cancer; prognosis; targeted therapy
ID MICROSATELLITE-INSTABILITY STATUS; RANDOMIZED PHASE-III; PRIMARY TUMOR;
   COLON; OXALIPLATIN; RECURRENCE; MUTATIONS; SURVIVAL; THERAPY; FOLFIRI
AB Aims Metastatic colorectal cancer (mCRC) with deficient DNA mismatch repair (dMMR) is a rare disease accounting only for 4-5% of the whole mCRC and its optimal treatment still remains unclear. We conducted a retrospective study to evaluate the outcome of chemotherapy with or without bevacizumab or cetuximab in this setting. Methods A total of 729 colorectal cancer patients with dMMR status were screened for eligibility. The Kaplan-Meier method, the log-rank test and Cox analysis were utilized for survival analyses. Results A total of 43 patients met the inclusion criteria and enrolled in the study. The median overall survival (OS) of entire cohort was 21.7 months. Chemotherapy plus bevacizumab group exhibited a tendency of substantially higher overall response rate (ORR) than chemotherapy alone group (63.6% vs. 23.8%, P = 0.053), whereas the ORR between chemotherapy plus cetuximab group and chemotherapy alone group were similar (28.6% vs. 23.8%, P = 1.000). Compared with chemotherapy alone group, bevacizumab combined group achieved a significantly longer progression-free survival (10.0 months vs. 4.8 months, P = 0.028), whereas cetuximab combined group was not (6.8 months vs. 4.8 months, P = 0.158). Although the median OS seemed to favor bevacizumab combined group, no significant differences were detected between the three arms (33.7, 21.7 and 15.3 months, respectively; P = 0.345). Prognostic analysis showed that primary tumor resection was the positive prognostic factor of OS (hazards ratio: 0.438; P = 0.041). Conclusion dMMR mCRC seems resistant to chemotherapy and cetuximab. Bevacizumab combined therapy shows a sign of potentially favorable outcome in this subtype.
C1 [Yu, Yue; Zhang, Wen; Sun, Yongkun; Yang, Lin; Cui, Chengxu; Zhou, Aiping] Chinese Acad Med Sci, Canc Hosp, Natl Clin Res Ctr Canc, Dept Med Oncol,Natl Canc Ctr, 17 Panjiayuan Nanli, Beijing 100021, Peoples R China.
   [Yu, Yue; Ying, Jianming; Zhang, Wen; Li, Weihua; Sun, Yongkun; Yang, Lin; Cui, Chengxu; Zeng, Yixin; Zhou, Aiping] Peking Union Med Coll, 17 Panjiayuan Nanli, Beijing 100021, Peoples R China.
   [Ying, Jianming; Li, Weihua] Chinese Acad Med Sci, Canc Hosp, Natl Clin Res Ctr Canc, Dept Pathol,Natl Canc Ctr, Beijing, Peoples R China.
   [Zeng, Yixin] Chinese Acad Med Sci, Canc Hosp, Natl Clin Res Ctr Canc, State Key Lab Mol Oncol,Natl Canc Ctr, 17 Panjiayuan Nanli, Beijing 100021, Peoples R China.
   [Zeng, Yixin] Sun Yat Sen Univ, Canc Ctr, Collaborat Innovat Ctr Canc Med, Dept Expt Res,State Key Lab Oncol Southern China, 651 Dongfengdong Rd, Guangzhou 510060, Guangdong, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Cancer Institute & Hospital - CAMS; Chinese Academy of Medical Sciences
   - Peking Union Medical College; Peking Union Medical College; Chinese
   Academy of Medical Sciences - Peking Union Medical College; Cancer
   Institute & Hospital - CAMS; Chinese Academy of Medical Sciences -
   Peking Union Medical College; Cancer Institute & Hospital - CAMS; State
   Key Lab Oncology South China; Sun Yat Sen University
RP Zhou, AP (corresponding author), Chinese Acad Med Sci, Canc Hosp, Natl Clin Res Ctr Canc, Dept Med Oncol,Natl Canc Ctr, 17 Panjiayuan Nanli, Beijing 100021, Peoples R China.; Zeng, YX; Zhou, AP (corresponding author), Peking Union Med Coll, 17 Panjiayuan Nanli, Beijing 100021, Peoples R China.; Zeng, YX (corresponding author), Chinese Acad Med Sci, Canc Hosp, Natl Clin Res Ctr Canc, State Key Lab Mol Oncol,Natl Canc Ctr, 17 Panjiayuan Nanli, Beijing 100021, Peoples R China.; Zeng, YX (corresponding author), Sun Yat Sen Univ, Canc Ctr, Collaborat Innovat Ctr Canc Med, Dept Expt Res,State Key Lab Oncol Southern China, 651 Dongfengdong Rd, Guangzhou 510060, Guangdong, Peoples R China.
EM zengyx@sysucc.org.cn; zhouap1825@126.com
RI Zhang, Wanying/IXD-8104-2023; Liu, Zhiwei/AAM-5300-2020
OI Yu, Yue/0000-0002-5408-4962
CR Alex AK, 2017, CLIN COLORECTAL CANC, V16, P228, DOI 10.1016/j.clcc.2016.11.001
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NR 24
TC 5
Z9 5
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1743-7555
EI 1743-7563
J9 ASIA-PAC J CLIN ONCO
JI Asia-Pac. J. Clin. Oncol.
PD JUN
PY 2019
VL 15
IS 3
BP 128
EP 135
DI 10.1111/ajco.13130
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IC4JO
UT WOS:000470931700005
PM 30693649
DA 2025-01-04
ER

PT J
AU Pappas, L
   Quintanilha, JCF
   Huang, RSP
   Parikh, AR
AF Pappas, Leontios
   Quintanilha, Julia C. F.
   Huang, Richard S. P.
   Parikh, Aparna R.
TI Genomic alterations associated with early-stage disease and early
   recurrence in patients with colorectal cancer
SO ONCOLOGIST
LA English
DT Article; Early Access
DE colorectal cancer; early-stage cancer; genomic alterations; cancer
   recurrence; molecular characterization
ID III COLON-CANCER; MICROSATELLITE INSTABILITY; 1ST-LINE TREATMENT; BRAF
   MUTATION; OPEN-LABEL; FLUOROURACIL; OXALIPLATIN; LEUCOVORIN; KRAS;
   CHEMOTHERAPY
AB Background: The molecular characterization of early-stage (1-3) colorectal cancer (CRC) remains incomplete, as opposed to metastatic disease, where comprehensive genomic profiling (CGP) is routinely performed. This study aimed to characterize the genomics of stages 1-3 versus IV CRC, and the genomics of patients recurring within 1 year of diagnosis. Patients and Methods: Patients from a de-identified CRC clinico-genomic database who received Foundation Medicine testing (FoundationOne/ FoundationOne CDx) during routine clinical care at approximately 280 US cancer clinics between March 2014 and June 2023 were included. Genomic alterations (GA) were compared by Fisher's exact test. Results: A total of 4702 patients were included; 1902 with stages 1-3 and 2800 with stage 4 disease. Among patients with stages 1-3 disease, 546 recurred within 1 year. Patients staged 1-3 had higher prevalence of microsatellite instability (MSI-H, 11.4% vs 4.5%, P < .001), tumor mutational burden (TMB) >= 10 Mut/Mb (14.6% vs 6.8%, P < .001), GA in RNF43 (11.2% vs 5.7%, P < .001), MSH6 (3.9% vs 1.7%, P < .001), MLH1 (2.3% vs 0.7%, P < .001), and MSH2 (1.5% vs 0.6%, P < .01) compared to those with stage 4 disease. Patients who recurred within 1 year had higher prevalence of MSI-H (13.2% vs 4.4%, P <.001),TMB >= 10 Mut/Mb (16.2% vs 6.9%, P < .001), BRAF V600E (17.2% vs 7.9%, P < .003), GA in RNF43 (13.7% vs 5.3%, P < .001), MSH6 (4.2% vs 1.6%, P = .035), and BRCA1/2 (6.2% vs 3.0%, P = .030). On recurrence, more patients received targeted therapy when CGP was performed before versus after first-line therapy (43% vs 19%, P < .001). Conclusions: Early-stage CRC patients can have distinct genomic profiles and CGP in this population can help expand access to targeted therapies.
C1 [Pappas, Leontios; Parikh, Aparna R.] Harvard Med Sch, Massachusetts Gen Hosp, Boston, MA USA.
   [Quintanilha, Julia C. F.; Huang, Richard S. P.] Fdn Med, Cambridge, MA USA.
C3 Harvard University; Harvard Medical School; Massachusetts General
   Hospital; Foundation Medicine
RP Parikh, AR (corresponding author), Massachusetts Gen Hosp, 55 Fruit St, Boston, MA 02114 USA.
EM Aparna.Parikh@MGH.HARVARD.EDU
OI Parikh, Aparna/0000-0002-5245-7841
FU Roche
FX Foundation Medicine, a wholly owned subsidiary of Roche, is a for-profit
   company and producer of FDA-regulated molecular diagnostics. Authors
   employed by Foundation Medicine were involved in the design and conduct
   of the study, analysis, interpretation of the data, preparation, review,
   and approval of the manuscript.
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NR 43
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PD 2024 NOV 12
PY 2024
DI 10.1093/oncolo/oyae269
EA NOV 2024
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA L8M3Z
UT WOS:001353205200001
PM 39531357
DA 2025-01-04
ER

PT J
AU Deng, T
   Duan, JJ
   Bai, M
   Zhang, L
   Li, HL
   Liu, R
   Ning, T
   Ge, SH
   Wang, X
   Yang, YC
   Ji, Z
   Wang, FX
   Ba, Y
AF Deng, Ting
   Duan, Jingjing
   Bai, Ming
   Zhang, Le
   Li, Hongli
   Liu, Rui
   Ning, Tao
   Ge, Shaohua
   Wang, Xia
   Yang, Yuchong
   Ji, Zhi
   Wang, Feixue
   Ba, Yi
TI Third-line treatment patterns and clinical outcomes for metastatic
   colorectal cancer: a retrospective real-world study
SO THERAPEUTIC ADVANCES IN CHRONIC DISEASE
LA English
DT Article
DE clinical outcomes; colorectal cancer; real-world evidence; third-line
   therapy; treatment patterns
ID FOLFOXIRI PLUS BEVACIZUMAB; 1ST-LINE TREATMENT; OPEN-LABEL; REVERSE
   SEQUENCE; RANDOMIZED-TRIAL; RAS MUTATIONS; DOUBLE-BLIND; PHASE-II;
   CHEMOTHERAPY; OXALIPLATIN
AB Background:There are multiple recommendations on the third-line therapy of metastatic colorectal cancer (mCRC); however, no consensus has been reached.Objectives:This study aimed to explore the patient demographics and the real-world third-line treatment landscape of mCRC.Design:A retrospective real-world cohort study.Methods:Electronic medical records of mCRC patients from Tianjin Medical University Cancer Institute and Hospital between 2013 and 2020 were collected. Upon descriptive, comparative, and survival analyses, a retrospective study was conducted to describe demographics and clinical outcomes of mCRC patients receiving third-line treatment.Results:Among 218 mCRC patients receiving third-line therapy, 65.5% received chemotherapy combined with or without targeted drugs, followed by anti-angiogenic monotherapy (18.4%), anti-epidermal growth factor receptor drugs (6.9%) and immunotherapy (6.4%). The overall response rate and disease control rate reached 10.2% and 59.2%, respectively; and median progression-free survival (PFS) and overall survival were 4.0 m and 10.7 m, respectively. After Cox multivariate analysis, we found that therapeutic regime was an independent prognostic factor. Compared to patients receiving anti-angiogenic monotherapy, those receiving chemotherapy combined with or without targeted drugs exhibited better prognosis. For patients whose PFS were longer in the front-line treatment, the PFS of third-line therapy was also relatively longer (p = 0.023). Multiple types of therapies (>3, p = 0.002) or multiple drugs (>5, p = 0.024) in the whole-course management of mCRC are indicators of longer survival.Conclusion:Chemotherapy combined with or without targeted therapy remained dominated third-line choice and showed favorable efficacy compared with anti-angiogenic monotherapy. With the application of more types and quantities of effective drugs, patients would achieve better survival.
C1 [Deng, Ting; Ba, Yi] Tianjin Med Univ, Natl Clin Res Ctr Canc, Tianjins Clin Res Ctr Canc, Dept GI Med Oncol,Canc Inst & Hosp,Key Lab Canc Pr, Huanhu West Rd, Tianjin 300060, Peoples R China.
   [Duan, Jingjing; Bai, Ming; Zhang, Le; Li, Hongli; Liu, Rui; Ning, Tao; Ge, Shaohua; Wang, Xia; Yang, Yuchong; Ji, Zhi; Wang, Feixue] Tianjin Med Univ, Natl Clin Res Ctr Canc, Dept GI Med Oncol, Tianjins Clin Res Ctr Canc,Canc Inst & Hosp,Key La, Tianjin 300060, Peoples R China.
C3 Tianjin Medical University; Tianjin Medical University
RP Deng, T; Ba, Y (corresponding author), Tianjin Med Univ, Natl Clin Res Ctr Canc, Tianjins Clin Res Ctr Canc, Dept GI Med Oncol,Canc Inst & Hosp,Key Lab Canc Pr, Huanhu West Rd, Tianjin 300060, Peoples R China.
EM xymcdengting@126.com; bayi@tjmuch.com
RI Wang, Feixue/HGC-1048-2022; LI, Hongli/JMQ-9352-2023
FU None.
FX None.
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NR 42
TC 0
Z9 0
U1 3
U2 6
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 2040-6223
EI 2040-6231
J9 THER ADV CHRONIC DIS
JI Ther. Adv. Chronic Dis.
PY 2023
VL 14
AR 20406223231197311
DI 10.1177/20406223231197311
PG 17
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA R6IJ3
UT WOS:001065369100001
PM 37720594
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Greally, M
   Kelly, CM
   Cercek, A
AF Greally, Megan
   Kelly, Ciara M.
   Cercek, Andrea
TI HER2: An emerging target in colorectal cancer
SO CURRENT PROBLEMS IN CANCER
LA English
DT Article
ID T-CELLS; BREAST-CANCER; OPEN-LABEL; MONOCLONAL-ANTIBODIES;
   PROGNOSTIC-FACTOR; TUMOR LOCATION; PHASE-I; SURVIVAL; CETUXIMAB;
   OVEREXPRESSION
AB Despite advances in the treatment of metastatic colorectal cancer (CRC) the 5-year survival of patients with this disease remains low. A small proportion of CRCs overexpress the HER2 oncogene and the effective targeting of this pathway in other malignancies such as breast and gastric cancer has led to efforts to determine if it can also be exploited as a target in CRC. Activation of the HER2 pathway as a bypass signalling pathway has been identified as a mechanism of resistance for antiepidermal growth factor receptor antibody therapy in both the first line and salvage settings. It has also been shown that RAS and BRAF wild type metastatic CRC enriches for the presence of HER2 amplification. This knowledge, in addition to preclinical data providing a rationale for dual anti-HER2 targeted therapy has led to several clinical trials. To date, recently published and presented early phase data provide promising evidence suggesting anti-HER2 therapy may have a potentially beneficial role in the treatment of HER2-positive metastatic CRC. Namely, the HERACLES-A and MyPathway studies have shown benefit in a small number of patients with the use of combination trastuzumab-lapatinib and trastuzumab-pertuzumab, respectively. However, data from larger clinical trials are required before HER2-directed therapy is incorporated into standard treatment paradigms for CRC. This review presents an overview of epidermal growth factor receptor and HER2 pathways in CRC and discusses preclinical and clinical studies carried out in this field to date. There is potential that with continued evolution of data in this area, HER2 may become a validated therapeutic target and thus, anti-HER2 therapy may become an additional treatment option for a small population of patients with metastatic CRC. (C) 2018 Elsevier Inc. All rights reserved.
C1 [Greally, Megan; Kelly, Ciara M.; Cercek, Andrea] Mem Sloan Kettering Canc Ctr, Dept Med, 1275 York Ave, New York, NY 10021 USA.
C3 Memorial Sloan Kettering Cancer Center
RP Greally, M (corresponding author), Mem Sloan Kettering Canc Ctr, 300 E 66th St,Off 1405, New York, NY 10065 USA.
EM greallym@mskcc.org
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NR 61
TC 71
Z9 75
U1 0
U2 6
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0147-0272
EI 1535-6345
J9 CURR PROB CANCER
JI Curr. Probl. Cancer
PD NOV-DEC
PY 2018
VL 42
IS 6
SI SI
BP 560
EP 571
DI 10.1016/j.currproblcancer.2018.07.001
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HF8AQ
UT WOS:000454463700003
PM 30100092
DA 2025-01-04
ER

PT J
AU Keikes, L
   Koopman, M
   Stuiver, MM
   Lemmens, VEPP
   van Oijen, MGH
   Punt, CJA
AF Keikes, Lotte
   Koopman, Miriam
   Stuiver, Martijn M.
   Lemmens, Valery E. P. P.
   van Oijen, Martijn G. H.
   Punt, Cornelis J. A.
TI Practice variation on hospital level in the systemic treatment of
   metastatic colorectal cancer in The Netherlands: a population-based
   study
SO ACTA ONCOLOGICA
LA English
DT Article
ID COMBINATION CHEMOTHERAPY; ELDERLY-PATIENTS; COST-EFFECTIVENESS;
   BEVACIZUMAB; PATTERNS; TRIAL; CAPECITABINE; OXALIPLATIN; IRINOTECAN;
   THERAPY
AB Introduction: Population-based data on the implementation of guidelines for cancer patients in daily practice are scarce, while practice variation may influence patient outcomes. Therefore, we evaluated treatment patterns and associated variables in the systemic treatment of metastatic colorectal cancer (mCRC) in the Netherlands. Material and methods: We selected a random sample of adult mCRC patients diagnosed from 2008 to 2015 from the National Cancer Registry in 20 (4 academic, 8 teaching and 8 regional) Dutch hospitals. We examined the influence of patient, demographic and tumour characteristics on the odds of being treated with systemic therapy according to the current guideline and assessed its association with survival. Results: Our study population consisted of 2222 mCRC patients of whom 1307 patients received systemic therapy for mCRC. Practice variation was most obvious in the use of bevacizumab and anti-EGFR therapy in patients with (K)RAS wild-type tumours. Administration rates did not differ between hospital types but fluctuated between individual hospitals for bevacizumab (8-92%; p < .0001) and anti-EGFR therapy (10-75%; p = .05). Bevacizumab administration was inversely correlated to higher age (OR:0.2; 95%CI: 0.1-0.3) comorbidity (OR:0.6; 95%CI: 0.5-0.8) and the presence of metachronous metastases (OR:0.5; 95%CI: 0.3-0.7), but patient characteristics did not differ between hospitals with low or high bevacizumab administration rates. The hazard ratios for exposure to bevacizumab and anti-EGFR therapy were 0.8 (95%CI: 0.7-0.9) and 0.6 (95%CI: 0.5-0.8), respectively. Discussion: We identified significant inter-hospital variation in targeted therapy administration for mCRC patients, which may affect outcome. Age and comorbidity were inversely correlated with non-administration of bevacizumab but did not explain inter-hospital practice variation. Our data suggest that practice variation is based on individual strategy of hospitals rather than guideline recommendations or patient-driven decisions. Individual hospital strategies are an additional factor that may explain the observed differences between real-life data and results obtained from clinical trials.
C1 [Keikes, Lotte; van Oijen, Martijn G. H.; Punt, Cornelis J. A.] Univ Amsterdam, Amsterdam UMC, Dept Med Oncol, Amsterdam, Netherlands.
   [Keikes, Lotte; Lemmens, Valery E. P. P.; van Oijen, Martijn G. H.] Netherlands Comprehens Canc Org, Dept Res, Utrecht, Netherlands.
   [Koopman, Miriam] Univ Utrecht, Univ Med Ctr, Dept Med Oncol, Utrecht, Netherlands.
   [Stuiver, Martijn M.] Univ Amsterdam, Amsterdam UMC, Dept Clin Epidemiol Biostat & Bioinformat, Amsterdam, Netherlands.
C3 University of Amsterdam; Utrecht University; Utrecht University Medical
   Center; University of Amsterdam
RP Keikes, L (corresponding author), Univ Amsterdam, Dept Med Oncol, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands.
EM l.keikes@amsterdamumc.nl
RI Stuiver, Martijn/AAE-6231-2021
FU Amgen; Roche; Servier; Merck Serono
FX This study was funded with unrestricted research grants from Amgen,
   Roche, Servier and Merck Serono.
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NR 32
TC 6
Z9 7
U1 0
U2 2
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0284-186X
EI 1651-226X
J9 ACTA ONCOL
JI Acta Oncol.
PD APR 2
PY 2020
VL 59
IS 4
BP 395
EP 403
DI 10.1080/0284186X.2020.1722320
EA FEB 2020
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KS3UF
UT WOS:000513601600001
PM 32048563
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Strickler, JH
   Loree, JM
   Ahronian, LG
   Parikh, AR
   Niedzwiecki, D
   Andresson, A
   Pereira, L
   McKinney, M
   Korn, WM
   Atreya, CE
   Banks, KC
   Nagy, RJ
   Meric-Bernstam, F
   Lanman, RB
   Talasaz, A
   Tsigelny, IF
   Corcoran, RB
   Kopetz, S
AF Strickler, John H.
   Loree, Jonathan M.
   Ahronian, Leanne G.
   Parikh, Aparna R.
   Niedzwiecki, Donna
   Andresson, Allan
   Pereira, Lima
   McKinney, Matthew
   Korn, W. Michael
   Atreya, Chloe E.
   Banks, Kimberly C.
   Nagy, Rebecca J.
   Meric-Bernstam, Funda
   Lanman, Richard B.
   Talasaz, AmirAli
   Tsigelny, Igor F.
   Corcoran, Ryan B.
   Kopetz, Scott
TI Genomic Landscape of Cell-Free DNA in Patients with Colorectal Cancer
SO CANCER DISCOVERY
LA English
DT Article
ID EGFR MONOCLONAL-ANTIBODIES; ACQUIRED-RESISTANCE; CETUXIMAB RESISTANCE;
   EXTRACELLULAR DOMAIN; CLONAL HEMATOPOIESIS; TARGETED THERAPY; KRAS
   MUTATIONS; HETEROGENEITY; EVOLUTION; BLOCKADE
AB "Liquid biopsy" approaches analyzing cell-free DNA (cfDNA) from the blood of patients with cancer are increasingly utilized in clinical practice. However, it is not yet known whether cfDNA sequencing from large cohorts of patients with cancer can detect genomic alterations at frequencies similar to those observed by direct tumor sequencing, and whether this approach can generate novel insights. Here, we report next-generation sequencing data from cfDNA of 1,397 patients with colorectal cancer. Overall, frequencies of genomic alterations detected in cfDNA were comparable to those observed in three independent tissue-based colorectal cancer sequencing compendia. Our analysis also identified a novel cluster of extracellular domain (ECD) mutations in EGFR, mediating resistance by blocking binding of anti-EGFR antibodies. Patients with EGFR ECD mutations displayed striking tumor heterogeneity, with 91% harboring multiple distinct resistance alterations (range, 1-13; median, 4). These results suggest that cfDNA profiling can effectively define the genomic landscape of cancer and yield important biological insights.
   SIGNIFICANCE: This study provides one of the first examples of how large-scale genomic profiling of cfDNA from patients with colorectal cancer can detect genomic alterations at frequencies comparable to those observed by direct tumor sequencing. Sequencing of cfDNA also generated insights into tumor heterogeneity and therapeutic resistance and identified novel EGFR ectodomain mutations. Cancer (C)2017 AACR.
C1 [Strickler, John H.; Niedzwiecki, Donna; McKinney, Matthew] Duke Univ, Med Ctr, Durham, NC USA.
   [Loree, Jonathan M.; Andresson, Allan; Pereira, Lima; Meric-Bernstam, Funda; Kopetz, Scott] Univ Texas MD Anderson Canc Ctr, 1515 Holcombe Blvd,Unit 426, Houston, TX 77030 USA.
   [Ahronian, Leanne G.; Parikh, Aparna R.; Corcoran, Ryan B.] Harvard Med Sch, Massachusetts Gen Hosp, Canc Ctr, Boston, MA USA.
   [Ahronian, Leanne G.; Parikh, Aparna R.; Corcoran, Ryan B.] Harvard Med Sch, Dept Med, Boston, MA USA.
   [Korn, W. Michael; Atreya, Chloe E.] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.
   [Korn, W. Michael] Caris Life Sci, Phoenix, AZ USA.
   [Banks, Kimberly C.; Nagy, Rebecca J.; Lanman, Richard B.; Talasaz, AmirAli] Guardant Hlth Inc, Redwood City, CA USA.
   [Tsigelny, Igor F.] Univ Calif San Diego, San Diego, CA 92103 USA.
   [Tsigelny, Igor F.] CureMatch Inc, San Diego, CA USA.
C3 Duke University; University of Texas System; UTMD Anderson Cancer
   Center; Harvard University; Massachusetts General Hospital; Harvard
   Medical School; Harvard University; Harvard Medical School; University
   of California System; University of California San Francisco; UCSF
   Medical Center; UCSF Helen Diller Family Comprehensive Cancer Center;
   Guardant Health, Inc.; University of California System; University of
   California San Diego
RP Kopetz, S (corresponding author), Univ Texas MD Anderson Canc Ctr, 1515 Holcombe Blvd,Unit 426, Houston, TX 77030 USA.; Corcoran, RB (corresponding author), Harvard Med Sch, 149 13th St, Boston, MA 02129 USA.
EM rbcorcoran@partners.org; skopetz@mdanderson.org
RI Kopetz, Scott/AAC-1387-2019; Meric-Bernstam, Funda/JRZ-1866-2023;
   Lanman, Richard/D-8290-2016; McKinney, Matthew/JPK-0745-2023; Pereira,
   Allan/N-7773-2016
OI Banks, Kimberly/0000-0002-1290-3114; Niedzwiecki,
   Donna/0000-0002-3566-0450; Strickler, John/0000-0001-7579-1175; Loree,
   Jonathan/0000-0001-8189-2132; Kopetz, Scott/0000-0001-9647-3416;
   Pereira, Allan/0000-0002-8573-7364
FU NIH [R01 CA184843]; CPRIT grant [RP150535]; ASCO Young Investigator
   Award; Canadian Association of Medical Oncologists Research Fellowship;
   Detweiler Fellowship; NIH/NCI [K08CA175143]; Damon Runyon Clinical
   Investigator Award; NIH/NCI Gastrointestinal Cancer SPORE [SPORE P50
   CA127003, R01CA208437, K08CA166510]; Stand Up To Cancer Colorectal
   Cancer Dream Team Translational Research Grant [SU2C-AACR-DT22-17]
FX The work is supported by NIH R01 CA184843 (to S. Kopetz), CPRIT grant
   RP150535 (to F. Meric-Bernstam), an ASCO Young Investigator Award,
   Canadian Association of Medical Oncologists Research Fellowship, and
   Detweiler Fellowship (to J.M. Loree), NIH/NCI K08CA175143 (to C.E.
   Atreya), and a Damon Runyon Clinical Investigator Award, NIH/NCI
   Gastrointestinal Cancer SPORE P50 CA127003, R01CA208437, and
   K08CA166510. Research was supported by a Stand Up To Cancer Colorectal
   Cancer Dream Team Translational Research Grant (grant number
   SU2C-AACR-DT22-17; to R.B. Corcoran). Research grants are administered
   by the American Association for Cancer Research, the scientific partner
   of SU2C.
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NR 34
TC 204
Z9 219
U1 1
U2 23
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
EI 2159-8290
J9 CANCER DISCOV
JI Cancer Discov.
PD FEB
PY 2018
VL 8
IS 2
BP 164
EP 173
DI 10.1158/2159-8290.CD-17-1009
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FV7OQ
UT WOS:000424774500022
PM 29196463
OA Green Submitted, Green Accepted, Bronze
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Qi, XY
   Hou, XY
   Wei, ZX
   Liu, DK
   Sun, Y
   Jiang, YH
   Liu, C
   Zhou, WH
   Yang, LP
   Liu, KJ
AF Qi, Xiaoyan
   Hou, Xuyang
   Wei, Zuxing
   Liu, Dekun
   Sun, Yin
   Jiang, Yuhong
   Liu, Chao
   Zhou, Weihan
   Yang, Leping
   Liu, Kuijie
TI Macrophage membrane-coated SN-38-encapsulated liposomes for efficient
   treatment of colorectal cancer
SO JOURNAL OF DRUG DELIVERY SCIENCE AND TECHNOLOGY
LA English
DT Article
DE Biomimetic; Macrophages; Colorectal cancer; Targeted therapy; SN-38
ID DRUG-DELIVERY; IN-VITRO; NANOPARTICLES; CAMPTOTHECIN; SN-38;
   NANOCARRIERS; FORMULATION; CONJUGATE; SN38
AB Background: SN-38, recognized as the primary active derivative of the pivotal chemotherapeutic agent CPT-11, demonstrates substantially enhanced efficacy in colorectal cancer (CRC) management compared to CPT-11. Nonetheless, challenges such as low stability, inadequate aqueous solubility, limited bioavailability, and nonspecific targeting to cancer cells hinder its clinical adoption. In the present research, we synthesized SN-38loaded liposomes cloaked with macrophage membranes (SN-38@MM-LPs) to assess their therapeutic potential and safety profile in addressing CRC. Methods: SN-38@MM-LPs were synthesized using an incubation extrusion technique, combining a macrophage membrane with liposomes (LPs). It was characterized by size, zeta potential, transmission electron microscopy observations, polydispersity index and coomassie bright blue staining. CCK-8, EdU, and flow cytometry assays were performed to evaluate the viability and apoptosis rates of HCT116 and HCT8 cells after treatment with SN38@MM-LPs. A cellular uptake assay was conducted to evaluate the internalization of SN-38@MM-LPs in vitro. Moreover, the biodistribution, therapeutic efficacy, and safety of SN-38@MM-LPs were further assessed in orthotopic HCT116 xenograft model mice. Results: Characterization results revealed that SN-38@MM-LPs possess a spherical morphology with a consistent size distribution (129 nm) and a drug loading efficiency of 5.54 +/- 0.73%. SN-38 curtailed the growth and promoted apoptosis in both HCT8 and HCT116 cells. The impact of SN-38 was accentuated when delivered via SN-38@LPs and SN-38@MM-LPs. Notably, in the orthotopic xenograft model, SN-38@MM-LPs manifested superior tumor-targeting capabilities and therapeutic outcomes. Additionally, SN-38@MM-LPs presented negligible hepatic toxicity. Conclusions: SN-38@MM-LPs showcased potent and targeted antitumor actions in CRC. Consequently, SN38@MM-LPs emerge as a potential nanoparticle formulation that could amplify the antitumor efficacy of SN38, simultaneously mitigating liver toxicity concerns.
C1 [Qi, Xiaoyan; Wei, Zuxing; Liu, Dekun; Jiang, Yuhong; Liu, Chao; Zhou, Weihan; Yang, Leping; Liu, Kuijie] Cent South Univ, Xiangya Hosp 2, Dept Gen Surg, Changsha 410011, Hunan, Peoples R China.
   [Hou, Xuyang] Cent South Univ, Xiangya Hosp 2, Dept Cardiovasc Surg, Changsha 410011, Hunan, Peoples R China.
   [Sun, Yin] Univ South China, Dept Pharmaceut Pharmacol, Hengyang, Hunan, Peoples R China.
C3 Central South University; Central South University; University of South
   China
RP Liu, KJ (corresponding author), Cent South Univ, Xiangya Hosp 2, Dept Gen Surg, Changsha 410011, Hunan, Peoples R China.
EM liukuijie@csu.edu.cn
RI Yang, Ye/GZM-4812-2022; JIANG, YUHONG/D-2099-2017
FU Hunan Provincial Health Commission [202204014332]; Hunan Provincial
   Innovation Platform and Talent Plan-2020 Hunan Young Talents
   [2020RC3062]
FX This study was funded by the Hunan Provincial Health Commission
   (202204014332) and Hunan Provincial Innovation Platform and Talent
   Plan-2020 Hunan Young Talents (2020RC3062) .
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NR 49
TC 3
Z9 3
U1 4
U2 20
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1773-2247
EI 2588-8943
J9 J DRUG DELIV SCI TEC
JI J. Drug Deliv. Sci. Technol.
PD JAN
PY 2024
VL 91
AR 104904
DI 10.1016/j.jddst.2023.104904
EA DEC 2023
PG 10
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DT6M3
UT WOS:001134364900001
OA hybrid
DA 2025-01-04
ER

PT J
AU Li, QY
   Pan, ZY
   Zhou, XK
AF Li, Qianyuan
   Pan, Zhiyun
   Zhou, Xiukou
TI Endothelial Cell-Derived Interleukin-6 Facilitated Colorectal Cancer
   Cell Migration and Invasion by Regulating Osteopontin in a Paracrine
   Manner
SO JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS
LA English
DT Article
DE colorectal cancer; metastasis; paracrine; interleukin-6; osteopontin;
   glycogen synthase kinase-3 beta-beta-catenin signaling pathway
ID MESENCHYMAL TRANSITION; TUMOR-GROWTH; LUNG-CANCER; METASTASIS;
   PROGRESSION; EXPRESSION; PROMOTE
AB Background: Patients with metastatic colorectal cancer (CRC) generally suffer from poor prognosis. Therefore, there is an urgent need to further delineate the mechanism of metastasis in CRC, which is of clinical significance for the development of more targeted therapy. This study aimed to explore the potential role of endothelial cells-derived interleukin-6 (IL-6) in CRC metastasis.Methods: Human umbilical vein endothelial cell (HUVEC)-conditioned medium and CRC-conditioned medium were prepared, with the latter being the control. Enzyme-linked immunosorbent assay was employed to detect IL-6 levels in HUVEC-conditioned or CRC-conditioned culture media. CRC cells were separately cultured in both media to investigate the effect of HUVECs on CRC metastasis using cell counting kit-8 assay, scratch test and Transwell assay. The role of HUVEC-derived IL-6 in CRC cells was investigated using rescue assay. The expressions of the osteopontin protein and the proteins in glycogen synthase kinase-3 beta (GSK3 beta)-beta-catenin signaling pathways were determined by Western blotting. To confirm the mediating role of osteopontin in the relationship between IL-6 and CRC, the expression of osteopontin in CRC cells was up-regulated.Results: IL-6 level was higher in HUVEC-conditioned medium than in CRC-conditioned medium (p < 0.001). CRC cells in the HUVEC-conditioned medium showed enhanced viability, migration and invasion (p < 0.05). HUVEC-secreted IL-6 facilitated malignant phenotypes and activated osteopontin and GSK3 beta-beta-catenin signaling pathway of CRC cells in a dose-dependent manner (p < 0.05). Moreover, osteopontin overexpression contributed to CRC metastasis in vitro and activated GSK3 beta-beta-catenin signaling pathway (p < 0.001), while such effect was abrogated by IL-6 silencing (p < 0.001).Conclusion: HUVEC-derived IL-6 facilitated the metastasis of CRC cells by regulating osteopontin in a paracrine manner.
C1 [Li, Qianyuan; Pan, Zhiyun; Zhou, Xiukou] Zhejiang Chinese Med Univ, Affiliated Hosp 1, Zhejiang Prov Hosp Chinese Med, Dept Anorectal Surg, Hangzhou 310006, Zhejiang, Peoples R China.
C3 Zhejiang Chinese Medical University
RP Li, QY (corresponding author), Zhejiang Chinese Med Univ, Affiliated Hosp 1, Zhejiang Prov Hosp Chinese Med, Dept Anorectal Surg, Hangzhou 310006, Zhejiang, Peoples R China.
EM liqianyuan_qy@163.com
CR Abd-Ellah A, 2018, SCI REP-UK, V8, DOI 10.1038/s41598-018-19822-z
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NR 38
TC 0
Z9 0
U1 0
U2 2
PU BIOLIFE SAS
PI SILVA MARINA (TE)
PA VIA S STEFANO 39 BIS, 64029 SILVA MARINA (TE), ITALY
SN 0393-974X
EI 1724-6083
J9 J BIOL REG HOMEOS AG
JI J. Biol. Regul. Homeost. Agents
PD JAN
PY 2024
VL 38
IS 1
BP 719
EP 732
DI 10.23812/j.biol.regul.homeost.agents.20243801.59
PG 14
WC Endocrinology & Metabolism; Immunology; Medicine, Research &
   Experimental; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Immunology; Research & Experimental
   Medicine; Physiology
GA GB2U1
UT WOS:001150140300001
DA 2025-01-04
ER

PT J
AU Lee, KS
   Lee, K
   Yun, S
   Moon, S
   Park, Y
   Han, JH
   Kim, CY
   Lee, HS
   Choe, G
AF Lee, Kyu Sang
   Lee, Kyoungyul
   Yun, Sumi
   Moon, Seyoung
   Park, Yujun
   Han, Jung Ho
   Kim, Chae-Yong
   Lee, Hye Seung
   Choe, Gheeyoung
TI Prognostic relevance of programmed cell death ligand 1 expression in
   glioblastoma
SO JOURNAL OF NEURO-ONCOLOGY
LA English
DT Article
DE Glioblastoma; Programmed cell death ligand 1; CD274;
   Immunohistochemistry; Prognosis
ID TUMOR-INFILTRATING LYMPHOCYTES; PD-L1 EXPRESSION; LUNG-CANCER;
   CLINICAL-OUTCOMES; COLORECTAL-CANCER; BRAIN-TUMORS; MICROGLIA;
   MUTATIONS; GLIOMAS; IMMUNOTHERAPY
AB The aim of this study was to determine the clinicopathological significance of programmed cell death ligand 1 (PD-L1) expression in glioblastoma (GBM). In a retrospective cohort of 115 consecutive patients with GBM, PD-L1 expression was determined using immunohistochemistry (IHC). Membranous and fibrillary PD-L1 staining of any intensity in > 5% neoplastic cells and tumour infiltrating immune cells (TIIs) was considered positive staining. In addition, isocitrate dehydrogenase-1 (IDH-1) (R132H) expression and cluster of differentiation 3 (CD3)-positive T-cell infiltration were investigated using IHC. O(6)-methylguanine-DNA methyltransferase (MGMT) promoter methylation assay and fluorescence in situ hybridization (FISH) for the assessment of 1p/19q deletion were performed. Expression of PD-L1 in tumour cells and TIIs was found in 37 (32.2%) and 6 (5.2%) patients, respectively. Kaplan-Meier analysis indicated that PD-L1 expression in tumour cells was significantly associated with poor overall survival (OS) (P = 0.017), though multivariate Cox analysis did not confirm this association (hazard ratio 1.204; P = 0.615). PD-L1 expression in TIIs did not correlate with the patient prognosis (P = 0.545). In addition, MGMT methylation and IDH-1 (R132H) expression were associated with a better prognosis (P < 0.001 and P = 0.024, respectively). The expression of PD-L1 was associated with CD3-positive T-cell infiltration (P < 0.001), and IDH-1 wild type status (P = 0.008). A deeper insight into PD-L1 expression could help to ensure the success of future immunotherapy in GBM. Our study suggested that PD-L1 target therapy might be beneficial for PD-L1-expressing GBM patients with a poor prognosis.
C1 [Lee, Kyu Sang; Moon, Seyoung; Park, Yujun; Lee, Hye Seung; Choe, Gheeyoung] Seoul Natl Univ, Bundang Hosp, Dept Pathol, 173-82 Gumi Ro, Seongnam Si 463707, Gyeonggi Do, South Korea.
   [Lee, Kyoungyul] Kangwon Natl Univ Hosp, Dept Pathol, 156 Baengnyeong Ro, Chuncheon Si 200722, Kangwon Do, South Korea.
   [Yun, Sumi] Samkwang Med Labs, Dept Diagnost Pathol, 57 Baumoe Ro 41 Gil, Seoul, South Korea.
   [Han, Jung Ho; Kim, Chae-Yong] Seoul Natl Univ, Bundang Hosp, Dept Neurosurg, 173-82 Gumi Ro, Seongnam Si 463707, Gyeonggi Do, South Korea.
C3 Seoul National University (SNU); Kangwon National University; Kangwon
   National University Hospital; Seoul National University (SNU)
RP Choe, G (corresponding author), Seoul Natl Univ, Bundang Hosp, Dept Pathol, 173-82 Gumi Ro, Seongnam Si 463707, Gyeonggi Do, South Korea.
EM gychoe@snu.ac.kr
RI PARK, YUJUN/ABA-4420-2021; KIM, CHAE-YONG/D-5769-2012; Lee, Hye
   Seung/G-6419-2011
OI Lee, Hye Seung/0000-0002-1667-7986; Choe, Gheeyoung/0000-0001-6547-5603;
   KIM, CHAE-YONG/0000-0001-9773-5553
FU Seoul National University Bundang Hospital research fund [11-2011-021]
FX This research was funded by the Seoul National University Bundang
   Hospital research fund (Grant Number: 11-2011-021).
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NR 50
TC 32
Z9 32
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-594X
EI 1573-7373
J9 J NEURO-ONCOL
JI J. Neuro-Oncol.
PD FEB
PY 2018
VL 136
IS 3
BP 453
EP 461
DI 10.1007/s11060-017-2675-6
PG 9
WC Oncology; Clinical Neurology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Neurosciences & Neurology
GA FV5US
UT WOS:000424648500005
PM 29147863
DA 2025-01-04
ER

PT J
AU Elkady, N
   Allam, DM
AF Elkady, Noha
   Allam, Dina M.
TI The Role of Galectin3, Tubulinβ, and Maspin in Promoting Tumor Budding
   in Colorectal Carcinoma and Their Clinical Implications
SO APPLIED IMMUNOHISTOCHEMISTRY & MOLECULAR MORPHOLOGY
LA English
DT Article
DE galectin3; tubulin beta and maspin; budding and colorectal cancer
ID EPITHELIAL-MESENCHYMAL TRANSITION; EXPRESSION; PROGRESSION; PROGNOSIS
AB Colorectal cancer (CRC) is a leading cause of death worldwide. Despite the advances in surgical and therapeutic management, tumor metastases and poor prognosis are still major problems. Tumor budding is a relevant prognostic factor in CRC, and it can predict tumor metastasis. Galectin3 is responsible for the development and progression of many cancers through the regulation of cell-cell/cell-matrix interactions and tumor cell invasion. Tubulin is a microtubule protein, and maspin is a serine protease inhibitor; both induce tumor cell invasion through the stimulation of epithelial-mesenchymal transition. This study aims to evaluate the relationship between the expression of galecin3, tubulin beta, and maspin in CRC and clinicopathological features, including tumor budding, their prognostic roles, and clinical implications using immunohistochemistry. Galectin3, tubulin beta, and maspin were detected in tumor cells in 95%, 65%, and 87.5% of cases and in stromal cells in 28.8%, 40%, and 0% of cases. High expression of galectin3 and tubulin beta expression either in tumor cells or stroma was significantly associated with aggressive tumor features such as lymph node metastasis, lymphovascular invasion, tumor budding, and advanced tumor stage. The nucleocytoplasmic expression of maspin in tumor cells showed a significant association with deeper tumor invasion, lymph node metastasis, tumor budding, and advanced tumor stage. Significant associations were found between high galectin3 tumor cell expression and nucleocytoplasmic maspin and shorter survival. High expression of galectin3, tubulin beta, and nucleocytoplasmic maspin were significantly associated with aggressive tumor features such as tumor invasion, metastasis, high tumor budding, and short survival in CRC. They could be used as biomarkers for tumor budding and tumor aggressiveness in CRC and may be considered for future target therapy.
C1 [Elkady, Noha; Allam, Dina M.] Menoufia Univ, Fac Med, Pathol Dept, Shibin Al Kawm 32511, Egypt.
C3 Egyptian Knowledge Bank (EKB); Menofia University
RP Allam, DM (corresponding author), Menoufia Univ, Fac Med, Pathol Dept, Shibin Al Kawm 32511, Egypt.
EM drnohaelkady@gmail.com; dn_llm_2006@yahoo.com
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NR 40
TC 2
Z9 2
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1541-2016
EI 1533-4058
J9 APPL IMMUNOHISTO M M
JI Appl. Immunohistochem.
PD MAR
PY 2024
VL 32
IS 3
BP 143
EP 150
DI 10.1097/PAI.0000000000001183
PG 8
WC Anatomy & Morphology; Medical Laboratory Technology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Anatomy & Morphology; Medical Laboratory Technology; Pathology
GA SG0P9
UT WOS:001233188700008
PM 38251657
DA 2025-01-04
ER

PT J
AU Hosseini, S
   Rejali, L
   Pezeshkian, Z
   Malekian, M
   Fatemi, N
   Peyravian, N
   Hadizadeh, M
   Mohsenifar, Z
   Khanabadi, B
   Farzam, M
   Sherkat, G
   Aghdaei, HA
   Mojarad, EN
   Bonab, MA
AF Hosseini, Shaghayegh
   Rejali, Leili
   Pezeshkian, Zahra
   Malekian, Mahtash
   Fatemi, Nayeralsadat
   Peyravian, Noshad
   Hadizadeh, Mahrooyeh
   Mohsenifar, Zhaleh
   Khanabadi, Binazir
   Farzam, Maral
   Sherkat, Ghazal
   Aghdaei, Hamid Asadzadeh
   Mojarad, Ehsan Nazemalhosseini
   Bonab, Maziar Ashrafian
TI Oncogenic Role of Connective Tissue Growth Factor Is Associated with
   Canonical TGF-β Cascade in Colorectal Cancer
SO GENES
LA English
DT Article
DE MMP-1; CTGF; canonical TGF-beta signalling; CRC
ID MATRIX METALLOPROTEINASE-1; SIGNALING PATHWAY; PROGNOSTIC-FACTOR; FACTOR
   CTGF/CCN2; EXPRESSION; MMP-1; CELLS; LIVER; CTGF; MIGRATION
AB TGF-beta signaling pathways promote tumour development and control several downstream genes such as CTGF and MMPs. This study aimed to investigate the association between CTGF and MMP-1 mRNA expressions with clinicopathological status and survival rate in colorectal cancer patients. We investigated expression levels of CTGF and MMP-1 genes in paraffin-embedded tumours and adjacent normal tissue blocks (ADJ) by Real Time-PCR. Then, the expression of Smad2 and Smad4 proteins in the TGF-beta canonical pathway was evaluated by immunohistochemistry. Finally, the correlation between CTGF, MMP-1, and the canonical TGF-beta-signalling pathway with the clinicopathological features was investigated. Expression levels of MMP-land CTGF were higher in tumours compared with adjacent normal tissues. Overexpression levels of MMP-1 and CTGF were associated with lymph node metastasis, distant metastasis, tumour histopathological grading, advanced stage, and poor survival (p < 0.05). Additionally, a significant association between the upregulation of MMP-1 and tumour location was noted. Upregulation of Smad2 and Smad4 proteins were also significantly correlated with lymph node metastasis, distant metastasis, advanced stage, and poor survival (p < 0.0001). This study showed that canonical TGF-beta signalling regulates both CTGF and MMP-1 expression and CRC progression. Moreover, TGF-beta signalling and its downstream genes could be used as novel biomarkers and novel approaches for targeted therapy in CRC.
C1 [Hosseini, Shaghayegh; Rejali, Leili; Pezeshkian, Zahra; Malekian, Mahtash; Fatemi, Nayeralsadat; Peyravian, Noshad; Khanabadi, Binazir; Aghdaei, Hamid Asadzadeh] Shahid Beheshti Univ Med Sci, Basic & Mol Epidemiol Gastrointestinal Disorders, Res Inst Gastroenterol & Liver Dis, Tehran 1985717411, Iran.
   [Hadizadeh, Mahrooyeh] Canterbury Christ Church Univ, Fac Hlth & Wellbeing, Canterbury CT1 1QU, Kent, England.
   [Mohsenifar, Zhaleh] Shahid Beheshti Univ Med Sci, Taleghani Hosp, Dept Pathol, Tehran 1983963113, Iran.
   [Farzam, Maral; Mojarad, Ehsan Nazemalhosseini] Shahid Beheshti Univ Med Sci, Gastroenterol & Liver Dis Res Ctr, Res Inst Gastroenterol & Liver Dis, Tehran 1985717411, Iran.
   [Sherkat, Ghazal] Islamic Azad Univ, Med Fac, Mashhad Branch, Mashhad 9187147578, Razavi Khorasan, Iran.
   [Bonab, Maziar Ashrafian] Kent & Medway Med Sch, Canterbury CT2 7FS, Kent, England.
C3 Shahid Beheshti University Medical Sciences; Canterbury Christ Church
   University; Shahid Beheshti University Medical Sciences; Shahid Beheshti
   University Medical Sciences; Islamic Azad University
RP Mojarad, EN (corresponding author), Shahid Beheshti Univ Med Sci, Gastroenterol & Liver Dis Res Ctr, Res Inst Gastroenterol & Liver Dis, Tehran 1985717411, Iran.; Bonab, MA (corresponding author), Kent & Medway Med Sch, Canterbury CT2 7FS, Kent, England.
EM shaghayeghhosseiny1990@gmail.com; leilirejali@gmail.com;
   zahrapezeshkian@yahoo.com; mahtash.malekian@yahoo.com;
   n_fatemi_1363@yahoo.com; n.peyravian@gmail.com;
   m.hadizadeh1176@canterbury.ac.uk; mohsenifar@sbmu.ac.ir;
   binazir.khanabadi74@gmail.com; marall_jeiilan@hotmail.com;
   gsherkat@yahoo.com; hamid.assadzadeh@gmail.com; ehsanmojarad@gmail.com;
   maziar.bonab@kmms.ac.uk
RI Pezeshkian, Zahra/GPC-5089-2022; Asadzadeh-Aghdaei, Hamid/AAD-4494-2022;
   Mohsenifar, Zhaleh/AAX-9347-2021; rejali, leili/ABA-1194-2020;
   Nazemalhosseini-Moja, ehsan/HGF-3165-2022
OI nazemalhosseini-mojarad, ehsan/0000-0001-8914-004X; Pezeshkian,
   Zahra/0000-0002-8945-9971
FU Gastroenterology and Liver Diseases Research Center, Research Institute
   for Gastroenterology and Liver Diseases, Shahid Beheshti University of
   Medical Sciences [858, 988]; Medical Ethical Committee of the RCGLD
   [IR.SBMU.RIGLD.REC.1396.947]
FX This project was completely supported and funded by the Gastroenterology
   and Liver Diseases Research Center, Research Institute for
   Gastroenterology and Liver Diseases, Shahid Beheshti University of
   Medical Sciences, with Grant Nos. 858 and 988, and the Medical Ethical
   Committee of the RCGLD, with Ethics No. IR.SBMU.RIGLD.REC.1396.947.
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NR 48
TC 4
Z9 4
U1 1
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4425
J9 GENES-BASEL
JI Genes
PD APR
PY 2022
VL 13
IS 4
AR 689
DI 10.3390/genes13040689
PG 13
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA 0R3FR
UT WOS:000785485900001
PM 35456495
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Van Cutsem, E
   Huijberts, S
   Grothey, A
   Yaeger, R
   Cuyle, PJ
   Elez, E
   Fakih, M
   Montagut, C
   Peeters, M
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   Wasan, H
   Desai, CJ
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   Gollerkeri, A
   Christy-Bittel, J
   Maharry, K
   Sandor, V
   Schellens, JH
   Kopetz, S
   Tabernero, J
AF Van Cutsem, Eric
   Huijberts, Sanne
   Grothey, Axel
   Yaeger, Rona
   Cuyle, Pieter-Jan
   Elez, Elena
   Fakih, Marwan
   Montagut, Clara
   Peeters, Marc
   Yoshino, Takayuki
   Wasan, Harpreet
   Desai, C. Jayesh
   Ciardiello, Fortunato
   Gollerkeri, Ashwin
   Christy-Bittel, Janna
   Maharry, Kati
   Sandor, Victor
   Schellens, Jan Hm
   Kopetz, Scott
   Tabernero, Josep
TI Binimetinib, Encorafenib, and Cetuximab Triplet Therapy for Patients
   With <i>BRAF</i> V600E-Mutant Metastatic Colorectal Cancer: Safety
   Lead-In Results From the Phase III BEACON Colorectal Cancer Study
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID FOLFOXIRI PLUS BEVACIZUMAB; 1ST-LINE TREATMENT; MEK INHIBITION;
   OPEN-LABEL; BRAF(V600E) INHIBITION; IMPROVED SURVIVAL; WILD-TYPE;
   VEMURAFENIB; DABRAFENIB; TRAMETINIB
AB PURPOSE To determine the safety and preliminary efficacy of selective combination targeted therapy for BRAF V600E-mutant metastatic colorectal cancer (mCRC) in the safety lead-in phase of the open-label, randomized, three-arm, phase III BEACON Colorectal Cancer trial (ClinicalTrials.gov identifier: NCT02928224; European Union Clinical Trials Register identifier: EudraCT2015-005805-35).
   PATIENTS AND METHODS Before initiation of the randomized portion of the BEACON Colorectal Cancer trial, 30 patients with BRAF V600E-mutant mCRC who had experienced treatment failure with one or two prior regimens were to be recruited to a safety lead-in of encorafenib 300 mg daily, binimetinib 45 mg twice daily, plus standard weekly cetuximab. The primary end point was safety, including the incidence of dose-limiting toxicities. Efficacy end points included overall response rate, progression-free survival, and overall survival.
   RESULTS Among the 30 treated patients, dose-limiting toxicities occurred in five patients and included serous retinopathy (n = 2), reversible decreased left ventricular ejection fraction (n = 1), and cetuximab-related infusion reactions (n = 2). The most common grade 3 or 4 adverse events were fatigue (13%), anemia (10%), increased creatine phosphokinase (10%), increased AST (10%), and urinary tract infections (10%). In 29 patients with BRAF V600E-mutant tumors (one patient had a non-BRAF V600E-mutant tumor and was not included in the efficacy analysis), the confirmed overall response rate was 48% (95% CI, 29.4% to 67.5%), median progression-free survival was 8.0 months (95% CI, 5.6 to 9.3 months), and median overall survival was 15.3 months (95% CI, 9.6 months to not reached), with median duration of follow-up of 18.2 months (range, 16.6 to 19.8 months).
   CONCLUSION In the safety lead-in, the safety and tolerability of the encorafenib, binimetinib, and cetuximab regimen is manageable and acceptable for initiation of the randomized portion of the study. The observed efficacy is promising compared with available therapies and, if confirmed in the randomized portion of the trial, could establish this regimen as a new standard of care for previously treated BRAF V600E-mutant mCRC. (C) 2019 by American Society of Clinical Oncology
C1 [Van Cutsem, Eric; Cuyle, Pieter-Jan] Univ Hosp Gasthuisberg Leuven, Leuven, Belgium.
   [Van Cutsem, Eric; Cuyle, Pieter-Jan] Katholieke Univ Leuven, Leuven, Belgium.
   [Huijberts, Sanne] Netherlands Canc Inst, Amsterdam, Netherlands.
   [Grothey, Axel] West Canc Ctr, Germantown, TN USA.
   [Yaeger, Rona] Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10021 USA.
   [Cuyle, Pieter-Jan] Imelda Gen Hosp, Bonheiden, Belgium.
   [Cuyle, Pieter-Jan] Univ Hosp Gasthuisberg, Leuven, Belgium.
   [Elez, Elena; Tabernero, Josep] Univ Autonoma Barcelona, Vall Hebron Inst Oncol, Barcelona, Spain.
   [Fakih, Marwan] City Hope Comprehens Canc Ctr, Duarte, CA USA.
   [Montagut, Clara] Univ Pompeu Fabra, Inst Hosp Mar Invest Med, Hosp Mar, Barcelona, Spain.
   [Peeters, Marc] Antwerp Univ Hosp, Edegem, Belgium.
   [Yoshino, Takayuki] Natl Canc Ctr Hosp East, Kashiwa, Chiba, Japan.
   [Wasan, Harpreet] Imperial Coll London, Hammersmith Hosp, London, England.
   [Desai, C. Jayesh] Peter MacCallum Canc Ctr, Melbourne, Vic, Australia.
   [Ciardiello, Fortunato] Univ Campania Luigi Vanvitelli, Naples, Italy.
   [Gollerkeri, Ashwin; Christy-Bittel, Janna; Maharry, Kati; Sandor, Victor] Array BioPharma Inc, Boulder, CO USA.
   [Schellens, Jan Hm] Univ Utrecht, Utrecht, Netherlands.
   [Kopetz, Scott] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
C3 KU Leuven; University Hospital Leuven; KU Leuven; Netherlands Cancer
   Institute; Memorial Sloan Kettering Cancer Center; Imeldaziekenhuis; KU
   Leuven; University Hospital Leuven; Vall d'Hebron Institut d'Oncologia
   (VHIO); Autonomous University of Barcelona; City of Hope; Hospital del
   Mar Research Institute; Hospital del Mar; Pompeu Fabra University;
   University of Antwerp; National Cancer Center - Japan; Imperial College
   London; Peter Maccallum Cancer Center; Universita della Campania
   Vanvitelli; Pfizer; Array BioPharma; Utrecht University; University of
   Texas System; UTMD Anderson Cancer Center
RP Kopetz, S (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, 1515 Holcombe Blvd,Unit 426, Houston, TX 77030 USA.
EM kopetz@mdanderson.org
RI Élez, Elena/AAH-2945-2019; Kopetz, Scott/AAC-1387-2019; Desai,
   Jayesh/AAV-1237-2021; Tabernero, Josep/AAG-5026-2019; Van+Cutsem,
   Eric/ABE-1762-2021; Schellens, Jan/O-8444-2016
OI Tabernero, Josep/0000-0002-2495-8139; Desai, Jayesh/0000-0003-4246-9344;
   Wasan, Harpreet/0000-0002-6268-2030; Elez, Elena/0000-0002-4653-6324;
   Fakih, Marwan/0000-0002-6554-5488
FU Array BioPharma
FX We thank the patients, their families, and the sites that participated
   in this study. For editorial support, funded by Array BioPharma, we
   thank Philip Sjostedt from The Medicine Group LLC, a Division of Bespoke
   Communications.
CR [Anonymous], 2018, J CLIN ONCOL S
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NR 53
TC 160
Z9 163
U1 0
U2 21
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
EI 1527-7755
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD JUN 10
PY 2019
VL 37
IS 17
BP 1460
EP +
DI 10.1200/JCO.18.02459
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IH7UW
UT WOS:000474710800003
PM 30892987
OA hybrid, Green Published, Green Accepted, Green Submitted
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Oliveira, SM
   Carvalho, PD
   Serra-Roma, A
   Oliveira, P
   Ribeiro, A
   Carvalho, J
   Martins, F
   Machado, AL
   Oliveira, MJ
   Velho, S
AF Oliveira, Susana Mendonca
   Carvalho, Patricia Dias
   Serra-Roma, Andre
   Oliveira, Patricia
   Ribeiro, Andreia
   Carvalho, Joana
   Martins, Flavia
   Machado, Ana Luisa
   Oliveira, Maria Jose
   Velho, Sergia
TI Fibroblasts Promote Resistance to KRAS Silencing in Colorectal Cancer
   Cells
SO CANCERS
LA English
DT Article
DE KRAS; colorectal cancer; fibroblasts; cancer stemness;
   epithelial-mesenchymal transition; therapy resistance
ID EPITHELIAL-MESENCHYMAL TRANSITION; STEM-CELLS; UP-REGULATION;
   EXPRESSION; INHIBITION; MICROENVIRONMENT; SUPPRESSION; REVEALS; MARKER;
   EMT
AB Simple Summary Novel therapies targeting KRAS offer treatment options for previously untreatable patients. However, in colorectal cancer (CRC), resistance to KRAS-targeted therapy develops rapidly, making it imperative to understand its underlying mechanisms. Cancer-associated fibroblasts (CAFs) contribute to therapy resistance by generating and maintaining the cancer stem cell niche. This study investigates whether CAF-secreted factors induce resistance to KRAS inhibition by enhancing cancer stemness. Our findings demonstrate that while KRAS silencing reduced the expression of stem cell markers and stemness, CAF-secreted factors counteracted those effects by activating pro-tumorigenic pathways, such as epithelial-to-mesenchymal transition, and increasing cell proliferation. Overall, we provide novel mechanistic insights into how CAF-secreted factors oppose KRAS silencing-induced growth inhibition, which may be crucial for improving CRC therapy.Abstract Colorectal cancer (CRC) responses to KRAS-targeted inhibition have been limited due to low response rates, the mechanisms of which remain unknown. Herein, we explored the cancer-associated fibroblasts (CAFs) secretome as a mediator of resistance to KRAS silencing. CRC cell lines HCT15, HCT116, and SW480 were cultured either in recommended media or in conditioned media from a normal colon fibroblast cell line (CCD-18Co) activated with rhTGF-beta 1 to induce a CAF-like phenotype. The expression of membrane stem cell markers was analyzed by flow cytometry. Stem cell potential was evaluated by a sphere formation assay. RNAseq was performed in KRAS-silenced HCT116 colonospheres treated with either control media or conditioned media from CAFs. Our results demonstrated that KRAS-silencing up-regulated CD24 and down-regulated CD49f and CD104 in the three cell lines, leading to a reduction in sphere-forming efficiency. However, CAF-secreted factors restored stem cell marker expression and increased stemness. RNA sequencing showed that CAF-secreted factors up-regulated genes associated with pro-tumorigenic pathways in KRAS-silenced cells, including KRAS, TGF beta, NOTCH, WNT, MYC, cell cycle progression and exit from quiescence, epithelial-mesenchymal transition, and immune regulation. Overall, our results suggest that resistance to KRAS-targeted inhibition might derive not only from cell-intrinsic causes but also from external elements, such as fibroblast-secreted factors.
C1 [Oliveira, Susana Mendonca; Carvalho, Patricia Dias; Serra-Roma, Andre; Oliveira, Patricia; Ribeiro, Andreia; Carvalho, Joana; Martins, Flavia; Machado, Ana Luisa; Oliveira, Maria Jose; Velho, Sergia] Univ Porto, I3S Inst Invest & Inovacao Saude, Rua Alfredo Allen 208, P-4200135 Porto, Portugal.
   [Oliveira, Susana Mendonca; Carvalho, Patricia Dias; Serra-Roma, Andre; Oliveira, Patricia; Ribeiro, Andreia; Carvalho, Joana; Martins, Flavia; Velho, Sergia] Univ Porto, IPATIMUP Inst Patol & Imunol Mol, Rua Julio Amaral Carvalho 45, P-4200135 Porto, Portugal.
   [Oliveira, Susana Mendonca; Martins, Flavia; Machado, Ana Luisa; Oliveira, Maria Jose] Univ Porto, FMUP Fac Med, Alameda Prof Hernani Monteiro, P-4200319 Porto, Portugal.
   [Oliveira, Susana Mendonca; Machado, Ana Luisa] Inst Politecn Porto, ESS PPORTO Escola Super Saude, Rua Dr Antonio Bernardino Almeida 400, P-4200072 Porto, Portugal.
   [Carvalho, Patricia Dias; Oliveira, Maria Jose] Univ Porto, ICBAS Inst Ciencias Biomed Abel Salazar, Rua Jorge Viterbo Ferreira 228, P-4050313 Porto, Portugal.
   [Oliveira, Maria Jose] Univ Porto, INEB Inst Nacl Engn Biomed, Rua Campo Alegre 823, P-4150177 Porto, Portugal.
   [Serra-Roma, Andre] Novartis Pharm AG, Biomed Res, Fabrikstr 2,Novartis Campus, CH-4056 Basel, Switzerland.
C3 Universidade do Porto; i3S - Instituto de Investigacao e Inovacao em
   Saude, Universidade do Porto; Universidade do Porto; Universidade do
   Porto; Instituto Politecnico do Porto; Universidade do Porto;
   Universidade do Porto; Novartis
RP Velho, S (corresponding author), Univ Porto, I3S Inst Invest & Inovacao Saude, Rua Alfredo Allen 208, P-4200135 Porto, Portugal.; Velho, S (corresponding author), Univ Porto, IPATIMUP Inst Patol & Imunol Mol, Rua Julio Amaral Carvalho 45, P-4200135 Porto, Portugal.
EM smendonca@ipatimup.pt; poliveira@ipatimup.pt; jcarvalho@ipatimup.pt;
   flaviam@ipatimup.pt; almachado@i3s.up.pt; mariajo@i3s.up.pt;
   svelho@i3s.up.pt
RI Machado, Ana Vera/K-6203-2012; Oliveira, M./D-9025-2013; Carvalho,
   Joana/J-9476-2013; Velho, Sergia/B-8501-2013; Oliveira, Maria
   Jose/K-3275-2013
OI Velho, Sergia/0000-0002-7104-8234; Oliveira, Maria
   Jose/0000-0002-0724-0272
FU Portuguese Foundation for Science and Technology (FCT)
FX The authors acknowledge the support of the i3S Genomics Scientific
   Platform, in particular Ana Mafalda Rocha. The authors also acknowledge
   Andre Maia from the BioSciences Screening i3S Scientific Platform and
   Catarina Meireles and Emilia Cardoso from the Translational Cytometry
   Unit (TraCy) i3S Scientific Platform.
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NR 65
TC 0
Z9 0
U1 1
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUL
PY 2024
VL 16
IS 14
AR 2595
DI 10.3390/cancers16142595
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZP7B3
UT WOS:001276554100001
PM 39061234
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Silva, MLS
AF Silva, Maria Luisa S.
TI Lectin-modified drug delivery systems - Recent applications in the
   oncology field
SO INTERNATIONAL JOURNAL OF PHARMACEUTICS
LA English
DT Review
DE Cancer; Aberrant glycosylation; Drug delivery systems; Lectins; Targeted
   therapy; Clinical translation
ID CONJUGATED PLGA NANOPARTICLES; HUMAN COLON-CANCER; ANTIBODY-MODIFIED
   LIPOSOMES; PLANT-LECTINS; MONOCLONAL-ANTIBODY; BREAST-CANCER; IN-VITRO;
   INCREASED EXPRESSION; TUMOR HETEROGENEITY; TARGETED DELIVERY
AB Chemotherapy with cytotoxic drugs remains the core treatment for cancer but, due to the difficulty to find general and usable biochemical differences between cancer cells and normal cells, many of these drugs are associated with lack of specificity, resulting in side effects and collateral cytotoxicity that impair patients' adherence to therapy. Novel cancer treatments in which the cytotoxic effect is maximized while adverse effects are reduced can be implemented by developing targeted therapies that exploit the specific features of cancer cells, such as the typical expression of aberrant glycans. Modification of drug delivery systems with lectins is one of the strategies to implement targeted chemotherapies, as lectins are able to specifically recognize and bind to cancer-associated glycans expressed at the surface of cancer cells, guiding the drug treatment towards these cells and not affecting healthy ones. In this paper, recent advances on the development of lectin-modified drug delivery systems for targeted cancer treatments are thoroughly reviewed, with a focus on their properties and performance in diverse applications, as well as their main advantages and limitations. The synthesis and analytical characterization of the cited lectin-modified drug delivery systems is also briefly described. A comparison with free-drug treatments and with antibody-modified drug delivery systems is presented, emphasizing the advantages of lectin-modified drug delivery systems. Main constraints and potential challenges of lectin-modified drug delivery systems, including key difficulties for clinical translation of these systems, and the required developments in this area, are also signalled.
C1 [Silva, Maria Luisa S.] Univ Aberta, Ctr Estudos Globais, Rua Escola Politecn 147, P-1269001 Lisbon, Portugal.
C3 Universidade Aberta
RP Silva, MLS (corresponding author), Univ Aberta, Ctr Estudos Globais, Rua Escola Politecn 147, P-1269001 Lisbon, Portugal.
EM MariaL.Silva@uab.pt
RI Nascimento, Laiane/JHT-1897-2023
OI Soares da Silva, Maria Luisa/0000-0002-1170-3962
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NR 228
TC 0
Z9 0
U1 2
U2 2
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0378-5173
EI 1873-3476
J9 INT J PHARMACEUT
JI Int. J. Pharm.
PD NOV 15
PY 2024
VL 665
AR 124685
DI 10.1016/j.ijpharm.2024.124685
EA SEP 2024
PG 28
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA G3R3Z
UT WOS:001315846500001
PM 39260750
DA 2025-01-04
ER

PT J
AU Kourie, HR
   Zouein, J
   Zalaquett, Z
   Chebly, A
   Nasr, L
   El Karak, F
   Sadek, M
   Safar, O
   Fouani, M
   Bitar, N
   Kachmar, K
   Nasr, F
   Farhat, F
   Makarem, J
   Kattan, J
   Taieb, J
AF Kourie, Hampig Raphael
   Zouein, Joseph
   Zalaquett, Ziad
   Chebly, Alain
   Nasr, Lewis
   El Karak, Fadi
   Sadek, Maroun
   Safar, Ousama
   Fouani, Mouin
   Bitar, Nizar
   Kachmar, Kamal
   Nasr, Fady
   Farhat, Fadi
   Makarem, Jawad
   Kattan, Joseph
   Taieb, Julien
TI Liquid biopsy as a tool for KRAS/NRAS/BRAF baseline testing in
   metastatic colorectal cancer
SO CLINICS AND RESEARCH IN HEPATOLOGY AND GASTROENTEROLOGY
LA English
DT Article
AB Background: The absence of KRAS and NRAS gene mutations (RAS wild type) in metastatic colorectal cancer (mCRC), is associated with a good response to targeted therapy with anti-EGFR receptor antibodies. The current gold standard for RAS mutational status identification is genetic testing on tissue biopsy samples. Objective: This study aimed to assess the relevance of liquid biopsy as a less invasive alternative to tissue biopsy for detecting KRAS/NRAS and BRAF mutations in patients with metastatic colorectal cancer (mCRC). The study also aimed to determine the concordance between liquid biopsy and tissue biopsy. Methods: This is a phase IV, observational, uncontrolled, non-comparative, non-randomized, open label study. RAS/BRAF status will be tested at baseline using tissue and liquid biopsy using the Idylla/Biocartis PCR-based device. The primary endpoint is the comparison of the RAS status based on liquid biopsy with the RAS status based on tissue biopsy. Results: 100 patients with mCRC were included in the study. 75 % of patients showed concordant results between liquid biopsy and tissue biopsy, while 25 % had discordant results. Liquid biopsy demonstrated a sensitivity of 62 % and a specificity of 93 %. The accuracy of liquid biopsy was 75 %, with a moderate agreement between the two tests. The most frequent mutations in concordant cases were in KRAS (41 %), followed by NRAS (4 %) and BRAF (3 %). Mutations were not detected in 42 % of tissue biopsy samples and 60 % of liquid biopsy samples. The presence of hepatic metastases did not significantly affect the concordance between the biopsy methods. Conclusion: Liquid biopsy using the Idylla (TM) system showed a relatively low sensitivity but high specificity for detecting KRAS/NRAS and BRAF mutations in mCRC patients. Despite some discordant cases, liquid biopsy remains a promising alternative to tissue biopsy due to its non-invasiveness, ability to provide multiple samples, and better representation of tumor heterogeneity.
C1 [Kourie, Hampig Raphael; Zouein, Joseph; Zalaquett, Ziad; Nasr, Lewis; El Karak, Fadi; Nasr, Fady; Kattan, Joseph] St Joseph Univ, Hotel Dieu France Univ Hosp, Hematol Oncol Dept, Blvd Alfred Naccache, Beirut, Lebanon.
   [Zouein, Joseph] Duke Univ, Med Ctr, Dept Med, Durham, NC USA.
   [Chebly, Alain] St Joseph Univ, Fac Med, Jacques Loiselet Ctr Med Genet & Genom CGGM, Beirut, Lebanon.
   [Chebly, Alain] St Joseph Univ, Higher Inst Publ Hlth, Beirut, Lebanon.
   [Sadek, Maroun] Lebanese Hosp Geitaoui, Hematol Oncol Dept, Beirut, Lebanon.
   [Safar, Ousama] Dar Amal Univ Hosp, Bekaa, Lebanon.
   [Fouani, Mouin] St George Hosp, Dept Radiol, Hadath, Lebanon.
   [Bitar, Nizar] Sahel Gen Hosp, Beirut, Lebanon.
   [Kachmar, Kamal] Minist Agr, Beirut, Lebanon.
   [Farhat, Fadi] Mt Lebanon Hosp, Aley, Lebanon.
   [Makarem, Jawad] Rafik Hariri Univ, Chouf, Lebanon.
   [Taieb, Julien] Hop Europe Georges Pompidou, Paris, France.
C3 Duke University; Assistance Publique Hopitaux Paris (APHP); Universite
   Paris Cite; Hopital Universitaire Europeen Georges-Pompidou - APHP
RP Kourie, HR (corresponding author), St Joseph Univ, Hotel Dieu France Univ Hosp, Hematol Oncol Dept, Blvd Alfred Naccache, Beirut, Lebanon.
EM hampig.kourie@usj.edu.lb
OI Zouein, Joseph/0000-0003-0078-8582
CR Chatila R, 2021, CANCER CONTROL, V28, DOI 10.1177/10732748211041221
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NR 22
TC 0
Z9 0
U1 3
U2 3
PU ELSEVIER MASSON, CORP OFF
PI PARIS
PA 65 CAMILLE DESMOULINS CS50083 ISSY-LES-MOULINEAUX, 92442 PARIS, FRANCE
SN 2210-7401
EI 2210-741X
J9 CLIN RES HEPATOL GAS
JI Clin. Res. Hepatol. Gastroenterol.
PD OCT
PY 2024
VL 48
IS 8
AR 102417
DI 10.1016/j.clinre.2024.102417
EA SEP 2024
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA H7G7U
UT WOS:001325094800001
PM 39009221
DA 2025-01-04
ER

PT J
AU Nowakowska, M
   Plonska-Gosciniak, E
   Szyszka, A
   Chrzanowski, L
   Krakowska, M
   Potemski, P
   Mizia-Stec, K
   Gasior, Z
   Bodys, A
   Sinski, M
   Goscinska-Szmagala, A
   Gosciniak, P
   Rózewicz, M
   Zaborska, B
   Braksator, W
   Kosior, D
   Kasprzak, JD
AF Nowakowska, Marta
   Plonska-Gosciniak, Edyta
   Szyszka, Andrzej
   Chrzanowski, Lukasz
   Krakowska, Magdalena
   Potemski, Piotr
   Mizia-Stec, Katarzyna
   Gasior, Zbigniew
   Bodys, Artur
   Sinski, Maciej
   Goscinska-Szmagala, Adrianna
   Gosciniak, Piotr
   Rozewicz, Monika
   Zaborska, Beata
   Braksator, Wojciech
   Kosior, Dariusz
   Kasprzak, Jaroslaw D.
TI Cardiovascular risk factors among cancer patients qualified for systemic
   treatment. Analysis of a cardiovascular disease-free cohort from the
   Polish multicentre study ONCOECHO
SO ARCHIVES OF MEDICAL SCIENCE
LA English
DT Article
DE cardiotoxicity; neoplasms; patient care team
ID VENTRICULAR SYSTOLIC DYSFUNCTION; METABOLIC SYNDROME; BREAST-CANCER;
   CHEMOTHERAPY; PREVALENCE; ECHOCARDIOGRAPHY; ASSOCIATION; WOMEN; ESC
AB Introduction: Cancer therapies are currently more efficient at increasing the survival of patients (pts) with cancer. Unfortunately, the cardiovascular (CV) complications of cancer therapies may adversely affect improving results of treatment. The aim of the study was to evaluate the prevalence of classical CV risk factors among pts with de novo diagnosis of cancer and thus identify the cohort of pts with potentially increased future risk of CV complications.
   Material and methods: The analysis is based on the database of the multi centre ONCOECHO study. Pts before systemic treatment (chemotherapy or targeted therapy) were included. The diagnostic datasets of resting electrocardiogram, blood samples, and transthoracic echocardiogram were analysed in 343 consecutive pts who were free from any cardiovascular disease that could adversely affect the introduced treatment.
   Results: Our cohort included 4.4% of pts with kidney cancer, 7.3% with colorectal cancer, 26.5% with haematological malignancies (HM), and 61.8% with breast cancer. The risk estimated by SCORE was 4.56 5.07%. Breast cancer pts had lower cardiovascular risk than those with HM (p = 0.001) and kidney cancer (p = 0.002). Additionally, the HM group had much higher levels of natriuretic peptides (p < 0.001) and creatinine (p = 0.008) than pts with breast cancer. The comparison with the NATPOL population data showed that our pts were more often smokers, hypertensives, and diabetics, but less frequently presented with hypercholesterolaemia.
   Conclusions: Patients with new diagnosis of cancer, who are candidates for potentially cardiotoxic medical treatment, have increased prevalence of significant cardiovascular risk factors and therefore should be followed by a multidisciplinary team during the therapeutic process.
C1 [Nowakowska, Marta; Chrzanowski, Lukasz; Kasprzak, Jaroslaw D.] Med Univ Lodz, Dept Cardiol, 1-3 Knaziewicza St, PL-91347 Lodz, Poland.
   [Plonska-Gosciniak, Edyta] Pomeranian Med Univ, Dept Cardiol, Szczecin, Poland.
   [Szyszka, Andrzej] Poznan Univ Med Sci, Dept Cardiol, Poznan, Poland.
   [Krakowska, Magdalena; Potemski, Piotr] Med Univ Lodz, Copernicus Mem Hosp, Oncol Dept, Chemotherapy Clin, Lodz, Poland.
   [Mizia-Stec, Katarzyna; Gasior, Zbigniew] Silesian Med Univ, Dept Cardiol, Katowice, Poland.
   [Bodys, Artur] Stefan Cardinal Wyszynski Reg Hosp, Dept Cardiol, Lublin, Poland.
   [Sinski, Maciej] Med Univ Warsaw, Dept Internal Med Hypertens & Angiol, Warsaw, Poland.
   [Goscinska-Szmagala, Adrianna] Amer Heart Poland, Tychy, Poland.
   [Gosciniak, Piotr] Pomeranian Med Univ, Independent Publ Clin Hosp 1, Independent Lab Noninvas Heart Diagnost Children, Szczecin, Poland.
   [Rozewicz, Monika] Cardinal Stefan Wyszynski Inst Cardiol, Dept Congenital Cardiac Defects, Warsaw, Poland.
   [Zaborska, Beata] Ctr Postgrad Med Educ, Dept Cardiol, Warsaw, Poland.
   [Braksator, Wojciech] Med Univ Warsaw, Dept Sports Cardiol & Noninvas Cardiac Diag, Warsaw, Poland.
   [Kosior, Dariusz] Cent Clin Hosp Minist Interior & Adm, Dept Cardiol & Hypertens, Warsaw, Poland.
C3 Medical University Lodz; Pomeranian Medical University; Poznan
   University of Medical Sciences; Medical University Lodz; Medical
   University Silesia; Medical University of Warsaw; Pomeranian Medical
   University; Centre of Postgraduate Medical Education - Poland; Medical
   University of Warsaw
RP Nowakowska, M (corresponding author), Med Univ Lodz, Dept Cardiol, 1-3 Knaziewicza St, PL-91347 Lodz, Poland.
EM now-mart@o2.pl
RI Szyszka, Andrzej/HPD-1547-2023; Kasprzak, Jaroslaw/S-4496-2016;
   Potemski, Piotr/LNR-5927-2024; Gościniak, Piotr/JVM-8428-2024;
   Mizia-Stec, Katarzyna/HLV-8003-2023; Braksator, Wojciech/N-2197-2018
OI Potemski, Piotr/0000-0001-7573-7347; Mizia-Stec,
   Katarzyna/0000-0001-6907-2799; Braksator, Wojciech/0000-0003-2201-4887;
   Zaborska, Beata/0000-0001-5513-8371; Kosior,
   Dariusz/0000-0002-7821-4442; Kasprzak, Jaroslaw D/0000-0002-5850-8187;
   Sinski, Maciej/0000-0001-8548-9762
FU Polish Cardiac Society
FX This research was supported by Polish Cardiac Society.
CR Bardia A, 2012, BREAST CANCER RES TR, V131, P907, DOI 10.1007/s10549-011-1843-1
   Dabrowski M, 2017, ARCH MED SCI, V13, P1025, DOI 10.5114/aoms.2016.58666
   Didkowska J, 2013, MORBIDITY MORTALITY
   Hanrahan EO, 2007, J CLIN ONCOL, V25, P4952, DOI 10.1200/JCO.2006.08.0499
   Healy LA, 2012, COLORECTAL DIS, V14, P157, DOI 10.1111/j.1463-1318.2011.02562.x
   Johnson CB, 2016, CAN J CARDIOL, V32, P900, DOI 10.1016/j.cjca.2016.04.008
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NR 22
TC 5
Z9 5
U1 0
U2 3
PU TERMEDIA PUBLISHING HOUSE LTD
PI POZNAN
PA KLEEBERGA ST 2, POZNAN, 61-615, POLAND
SN 1734-1922
EI 1896-9151
J9 ARCH MED SCI
JI Arch. Med. Sci.
PD OCT
PY 2020
VL 16
IS 6
BP 1295
EP 1303
DI 10.5114/aoms.2020.100401
PG 9
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA OM3IB
UT WOS:000585918400004
PM 33224328
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yang, F
   Fu, ZY
   Yang, MZ
   Sun, CX
   Li, YF
   Chu, JH
   Zhang, YH
   Li, W
   Huang, X
   Li, J
   Wu, H
   Ding, XR
   Yin, YM
AF Yang, Fan
   Fu, Ziyi
   Yang, Mengzhu
   Sun, Chunxiao
   Li, Yongfei
   Chu, Jiahui
   Zhang, Yanhong
   Li, Wei
   Huang, Xiang
   Li, Jun
   Wu, Hao
   Ding, Xiaorong
   Yin, Yongmei
TI Expression pattern of microRNAs related with response to trastuzumab in
   breast cancer
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Article
DE breast cancer; miRNA; trastuzumab resistance
ID EPITHELIAL-MESENCHYMAL TRANSITION; COLORECTAL-CANCER; HER2-TARGETED
   THERAPY; NEOADJUVANT TREATMENT; UP-REGULATION; CELLS; RESISTANCE;
   CHEMOTHERAPY; PATHWAY; SUPPRESSES
AB BackgroundAlthough an immense effort has been made to develop a novel biomarker for response to trastuzumab, no reliable biomarkers are available to guide management, expect for HER2. The aim of this study was to examine the relationship between microRNA (miRNA) expression and resistance to trastuzumab.
   MethodsDifferentially expressed miRNAs between trastuzumab-resistant and trastuzumab-sensitive cell lines were analyzed using microarrays. We performed Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses to determine the functions of differentially expressed miRNA and their targeted genes. Furthermore, the protein-protein interactions (PPI) network was analyzed. Serum samples were collected from patients with HER2-positive breast cancer who were treated with trastuzumab. We validated the miRNAs expression levels by quantitative reverse-transcription polymerase chain reaction (qRT-PCR) in these serums. Receiver operating characteristic (ROC) curve analysis was performed to evaluate the predictive performance of the miRNA.
   ResultsUsing miRNA microarrays, 151 miRNAs that significant differentially expressed between the trastuzumab-resistant and sensitive cells were identified, including 46 upregulated and 105 downregulated miRNAs. Results of real-time PCR confirmed seven miRNAs in cell lines. PI3K-Akt signaling pathway was involved in regulating biological function according to KEGG analysis. Compared with the serums of trastuzumab-sensitive patients, three miRNAs, namely miR-200b, miR-135b, and miR-29a, were identified to be upregulated, and miR-224 was downregulated in the trastuzumab-resistant serums. ROC analysis showed that four miRNAs were correlated with trastuzumab resistance. Furthermore, three subnetwork modules of PPI network were obtained.
   ConclusionThe results indicated that miRNAs were reliable predictive biomarkers for response to trastuzumab.
C1 [Yang, Fan; Fu, Ziyi; Yang, Mengzhu; Sun, Chunxiao; Li, Yongfei; Chu, Jiahui; Zhang, Yanhong; Li, Wei; Huang, Xiang; Li, Jun; Wu, Hao; Ding, Xiaorong; Yin, Yongmei] Nanjing Med Univ, Affiliated Hosp 1, Dept Oncol, Nanjing, Jiangsu, Peoples R China.
   [Yang, Fan; Yang, Mengzhu; Sun, Chunxiao; Li, Yongfei; Chu, Jiahui; Zhang, Yanhong; Ding, Xiaorong] Nanjing Med Univ, Clin Coll 1, Nanjing, Jiangsu, Peoples R China.
   [Fu, Ziyi] Nanjing Med Univ, Nanjing Matern & Child Hlth Care Hosp, Affiliated Obstet & Gynecol Hosp, Nanjing Maternal & Child Hlth Inst, Nanjing, Jiangsu, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University; Nanjing Medical
   University
RP Yin, YM (corresponding author), Nanjing Med Univ, Affiliated Hosp 1, 300 Guangzhou Rd, Nanjing 210029, Jiangsu, Peoples R China.
EM ymyin@njmu.edu.cn
RI Fu, Ziyi/ABB-8091-2022; LI, WEI/JUE-9796-2023; yin,
   yongmei/KVZ-0566-2024
FU collaborative innovation center for tumor individualization focuses on
   open topics [JX21817902/008]; 333 Project of Jiangsu Province
   [BRA2015470, BRA2017534]; High-level innovation team of Nanjing Medical
   University [JX102GSP201727]; Project of China key research and
   development program precision medicine research [2016YFC0905901]; Key
   medical talents [ZDRCA2016023]; National Key Research and Development
   Program of China [ZDZX2017ZL-01]; Wu Jieping Foundation [320.6750.17006]
FX The collaborative innovation center for tumor individualization focuses
   on open topics, Grant/Award Number: JX21817902/008; 333 Project of
   Jiangsu Province, Grant/Award Numbers: BRA2015470, BRA2017534;
   High-level innovation team of Nanjing Medical University, Grant/Award
   Number: JX102GSP201727; Project of China key research and development
   program precision medicine research, Grant/Award Number: 2016YFC0905901;
   Key medical talents, Grant/Award Number: ZDRCA2016023; National Key
   Research and Development Program of China, Grant/Award Number:
   ZDZX2017ZL-01; Wu Jieping Foundation, Grant/Award Number: 320.6750.17006
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NR 59
TC 9
Z9 9
U1 0
U2 17
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9541
EI 1097-4652
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD SEP
PY 2019
VL 234
IS 9
BP 16102
EP 16113
DI 10.1002/jcp.28268
PG 12
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA IB3NM
UT WOS:000470174200149
PM 30770556
DA 2025-01-04
ER

PT J
AU Wang, YS
   Zhang, J
   Li, L
   Xu, X
   Zhang, Y
   Teng, ZW
   Wu, FH
AF Wang, Yansheng
   Zhang, Jun
   Li, Li
   Xu, Xin
   Zhang, Yong
   Teng, Zhaowei
   Wu, Feihu
TI Identification of Molecular Targets for Predicting Colon Adenocarcinoma
SO MEDICAL SCIENCE MONITOR
LA English
DT Article
DE Adenocarcinoma; Gene Expression Profiling; Gene Regulatory Networks
ID PROGESTERONE-RECEPTOR STATUS; COLORECTAL-CANCER; MICRORNA; EXPRESSION;
   CALCIUM; GENES; RESISTANCE; CYTOSCAPE; PROGNOSIS; APOPTOSIS
AB Background: Colon adenocarcinoma mostly happens at the junction of the rectum and is a common gastrointestinal malignancy. Accumulated evidence has indicated that colon adenocarcinoma develops by genetic alterations and is a complicated disease. The aim of this study was to screen differentially expressed miRNAs (DEMs) and genes with diagnostic and prognostic potentials in colon adenocarcinoma.
   Material/Methods: In this study we screened DEMs and their target genes (DEGs) between 100 colon adenocarcinoma and normal samples in The Cancer Genome Atlas (TCGA) database by using the DEseq toolkit in Bioconductor. Then Go enrichment and KEGG pathway analysis were performed on the selected differential genes by use of the DAVID online tool. A regulation network of miRNA-gene was constructed and analyzed by Cytoscape. Finally, we performed ROC analysis of 8 miRNAs and ROC curves were drawn.
   Results: A total of 159 DEMs and 1921 DEGs were screened, and 1881 pairs of miRNA-target genes with significant negative correlations were also obtained. A regulatory network of miRNA-gene, including 60 cancer-related genes and 47 miRNAs, was successfully constructed. In addition, 5 clusters with several miRNAs regulating a set of target genes simultaneously were identified through cluster analysis. There were 8 miRNAs involved in these 5 clusters, and these miRNAs could serve as molecular biomarkers to distinguish colon adenocarcinoma and normal samples indicated by ROC analysis.
   Conclusions: The identified 8 miRNAs were closely associated with colon adenocarcinoma, which may have great clinical value as diagnostic and prognostic biomarkers and provide new ideas for targeted therapy.
C1 [Wang, Yansheng; Zhang, Jun; Li, Li; Xu, Xin; Zhang, Yong] Kunming Med Univ, Affiliated Hosp 6, Peoples Hosp Yuxi City, Dept Gen Surg, Yuxi, Yunan, Peoples R China.
   [Teng, Zhaowei] Kunming Med Coll, Affiliated Hosp 6, Peoples Hosp Yuxi City, Dept Orthoped Surg, Yuxi, Yunan, Peoples R China.
   [Wu, Feihu] Kunming Med Coll, Affiliated Hosp 6, Peoples Hosp Yuxi City, Yuxi, Yunan, Peoples R China.
C3 Kunming Medical University; Kunming Medical University; Kunming Medical
   University
RP Teng, ZW (corresponding author), Kunming Med Coll, Affiliated Hosp 6, Peoples Hosp Yuxi City, Dept Orthoped Surg, Yuxi, Yunan, Peoples R China.; Wu, FH (corresponding author), Kunming Med Coll, Affiliated Hosp 6, Peoples Hosp Yuxi City, Yuxi, Yunan, Peoples R China.
EM feihuwufh@163.com
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NR 34
TC 16
Z9 16
U1 0
U2 12
PU INT SCIENTIFIC INFORMATION, INC
PI MELVILLE
PA 150 BROADHOLLOW RD, STE 114, MELVILLE, NY 11747 USA
EI 1643-3750
J9 MED SCI MONITOR
JI Med. Sci. Monitor
PD FEB 12
PY 2016
VL 22
BP 460
EP 468
DI 10.12659/MSM.895881
PG 9
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA DD4SL
UT WOS:000369912800001
PM 26868022
OA Green Published
DA 2025-01-04
ER

PT J
AU Khalili-Hezarjaribi, H
   Bahrami, AR
   Saljooghi, AS
   Matin, MM
AF Khalili-Hezarjaribi, Hojjat
   Bahrami, Ahmad Reza
   Saljooghi, Amir Sh.
   Matin, Maryam M.
TI Modified mesoporous silica nanocarriers containing superparamagnetic
   iron oxide nanoparticle, 5-fluorouracil or oxaliplatin, and metformin as
   a radiosensitizer, significantly impact colorectal cancer radiation
   therapy
SO INTERNATIONAL JOURNAL OF PHARMACEUTICS
LA English
DT Article
DE Colorectal cancer; Superparamagnetic iron oxide nanoparticle; Mesoporous
   silica nanoparticle; Metformin; Folic acid; Targeted therapy;
   Radiosensitizer
ID GOLD NANOPARTICLES; MAGNETIC NANOPARTICLES; FOLIC-ACID; DRUG; DELIVERY;
   DOXORUBICIN; EUDRAGIT; SURFACE; SPIONS; AGENT
AB This study investigates the anticancer effects of SPION-based silica nanoparticles carrying 5-fluorouracil (5-FU) or oxaliplatin (OX), and metformin (MET) on colorectal cancer cells. Nanocarriers were equipped with pHresponsive gold gatekeepers for controlled release, PEGylation for longer circulation, and folic acid (FA) for targeted delivery. The effects were evaluated by investigating cell viability, cellular uptake, flow cytometry, and clonogenic assay in vitro. The efficacy of the system was also tested in vivo on C57BL/6 mice bearing HT-29 tumors, and potential side effects were evaluated. Nanocarriers were synthesized with hydrodynamic diameters of 79.8 nm for 5-FU and 85.2 nm for OX; zeta potentials of -21 and -22 mV, respectively, and remained stable after 72 h. Encapsulation efficiencies were 85 % for 5-FU, 80 % for OX, and 83 % for MET, with loading capacities of 44 %, 38 %, and 41 %, respectively. Drug release in acidic buffer was 38.7 % for 5-FU, 32.8 % for OX, and 43.5 % for MET. MTT assay showed increased toxicity due to FA conjugation, while PEGylation reduced the hemolysis activity. Targeted nanocarriers demonstrated superior cellular uptake and tumor localization compared to non-targeted variants. The combination of 5-FU-MET and OX-MET nanocarriers with radiation therapy (RT) demonstrated the greatest effect on their antitumor activity, accompanied by minimal side effects indicating effective tumor targeting in vivo. MRI and CT imaging further supported these findings. This study underscores the synergistic impact of MET alongside RT on the inhibition of cancer cells and tumor growth for both targeted 5-FU and OX nanocarriers reflecting the significant radiosensitizing properties of MET.
C1 [Khalili-Hezarjaribi, Hojjat; Bahrami, Ahmad Reza; Matin, Maryam M.] Ferdowsi Univ Mashhad, Fac Sci, Dept Biol, Mashhad, Iran.
   [Bahrami, Ahmad Reza] Ferdowsi Univ Mashhad, Inst Biotechnol, Ind Biotechnol Res Grp, Mashhad, Iran.
   [Saljooghi, Amir Sh.] Ferdowsi Univ Mashhad, Fac Sci, Dept Chem, Mashhad, Iran.
   [Saljooghi, Amir Sh.; Matin, Maryam M.] Ferdowsi Univ Mashhad, Inst Biotechnol, Novel Diagnost & Therapeut Res Grp, Mashhad, Iran.
C3 Ferdowsi University Mashhad; Ferdowsi University Mashhad; Ferdowsi
   University Mashhad; Ferdowsi University Mashhad
RP Matin, MM (corresponding author), Ferdowsi Univ Mashhad, Fac Sci, Dept Biol, Mashhad, Iran.; Matin, MM (corresponding author), Ferdowsi Univ Mashhad, Inst Biotechnol, Novel Diagnost & Therapeut Res Grp, Mashhad, Iran.
EM matin@um.ac.ir
RI Saljooghi, Amir/AAB-6042-2021; M. Matin, Maryam/W-1884-2017
OI M. Matin, Maryam/0000-0002-7949-7712
FU Ferdowsi University of Mashhad [3/55374]
FX The authors express their gratitude to Ferdowsi University of Mashhad
   for providing financial support (grant number 3/55374) for this project.
   In addition, the authors extend their special thanks to Reza
   Radiotherapy and Oncology Center for their invaluable support. The
   authors also wish to extend their sincere appreciation to Elaheh
   Valizadeh-Kakhki, Dr. Sonia Iranpour, Amir Abrishami, and Mohammad Hasan
   Mollaei for their significant contribution and unwavering support
   throughout this study.
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NR 82
TC 0
Z9 0
U1 6
U2 6
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0378-5173
EI 1873-3476
J9 INT J PHARMACEUT
JI Int. J. Pharm.
PD DEC 5
PY 2024
VL 666
AR 124838
DI 10.1016/j.ijpharm.2024.124838
EA OCT 2024
PG 19
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA K5K0M
UT WOS:001344247100001
PM 39419365
DA 2025-01-04
ER

PT J
AU Fukuoka, K
   Nara, S
   Honma, Y
   Kishi, Y
   Esaki, M
   Shimada, K
AF Fukuoka, Kengo
   Nara, Satoshi
   Honma, Yoshitaka
   Kishi, Yoji
   Esaki, Minoru
   Shimada, Kazuaki
TI Hepatectomy for Colorectal Cancer Liver Metastases in the Era of Modern
   Preoperative Chemotherapy: Evaluation of Postoperative Complications
SO WORLD JOURNAL OF SURGERY
LA English
DT Article
ID OXALIPLATIN-BASED CHEMOTHERAPY; HEPATIC RESECTION; MAJOR HEPATECTOMY;
   PERIOPERATIVE CHEMOTHERAPY; PATHOLOGICAL RESPONSE; INCREASE MORBIDITY;
   BEVACIZUMAB; SURGERY; MORTALITY; STEATOHEPATITIS
AB Recently, an increasing number of patients with liver metastases from colorectal cancer have received chemotherapy before hepatectomy. However, the effect of chemotherapy on postoperative short-term outcome is not well defined.
   We retrospectively investigated the postoperative complications of 439 patients who underwent hepatectomy for colorectal liver metastases in our division from 2005 to 2014. Patients were classified into two groups according to the presence (Cx; 84 patients) or absence (NCx; 355 patients) of preoperative chemotherapy. Univariate and multivariate analyses were conducted to determine the predictive factors for postoperative complications.
   There was neither mortality nor liver failure after surgery. There was no significant difference in the frequency of postoperative complications between Groups Cx and NCx [29 vs 26 % for all complications; both 6 % for bile leakage that required therapeutic intervention; and 2 vs 3 % for Clavien-Dindo (CD) Grade IIIa, respectively]. In Group Cx, morbidity rates were similar among patients with different chemotherapy regimens. Chemotherapy-related factors (administration of bevacizumab, oxaliplatin or irinotecan, duration of chemotherapy > 150 days, and timing of hepatectomy) were not significantly associated with clinically relevant bile leakage and CD IIIa in multivariate analysis.
   Even after combination chemotherapy including targeted therapy, hepatectomy for colorectal liver metastases can be performed safely without increasing morbidity or mortality, if the patients fulfill the conventional criteria for surgery.
C1 [Fukuoka, Kengo; Nara, Satoshi; Kishi, Yoji; Esaki, Minoru; Shimada, Kazuaki] Natl Canc Ctr, Hepatobiliary & Pancreat Surg Div, Chuo Ku, 5-1-1 Tsukiji, Tokyo 1040045, Japan.
   [Honma, Yoshitaka] Natl Canc Ctr, Gastrointestinal Med Oncol Div, Tokyo, Japan.
C3 National Cancer Center - Japan; National Cancer Center - Japan
RP Nara, S (corresponding author), Natl Canc Ctr, Hepatobiliary & Pancreat Surg Div, Chuo Ku, 5-1-1 Tsukiji, Tokyo 1040045, Japan.
EM sanara@ncc.go.jp
RI Nara, Satoshi/G-1238-2011
OI Nara, Satoshi/0000-0002-3516-8765
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NR 38
TC 14
Z9 16
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0364-2313
EI 1432-2323
J9 WORLD J SURG
JI World J.Surg.
PD APR
PY 2017
VL 41
IS 4
BP 1073
EP 1081
DI 10.1007/s00268-016-3724-6
PG 9
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA EP7VN
UT WOS:000397585400026
PM 27679508
DA 2025-01-04
ER

PT J
AU Ducreux, M
   Chamseddine, A
   Laurent-Puig, P
   Smolenschi, C
   Hollebecque, A
   Dartigues, P
   Samallin, E
   Boige, V
   Malka, D
   Gelli, M
AF Ducreux, Michel
   Chamseddine, Ali
   Laurent-Puig, Pierre
   Smolenschi, Cristina
   Hollebecque, Antoine
   Dartigues, Peggy
   Samallin, Emmanuelle
   Boige, Valerie
   Malka, David
   Gelli, Maximiliano
TI Molecular targeted therapy of BRAF-mutant colorectal cancer
SO THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
LA English
DT Review
DE BRAF inhibitors; BRAF mutation; chemotherapy; colorectal cancer
ID FOLFOXIRI PLUS BEVACIZUMAB; MICROSATELLITE INSTABILITY; 1ST-LINE
   TREATMENT; COLON-CANCER; RAS MUTATIONS; OPEN-LABEL; METASTATIC MELANOMA;
   POOLED ANALYSIS; ONCOGENIC BRAF; PHASE IB
AB Over the past two decades, the molecular characterization of metastatic colorectal cancer (mCRC) has been revolutionized by the routine implementation of RAS and BRAF tests. As a result, it is now known that patients with mCRC harboring BRAF mutations experience a poor prognosis. Although it accounts for only 10% of mCRC, this group is heterogeneous; only the BRAF-V600E mutation, also observed in melanoma, is associated with a very poor prognosis. In terms of treatment, these patients do not benefit from therapeutics targeting the epidermal growth factor receptor (EGFR). In first-line chemotherapy, there are two main options; the first one is to use a triple chemotherapy combination of 5-fluorouracil, irinotecan, and oxaliplatin, with the addition of bevacizumab, because post hoc analysis of randomized trials have reported interesting results. The other option is to use double chemotherapy plus bevacizumab, since anti-EGFR seems to have modest activity in these patients. Only a small percentage of patients who experience failure of this first-line treatment receive second-line treatment. Monotherapy with BRAF inhibitors has failed in this setting, and different combinations have also been tested. Using the rationale that BRAF inhibitor monotherapy fails due to feedback activation of the EGFR pathway, BRAF inhibitors have been combined with anti-EGFR agents plus or minus MEK inhibitors; however, the results did not live up to the hopes raised by the concept. To date, the best results in second-line treatment have been obtained with a combination of vemurafenib, cetuximab, and irinotecan. Despite these advances, further improvements are needed.
C1 [Ducreux, Michel] Univ Paris Saclay, Gustave Roussy Canc Campus Grand Paris, Dept Oncol Med, 114 Rue Edouard Vaillant, F-94805 Villejuif, France.
   [Chamseddine, Ali; Smolenschi, Cristina; Hollebecque, Antoine; Boige, Valerie; Malka, David] Gustave Roussy Canc Campus Grand Paris, Dept Oncol Med, Villejuif, France.
   [Laurent-Puig, Pierre] Hop Europeen Georges Pompidou, AP HP, Dept Biol, Paris, France.
   [Laurent-Puig, Pierre] Univ Paris 05, Paris, France.
   [Laurent-Puig, Pierre] INSERM, UMRS 1147, Paris, France.
   [Hollebecque, Antoine] Gustave Roussy Canc Campus Grand Paris, DITEP, Villejuif, France.
   [Dartigues, Peggy] Gustave Roussy Canc Campus Grand Paris, Dept Biopathol, Villejuif, France.
   [Samallin, Emmanuelle] Inst Reg Canc Montpellier ICM, Dept Oncol Digest, Montpellier, France.
   [Gelli, Maximiliano] Gustave Roussy Canc Campus Grand Paris, Dept Chirurg Viscerale, Villejuif, France.
C3 Universite Paris Saclay; UNICANCER; Gustave Roussy; UNICANCER; Gustave
   Roussy; Assistance Publique Hopitaux Paris (APHP); Universite Paris
   Cite; Hopital Universitaire Europeen Georges-Pompidou - APHP; Universite
   Paris Cite; Universite Paris Cite; Institut National de la Sante et de
   la Recherche Medicale (Inserm); UNICANCER; Gustave Roussy; UNICANCER;
   Gustave Roussy; Universite de Montpellier; UNICANCER; Gustave Roussy
RP Ducreux, M (corresponding author), Univ Paris Saclay, Gustave Roussy Canc Campus Grand Paris, Dept Oncol Med, 114 Rue Edouard Vaillant, F-94805 Villejuif, France.
EM michel.ducreux@gustaveroussy.fr
RI CHAMSEDDINE, Ali/JAX-3890-2023; Gelli, Maximiliano/K-8340-2019; Malka,
   David/HJA-5870-2022; CHAMSEDDINE, Ali N./P-5601-2018; Hollebecque,
   Antoine/M-2695-2013; Laurent-Puig, Pierre/B-2226-2013
OI CHAMSEDDINE, Ali N./0000-0001-5701-4268; Hollebecque,
   Antoine/0000-0003-2869-7551; Gelli, Maximiliano/0000-0001-9807-4021;
   Laurent-Puig, Pierre/0000-0001-8475-5459
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NR 96
TC 73
Z9 79
U1 0
U2 4
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1758-8340
EI 1758-8359
J9 THER ADV MED ONCOL
JI Ther. Adv. Med. Oncol.
PD JUN
PY 2019
VL 11
AR 1758835919856494
DI 10.1177/1758835919856494
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IN4SK
UT WOS:000478666000001
PM 31244912
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Ma, J
   Zhu, J
   Yu, SH
   Zhou, CP
   Duan, SQ
   Zhang, YM
AF Ma, Jun
   Zhu, Juan
   Yu, Shuihong
   Zhou, Chaoping
   Duan, Shuqiang
   Zhang, Yaming
TI An ileal gastrointestinal stromal tumor misdiagnosed as pelvic
   metastases from rectal cancer: a case report
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE rectal cancer; GIST; synchronous tumors; surgery; metastases
ID ADENOCARCINOMA; CARCINOMA
AB With the advancement of imaging and pathological diagnostic methods, it is not uncommon to see synchronous gastrointestinal stromal tumors (GIST) and other primary cancers, the most common of which are synchronous gastric cancer and gastric GIST. However, synchronous advanced rectal cancer and high-risk GIST in the terminal ileum are extremely rare, and they are easily misdiagnosed as rectal cancer with pelvic metastases due to their special location near iliac vessels. Herein, we report a 55-year-old Chinese woman with rectal cancer. Preoperative imaging revealed a middle and lower rectal lesion with a right pelvic mass (considered possible metastasis from rectal cancer). Through multidisciplinary discussions, we suspected the possibility of rectal cancer synchronous with a GIST in the terminal ileum. Intraoperative exploration by laparoscopy revealed a terminal ileal mass with pelvic adhesion, a rectal mass with plasma membrane depression, and no abdominal or liver metastases. Laparoscopic radical proctectomy (DIXON) plus partial small bowel resection plus prophylactic loop ileostomy was performed, and the pathological report confirmed the coexistence of advanced rectal cancer and a high-risk ileal GIST. The patient was treated with the chemotherapy (CAPEOX regimen) plus targeted therapy(imatinib) after surgery, and no abnormalities were observed on the follow-up examination. Synchronous rectal cancer and ileal GIST are rare and easily misdiagnosed as a rectal cancer with pelvic metastases, and careful preoperative imaging analysis and prompt laparoscopic exploration are required to determine the diagnosis and prolong patient survival.
C1 [Ma, Jun; Zhou, Chaoping; Zhang, Yaming] Anqing Municipal Hosp, Dept Gen Surg, Anqing, Peoples R China.
   [Zhu, Juan] Anqing Municipal Hosp, Dept Imaging, Anqing, Peoples R China.
   [Yu, Shuihong] Anqing Med & Pharmaceut Coll, Res & Expt Ctr, Anqing, Peoples R China.
   [Duan, Shuqiang] Anqing Municipal Hosp, Dept Pathol, Anqing, Peoples R China.
RP Zhang, YM (corresponding author), Anqing Municipal Hosp, Dept Gen Surg, Anqing, Peoples R China.
EM zhangyaming2014@163.com
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NR 19
TC 1
Z9 1
U1 1
U2 6
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD APR 25
PY 2023
VL 13
AR 1164391
DI 10.3389/fonc.2023.1164391
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA F6ZC6
UT WOS:000983796700001
PM 37182150
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Saorin, A
   Di Gregorio, E
   Buonadonna, A
   Miolo, G
   Corona, G
AF Saorin, Asia
   Di Gregorio, Emanuela
   Buonadonna, Angela
   Miolo, Gianmaria
   Corona, Giuseppe
TI The Riddle of Cetuximab-Related Skin Toxicity: <SUP>1</SUP>H-NMR Sebum
   Analysis Revealed Dynamic Lipid Alterations Associated with Skin
   Toxicity Development in Metastatic Colorectal Cancer Patients
SO CANCERS
LA English
DT Article
DE cetuximab; cancer; sebum; H-1-NMR; skin; toxicity; lipidomics
ID RASH; SQUALENE; ANTIBODY
AB The epidermal growth factor receptor inhibitor (EGFRIs) treatments are commonly associated with the development of adverse skin effects. This study aims to investigate the lipid composition change in sebum during cetuximab-based treatment in an attempt to identify specific metabolic signatures useful in predicting the occurrence of severe skin toxicity. Sebum from 30 metastatic colorectal cancer (mCRC) patients was collected at three time points during the targeted therapy by the application of Sebutape (R) on the forehead, and the major lipid classes were analyzed and quantified by H-1-NMR. Univariate analysis was performed to reveal significant alterations among patients in sebum production as well as lipid composition and over the course of cetuximab therapy. A transient but significant decrease in sebum production associated with a reduction in the relative content of triglycerides (TG) and squalene (SQ) was found to be induced by cetuximab administration. The reduction of these two lipid classes was also found to be associated with the severity of skin rash experienced by patients. The results of this study indicate that cetuximab-based treatment can reduce sebum gland activity, leading to an overall decrease in sebum production and the induction of specific modifications to its composition. The extent of the loss of skin barrier function may be important for determining the severity of skin toxicity development.
C1 [Saorin, Asia; Di Gregorio, Emanuela; Corona, Giuseppe] IRCCS, Ctr Riferimento Oncol Aviano CRO, Immunopathol & Canc Biomarkers Unit, I-33081 Aviano, Italy.
   [Saorin, Asia] Ca Foscari Univ Venice, Dept Mol Sci & Nanosyst, I-30170 Venice, Italy.
   [Buonadonna, Angela; Miolo, Gianmaria] IRCCS, Ctr Riferimento Oncol Aviano CRO, Med Oncol & Canc Prevent Unit, I-33081 Aviano, Italy.
C3 IRCCS Aviano (CRO); Universita Ca Foscari Venezia; IRCCS Aviano (CRO)
RP Corona, G (corresponding author), IRCCS, Ctr Riferimento Oncol Aviano CRO, Immunopathol & Canc Biomarkers Unit, I-33081 Aviano, Italy.
EM giuseppe.corona@cro.it
RI Di Gregorio, Emanuela/ABF-5351-2020; Buonadonna, Angela/ABE-2374-2020;
   Corona, Giuseppe/AAF-3534-2019; Miolo, Gianmaria/AAC-2351-2020; SAORIN,
   ASIA/ABF-9196-2020
OI Corona, Giuseppe/0000-0003-3619-7709; Miolo,
   Gianmaria/0000-0001-5084-295X; SAORIN, ASIA/0000-0002-4312-7795
FU Italian Ministry of Health-Ricerca Corrente
FX This work was supported by the Italian Ministry of Health-Ricerca
   Corrente.
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NR 37
TC 2
Z9 2
U1 3
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD NOV
PY 2022
VL 14
IS 21
AR 5308
DI 10.3390/cancers14215308
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 6B0WN
UT WOS:000881064600001
PM 36358726
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kalia, M
AF Kalia, Madhu
TI Biomarkers for personalized oncology: recent advances and future
   challenges
SO METABOLISM-CLINICAL AND EXPERIMENTAL
LA English
DT Article
DE Genomic biomarkers; Protein profiling; Molecular carcinogenesis;
   Pharmacogenomics
ID CHRONIC MYELOID-LEUKEMIA; SURROGATE END-POINTS; MOLECULAR DIAGNOSTICS;
   ENDOCRINE THERAPY; LUNG-CANCER; INHIBITION; IMATINIB; WAR
AB Cancer is a group of diseases characterized by the uncontrolled growth and spread of abnormal cells and oncology is a branch of medicine that deals with tumors. The last decade has seen significant advances in the development of biomarkers in oncology that play a critical role in understanding molecular and cellular mechanisms which drive tumor initiation, maintenance and progression. Clinical molecular diagnostics and biomarker discoveries in oncology are advancing rapidly as we begin to understand the complex mechanisms that transform a normal cell into an abnormal one. These discoveries have fueled the development of novel drug targets and new treatment strategies. The standard of care for patients with advanced-stage cancers has shifted away from an empirical treatment strategy based on the clinical pathological profile to one where a biomarker driven treatment algorithm based on the molecular profile of the tumor is used. Recent advances in multiplex genotyping technologies and high-throughput genomic profiling by next-generation sequencing make possible the rapid and comprehensive analysis of the cancer genome of individual patients even from very little tumor biopsy material. Predictive (diagnostic) biomarkers are helpful in matching targeted therapies with patients and in preventing toxicity of standard (systemic) therapies. Prognostic biomarkers identify somatic germ line mutations, changes in DNA methylation, elevated levels of microRNA (miRNA) and circulating tumor cells (CTC) in blood. Predictive biomarkers using molecular diagnostics are currently in use in clinical practice of personalized oncotherapy for the treatment of five diseases: chronic myeloid leukemia, colon, breast, lung cancer and melanoma and these biomarkers are being used successfully to evaluate benefits that can be achieved through targeted therapy. Examples of these molecularly targeted biomarker therapies are: tyrosine ldnase inhibitors in chronic myeloid leukemia and gastrointestinal tumors; anaplastic lymphoma kinase (ALK) inhibitors in lung cancer with EML4-ALk fusion; HER2/neu blockage in HER2/neu-positive breast cancer; and epidermal growth factor receptors (EGER) inhibition in EGFR-mutated lung cancer. This review presents the current state of our knowledge of biomarkers in five selected cancers: chronic myeloid leukemia, colorectal cancer, breast cancer, non-small cell lung cancer and melanoma. (C) 2015 Elsevier Inc. All rights reserved.
C1 Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
C3 Jefferson University
RP Kalia, M (corresponding author), Thomas Jefferson Univ, Suite 520,1020 Walnut St, Philadelphia, PA 19107 USA.
EM madhu.kalia@jefferson.edu
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NR 36
TC 172
Z9 194
U1 0
U2 162
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0026-0495
EI 1532-8600
J9 METABOLISM
JI Metab.-Clin. Exp.
PD MAR
PY 2015
VL 64
IS 3
SU 1
BP S16
EP S21
DI 10.1016/j.metabol.2014.10.027
PG 6
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA CA2QP
UT WOS:000348752800004
PM 25468140
DA 2025-01-04
ER

PT J
AU Buikhuisen, JY
   Barila, PMG
   Torang, A
   Dekker, D
   de Jong, JH
   Cameron, K
   Vitale, S
   Stassi, G
   van Hooff, SR
   Castro, MAA
   Vermeulen, L
   Medema, JP
AF Buikhuisen, Joyce Y.
   Gomez Barila, Patricia M.
   Torang, Arezo
   Dekker, Danielle
   de Jong, Joan H.
   Cameron, Kate
   Vitale, Sara
   Stassi, Giorgio
   van Hooff, Sander R.
   Castro, Mauro A. A.
   Vermeulen, Louis
   Medema, Jan Paul
TI AKT3 Expression in Mesenchymal Colorectal Cancer Cells Drives Growth and
   Is Associated with Epithelial-Mesenchymal Transition
SO CANCERS
LA English
DT Article
DE mesenchymal CRC; CMS; AKT3; growth
ID CONSENSUS MOLECULAR SUBTYPES; KINASE-B-GAMMA; COLON-CANCER; MAGI3-AKT3
   FUSION; TUMOR-GROWTH; BREAST; HETEROGENEITY; OVEREXPRESSION; METASTASIS;
   ACTIVATION
AB Simple Summary
   Colorectal cancer can be subdivided into four distinct subtypes that are characterised by different clinical features and responses to therapies currently used in the clinic to treat this disease. One of those subtypes, called CMS4, is associated with a worse prognosis and poor response to therapies compared to other subtypes. We therefore set out to explore what proteins are differentially expressed and used in CMS4 to find potential new targets for therapy. We found that protein AKT3 is highly expressed in CMS4, and that active AKT3 inhibits a protein that stalls growth of cancer cells (p27(KIP1)). We can target AKT3 with inhibitors which leads to strongly reduced growth of cancer cell lines that are categorised as CMS4. Furthermore, our data suggests that high AKT3 expression in tumour cells may be used to identify poor prognosis colorectal cancer patients. Future research should point out if high AKT3 expression can be used to select colorectal cancer patients that have a poor prognosis but that could benefit from AKT3-targeted treatment.
   Colorectal cancer (CRC) is a heterogeneous disease that can currently be subdivided into four distinct consensus molecular subtypes (CMS) based on gene expression profiling. The CMS4 subtype is marked by high expression of mesenchymal genes and is associated with a worse overall prognosis compared to other CMSs. Importantly, this subtype responds poorly to the standard therapies currently used to treat CRC. We set out to explore what regulatory signalling networks underlie the CMS4 phenotype of cancer cells, specifically, by analysing which kinases were more highly expressed in this subtype compared to others. We found AKT3 to be expressed in the cancer cell epithelium of CRC specimens, patient derived xenograft (PDX) models and in (primary) cell cultures representing CMS4. Importantly, chemical inhibition or knockout of this gene hampers outgrowth of this subtype, as AKT3 controls expression of the cell cycle regulator p27(KIP1). Furthermore, high AKT3 expression was associated with high expression of epithelial-mesenchymal transition (EMT) genes, and this observation could be expanded to cell lines representing other carcinoma types. More importantly, this association allowed for the identification of CRC patients with a high propensity to metastasise and an associated poor prognosis. High AKT3 expression in the tumour epithelial compartment may thus be used as a surrogate marker for EMT and may allow for a selection of CRC patients that could benefit from AKT3-targeted therapy.
C1 [Buikhuisen, Joyce Y.; Gomez Barila, Patricia M.; Torang, Arezo; Dekker, Danielle; de Jong, Joan H.; Cameron, Kate; van Hooff, Sander R.; Vermeulen, Louis; Medema, Jan Paul] Univ Amsterdam, Amsterdam UMC, Canc Ctr Amsterdam, Ctr Expt Mol Med,Lab Expt Oncol & Radiobiol, NL-1105 AZ Amsterdam, Netherlands.
   [Buikhuisen, Joyce Y.; Gomez Barila, Patricia M.; Torang, Arezo; Dekker, Danielle; de Jong, Joan H.; Cameron, Kate; van Hooff, Sander R.; Vermeulen, Louis; Medema, Jan Paul] Oncode Inst, NL-3521 AL Utrecht, Netherlands.
   [Vitale, Sara] Univ Cattolica Sacro Cuore, Ist Patol Gen, Dipartimento Med & Chirurg Traslaz, I-20123 Milan, Italy.
   [Vitale, Sara] Ist Super Sanita, Dept Oncol & Mol Med, I-00161 Rome, Italy.
   [Stassi, Giorgio] Univ Palermo, Dept Surg Oncol & Stomatol Sci, Cellular & Mol Oncol Sect, I-90127 Palermo, Italy.
   [Castro, Mauro A. A.] Univ Fed Parana, Bioinformat & Syst Biol Lab, BR-81520260 Curitiba, Parana, Brazil.
   [van Hooff, Sander R.] Princess Maxima Ctr Pediat Oncol, NL-3584 CS Utrecht, Netherlands.
C3 Vrije Universiteit Amsterdam; University of Amsterdam; Catholic
   University of the Sacred Heart; Istituto Superiore di Sanita (ISS);
   University of Palermo; Universidade Federal do Parana
RP Medema, JP (corresponding author), Univ Amsterdam, Amsterdam UMC, Canc Ctr Amsterdam, Ctr Expt Mol Med,Lab Expt Oncol & Radiobiol, NL-1105 AZ Amsterdam, Netherlands.; Medema, JP (corresponding author), Oncode Inst, NL-3521 AL Utrecht, Netherlands.
EM j.y.buikhuisen@amsterdamumc.nl; p.m.gomezbarila@amsterdamumc.nl;
   a.torang@amsterdamumc.nl; danielle.dekker@amsterdamumc.nl;
   j.h.dejong@amsterdamumc.nl; k.cameron@amsterdamumc.nl;
   sara.vitale@unicatt.it; giorgio.stassi@unipa.it;
   S.R.vanHooff-3@prinsesmaximacentrum.nl; mauro.castro@ufpr.br;
   l.vermeulen@amsterdamumc.nl; j.p.medema@amsterdamumc.nl
RI Vitale, Sara/AAB-9588-2019; Stassi, Giorgio/JAZ-0703-2023; Vermeulen,
   Louis/B-7488-2008; Castro, Mauro/A-5467-2008
OI Torang, Arezo/0000-0002-7912-3964; Buikhuisen,
   Joyce/0000-0002-1181-737X; Stassi, Giorgio/0000-0002-1016-9059; Gomez
   Barila, Patricia/0000-0003-3878-3373; Castro, Mauro/0000-0003-4942-8131;
   Dekker, Danielle/0000-0003-2589-0620; vitale, sara/0000-0002-9011-9042;
   Medema, Jan Paul/0000-0003-3045-2924
FU KoninginWilhelmina Fonds Dutch Cancer Society [UVA2014-7245, 10150];
   Oncode Institute; AMC Graduate School PhD Scholarship
FX This work was supported by the KoninginWilhelmina Fonds Dutch Cancer
   Society (grants UVA2014-7245 and 10150) and Oncode Institute. L.V. is a
   New York Stem Cell Foundation-Robertson Investigator. J.Y.B. was
   partially funded by the AMC Graduate School PhD Scholarship.
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NR 74
TC 20
Z9 21
U1 0
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD FEB
PY 2021
VL 13
IS 4
AR 801
DI 10.3390/cancers13040801
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QO8FJ
UT WOS:000623373400001
PM 33673003
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Choi, YJ
   Choi, CY
   Rhie, SJ
   Shin, S
AF Choi, Yeo Jin
   Choi, Chang-Young
   Rhie, Sandy Jeong
   Shin, Sooyoung
TI Safety Assessment on Serious Adverse Events of Targeted Therapeutic
   Agents Prescribed for RAS Wild-Type Metastatic Colorectal Cancer:
   Systematic Review and Network Meta-Analysis
SO INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH
LA English
DT Review
DE adverse events; bevacizumab; cetuximab; colorectal cancer; metastatic
   cancer; panitumumab; pharmacovigilance
ID PHASE-II; VENOUS THROMBOEMBOLISM; BEVACIZUMAB; CETUXIMAB; PANITUMUMAB;
   RISK; CHEMOTHERAPY; MULTICENTER; THERAPIES; ANTIBODY
AB Despite substantially elevated risk of serious adverse events (SAEs) from targeted therapy in combination with chemotherapy, comprehensive pharmacovigilance research is limited. This study aims to systematically assess SAE risks of commonly prescribed targeted agents (bevacizumab, cetuximab, and panitumumab) in patients with rat sarcoma viral oncogene homolog (RAS) wild-type metastatic colon cancer. Keyword searches of Cochrane Library, Clinical Key and MEDLINE were conducted per PRISMA-NMA guidelines. Frequentist network meta-analysis was performed with eight randomized controlled trials to compare relative risk (RR) of 21 SAE profiles. The risks of hematological, gastrointestinal, neurological SAE were insignificant among targeted agents (p > 0.05). The risk of serious hypertension was substantially elevated in bevacizumab-based chemotherapy (p < 0.05), whereas panitumumab-based chemotherapy had markedly elevated risk of serious thromboembolism (RR 3.65; 95% CI 1.30-10.26). Although both cetuximab and panitumumab demonstrated increased risk of serious dermatological and renal toxicities, panitumumab-based chemotherapy has relatively higher risk of skin toxicity (RR 15.22; 95% CI 7.17-32.35), mucositis (RR 3.18; 95% CI 1.52-6.65), hypomagnesemia (RR 20.10; 95% CI 5.92-68.21), and dehydration (RR 2.81; 95% CI 1.03-7.67) than cetuximab-based chemotherapy. Thus, further studies on risk stratification and SAE management are warranted for safe administration of targeted agents.
C1 [Choi, Yeo Jin] Kyung Hee Univ, Dept Pharm, Coll Pharm, Seoul 02447, South Korea.
   [Choi, Yeo Jin] Kyung Hee Univ, Grad Sch, Dept Regulatory Sci, Seoul 02447, South Korea.
   [Choi, Chang-Young] Ajou Univ, Med Ctr, Dept Internal Med, Suwon 16499, South Korea.
   [Rhie, Sandy Jeong] Ewha Womans Univ, Grad Sch Converging Clin & Publ Hlth, Seoul 03670, South Korea.
   [Rhie, Sandy Jeong] Ewha Womans Univ, Grad Sch Pharmaceut Sci, Coll Pharm, Seoul 03760, South Korea.
   [Shin, Sooyoung] Ajou Univ, Dept Pharm, Coll Pharm, Suwon 16499, South Korea.
C3 Kyung Hee University; Kyung Hee University; Ajou University; Ewha Womans
   University; Ewha Womans University; Ajou University
RP Choi, YJ (corresponding author), Kyung Hee Univ, Dept Pharm, Coll Pharm, Seoul 02447, South Korea.; Choi, YJ (corresponding author), Kyung Hee Univ, Grad Sch, Dept Regulatory Sci, Seoul 02447, South Korea.; Shin, S (corresponding author), Ajou Univ, Dept Pharm, Coll Pharm, Suwon 16499, South Korea.
EM yeojin.choi@khu.ac.kr; changchoi1216@gmail.com; sandy.rhie@ewha.ac.kr;
   syshin@ajou.ac.kr
RI Choi, Yeo Jin/JXM-0329-2024
OI Rhie, Jeong Yeon/0000-0003-2554-3370; Shin,
   Sooyoung/0000-0003-2388-1122; Choi, Yeo Jin/0000-0002-0635-4374
FU National Research Foundation (NRF) - Ministry of Education
   [2021R1I1A1A01044500]; Ministry of Science and ICT [2021R1C1C1003735,
   2020R1A2C1009224]; Ministry of Food and Drug Safety [21153MFDS601-1]
FX This research was partially supported by a grant (No. 21153MFDS601-1)
   from the Ministry of Food and Drug Safety in 2021 and National Research
   Foundation (NRF), grant-funded by Ministry of Education (No.
   2021R1I1A1A01044500) and the Ministry of Science and ICT (No.
   2021R1C1C1003735 and 2020R1A2C1009224).
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NR 56
TC 5
Z9 5
U1 3
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1660-4601
J9 INT J ENV RES PUB HE
JI Int. J. Environ. Res. Public Health
PD AUG
PY 2022
VL 19
IS 15
AR 9196
DI 10.3390/ijerph19159196
PG 18
WC Environmental Sciences; Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
   Health
GA 3S1PB
UT WOS:000839373700001
PM 35954563
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Dang, J
   He, ZY
   Cui, X
   Fan, JC
   Hambly, DJ
   Hambly, BD
   Li, X
   Bao, SS
AF Dang, Jie
   He, Zhiyun
   Cui, Xiang
   Fan, Jingchun
   Hambly, David J.
   Hambly, Brett D.
   Li, Xun
   Bao, Shisan
TI The Role of IL-37 and IL-38 in Colorectal Cancer
SO FRONTIERS IN MEDICINE
LA English
DT Review
DE IL-37; IL-38; colorectal cancer; TAM; TAN
ID INFLAMMATION; IMMUNITY; CYTOKINE; SUPPRESSION; STATISTICS; ANTAGONIST;
   ACTIVATION; COLITIS; MEMBERS; CELLS
AB Colorectal cancer (CRC) is a major killer. Dysregulation of IL-37 and IL-38, both anti-inflammatory cytokines, is observed in auto-immune diseases. The precise regulatory mechanisms of IL-37/IL-38 during the development of CRC remains unclear, but chronic intestinal inflammation is involved in the carcinogenesis of CRC. Constitutive production of colonic IL-37 and IL-38 is substantially reduced in CRC, consistent with an inverse correlation with CRC differentiation. Reduced colonic IL-37 and IL-38 is relating to CRC invasion and distant metastasis, suggesting a protective role for IL-38 within the tumor micro-environment. IL-38 is reduced in right-sided CRC compared to left-sided CRC, which is in line with multiple risk factors for right-sided CRC, including the embryonic development of the colon, and genetic differences in CRC between these two sides. Finally, colonic IL-37 and tumor associated neutrophils (TAN) seem to be independent biomarkers of prognostic value, whereas colonic IL-38 seems to be a reliable and independent biomarker in predicting the 5-year survival post-surgery in CRC. However, there is room for improvement in available studies, including the extension of these studies to different regions/countries incorporating different races, evaluation of the role of multi-drug resistance, and different subsets of CRC. It would be useful to determine the kinetics of circulating IL-38 and its relationship with drug resistance/targeted therapy. The measurement of colonic IL-38 at the molecular and cellular level is required to explore the contribution of IL-38 pathways during the development of CRC. These approaches could provide insight for the development of personalized medicine.
C1 [Dang, Jie] Lanzhou Univ, Child & Adolescent Hlth Management Ctr, Hosp 2, Lanzhou, Peoples R China.
   [He, Zhiyun; Li, Xun] Lanzhou Univ, Dept Gen Surg, Hosp 1, Lanzhou, Peoples R China.
   [Cui, Xiang] Lanzhou Univ, Dept Gen Surg, Hosp 2, Lanzhou, Peoples R China.
   [Fan, Jingchun; Hambly, Brett D.; Bao, Shisan] Gansu Univ Chinese Med, Sch Publ Hlth, Dept Epidemiol & Evidence Based Med, Ctr Evidence Based Med, Lanzhou, Peoples R China.
   [Hambly, David J.] Gold Coast Univ Hosp, Resident Training Program, Southport, Qld, Australia.
   [Hambly, David J.] Torrens Univ Australia, Ctr Hlth Futures, Sydney, NSW, Australia.
C3 Lanzhou University; Lanzhou University; Lanzhou University; Gansu
   University of Chinese Medicine; Gold Coast University Hospital; Torrens
   University Australia
RP Li, X (corresponding author), Lanzhou Univ, Dept Gen Surg, Hosp 1, Lanzhou, Peoples R China.; Bao, SS (corresponding author), Gansu Univ Chinese Med, Sch Publ Hlth, Dept Epidemiol & Evidence Based Med, Ctr Evidence Based Med, Lanzhou, Peoples R China.
EM 154964740@qq.com; profbao@hotmail.com
RI Bao, Shisan/C-6072-2014; Hambly, Brett/B-1965-2009
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NR 66
TC 8
Z9 8
U1 0
U2 9
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-858X
J9 FRONT MED-LAUSANNE
JI Front. Med.
PD FEB 2
PY 2022
VL 9
AR 811025
DI 10.3389/fmed.2022.811025
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA ZF8YT
UT WOS:000759855900001
PM 35186997
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Davis, TB
   Gupta, S
   Yang, ML
   Pflieger, L
   Rajan, M
   Wang, HM
   Thota, R
   Yeatman, TJ
   Pledger, WJ
AF Davis, Thomas Benjamin
   Gupta, Shilpa
   Yang, Mingli
   Pflieger, Lance
   Rajan, Malini
   Wang, Heiman
   Thota, Ramya
   Yeatman, Timothy J.
   Pledger, Warren Jackson
TI Ras Pathway Activation and MEKi Resistance Scores Predict the Efficiency
   of MEKi and SRCi Combination to Induce Apoptosis in Colorectal Cancer
SO CANCERS
LA English
DT Article
DE colorectal cancer (CRC); drug resistance; biomarkers; drugs sensitivity
   selection; MEK inhibition; SRC inhibition; gene expression; gene
   signature score; consensus molecular subtype (CMS)
ID CONSENSUS MOLECULAR SUBTYPES; COLON-CANCER; ADAPTIVE RESISTANCE; C-SRC;
   IDENTIFICATION; SENSITIVITY; EXPRESSION; SECONDARY; THERAPY; KINASE
AB Simple Summary Inhibition of MEK has been proposed as a means to address mutant RAS colorectal cancer (CRC). However, MEK inhibitor adaptive resistance has led to reduced clinical utility of this new drug. Our studies have suggested the potential for the addition of an SRC inhibitor to prevent the development of resistance to MEK inhibitors. Moreover, we have identified that gene expression signature scores for RAS pathway activation, and MEK inhibitor resistance may be useful biomarkers in determining CRC drug sensitivity to the novel combination of Trametinib and Dasatinib. Colorectal cancer (CRC) is the second leading cause of cancer death in the United States. The RAS pathway is activated in more than 55% of CRC and has been targeted for therapeutic intervention with MEK inhibitors. Unfortunately, many patients have de novo resistance, or can develop resistance to this new class of drugs. We have hypothesized that much of this resistance may pass through SRC as a common signal transduction node, and that inhibition of SRC may suppress MEK inhibition resistance mechanisms. CRC tumors of the Consensus Molecular Subtype (CMS) 4, enriched in stem cells, are difficult to successfully treat and have been suggested to evade traditional chemotherapy agents through resistance mechanisms. Here, we evaluate targeting two pathways simultaneously to produce an effective treatment by overcoming resistance. We show that combining Trametinib (MEKi) with Dasatinib (SRCi) provides enhanced cell death in 8 of the 16 tested CRC cell lines compared to treatment with either agent alone. To be able to select sensitive cells, we simultaneously evaluated a validated 18-gene RAS pathway activation signature score along with a 13-gene MEKi resistance signature score, which we hypothesize predict tumor sensitivity to this dual targeted therapy. We found the cell lines that were sensitive to the dual treatment were predominantly CMS4 and had both a high 18-gene and a high 13-gene score, suggesting these cell lines had potential for de novo MEKi sensitivity but were subject to the rapid development of MEKi resistance. The 13-gene score is highly correlated to a score for SRC activation, suggesting resistance is dependent on SRC. Our data show that gene expression signature scores for RAS pathway activation and for MEKi resistance may be useful in determining which CRC tumors will respond to the novel drug combination of MEKi and SRCi.
C1 [Davis, Thomas Benjamin; Gupta, Shilpa; Yang, Mingli; Rajan, Malini; Wang, Heiman; Yeatman, Timothy J.; Pledger, Warren Jackson] Univ Utah, Dept Surg, Salt Lake City, UT 84132 USA.
   [Pflieger, Lance] Intermt Healthcare, Precis Genom Translat Sci Ctr, Murray, UT 84107 USA.
   [Thota, Ramya] Intermt Healthcare, Oncol Clin Program, Murray, UT 84107 USA.
   [Yeatman, Timothy J.; Pledger, Warren Jackson] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
C3 Utah System of Higher Education; University of Utah; Intermountain
   Healthcare; Intermountain Medical Center; Intermountain Healthcare;
   Intermountain Medical Center; Utah System of Higher Education;
   University of Utah; Huntsman Cancer Institute
RP Davis, TB; Pledger, WJ (corresponding author), Univ Utah, Dept Surg, Salt Lake City, UT 84132 USA.; Pledger, WJ (corresponding author), Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
EM thomas.davis@utah.edu; u0878193@utah.edu; minglyang@utah.edu;
   lance.pflieger@imail.org; mrajan@u2m2.utah.edu; heiman.wang@utah.edu;
   ramya.thota@imail.org; yeatman7383@gmail.com; jack.pledger@utah.edu
RI Yeatman, Timothy/LJK-6730-2024; Rajan, Malini/AAV-5433-2021
OI Yang, Mingli/0000-0002-4781-690X
FU National Institutes of Health [UH2CA227955, UH3CA227955, R21CA252436,
   R21CA255312, R21 CA256372]; Intermountain Healthcare; National Cancer
   Institute [UH3CA227955] Funding Source: NIH RePORTER
FX This work is supported by National Institutes of Health grants
   UH2CA227955 (TJY) and UH3CA227955 (TJY) as well as R21CA252436 (TJY),
   R21CA255312 (TJY) and R21 CA256372 (TJY); This work is also supported by
   the fund from Intermountain Healthcare.
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NR 38
TC 4
Z9 4
U1 0
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD MAR
PY 2022
VL 14
IS 6
AR 1451
DI 10.3390/cancers14061451
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 0D4PR
UT WOS:000775979600001
PM 35326598
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zeng, Q
   Xie, L
   Zhou, N
   Liu, M
   Song, XR
AF Zeng, Qian
   Xie, Li
   Zhou, Na
   Liu, Min
   Song, Xianrang
TI Detection of <i>PIK3CA</i> Mutations in Plasma DNA of Colorectal Cancer
   Patients by an Ultra-Sensitive PNA-Mediated PCR
SO MOLECULAR DIAGNOSIS & THERAPY
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; CIRCULATING TUMOR-CELLS; BREAST-CANCER; KRAS
   MUTATIONS; HIGH-FREQUENCY; LUNG-CANCER; GENE; BRAF; CARCINOMAS;
   HETEROGENEITY
AB Background Mutant Phosphatidylinositol-4, 5-bisphosphate 3-kinase, catalytic subunit alpha (PIK3CA) has been shown to be associated with the occurrence, development and prognosis in colorectal cancer (CRC). However, its detection has been limited because of complicated procedures and the low sensitivity of the present approaches.
   Methods We established an ultra-sensitive peptide nucleic acid-mediated polymerase chain reaction (PNA-PCR) assay to detect PIK3CA gene mutation in exon 9 and exon 20 with cell-free DNA (cfDNA). Using this technology, we detected the mutation status of PIK3CA in 128 colorectal cancer patients. 6 CRC patients receiving targeted therapy were chosen at random to undergo continuous PIK3CA mutation detection.
   Results The results showed that the sensitivity of PNA-PCR clamping method was 0.1% for the exon 9 and 0.2% for the exon 20 variant alleles. When the PIK3CA mutation status was determined by PNA-PCR plus sequencing, 38.3% (49/128) of CRC carried at least one mutation, either E545Kor H1047R. The clinic-pathological parameters of age (p = 0.358), gender (p = 0.622), disease stage (p = 0.353) and disease location (p = 0.307) were not associated with the PIK3CA mutation. In the continuous monitoring study, we found that the gene status was associated with the effect of treatment. Furthermore, when the PIK3CA variant was determined by only the PNA-PCR method, there was a good linear relationship between Delta Cp values and the proportion of variant DNA. The accuracy of PNA-PCR was 93.75 and 92.27% respectively when the cut-off values of Delta Cp at 9.0 and 8.0 were set for determining the E545K and H1047R mutations.
   Conclusions A simple, noninvasive, ultra-sensitive PNA-PCR technology was developed and was especially suitable for the dynamic detection of PIK3CA variants using cfDNA.
C1 [Zeng, Qian; Xie, Li; Zhou, Na; Liu, Min; Song, Xianrang] Shandong Canc Hosp & Inst, Clin Lab, 440 Ji Yan Rd, Jinan 250117, Shandong, Peoples R China.
   [Zeng, Qian; Zhou, Na] Shandong Univ, Clin Lab, Qilu Childrens Hosp, 23976 Jing Shi Rd, Jinan 250022, Shandong, Peoples R China.
C3 Shandong First Medical University & Shandong Academy of Medical
   Sciences; Shandong University
RP Song, XR (corresponding author), Shandong Canc Hosp & Inst, Clin Lab, 440 Ji Yan Rd, Jinan 250117, Shandong, Peoples R China.
EM 1kurama@163.com; l_xie2001@126.com; 729949080@qq.com; kellyminy@126.com;
   sxr@vip.163.com
FU National Science Foundation of China [81371886]
FX This study was supported by Grants from the National Science Foundation
   of China (No. 81371886).
CR [Anonymous], ONCOTARGET
   [Anonymous], 2016, Oncotarget
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NR 35
TC 10
Z9 11
U1 3
U2 19
PU ADIS INT LTD
PI NORTHCOTE
PA 5 THE WAREHOUSE WAY, NORTHCOTE 0627, AUCKLAND, NEW ZEALAND
SN 1177-1062
EI 1179-2000
J9 MOL DIAGN THER
JI Mol. Diagn. Ther.
PD AUG
PY 2017
VL 21
IS 4
BP 443
EP 451
DI 10.1007/s40291-017-0269-9
PG 9
WC Genetics & Heredity; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity; Pharmacology & Pharmacy
GA FA5ST
UT WOS:000405504700009
PM 28247181
DA 2025-01-04
ER

PT J
AU Dercle, L
   Lu, L
   Lichtenstein, P
   Yang, H
   Wang, DL
   Zhu, JG
   Wu, FY
   Piessevaux, H
   Schwartz, LH
   Zhao, BS
AF Dercle, Laurent
   Lu, Lin
   Lichtenstein, Philip
   Yang, Hao
   Wang, Deling
   Zhu, Jianguo
   Wu, Feiyun
   Piessevaux, Hubert
   Schwartz, Lawrence H.
   Zhao, Binsheng
TI Impact of Variability in Portal Venous Phase Acquisition Timing in Tumor
   Density Measurement and Treatment Response Assessment: Metastatic
   Colorectal Cancer as a Paradigm
SO JCO CLINICAL CANCER INFORMATICS
LA English
DT Article
ID RENAL-CELL CARCINOMA; CONTRAST ENHANCEMENT; COMPUTED-TOMOGRAPHY;
   IMATINIB MESYLATE; TARGETED THERAPY; EAU GUIDELINES; RAS MUTATIONS;
   SOLID TUMORS; CT SCANS; CETUXIMAB
AB Purpose New response patterns to anticancer drugs have led tumor size-based response criteria to shift to also include density measurements. Choi criteria, for instance, categorize antiangiogenic therapy response as a decrease in tumor density > 15% at the portal venous phase (PVP). We studied the effect that PVP timing has on measurement of the density of liver metastases (LM) from colorectal cancer (CRC).
   Methods Pretreatment PVP computed tomography images from 291 patients with LM-CRC from the CRYSTAL trial (Cetuximab Combined With Irinotecan in First-Line Therapy for Metastatic Colorectal Cancer; ClinicalTrials.gov identifier: NCT00154102) were included. Four radiologists independently scored the scans' timing according to a three-point scoring system: early, optimal, late PVP. Using this, we developed, by machine learning, a proprietary computer-aided quality-control algorithm to grade PVP timing. The reference standard was a computer-refined consensus. For each patient, we contoured target liver lesions and calculated their mean density.
   Results Contrast-product administration data were not recorded in the digital imaging and communications in medicine headers for injection volume (94%), type (93%), and route (76%). The PVP timing was early, optimal, and late in 52, 194, and 45 patients, respectively. The mean (95% CI) accuracy of the radiologists for detection of optimal PVP timing was 81.7% (78.3 to 85.2) and was outperformed by the 88.6% (84.8 to 92.4) computer accuracy. The mean +/- standard deviation of LM-CRC density was 68 +/- 15 Hounsfield units (HU) overall and 59.5 +/- 14.9 HU, 71.4 +/- 14.1 HU, 62.4 +/- 12.5 HU at early, optimal, and late PVP timing, respectively. LM-CRC density was thus decreased at nonoptimal PVP timing by 14.8%: 16.7% at early PVP (P < .001) and 12.6% at late PVP (P < .001).
   Conclusion Nonoptimal PVP timing should be identified because it significantly decreased tumor density by 14.8%. Our computer-aided quality-control system outperformed the accuracy, reproducibility, and speed of radiologists' visual scoring. PVP-timing scoring could improve the extraction of tumor quantitative imaging biomarkers and the monitoring of anticancer therapy efficacy at the patient and clinical trial levels. (c) 2017 by American Society of Clinical Oncology.
C1 [Dercle, Laurent; Lu, Lin; Lichtenstein, Philip; Yang, Hao; Zhu, Jianguo; Wu, Feiyun; Schwartz, Lawrence H.; Zhao, Binsheng] Columbia Univ, Med Ctr, New York, NY USA.
   [Dercle, Laurent; Lu, Lin; Lichtenstein, Philip; Yang, Hao; Zhu, Jianguo; Wu, Feiyun; Schwartz, Lawrence H.; Zhao, Binsheng] Presbyterian Hosp, New York, NY USA.
   [Dercle, Laurent] Univ Paris Saclay, UMR1015, Gustave Roussy, Villejuif, France.
   [Wang, Deling] Sun Yat Sen Univ, Canc Ctr, Guangzhou, Guangdong, Peoples R China.
   [Wang, Deling] Collaborat Innovat Ctr Canc Med, Guangzhou, Guangdong, Peoples R China.
   [Wang, Deling] State Key Lab Oncol South China, Hong Kong, Peoples R China.
   [Piessevaux, Hubert] Clin Univ St Luc, Brussels, Belgium.
C3 Columbia University; NewYork-Presbyterian Hospital; Universite Paris
   Saclay; UNICANCER; Gustave Roussy; Sun Yat Sen University; State Key Lab
   Oncology South China; Universite Catholique Louvain; Cliniques
   Universitaires Saint-Luc
RP Dercle, L (corresponding author), Columbia Univ, Dept Radiol, Med Ctr, New York Presbyterian Hosp, 630 W 168th St, New York, NY 10027 USA.
EM laurent.dercle@gmail.com
RI Piessevaux, Hubert/N-9558-2019; Dercle, Laurent/C-9740-2018
OI Dercle, Laurent/0000-0002-1322-0710; Piessevaux,
   Hubert/0000-0003-1193-0601
FU National Institutes of Health [U01 CA140207]; Philanthropia Fundation,
   Geneva, Switzerland; Fondation ARC, Villejuif, France
FX Supported by National Institutes of Health Grant No. U01 CA140207 and by
   a grant from the Philanthropia Fundation, Geneva, Switzerland (to L.D.)
   and the Fondation ARC, Villejuif, France (to L.D.).
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NR 45
TC 19
Z9 19
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 2473-4276
J9 JCO CLIN CANCER INFO
JI JCO Clin. Cancer Info.
PY 2017
VL 1
DI 10.1200/CCI.17.00108
PG 13
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA VI1ZO
UT WOS:000462302500003
PM 30657405
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Karpisheh, V
   Joshi, N
   Zekiy, AO
   Beyzai, B
   Hojjat-Farsangi, M
   Namdar, A
   Edalati, M
   Jadidi-Niaragh, F
AF Karpisheh, Vahid
   Joshi, Navneet
   Zekiy, Angelina Olegovna
   Beyzai, Behzad
   Hojjat-Farsangi, Mohammad
   Namdar, Afshin
   Edalati, Mahdi
   Jadidi-Niaragh, Farhad
TI EP4 receptor as a novel promising therapeutic target in colon cancer
SO PATHOLOGY RESEARCH AND PRACTICE
LA English
DT Article
DE cyclooxygenase-2 (COX-2); Prostaglandin E2 (PGE2); EP4 receptor; Colon
   cancer; Treatment
ID POSSIBLE AUTOCRINE/PARACRINE REGULATION; PROSTAGLANDIN E-2 SYNTHESIS;
   NEOPLASTIC CELL-FUNCTION; ELEMENT-BINDING PROTEIN; GROWTH-FACTOR
   RECEPTOR; COLORECTAL-CANCER; PROSTANOID RECEPTORS; CYCLOOXYGENASE-2
   EXPRESSION; RESPONSE ELEMENT; DRUG-RESISTANCE
AB The most prevalent malignancy that can occur in the gastrointestinal tract is colon cancer. The current treatment options for colon cancer patients include chemotherapy, surgery, radiotherapy, immunotherapy, and targeted therapy. Although the chance of curing the disease in the early stages is high, there is no cure for almost all patients with advanced and metastatic disease. It has been found that over-activation of cyclooxygenase 2 (COX-2), followed by the production of prostaglandin E2 (PGE2) in patients with colon cancer are significantly increased. The tumorigenic function of COX-2 is mainly due to its role in the production of PGE2. PGE2, as a main generated prostanoid, has an essential role in growth and survival of colon cancer cell's. PGE2 exerts various effects in colon cancer cells including enhanced expansion, angiogenesis, survival, invasion, and migration. The signaling of PGE2 via the EP4 receptor has been shown to induce colon tumorigenesis. Moreover, the expression levels of the EP4 receptor significantly affect tumor growth and development. Overexpression of EP4 by various mechanisms increases survival and tumor vasculature in colon cancer cells. It seems that the pathway starting with COX2, continuing with PGE2, and ending with EP4 can promote the spread and growth of colon cancer. Therefore, targeting the COX-2/PGE2/EP4 axis can be considered as a worthy therapeutic approach to treat colon cancer. In this review, we have examined the role and different mechanisms that the EP4 receptor is involved in the development of colon cancer.
C1 [Karpisheh, Vahid; Jadidi-Niaragh, Farhad] Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran.
   [Karpisheh, Vahid] Tabriz Univ Med Sci, Student Res Comm, Tabriz, Iran.
   [Joshi, Navneet] Mody Univ Sci & Technol, Dept Biosci, Lakshmangarh, Rajasthan, India.
   [Zekiy, Angelina Olegovna] Sechenov First Moscow State Med Univ, Dept Prosthet Dent, Moscow, Russia.
   [Beyzai, Behzad] Tabriz Univ Med Sci, Drug Appl Res Ctr, Tabriz, Iran.
   [Hojjat-Farsangi, Mohammad] Karolinska Inst, Dept Oncol Pathol, Bioclinicum, Stockholm, Sweden.
   [Namdar, Afshin] Univ Alberta, Cross Canc Inst, Dept Oncol, Edmonton, AB, Canada.
   [Edalati, Mahdi] Tabriz Univ Med Sci, Paramed Fac, Dept Lab Sci, Tabriz, Iran.
   [Jadidi-Niaragh, Farhad] Tabriz Univ Med Sci, Dept Immunol, Fac Med, Tabriz, Iran.
C3 Tabriz University of Medical Science; Tabriz University of Medical
   Science; Mody University of Science & Technology; Sechenov First Moscow
   State Medical University; Tabriz University of Medical Science;
   Karolinska Institutet; University of Alberta; Tabriz University of
   Medical Science; Tabriz University of Medical Science
RP Jadidi-Niaragh, F (corresponding author), Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran.; Joshi, N (corresponding author), Mody Univ Sci & Technol, Dept Biosci, Lakshmangarh, Rajasthan, India.; Jadidi-Niaragh, F (corresponding author), Tabriz Univ Med Sci, Dept Immunol, Fac Med, Tabriz, Iran.
EM navybiotech@gmail.com; jadidif@tbzmed.ac.ir
RI Joshi, Navneet/GLU-7414-2022; Fathabad, Edalati/AAL-9360-2020;
   Jadidi-Niaragh, Farhad/D-3985-2017; Hojat Farsangi, Mohammad/E-8171-2018
OI Joshi, Navneet/0000-0003-0155-3785; Hojat Farsangi,
   Mohammad/0000-0002-0589-5523; karpisheh, vahid/0000-0003-0042-3874
FU National Institute for Medical Research Development, NIMAD [976852];
   Tabriz University of Medical Sciences [66020]
FX We would like to thank the National Institute for Medical Research
   Development, NIMAD, for financial support of this study (grant number:
   976852). We are also very grateful to Tabriz University of Medical
   Sciences for supporting this study (grant number: 66020).
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NR 146
TC 25
Z9 25
U1 2
U2 19
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0344-0338
J9 PATHOL RES PRACT
JI Pathol. Res. Pract.
PD DEC
PY 2020
VL 216
IS 12
AR 153247
DI 10.1016/j.prp.2020.153247
PG 11
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA PC6XM
UT WOS:000597141600001
PM 33190014
DA 2025-01-04
ER

PT J
AU Tong, YX
   Huang, YA
   Zhang, YC
   Zeng, XT
   Yan, M
   Xia, ZS
   Lai, DM
AF Tong, Yixin
   Huang, Yuan
   Zhang, Yuchao
   Zeng, Xiangtai
   Yan, Mei
   Xia, Zhongsheng
   Lai, Dongming
TI DPP3/CDK1 contributes to the progression of colorectal cancer through
   regulating cell proliferation, cell apoptosis, and cell migration
SO CELL DEATH & DISEASE
LA English
DT Article
ID DIPEPTIDYL-PEPTIDASE-III; TARGETED THERAPY; CDK1; INHIBITOR; P21
AB At present, colorectal cancer (CRC) has become a serious threat to human health in the world. Dipeptidyl peptidase 3 (DPP3) is a zinc-dependent hydrolase that may be involved in several physiological processes. However, whether DPP3 affects the development and progression of CRC remains a mystery. This study is the first to demonstrate the role of DPP3 in CRC. Firstly, the results of immunohistochemistry analysis showed the upregulation of DPP3 in CRC tissues compared with normal tissues, which is statistically analyzed to be positively correlated with lymphatic metastasis, pathological stage, positive number of lymph nodes. Moreover, the high expression of DPP3 predicts poor prognosis in CRC patients. In addition, the results of cell dysfunction experiments clarified that the downregulation of DPP3 significantly inhibited cell proliferation, colony formation, cell migration, and promoted apoptosis in vitro. DPP3 depletion could induce cell apoptosis by upregulating the expression of BID, BIM, Caspase3, Caspase8, HSP60, p21, p27, p53, and SMAC. In addition, downregulation of DPP3 can reduce tumorigenicity of CRC cells in vivo. Furthermore, CDK1 is determined to be a downstream target of DPP3-mediated regulation of CRC by RNA-seq, qPCR, and WB. The interaction between DPP3 and CDK1 shows mutual regulation. Specifically, downregulation of DPP3 can accentuate the effects of CDK1 knockdown on the function of CRC cells. Overexpression of CDK1 alleviates the inhibitory effects of DPP3 knockdown in CRC cells. In summary, DPP3 has oncogene-like functions in the development and progression of CRC by targeting CDK1, which may be an effective molecular target for the prognosis and treatment of CRC.
C1 [Tong, Yixin; Yan, Mei; Xia, Zhongsheng; Lai, Dongming] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Gastrointestinal Surg, 107 Yanjiang West Rd, Guangzhou, Guangdong, Peoples R China.
   [Huang, Yuan] Huazhong Univ, Dept Tongji Med Coll, 1095 Jiefang Dadao, Wuhan, Hubei, Peoples R China.
   [Zhang, Yuchao] Fudan Univ, Zhongshan Hosp, Dept Endoscopy Ctr, 180 Fenglin Rd, Shanghai, Peoples R China.
   [Zeng, Xiangtai] Gannan Med Univ, Dept Affiliated Hosp 1, 23 Qingnian Rd, Ganzhou, Jiangxi, Peoples R China.
C3 Sun Yat Sen University; Fudan University; Gannan Medical University
RP Xia, ZS; Lai, DM (corresponding author), Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Gastrointestinal Surg, 107 Yanjiang West Rd, Guangzhou, Guangdong, Peoples R China.
EM xiazhsh@163.com; laidm@mail.sysu.edu.cn
RI Chen, Tao/G-5925-2010
FU Guangdong Science and Technology Foundation of China [2012B031800377];
   National Natural Science Foundation of China [81772268]; Guangdong
   Natural Science Foundation of China [2017A030313815]
FX This paper presents independent research funded by the Guangdong Science
   and Technology Foundation of China (No. 2012B031800377), National
   Natural Science Foundation of China (No. 81772268); Guangdong Natural
   Science Foundation of China (No. 2017A030313815).
CR Abbas T, 2009, NAT REV CANCER, V9, P400, DOI 10.1038/nrc2657
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NR 36
TC 37
Z9 37
U1 1
U2 21
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD MAY 22
PY 2021
VL 12
IS 6
AR 529
DI 10.1038/s41419-021-03796-4
PG 12
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA SM5NL
UT WOS:000657651900005
PM 34023852
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kadyr, S
   Zhuraliyeva, A
   Yermekova, A
   Makhambetova, A
   Kaldybekov, DB
   Mun, EA
   Bulanin, D
   Askarova, SN
   Umbayev, BA
AF Kadyr, Sanazar
   Zhuraliyeva, Altyn
   Yermekova, Aislu
   Makhambetova, Aigerim
   Kaldybekov, Daulet B.
   Mun, Ellina A.
   Bulanin, Denis
   Askarova, Sholpan N.
   Umbayev, Bauyrzhan A.
TI PLGA-PEG Nanoparticles Loaded with Cdc42 Inhibitor for Colorectal Cancer
   Targeted Therapy
SO PHARMACEUTICS
LA English
DT Article
DE Cdc42; CASIN; colorectal cancer; PLGA-PEG-COOH; nanoparticles
ID HETEROGENEITY; ACTIVATION; RESISTANCE; APOPTOSIS; DELIVERY; MEK/ERK;
   HCT116; TUMOR
AB Background/Objectives: An inhibitor of small Rho GTPase Cdc42, CASIN, has been shown to reduce cancer cell proliferation, migration, and invasion, yet it has several limitations, including rapid drug elimination and low bioavailability, which prevents its systemic administration. In this study, we designed and characterized a nanoparticle-based delivery system for CASIN encapsulated within poly(lactide-co-glycolide)-block-poly(ethylene glycol)-carboxylic acid endcap nanoparticles (PLGA-PEG-COOH NPs) for targeted inhibition of Cdc42 activity in colon cancer. Methods: We applied DLS, TEM, and UV-vis spectroscopy methods to characterize the size, polydispersity index, zeta potential, encapsulation efficiency, loading capacity, and in vitro drug release of the synthesized nanoparticles. The CCK-8 cell viability test was used to study colorectal cancer cell growth in vitro. Results: We showed that CASIN-PLGA-PEG-COOH NPs were smooth, spherical, and had a particle size of 86 +/- 1 nm, with an encapsulation efficiency of 66 +/- 5% and a drug-loading capacity of 5 +/- 1%. CASIN was gradually released from NPs, reaching its peak after 24 h, and could effectively inhibit the proliferation of HT-29 (IC50 = 19.55 mu M), SW620 (IC50 = 9.33 mu M), and HCT116 (IC50 = 10.45 mu M) cells in concentrations ranging between 0.025-0.375 mg/mL. CASIN-PLGA-PEG-COOH NPs demonstrated low hemolytic activity with a hemolytic ratio of less than 1% for all tested concentrations. Conclusion: CASIN-PLGA-PEG-COOH NPs have high encapsulation efficiency, sustained drug release, good hemocompatibility, and antitumor activity in vitro. Our results suggest that PLGA-PEG-COOH nanoparticles loaded with CASIN show potential as a targeted treatment for colorectal cancer and could be recommended for further in vivo evaluation.
C1 [Kadyr, Sanazar; Bulanin, Denis] Nazarbayev Univ, Sch Med, Astana 010000, Kazakhstan.
   [Zhuraliyeva, Altyn; Yermekova, Aislu; Makhambetova, Aigerim; Askarova, Sholpan N.; Umbayev, Bauyrzhan A.] Nazarbayev Univ, Lab Bioengn & Regenerat Med, Natl Lab Astana, Astana 010000, Kazakhstan.
   [Kaldybekov, Daulet B.] Al Farabi Kazakh Natl Univ, Dept Chem & Chem Technol, Alma Ata 050040, Kazakhstan.
   [Mun, Ellina A.] Nazarbayev Univ, Sch Sci & Humanities, Astana 010000, Kazakhstan.
C3 Nazarbayev University; Nazarbayev University; Al-Farabi Kazakh National
   University; Nazarbayev University
RP Umbayev, BA (corresponding author), Nazarbayev Univ, Lab Bioengn & Regenerat Med, Natl Lab Astana, Astana 010000, Kazakhstan.
EM sanazar.kadyr@nu.edu.kz; altyn.zhuraliyeva@nu.edu.kz;
   aislu.yermekova@nu.edu.kz; aigerim.makhambetova@nu.edu.kz;
   dauletchem@gmail.com; ellina.mun@nu.edu.kz; dbulanin@nu.edu.kz;
   shaskarova@nu.edu.kz; bauyrzhan.umbayev@nu.edu.kz
RI Umbayev, Bauyrzhan/AAR-1900-2020; Mun, Ellina/AAS-3133-2020; Kadyr,
   Sanazar/HJA-0381-2022; Askarova, Sholpan/P-1091-2017; Kaldybekov,
   Daulet/F-1321-2014
OI Askarova, Sholpan/0000-0001-6161-1671; Umbayev,
   Bauyrzhan/0000-0002-0286-7252; Mun, Ellina/0000-0001-8625-9563; Kadyr,
   Sanazar/0009-0001-3958-5777; Kaldybekov, Daulet/0000-0002-7191-5465
FU Committee of Science of the Ministry of Science and Higher Education of
   the Republic of Kazakhstan; Nazarbayev University, Collaborative
   Research Project (CRP) [211123CRP1611];  [AP14871939]
FX This research has been funded by the Committee of Science of the
   Ministry of Science and Higher Education of the Republic of Kazakhstan
   (Grant No. AP14871939) and Nazarbayev University, Collaborative Research
   Project (CRP) Grant No. 211123CRP1611.
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NR 38
TC 0
Z9 0
U1 3
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1999-4923
J9 PHARMACEUTICS
JI Pharmaceutics
PD OCT
PY 2024
VL 16
IS 10
AR 1301
DI 10.3390/pharmaceutics16101301
PG 13
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA K1X8M
UT WOS:001341888000001
PM 39458630
OA gold
DA 2025-01-04
ER

PT J
AU Mohamed, MS
   Abdelhamid, AO
   Almutairi, FM
   Ali, AG
   Bishr, MK
AF Mohamed, Mervat S.
   Abdelhamid, Abdou O.
   Almutairi, Fahad M.
   Ali, Ayat G.
   Bishr, Mai K.
TI Induction of apoptosis by pyrazolo[3,4-<i>d</i>]pyridazine derivative in
   lung cancer cells via disruption of <i>Bcl</i>-<i>2</i>/<i>Bax</i>
   expression balance
SO BIOORGANIC & MEDICINAL CHEMISTRY
LA English
DT Article
DE Pyrazolo[3,4-d]pyridazine derivatives; Molecular modeling; Cytotoxicity;
   Apoptosis; Apoptotic regulators
ID IAP PROTEINS; INHIBITOR; REGULATORS; FAMILY
AB In the rapidly expanding era of cancer target therapy, regulators of apoptosis are emerging as attractive therapeutic targets. X-linked inhibitor of apoptosis (XIAP) is of specific interest owing to its characteristic overexpression in a wide variety of neoplasms, with a resultant survival advantage for tumor cells and treatment resistance. In this study, we examined three pyrazolo [3,4-d] pyridazine derivatives (PPDs) through molecular modeling and studied their modes of interaction with XIAP-BIR3 domain. PPD-1, which possessed the highest binding affinity with XIAP, was tested on A549 (lung cancer cell line); HCT-116 (colorectal carcinoma cell line); HEPG2 (liver carcinoma cell line), HFB4 (normal human skin melanocyte cell line) and WI-38 (human embryonic lung fibroblasts). In comparison to cisplatin as a positive control, PPD-1 yielded remarkable cytotoxicity on all cancer cell lines, with the highest anti-tumor activity on A549 and a favorable therapeutic ratio. Flow cytometry studies concluded that PPD-1 treatment induces Sub G1 and G2/M cell cycle arrest and apoptosis. The percentage of apoptotic cells in PPD-1 treated A549 cells was considerably higher than that in untreated cells (10.06% vs 0.57%, respectively). To further investigate the mechanism of induction of apoptosis by PPD-1, Real time-PCR was used to quantify the expression levels of key apoptotic regulators. Significant overexpression of the effector capsase-3, pro-apoptotic bax and tumor suppressor gene p53 were noted as compared to untreated cells (7.19 folds, 7.28 folds, and 5.08 folds, respectively). Moreover, PPD-1 inhibited the expression of the antiapoptotic bcl-2 gene to 0.22 folds. These findings demonstrate that PPD-1 treatment disrupts the Bcl-2/BAX balance in lung cancer cell lines, leading to apoptosis induction possibly through intrinsic mitochondria- dependent pathway. These novel insights elucidate the mechanism of PPD-1 cytotoxicity in lung cancer cell lines and offer a promising therapeutic approach that needs further study. (C) 2017 Elsevier Ltd. All rights reserved.
C1 [Mohamed, Mervat S.; Almutairi, Fahad M.] Univ Tabuk, Dept Biochem, Fac Sci, Tabuk, Saudi Arabia.
   [Mohamed, Mervat S.] Cairo Univ, Dept Chem, Biochem Special, Fac Sci, Giza, Egypt.
   [Abdelhamid, Abdou O.] Cairo Univ, Dept Chem, Organ Chem Special, Fac Sci, Giza, Egypt.
   [Ali, Ayat G.] El Sahel Teaching Hosp, Dept Biochem, Cairo, Egypt.
   [Bishr, Mai K.] Childrens Canc Hosp Egypt CCHE, Dept Radiotherapy, Cairo, Egypt.
C3 University of Tabuk; Egyptian Knowledge Bank (EKB); Cairo University;
   Egyptian Knowledge Bank (EKB); Cairo University; Egyptian Knowledge Bank
   (EKB); General Organization of Teaching Hospitals & Institutes (GOTHI);
   Children's Cancer Hospital 57357
EM Mervat@ut.edu.sa
RI M AlMutairi, Fahad/HSG-9364-2023
OI Bishr, Mai/0000-0002-9124-7492; Gamal, Ayat/0000-0003-3254-3782;
   Almutairi, Fahad M./0000-0001-6951-1114
FU University of Tabuk, Kingdom of Saudi Arabia [S - 1438-0013]
FX This work is supported by a research grant S - 1438-0013 from University
   of Tabuk, Kingdom of Saudi Arabia to Mervat S. Mohamed.
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NR 28
TC 31
Z9 33
U1 0
U2 10
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0968-0896
EI 1464-3391
J9 BIOORGAN MED CHEM
JI Bioorg. Med. Chem.
PD FEB 1
PY 2018
VL 26
IS 3
BP 623
EP 629
DI 10.1016/j.bmc.2017.12.026
PG 7
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry,
   Organic
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA FW8BA
UT WOS:000425550800009
PM 29290491
DA 2025-01-04
ER

PT J
AU Konda, JD
   Olivero, M
   Musiani, D
   Lamba, S
   Di Renzo, MF
AF Konda, John D.
   Olivero, Martina
   Musiani, Daniele
   Lamba, Simona
   Di Renzo, Maria F.
TI Heat-shock protein 27 (HSP27, HSPB1) is synthetic lethal to cells with
   oncogenic activation of MET, EGFR and BRAF
SO MOLECULAR ONCOLOGY
LA English
DT Article
DE oncogenes; small heat-shock proteins; target therapy
ID CANCER-CELLS; CONFERS RESISTANCE; KINASE INHIBITORS; PANCREATIC-CANCER;
   PROSTATE-CANCER; BREAST-CANCER; IN-VIVO; CHEMOTHERAPY; DEATH; APOPTOSIS
AB The small heat-shock protein of 27 kDa (HSP27) is highly expressed in many cancers and is associated with aggressive tumour behaviour, metastasis, poor prognosis and resistance to chemotherapy. We aimed at assessing the role of HSP27 in modulating responses to target therapies. We selected several oncogene-addicted cancer cell lines, which undergo either cell cycle blockade or cell death in response to agents that target the specific oncogene. Surprisingly, HSP27 suppression alone resulted in the apoptotic death of MET-addicted EBC-1 lung cancer cells, epidermal growth factor receptor (EGFR)-addicted colorectal carcinoma (CRC) DiFi cells and BRAF-addicted CRC COLO205 and OXCO-1 and melanoma COLO741 cells, all of which also undergo death when treated with the specific targeted agent. In other cell lines, such as MET-addicted gastric carcinoma MKN45 and EGFR-addicted CRC SW48 lines, where oncogene inhibition only blocked proliferation, HSP27 knockdown made targeted agents switch from cytostatic to cytotoxic activity. Mechanistically, the more the cells were susceptible to HSP27 suppression, the more they were primed for death, as demonstrated by increased levels of mitochondrial outer membrane permeabilization. Priming for death was accompanied by the increase in pro-apoptotic proteins of the BCL2 family and of active caspase-3 and lamin B. Together, these data suggest that oncogene-addicted cells require HSP27 for survival and that HSP27 might interfere with the effectiveness of targeted agents.
C1 [Konda, John D.; Olivero, Martina; Musiani, Daniele; Di Renzo, Maria F.] Univ Turin, Dept Oncol, Turin, Italy.
   [Konda, John D.; Olivero, Martina; Musiani, Daniele; Lamba, Simona; Di Renzo, Maria F.] IRCCS, FPO, Candiolo Canc Inst, Turin, Italy.
C3 University of Turin; IRCCS Fondazione del Piemonte per l'Oncologia
RP Di Renzo, MF (corresponding author), Univ Turin, IRCCS, FPO, Candiolo Canc Inst, SP 142,Km 3-95, I-10060 Turin, Italy.
EM mariaflavia.direnzo@unito.it
RI Musiani, Daniele/N-8121-2017; Olivero, Martina/J-4811-2018; DI RENZO,
   Maria Flavia/B-6091-2012
OI Musiani, Daniele/0000-0001-6851-2633; Konda, John
   David/0000-0002-9552-1321; Olivero, Martina/0000-0002-6815-3498; DI
   RENZO, Maria Flavia/0000-0002-5093-3373; Lamba, Simona
   Elena/0000-0003-3207-1594
FU IG of the Italian Association of Cancer Research (AIRC) [17473]
FX This work has been supported by the following grants: 2015 IG grant#
   17473 of the Italian Association of Cancer Research (AIRC) to MFD.
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NR 54
TC 29
Z9 33
U1 1
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1878-0261
J9 MOL ONCOL
JI Mol. Oncol.
PD JUN
PY 2017
VL 11
IS 6
BP 599
EP 611
DI 10.1002/1878-0261.12042
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FA9BR
UT WOS:000405741400001
PM 28182330
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Car, I
   Dittmann, A
   Vasieva, O
   Bockor, L
   Grbcic, P
   Pitesa, N
   Klobucar, M
   Pavelic, SK
   Sedic, M
AF Car, Iris
   Dittmann, Antje
   Vasieva, Olga
   Bockor, Luka
   Grbcic, Petra
   Pitesa, Nikolina
   Klobucar, Marko
   Pavelic, Sandra Kraljevic
   Sedic, Mirela
TI Ezrin Inhibition Overcomes Acquired Resistance to Vemurafenib in
   BRAFV600E-Mutated Colon Cancer and Melanoma Cells In Vitro
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE BRAFV600E; colon cancer; melanoma; BRAF inhibitor; vemurafenib; ezrin;
   actin cytoskeleton; ezrin inhibitor; NSC305787
ID METASTATIC COLORECTAL-CANCER; EGFR INHIBITION; COMBINED BRAF;
   COMBINATION; EXPRESSION; MODELS; TRIAL
AB Despite the advancements in targeted therapy for BRAFV600E-mutated metastatic colorectal cancer (mCRC), the development of resistance to BRAFV600E inhibition limits the response rate and durability of the treatment. Better understanding of the resistance mechanisms to BRAF inhibitors will facilitate the design of novel pharmacological strategies for BRAF-mutated mCRC. The aim of this study was to identify novel protein candidates involved in acquired resistance to BRAFV600E inhibitor vemurafenib in BRAFV600E-mutated colon cancer cells using an integrated proteomics approach. Bioinformatic analysis of obtained proteomics data indicated actin-cytoskeleton linker protein ezrin as a highly ranked protein significantly associated with vemurafenib resistance whose overexpression in the resistant cells was additionally confirmed at the gene and protein level. Ezrin inhibition by NSC305787 increased anti-proliferative and pro-apoptotic effects of vemurafenib in the resistant cells in an additive manner, which was accompanied by downregulation of CD44 expression and inhibition of AKT/c-Myc activities. We also detected an increased ezrin expression in vemurafenib-resistant melanoma cells harbouring the BRAFV600E mutation. Importantly, ezrin inhibition potentiated anti-proliferative and pro-apoptotic effects of vemurafenib in the resistant melanoma cells in a synergistic manner. Altogether, our study suggests a role of ezrin in acquired resistance to vemurafenib in colon cancer and melanoma cells carrying the BRAFV600E mutation and supports further pre-clinical and clinical studies to explore the benefits of combined BRAF inhibitors and actin-targeting drugs as a potential therapeutic approach for BRAFV600E-mutated cancers.
C1 [Car, Iris; Bockor, Luka; Klobucar, Marko; Sedic, Mirela] Inst Anthropol Res, Ctr Appl Bioanthropol, Ljudevita Gaja 32, Zagreb 10000, Croatia.
   [Dittmann, Antje] Swiss Fed Inst Technol, Funct Genom Ctr Zurich, Winterthurerstr 190,Y59 H38, CH-8057 Zurich, Switzerland.
   [Vasieva, Olga] INGENET Ltd, 27 Market St, Hoylake CH47 2BG, Wirral, England.
   [Grbcic, Petra] Juraj Dobrila Univ Pula, Fac Med, Zagrebacka Ul 30, Pula 52100, Croatia.
   [Pitesa, Nikolina] Rudjer Boskovic Inst, Div Mol Med, Bijenicka Cesta 54, Zagreb 10000, Croatia.
   [Pavelic, Sandra Kraljevic] Univ Rijeka, Fac Hlth Studies, Viktora Cara Emina 5, Rijeka 51000, Croatia.
C3 Institute for Anthropological Research Zagreb; Swiss Federal Institutes
   of Technology Domain; ETH Zurich; University of Juraj Dobrila Pula;
   Rudjer Boskovic Institute; University of Rijeka
RP Sedic, M (corresponding author), Inst Anthropol Res, Ctr Appl Bioanthropol, Ljudevita Gaja 32, Zagreb 10000, Croatia.
EM iris.car@inantro.hr; antje.dittmann@fgcz.ethz.ch; ovasieva@ingenets.com;
   luka.bockor@inantro.hr; petra.grbcic@gmail.com; nikolina.rincic@irb.hr;
   m.klobucar186@gmail.com; sandrakp@uniri.hr; mirela.sedic@inantro.hr
RI Klobučar, Marko/S-4170-2018; Bočkor, Luka/IZP-9117-2023; Grbčić,
   Petra/JFJ-7685-2023; SEDIC, MIRELA/R-4346-2018; Kraljevic Pavelic,
   Sandra/J-3864-2012; Grbcic, Petra/Q-6531-2018
OI SEDIC, MIRELA/0000-0003-4679-1541; Dittmann, Antje/0000-0002-2570-5192;
   Kraljevic Pavelic, Sandra/0000-0003-0491-673X; Grbcic,
   Petra/0000-0002-5711-6237; Bockor, Luka/0000-0002-2096-0944
FU We acknowledge the access to the equipment owned by the Institute for
   Anthropological Research in Zagreb within the project "Centre for
   Applied Bioanthropology", project ID K.K.01.1.1.02.0002, funded by the
   European Fund for Regional Development.; Institute for Anthropological
   Research in Zagreb within the project "Centre for Applied
   Bioanthropology"; European Fund for Regional Development; 
   [01.1.1.02.0002]
FX We acknowledge the access to the equipment owned by the Institute for
   Anthropological Research in Zagreb within the project "Centre for
   Applied Bioanthropology", project ID K.K.01.1.1.02.0002, funded by the
   European Fund for Regional Development.
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NR 44
TC 0
Z9 0
U1 1
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD AUG
PY 2023
VL 24
IS 16
AR 12906
DI 10.3390/ijms241612906
PG 25
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA Q3PR6
UT WOS:001056676300001
PM 37629086
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wong, JJW
   Selbo, PK
AF Wong, Judith Jing Wen
   Selbo, Pal Kristian
TI Light-controlled elimination of PD-L1+cells
SO JOURNAL OF PHOTOCHEMISTRY AND PHOTOBIOLOGY B-BIOLOGY
LA English
DT Article
DE PD-L1; Saporin; Photochemical internalization; Immune checkpoint
   therapy; Immunotoxin; Targeted therapy; Cancer; Drug delivery
ID PHOTOCHEMICAL INTERNALIZATION; PHOTODYNAMIC THERAPY; ANTI-PD-L1
   ANTIBODY; IN-VITRO; CANCER; CELLS; PD-L1; IMMUNOTOXINS; EXPRESSION;
   SAFETY
AB The programmed death ligand-1 (PD-L1), also known as CD274 or B7-H1, is mainly expressed on cancer cells and/or immunosuppressive cells in the tumor microenvironment (TME) and plays an essential role in tumor progression and immune escape. Immune checkpoint inhibitors (ICIs) of the PD-1/PD-L1 axis have shown impressive clinical success, however, the majority of the patients do not respond to immune checkpoint therapy (ICT). Thus, to overcome ICT resistance there is a high need for potent and novel strategies that simultaneously target both tumor cells and immunosuppressive cells in the TME. In this study, we show that the intracellular light-controlled drug delivery method photochemical internalization (PCI) induce specific and strongly enhanced cytotoxic effects of the PD-L1-targeting immunotoxin, anti-PD-L1-saporin (Anti-PDL1-SAP), in the PD-L1+ triple negative breast cancer MDA-MB-231 cell line, while no enhanced efficacy was obtained in the PD-L1 negative control cell line MDA-MB-453. Using fluorescence microscopy, we reveal that the anti-PD-L1 antibody binds to PD-L1 on the surface of the MDA-MD-231 cells and overnight accumulates in late endosomes and lysosomes where it co-localizes with the PCI photosensitizer fimaporfin (TPCS2a). Moreover, light-controlled endosomal/ lysosomal escape of the anti-PD-L1 antibody and fimaporfin into the cytosol was obtained. We also confirm that the breast MDA-MB-468 and the prostate PC-3 and DU-145 cancer cell lines have subpopulations with PD-L1 expression. In addition, we show that interferon-gamma strongly induce PD-L1 expression in the per se PD-L1 negative CT26.WT cells and enhance the PD-L1 expression in MC-38 cells, of which both are murine colon cancer cell lines. In conclusion, our work provides an in vitro proof-of-concept of PCI-enhanced targeting and eradication of PD-L1 positive immunosuppressive cells. This light-controlled combinatorial strategy has a potential to advance cancer immunotherapy and should be explored in preclinical studies.
C1 [Wong, Judith Jing Wen; Selbo, Pal Kristian] Oslo Univ Hosp, Norwegian Radium Hosp, Inst Canc Res, Dept Radiat Biol, Oslo, Norway.
C3 University of Oslo
RP Selbo, PK (corresponding author), Oslo Univ Hosp, Norwegian Radium Hosp, Inst Canc Res, Dept Radiat Biol, Oslo, Norway.
EM judwon@rr-research.no; selbo@rr-research.no
RI Selbo, Pal Kristian/B-4638-2009
OI Selbo, Pal Kristian/0000-0002-5310-057X; Wong, Judith Jing
   Wen/0000-0001-8016-8695
FU South-Eastern Norway Regional Health Authority [2017068, 2016023];
   Norwegian Radium Hospital Research Foundation [FU0803, SE2002]
FX The present work was financially supported by South-Eastern Norway
   Regional Health Authority (funding number: 2017068 (P.K.S.) and 2016023
   (J.J.W.W.)), The Norwegian Radium Hospital Research Foundation (funding
   number: FU0803 (P.K.S) and SE2002 (J.J.W.W.)).
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NR 61
TC 4
Z9 4
U1 1
U2 13
PU ELSEVIER SCIENCE SA
PI LAUSANNE
PA PO BOX 564, 1001 LAUSANNE, SWITZERLAND
SN 1011-1344
EI 1873-2682
J9 J PHOTOCH PHOTOBIO B
JI J. Photochem. Photobiol. B-Biol.
PD DEC
PY 2021
VL 225
AR 112355
DI 10.1016/j.jphotobiol.2021.112355
EA NOV 2021
PG 9
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA XA4KQ
UT WOS:000720618300003
PM 34768077
OA Green Published, hybrid, Green Submitted
DA 2025-01-04
ER

PT J
AU Zhou, YL
   Peng, XT
   Fang, C
   Peng, X
   Tang, JN
   Wang, ZL
   Long, Y
   Chen, JL
   Peng, YH
   Zhang, ZW
   Zhou, YM
   Tang, J
   Liao, JZ
   Xiao, DS
   Tao, YG
   Shi, Y
   Liu, S
AF Zhou, Yanling
   Peng, Xintong
   Fang, Cheng
   Peng, Xin
   Tang, Jianing
   Wang, Zuli
   Long, Yao
   Chen, Jielin
   Peng, Yuanhao
   Zhang, Zewen
   Zhou, Yanmin
   Tang, Jun
   Liao, Jingzhong
   Xiao, Desheng
   Tao, Yongguang
   Shi, Ying
   Liu, Shuang
TI Histones Methyltransferase NSD3 Inhibits Lung Adenocarcinoma Glycolysis
   Through Interacting with PPP1CB to Decrease STAT3 Signaling Pathway
SO ADVANCED SCIENCE
LA English
DT Article
DE glycolysis; histones methyltransferase; lung adenocarcinoma; STAT3
   signaling pathway
ID PROMOTES AEROBIC GLYCOLYSIS; COLORECTAL-CANCER; EXPRESSION;
   TUMORIGENESIS; CARCINOMA; THERAPY; BINDING; GENE; HK2
AB Histones methyltransferase NSD3 targeting H3K36 is frequently disordered and mutant in various cancers, while the function of NSD3 during cancer initiation and progression remains unclear. In this study, it is proved that downregulated level of NSD3 is linked to clinical features and poor survival in lung adenocarcinoma. In vivo, NSD3 inhibited the proliferation, immigration, and invasion ability of lung adenocarcinoma. Meanwhile, NSD3 suppressed glycolysis by inhibiting HK2 translation, transcription, glucose uptake, and lactate production in lung adenocarcinoma. Mechanistically, as an intermediary, NSD3 binds to PPP1CB and p-STAT3 in protein levels, thus forming a trimer to dephosphorylate the level of p-STAT3 by PPP1CB, leading to the suppression of HK2 transcription. Interestingly, the phosphorylation function of PPP1CB is related to the concentration of carbon dioxide and pH value in the culture environment. Together, this study revealed the critical non-epigenetic role of NSD3 in the regulation of STAT3-dependent glycolysis, providing a piece of compelling evidence for targeting the NSD3/PPP1CB/p-STAT3 in lung adenocarcinoma.
   This research clarifies the crucial role of NSD3 in lung adenocarcinoma that is correlated with NSD3/PPP1CB/p-STAT3 dimer formation, revealing the correlation between non-epigenetic functions of NSD3 and tumor cell metabolism, suggesting the potential of NSD3 in targeted therapy in lung adenocarcinoma. image
C1 [Zhou, Yanling; Zhou, Yanmin; Liu, Shuang] Cent South Univ, Natl Clin Res Ctr Geriatr Disorders, Inst Med Sci, Dept Oncol,Inst Med Sci,Xiangya Hosp, Changsha 410008, Hunan, Peoples R China.
   [Zhou, Yanling] Cent South Univ, Xiangya Hosp, Dept Hematol, Changsha 410008, Hunan, Peoples R China.
   [Peng, Xintong; Long, Yao; Peng, Yuanhao; Zhang, Zewen; Tang, Jun; Tao, Yongguang; Shi, Ying; Liu, Shuang] Cent South Univ, Xiangya Hosp, Key Lab Carcinogenesis & Canc Invas, Minist Educ,Dept Pathol, Changsha 410008, Hunan, Peoples R China.
   [Peng, Xintong; Long, Yao; Peng, Yuanhao; Zhang, Zewen; Tang, Jun; Tao, Yongguang; Shi, Ying] Cent South Univ, Canc Res Inst, Sch Basic Med, Changsha 410028, Hunan, Peoples R China.
   [Fang, Cheng] Cent South Univ, Xiangya Hosp, Dept Cardiac Surg, Changsha 410008, Hunan, Peoples R China.
   [Peng, Xin; Chen, Jielin; Xiao, Desheng; Liu, Shuang] Cent South Univ, Xiangya Hosp, Dept Pathol, Changsha 410008, Hunan, Peoples R China.
   [Tang, Jianing] Cent South Univ, Xiangya Hosp, Dept Liver Surg, Changsha 410008, Hunan, Peoples R China.
   [Wang, Zuli] Guizhou Med Univ, Ctr Tissue Engn & Stem Cell Res, Guiyang 561113, Guizhou, Peoples R China.
   [Liao, Jingzhong] Cent South Univ, Xiangya Hosp, Dept Lab Med, Changsha 410008, Hunan, Peoples R China.
C3 Central South University; Central South University; Central South
   University; Central South University; Central South University; Central
   South University; Central South University; Guizhou Medical University;
   Central South University
RP Liu, S (corresponding author), Cent South Univ, Natl Clin Res Ctr Geriatr Disorders, Inst Med Sci, Dept Oncol,Inst Med Sci,Xiangya Hosp, Changsha 410008, Hunan, Peoples R China.; Shi, Y; Liu, S (corresponding author), Cent South Univ, Xiangya Hosp, Key Lab Carcinogenesis & Canc Invas, Minist Educ,Dept Pathol, Changsha 410008, Hunan, Peoples R China.; Shi, Y (corresponding author), Cent South Univ, Canc Res Inst, Sch Basic Med, Changsha 410028, Hunan, Peoples R China.; Liu, S (corresponding author), Cent South Univ, Xiangya Hosp, Dept Pathol, Changsha 410008, Hunan, Peoples R China.
EM yingshi@csu.edu.cn; shuangliu2016@csu.edu.cn
RI Zhang, Zewen/AAX-4336-2020; Chen, Songlin/HTL-7344-2023
FU Natural Science Foundation of Hunan Province [2024JJ6683, 2021JJ30907,
   2024JJ3048]; National Natural Science Foundation of China [82372598,
   81872285, 82072594, 82073097, 81874139, 82073136, 81772927, 82203160]
FX This work was supported by the Natural Science Foundation of Hunan
   Province (No. 2024JJ6683, 2021JJ30907, 2024JJ3048) and by the National
   Natural Science Foundation of China (No. 82372598, 81872285, 82072594,
   82073097, 81874139, 82073136, 81772927, 82203160).
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NR 58
TC 0
Z9 0
U1 7
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2198-3844
J9 ADV SCI
JI Adv. Sci.
PD OCT
PY 2024
VL 11
IS 38
DI 10.1002/advs.202400381
EA AUG 2024
PG 15
WC Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials
   Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA J4B6U
UT WOS:001286630200001
PM 39119928
OA gold
DA 2025-01-04
ER

PT J
AU Wang, M
   Yu, F
   Li, PF
AF Wang, Man
   Yu, Fei
   Li, Peifeng
TI Intratumor microbiota in cancer pathogenesis and immunity: from
   mechanisms of action to therapeutic opportunities
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE tumor microenvironment; intratumoral microbiota; cancer pathogenesis;
   tumor immunity; cancer metabolism; microbiota-targeted therapy
ID COLORECTAL-CANCER; TUMOR MICROBIOME; PROMOTES; CELLS; IMMUNOTHERAPY;
   ONCOGENESIS; RESISTANCE; EXPRESSION; GROWTH
AB Microbial species that dwell human bodies have profound effects on overall health and multiple pathological conditions. The tumor microenvironment (TME) is characterized by disordered vasculature, hypoxia, excessive nutrition and immunosuppression. Thus, it is a favorable niche for microbial survival and growth. Multiple lines of evidence support the existence of microorganisms within diverse types of cancers. Like gut microbiota, intratumoral microbes have been tightly associated with cancer pathogenesis. Intratumoral microbiota can affect cancer development through various mechanisms, including induction of host genetic mutation, remodeling of the immune landscape and regulation of cancer metabolism and oncogenic pathways. Tumor-associated microbes modulate the efficacy of anticancer therapies, suggesting their potential utility as novel targets for future intervention. In addition, a growing body of evidence has manifested the diagnostic, prognostic, and therapeutic potential of intratumoral microorganisms in cancer. Nevertheless, our knowledge of the diversity and biological function of intratumoral microbiota is still incomplete. A deeper appreciation of tumor microbiome will be crucial to delineate the key pathological mechanisms underlying cancer progression and hasten the development of personalized treatment approaches. Herein, we summarize the most recent progress of the research into the emerging roles of intratumoral microbiota in cancer and towards clarifying the sophisticated mechanisms involved. Moreover, we discuss the effect of intratumoral microbiota on cancer treatment response and highlight its potential clinical implications in cancer.
C1 [Wang, Man; Yu, Fei; Li, Peifeng] Qingdao Univ, Affiliated Hosp, Inst Translat Med, Coll Med, Qingdao, Peoples R China.
C3 Qingdao University
RP Wang, M; Li, PF (corresponding author), Qingdao Univ, Affiliated Hosp, Inst Translat Med, Coll Med, Qingdao, Peoples R China.
EM wangman@qdu.edu.cn; peifli@qdu.edu.cn
RI Li, Peifeng/E-9421-2015; Yu, Fei/AAA-4487-2020; wang,
   manning/AAH-8148-2019
FU The authors declare financial support was received for the research,
   authorship, and/or publication of this article. This work was supported
   by the grant from the Natural Science Foundation of Shandong Province,
   China (No. ZR2021MH018). [ZR2021MH018]; Natural Science Foundation of
   Shandong Province, China
FX The authors declare financial support was received for the research,
   authorship, and/or publication of this article. This work was supported
   by the grant from the Natural Science Foundation of Shandong Province,
   China (No. ZR2021MH018).
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NR 122
TC 15
Z9 15
U1 6
U2 24
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD OCT 6
PY 2023
VL 14
AR 1269054
DI 10.3389/fimmu.2023.1269054
PG 25
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA U6OI3
UT WOS:001085972600001
PM 37868956
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Touma, J
   Pantalone, MR
   Rahbar, A
   Liu, Y
   Vetvik, K
   Sauer, T
   Söderberg-Naucler, C
   Geisler, J
AF Touma, Joel
   Pantalone, Mattia Russel
   Rahbar, Afsar
   Liu, Yan
   Vetvik, Katja
   Sauer, Torill
   Soderberg-Naucler, Cecilia
   Geisler, Juergen
TI Human Cytomegalovirus Protein Expression Is Correlated with Shorter
   Overall Survival in Breast Cancer Patients: A Cohort Study
SO VIRUSES-BASEL
LA English
DT Article
DE breast cancer; human cytomegalovirus; HCMV; prognosis; overall survival
ID COLORECTAL-CANCER; HIGH PREVALENCE; OVARIAN-CANCER; GLIOBLASTOMA;
   REACTIVATION; MECHANISMS; INFECTION; DISEASE; CELLS
AB Background: Human cytomegalovirus (HCMV) is increasingly suggested to be involved in human carcinogenesis and onco-modulation due to its ability to contribute to all hallmarks of cancer. Growing evidence demonstrates a link between HCMV infection and various malignancies, including breast cancer, which incidence and mortality are still on the rise. The etiology of breast cancer remains mostly unclear, leaving 80% of breast cancer cases considered to be sporadic. Identifying novel risk- and prognostic factors for improved breast cancer treatment and increased survival rates, were the objectives of this study. Methods: Automated immunohistochemical staining results for HCMV proteins in 109 breast tumors and lymph node metastasis were correlated with clinical follow-up data (>10 years). Statistical analyses for median Overall Survival (OS) were performed. Results: Survival analyses revealed shorter median OS for patients with HCMV-IE positive tumors of 118.4 months compared to 202.4 months for HCMV-IE negative tumors. A higher number of HCMV-LA positive cells in the tumors was also associated with a shorter OS in patients (146.2 months vs. 151.5 months). Conclusions: Our findings suggest a link between HCMV-infections and breast cancer prognosis, which paves the way for potential novel clinical intervention and targeted therapy that may prolong the overall survival of selected patients with breast cancer.
C1 [Touma, Joel; Vetvik, Katja; Sauer, Torill; Geisler, Juergen] Univ Oslo, Campus Akershus Univ Hosp AHUS, Inst Clin Med, N-1478 Nordbyhagen, Norway.
   [Touma, Joel; Geisler, Juergen] Akershus Univ Hosp AHUS, Dept Oncol, N-1478 Nordbyhagen, Norway.
   [Pantalone, Mattia Russel; Rahbar, Afsar; Soderberg-Naucler, Cecilia] Karolinska Inst, Dept Med, Microbial Pathogenesis Unit, S-17164 Solna, Sweden.
   [Pantalone, Mattia Russel; Rahbar, Afsar; Soderberg-Naucler, Cecilia] Karolinska Univ Hosp, Dept Neurol, S-17177 Stockholm, Sweden.
   [Liu, Yan] Univ Oslo, Dept Clin Mol Biol, N-0315 Oslo, Norway.
   [Liu, Yan] Akershus Univ Hosp AHUS, Dept Clin Mol Biol EpiGen, N-1478 Nordbyhagen, Norway.
   [Vetvik, Katja] Akershus Univ Hosp AHUS, Dept Breast & Endocrine Surg, N-1478 Nordbyhagen, Norway.
   [Sauer, Torill] Akershus Univ Hosp AHUS, Dept Pathol, N-1478 Nordbyhagen, Norway.
   [Soderberg-Naucler, Cecilia] Turku Univ, Inst Biomed, Unit Infect & Immunol, MedCity Res Lab, Turku 20520, Finland.
C3 University of Oslo; Karolinska Institutet; Karolinska Institutet;
   Karolinska University Hospital; University of Oslo; University of Turku
RP Geisler, J (corresponding author), Univ Oslo, Campus Akershus Univ Hosp AHUS, Inst Clin Med, N-1478 Nordbyhagen, Norway.; Geisler, J (corresponding author), Akershus Univ Hosp AHUS, Dept Oncol, N-1478 Nordbyhagen, Norway.; Söderberg-Naucler, C (corresponding author), Karolinska Inst, Dept Med, Microbial Pathogenesis Unit, S-17164 Solna, Sweden.; Söderberg-Naucler, C (corresponding author), Karolinska Univ Hosp, Dept Neurol, S-17177 Stockholm, Sweden.; Söderberg-Naucler, C (corresponding author), Turku Univ, Inst Biomed, Unit Infect & Immunol, MedCity Res Lab, Turku 20520, Finland.
EM juergen.geisler@medisin.uio.no
RI Naucler, Cecilia/LGZ-9780-2024; Pantalone, Mattia/ABC-3147-2020; Bartek,
   Jiri/G-5870-2014; Geisler, Jurgen/AAI-4613-2020; Sauer,
   Torill/H-7041-2019
OI Pantalone, Mattia Russel/0000-0002-2706-4683; Soderberg-Naucler,
   Cecilia/0000-0001-8955-3610; Sauer, Torill/0000-0002-8305-3639; Geisler,
   Jurgen/0000-0001-6239-3856; Vetvik, Katja/0000-0003-2454-5585
FU South-Eastern Norway Regional Health Authority (HSO) [2016046]; Bodil
   and Magnes Cancer Research Fund (Oslo, Norway)
FX This research was funded by the South-Eastern Norway Regional Health
   Authority (HSO), project no. 2016046 (Ph.D.-project for J.T.). Generous
   funding by Bodil and Magnes Cancer Research Fund (Oslo, Norway) is
   highly appreciated.
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NR 71
TC 7
Z9 7
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1999-4915
J9 VIRUSES-BASEL
JI Viruses-Basel
PD MAR
PY 2023
VL 15
IS 3
AR 732
DI 10.3390/v15030732
PG 13
WC Virology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Virology
GA C1RC4
UT WOS:000959763500001
PM 36992442
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Balasubramanian, S
   Priyathersini, N
   Johnson, T
AF Balasubramanian, Subalakshmi
   Priyathersini, Nagarajan
   Johnson, Thanka
TI Expression of Vascular Endothelial Growth Factor (VEGF) in Colorectal
   Adenoma and Carcinoma in a Tertiary Care Center
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Article
DE colorectal cancer; adenocarcinoma; adenoma; vegf; angiogenesis
ID ANGIOGENIC SWITCH; CANCER; METASTASIS
AB Introduction: Colorectal cancer is one of the malignancies in which angiogenesis has been implicated and its importance at different stages of malignant disease. Neovascularization begins when the angiogenic switch is turned on and when angiogenesis activators outweigh angiogenic inhibitors. The process of blood vessel formation is regulated through several growth factor systems. The vascular endothelial growth factor (VEGF) system is one of the important ones and may consequently be a key system in relation to different aspects of colorectal carcinoma treatment. Because of the well-defined steps in its progression (adenoma -Tis -T1 invasive cancer-T2 advanced cancer with metastases), colorectal cancer (CRC) represents a model for investigating the effects of angiogenesis throughout tumor development. The aim of this study is to determine the role of VEGF expression by immunohistochemistry (IHC) in normal epithelium, dysplasia, carcinoma of colorectal specimens and to correlate the same with tumor grade, stage, nodal status, and metastasis. Methods: This is a retrospective study on paraffin blocks of 50 colon cancer specimens, 40 adenoma specimens, and 10 normal colonic mucosa specimens. Immunohistochemical stain for VEGF was done on the sections along with controls. Monoclonal antibody detected against VEGF antigen was observed in the cytoplasm of the tumor cells and the intensity of VEGF expression in individual tumor cells was scored on a scale of 0 (no staining) to 3 (strong intensity), and the percentage of cells with VEGF staining at each intensity was estimated from 0 to 100. Pearson's Chi-squared test and Mann-Whitney test were used to determine significant clinicopathological differences between VEGF expression in positive and negative tumors. Results: In normal epithelium, VEGF immunoreactivity was seen in all 10 cases with high intensity. Among adenomas, VEGF expression was seen in 26 (65%) of the 40 cases. Out of which in tubular adenomas VEGF expression was seen in 13 cases (60%) and negative in eight cases (40%). In tubulo villous adenoma, VEGF expression was seen in nine cases (60%) and negative in six cases (40%). Villous adenomas showed VEGF expression in all four cases (100%). In adenocarcinoma, VEGF expression was seen to be expressed in 42 cases (84%) and negative in eight cases (16%) and expression was higher in low-grade carcinomas (70%) compared to high-grade carcinomas. A significant difference in the expression of VEGF among adenomas and carcinomas was observed with higher intensity present in adenoma when compared to carcinoma. Conclusion: Expression of VEGF could be considered as an early carcinogenic factor in colorectal carcinomas as it is expressed in higher intensity in the precancerous lesion and low-grade and stage 1 adenocarcinoma. Hence, we infer that early colorectal carcinomas are an important model for targeted therapy with antiangiogenic factors for VEGF.
C1 [Balasubramanian, Subalakshmi; Priyathersini, Nagarajan] Sri Ramachandra Inst Higher Educ & Res, Pathol, Chennai, Tamil Nadu, India.
   [Johnson, Thanka] Sree Balaji Med Coll & Hosp, Pathol, Chennai, Tamil Nadu, India.
C3 Sri Ramachandra Institute of Higher Education & Research; Bharath
   Institute of Higher Education & Research; Sree Balaji Medical College &
   Hospital
RP Priyathersini, N (corresponding author), Sri Ramachandra Inst Higher Educ & Res, Pathol, Chennai, Tamil Nadu, India.
EM nagarajan.priyathersini@gmail.com
RI Johnson, Thanka/AAZ-6336-2021
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NR 21
TC 3
Z9 3
U1 0
U2 2
PU CUREUS INC
PI PALO ALTO
PA PO BOX 61002, PALO ALTO, CA 94306 USA
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD NOV 11
PY 2022
VL 14
IS 11
AR e31393
DI 10.7759/cureus.31393
PG 12
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA 8I6UL
UT WOS:000921867000038
PM 36514651
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Jahangiri, L
   Ishola, T
   Pucci, P
   Trigg, RM
   Pereira, J
   Williams, JA
   Cavanagh, ML
   Gkoutos, GV
   Tsaprouni, L
   Turner, SD
AF Jahangiri, Leila
   Ishola, Tala
   Pucci, Perla
   Trigg, Ricky M.
   Pereira, Joao
   Williams, John A.
   Cavanagh, Megan L.
   Gkoutos, Georgios V.
   Tsaprouni, Loukia
   Turner, Suzanne D.
TI The Role of Autophagy and lncRNAs in the Maintenance of Cancer Stem
   Cells
SO CANCERS
LA English
DT Review
DE cancer stem cells (CSCs); tumour microenvironment; solid cancers;
   haematological malignancies; autophagy; LncRNAs
ID LONG NONCODING RNA; ACUTE MYELOID-LEUKEMIA; SIDE POPULATION CELLS;
   PANCREATIC-CANCER; COLORECTAL-CANCER; INITIATING CELLS; HYPOXIC STRESS;
   SELF-RENEWAL; OF-ORIGIN; C-MYC
AB Simple Summary
   Cancer stem cells (CSCs) represent a distinct cancer subpopulation that can influence the tumour microenvironment, in addition to cancer progression and relapse. A multitude of factors including CSC properties, long noncoding RNAs (lncRNAs), and autophagy play pivotal roles in maintaining CSCs. We discuss the methods of detection of CSCs and how our knowledge of regulatory and cellular processes, and their interaction with the microenvironment, may lead to more effective targeting of these cells. Autophagy and lncRNAs can regulate several cellular functions, thereby promoting stemness factors and CSC properties, hence understanding this triangle and its associated signalling networks can lead to enhanced therapy response, while paving the way for the development of novel therapeutic approaches.
   Cancer stem cells (CSCs) possess properties such as self-renewal, resistance to apoptotic cues, quiescence, and DNA-damage repair capacity. Moreover, CSCs strongly influence the tumour microenvironment (TME) and may account for cancer progression, recurrence, and relapse. CSCs represent a distinct subpopulation in tumours and the detection, characterisation, and understanding of the regulatory landscape and cellular processes that govern their maintenance may pave the way to improving prognosis, selective targeted therapy, and therapy outcomes. In this review, we have discussed the characteristics of CSCs identified in various cancer types and the role of autophagy and long noncoding RNAs (lncRNAs) in maintaining the homeostasis of CSCs. Further, we have discussed methods to detect CSCs and strategies for treatment and relapse, taking into account the requirement to inhibit CSC growth and survival within the complex backdrop of cellular processes, microenvironmental interactions, and regulatory networks associated with cancer. Finally, we critique the computationally reinforced triangle of factors inclusive of CSC properties, the process of autophagy, and lncRNA and their associated networks with respect to hypoxia, epithelial-to-mesenchymal transition (EMT), and signalling pathways.
C1 [Jahangiri, Leila; Ishola, Tala; Cavanagh, Megan L.; Tsaprouni, Loukia] Birmingham City Univ, Dept Life Sci, Birmingham B15 3TN, W Midlands, England.
   [Jahangiri, Leila; Pucci, Perla; Trigg, Ricky M.; Turner, Suzanne D.] Univ Cambridge, Dept Pathol, Div Cellular & Mol Pathol, Cambridge CB2 0QQ, England.
   [Trigg, Ricky M.] GlaxoSmithKline, Dept Funct Genom, Stevenage SG1 2NY, Herts, England.
   [Pereira, Joao] Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
   [Williams, John A.; Gkoutos, Georgios V.] Univ Hosp Birmingham NHS Fdn Trust, Inst Translat Med, Birmingham B15 2TH, W Midlands, England.
   [Williams, John A.; Gkoutos, Georgios V.] Univ Birmingham, Coll Med & Dent Sci, Inst Canc & Genom Sci, Birmingham B15 2SY, W Midlands, England.
   [Gkoutos, Georgios V.] Med Res Council Harwell Inst, Mammalian Genet Unit, Didcot OX11 0RD, Oxon, England.
   [Gkoutos, Georgios V.] Univ Birmingham, MRC Hlth Data Res Midlands, Birmingham B15 2TT, W Midlands, England.
   [Gkoutos, Georgios V.] NIHR Expt Canc Med Ctr, Birmingham B15 2TT, W Midlands, England.
   [Gkoutos, Georgios V.] NIHR Surg Reconstruct & Microbiol Res Ctr, Birmingham B15 2TT, W Midlands, England.
   [Gkoutos, Georgios V.] NIHR Biomed Res Ctr, Birmingham B15 2TT, W Midlands, England.
   [Turner, Suzanne D.] Masaryk Univ, Cent European Inst Technol CEITEC, Brno 62500, Czech Republic.
C3 Birmingham City University; University of Cambridge; GlaxoSmithKline;
   Harvard University; Harvard Medical School; Massachusetts General
   Hospital; University of Birmingham; University of Birmingham; University
   of Birmingham; Masaryk University Brno
RP Jahangiri, L (corresponding author), Birmingham City Univ, Dept Life Sci, Birmingham B15 3TN, W Midlands, England.; Jahangiri, L (corresponding author), Univ Cambridge, Dept Pathol, Div Cellular & Mol Pathol, Cambridge CB2 0QQ, England.; Gkoutos, GV (corresponding author), Univ Hosp Birmingham NHS Fdn Trust, Inst Translat Med, Birmingham B15 2TH, W Midlands, England.; Gkoutos, GV (corresponding author), Univ Birmingham, Coll Med & Dent Sci, Inst Canc & Genom Sci, Birmingham B15 2SY, W Midlands, England.; Gkoutos, GV (corresponding author), Med Res Council Harwell Inst, Mammalian Genet Unit, Didcot OX11 0RD, Oxon, England.; Gkoutos, GV (corresponding author), Univ Birmingham, MRC Hlth Data Res Midlands, Birmingham B15 2TT, W Midlands, England.; Gkoutos, GV (corresponding author), NIHR Expt Canc Med Ctr, Birmingham B15 2TT, W Midlands, England.; Gkoutos, GV (corresponding author), NIHR Surg Reconstruct & Microbiol Res Ctr, Birmingham B15 2TT, W Midlands, England.; Gkoutos, GV (corresponding author), NIHR Biomed Res Ctr, Birmingham B15 2TT, W Midlands, England.
EM leila.jahangiri@bcu.ac.uk; tala.ishola@bcu.ac.uk; pp504@cam.ac.uk;
   ricky.m.trigg@gsk.com; jtavaresdasilvapereira@mgh.harvard.edu;
   megan.cavanagh@mail.bcu.ac.uk; g.gkoutos@bham.ac.uk;
   loukia.tsaprouni@bcu.ac.uk; sdt36@cam.ac.uk
RI Gkoutos, Georgios/AAS-9936-2020; Jahangiri, Leila/AAA-9786-2022; da
   Silva Pereira, Joao/D-8298-2013; Pucci, Perla/AAJ-3806-2021; Williams,
   John/AAI-4043-2020; Turner, Suzanne/K-4405-2013
OI Turner, Suzanne/0000-0002-8439-4507; Olley-Williams,
   Jackie/0000-0002-0357-5454; Pucci, Perla/0000-0003-1264-3487; Pereira,
   Joao/0000-0002-5587-7593; Jahangiri, Leila/0000-0003-0235-8447; Ishola,
   Dr. Tala/0000-0002-3067-0553; Gkoutos, Georgios/0000-0002-2061-091X;
   Tsaprouni, Loukia/0000-0002-4740-3099
FU NIHR Birmingham ECMC; NIHR Birmingham SRMRC; Nanocommons Horizon 2020-EU
   [731032]; NIHR Birmingham Biomedical Research Centre; MRC HDR UK
   [HDRUK/CFC/01]; UK Research and Innovation, Department of Health and
   Social Care (England)
FX G.V.G. acknowledges support from the NIHR Birmingham ECMC, NIHR
   Birmingham SRMRC, Nanocommons Horizon 2020-EU (731032), the NIHR
   Birmingham Biomedical Research Centre, and the MRC HDR UK
   (HDRUK/CFC/01), an initiative funded by UK Research and Innovation,
   Department of Health and Social Care (England) and the devolved
   administrations, and leading medical research charities. The views
   expressed in this publication are those of the authors and not
   necessarily those of the NHS, the National Institute for Health
   Research, the Medical Research Council, or the Department of Health.
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NR 198
TC 11
Z9 11
U1 0
U2 10
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD MAR
PY 2021
VL 13
IS 6
AR 1239
DI 10.3390/cancers13061239
PG 31
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RE8BN
UT WOS:000634372400001
PM 33799834
OA Green Published, Green Accepted, gold
DA 2025-01-04
ER

PT J
AU Pan, QZ
   Zhao, JJ
   Liu, L
   Zhang, DS
   Wang, LP
   Hu, WW
   Weng, DS
   Xu, X
   Li, YZ
   Tang, Y
   Zhang, WH
   Li, JY
   Zheng, X
   Wang, QJ
   Li, YQ
   Xiang, T
   Zhou, L
   Yang, SN
   Wu, C
   Huang, RX
   He, J
   Du, WJ
   Chen, LJ
   Wu, YN
   Xu, B
   Shen, Q
   Zhang, Y
   Jiang, JT
   Ren, XB
   Xia, JC
AF Pan, Qiu-Zhong
   Zhao, Jing-Jing
   Liu, Liang
   Zhang, Dong-Sheng
   Wang, Li-Ping
   Hu, Wen-Wei
   Weng, De-Sheng
   Xu, Xiang
   Li, Yi-Zhuo
   Tang, Yan
   Zhang, Wei-Hong
   Li, Jie-Yao
   Zheng, Xiao
   Wang, Qi-Jing
   Li, Yong-Qiang
   Xiang, Tong
   Zhou, Li
   Yang, Shuang-Ning
   Wu, Chen
   Huang, Rong-Xing
   He, Jia
   Du, Wei-Jiao
   Chen, Lu-Jun
   Wu, Yue-Na
   Xu, Bin
   Shen, Qiong
   Zhang, Yi
   Jiang, Jing-Ting
   Ren, Xiu-Bao
   Xia, Jian-Chuan
TI XELOX (capecitabine plus oxaliplatin) plus bevacizumab (anti-VEGF-A
   antibody) with or without adoptive cell immunotherapy in the treatment
   of patients with previously untreated metastatic colorectal cancer: a
   multicenter, open-label, randomized, controlled, phase 3 trial
SO SIGNAL TRANSDUCTION AND TARGETED THERAPY
LA English
DT Article
ID INDUCED KILLER-CELLS; 1ST-LINE TREATMENT; THERAPY; CHEMOTHERAPY;
   EFFICACY; SAFETY; CYTOTOXICITY; MECHANISM; FOLFOX; TUMORS
AB Fluoropyrimidine-based combination chemotherapy plus targeted therapy is the standard initial treatment for unresectable metastatic colorectal cancer (mCRC), but the prognosis remains poor. This phase 3 trial (ClinicalTrials.gov: NCT03950154) assessed the efficacy and adverse events (AEs) of the combination of PD-1 blockade-activated DC-CIK (PD1-T) cells with XELOX plus bevacizumab as a first-line therapy in patients with mCRC. A total of 202 participants were enrolled and randomly assigned in a 1:1 ratio to receive either first-line XELOX plus bevacizumab (the control group, n = 102) or the same regimen plus autologous PD1-T cell immunotherapy (the immunotherapy group, n = 100) every 21 days for up to 6 cycles, followed by maintenance treatment with capecitabine and bevacizumab. The main endpoint of the trial was progression-free survival (PFS). The median follow-up was 19.5 months. Median PFS was 14.8 months (95% CI, 11.6-18.0) for the immunotherapy group compared with 9.9 months (8.0-11.8) for the control group (hazard ratio [HR], 0.60 [95% CI, 0.40-0.88]; p = 0.009). Median overall survival (OS) was not reached for the immunotherapy group and 25.6 months (95% CI, 18.3-32.8) for the control group (HR, 0.57 [95% CI, 0.33-0.98]; p = 0.043). Grade 3 or higher AEs occurred in 20.0% of patients in the immunotherapy group and 23.5% in the control groups, with no toxicity-associated deaths reported. The addition of PD1-T cells to first-line XELOX plus bevacizumab demonstrates significant clinical improvement of PFS and OS with well tolerability in patients with previously untreated mCRC.
C1 [Pan, Qiu-Zhong; Zhao, Jing-Jing; Zhang, Dong-Sheng; Weng, De-Sheng; Tang, Yan; Wang, Qi-Jing; Li, Yong-Qiang; Xiang, Tong; Huang, Rong-Xing; He, Jia; Wu, Yue-Na; Xia, Jian-Chuan] Sun Yat sen Univ, Guangdong Prov Clin Res Ctr Canc, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China,Canc Ctr, Guangzhou 510060, Guangdong, Peoples R China.
   [Pan, Qiu-Zhong; Zhao, Jing-Jing; Weng, De-Sheng; Tang, Yan; Wang, Qi-Jing; Li, Yong-Qiang; Huang, Rong-Xing; He, Jia; Wu, Yue-Na; Xia, Jian-Chuan] Sun Yat Sen Univ, Ctr Canc, Dept Biotherapy, Guangzhou 510060, Guangdong, Peoples R China.
   [Liu, Liang; Zhang, Wei-Hong; Zhou, Li; Du, Wei-Jiao; Ren, Xiu-Bao] Tianjin Med Univ, Canc Inst & Hosp, Natl Clin Res Ctr Canc, Tianjin 300060, Peoples R China.
   [Liu, Liang; Zhang, Wei-Hong; Zhou, Li; Du, Wei-Jiao; Ren, Xiu-Bao] Key Lab Canc Immunol & Biotherapy, Tianjin 300060, Peoples R China.
   [Liu, Liang; Zhang, Wei-Hong; Zhou, Li; Du, Wei-Jiao; Ren, Xiu-Bao] Tianjin Med Univ, Dept Biotherapy Immunol, Canc Inst & Hosp, Tianjin 300060, Peoples R China.
   [Zhang, Dong-Sheng] Sun Yat Sen Univ, Ctr Canc, Dept Med Oncol, Guangzhou 510060, Peoples R China.
   [Wang, Li-Ping; Li, Jie-Yao; Yang, Shuang-Ning; Zhang, Yi] Zhengzhou Univ, Dept Pathol, Affiliated Hosp 1, Zhengzhou 450052, Peoples R China.
   [Hu, Wen-Wei; Zheng, Xiao; Wu, Chen; Chen, Lu-Jun; Xu, Bin; Shen, Qiong; Jiang, Jing-Ting] Soochow Univ, Affiliated Hosp 3, Dept Tumor Biol Treatment, Changzhou 213003, Jiangsu, Peoples R China.
   [Hu, Wen-Wei; Zheng, Xiao; Wu, Chen; Chen, Lu-Jun; Xu, Bin; Shen, Qiong; Jiang, Jing-Ting] Jiangsu Engn Res Ctr Tumor Immunotherapy, Changzhou 213003, Jiangsu, Peoples R China.
   [Hu, Wen-Wei; Zheng, Xiao; Wu, Chen; Chen, Lu-Jun; Xu, Bin; Shen, Qiong; Jiang, Jing-Ting] Soochow Univ, Inst Cell Therapy, Changzhou 213003, Jiangsu, Peoples R China.
   [Xu, Xiang] Army Med Univ, Daping Hosp, Dept Stem Cell & Regenerat Med, State Key Lab Trauma Burn & Combined Injury, Chongqing 400042, Peoples R China.
   [Li, Yi-Zhuo] Sun Yat Sen Univ, Ctr Canc, Imaging Diag & Intervent Ctr, Guangzhou 510060, Guangdong, Peoples R China.
C3 State Key Lab Oncology South China; Sun Yat Sen University; Sun Yat Sen
   University; Tianjin Medical University; Tianjin Medical University; Sun
   Yat Sen University; Zhengzhou University; Soochow University - China;
   Soochow University - China; Army Medical University; Sun Yat Sen
   University
RP Xia, JC (corresponding author), Sun Yat sen Univ, Guangdong Prov Clin Res Ctr Canc, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China,Canc Ctr, Guangzhou 510060, Guangdong, Peoples R China.; Xia, JC (corresponding author), Sun Yat Sen Univ, Ctr Canc, Dept Biotherapy, Guangzhou 510060, Guangdong, Peoples R China.; Ren, XB (corresponding author), Tianjin Med Univ, Canc Inst & Hosp, Natl Clin Res Ctr Canc, Tianjin 300060, Peoples R China.; Ren, XB (corresponding author), Key Lab Canc Immunol & Biotherapy, Tianjin 300060, Peoples R China.; Ren, XB (corresponding author), Tianjin Med Univ, Dept Biotherapy Immunol, Canc Inst & Hosp, Tianjin 300060, Peoples R China.; Zhang, Y (corresponding author), Zhengzhou Univ, Dept Pathol, Affiliated Hosp 1, Zhengzhou 450052, Peoples R China.; Jiang, JT (corresponding author), Soochow Univ, Affiliated Hosp 3, Dept Tumor Biol Treatment, Changzhou 213003, Jiangsu, Peoples R China.; Jiang, JT (corresponding author), Jiangsu Engn Res Ctr Tumor Immunotherapy, Changzhou 213003, Jiangsu, Peoples R China.; Jiang, JT (corresponding author), Soochow Univ, Inst Cell Therapy, Changzhou 213003, Jiangsu, Peoples R China.
EM yizhang@zzu.edu.cn; jiangjingting@suda.edu.cn; renxiubao@tjmuch.com;
   xiajch@mail.sysu.edu.cn
RI Wang, Liping/JRY-1318-2023; WANG, QIFENG/D-1094-2015; Dongsheng,
   ZHANG/AAL-6913-2020; wu, chen/LPQ-7578-2024
FU National Natural Science Foundation of China (National Science
   Foundation of China) [2018YFC1313400]; National Key R&D Program of China
   [81773110]; National Natural Science Foundation of China
FX This study was funded by the National Key R&D Program of China for J-CX
   (grant number 2018YFC1313400), the National Natural Science Foundation
   of China for J.-C.X. (grant number 81773110). We express our gratitude
   to all participating patients and their families, as well as to the
   study groups and investigators from the participating centers.
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NR 43
TC 7
Z9 7
U1 8
U2 12
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2095-9907
EI 2059-3635
J9 SIGNAL TRANSDUCT TAR
JI Signal Transduct. Target. Ther.
PD APR 3
PY 2024
VL 9
IS 1
AR 79
DI 10.1038/s41392-024-01788-2
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA MX7O3
UT WOS:001197002600001
PM 38565886
OA gold
DA 2025-01-04
ER

PT J
AU Chen, X
   Liu, B
   Zhao, ZR
   He, M
   Yu, KY
AF Chen, Xin
   Liu, Bo
   Zhao, Zengren
   He, Meng
   Yu, Kuaiyun
TI <i>HSH2D</i> Promotes the Progression and Chemoresistance of CRC by
   Regulating the<i> YAP1</i>
SO JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS
LA English
DT Article
DE HSH2D; YAP1; CRC progression; chemotherapy resistance; targeted therapy
ID CELL LUNG-CANCER; COLORECTAL-CANCER; YAP1; RESISTANCE
AB Background: Colorectal cancer (CRC) stands out as one of the most widespread and life -threatening malignancies globally. In recent years, significant attention has been directed towards the Yes -associated protein 1 (YAP1), identified as the central effector molecule in the Hippo signaling pathway, highlighting its crucial involvement in CRC development. Nevertheless, the role of hematopoietic SH2 domain -containing (HSH2D) in CRC, and its impact on tumor progression and resistance to chemotherapy by modulating YAP1, remains unclear. Therefore, this study aims to explore the role of HSH2D in CRC and assess its potential therapeutic significance. Methods: The study included the analysis of HSH2D expression levels in CRC tissues and cells by immunohistochemistry and western blot techniques. The influence of HSH2D on CRC cell proliferation and migration was examined using RNA interference and overexpression systems. The regulatory impact of HSH2D on YAP1 expression was assessed through real-time reverse transcriptase-polymerase chain reaction (RT-qPCR) and immunoblotting. In vitro cell experiments were conducted to unravel the mechanism by which HSH2D promotes CRC progression through YAP1. Lastly, the study investigated the role of HSH2D in modulating the sensitivity of CRC cells to cisplatin by chemosensitivity experiments. Results: The experimental findings demonstrated a notable elevation in HSH2D expression within both CRC tissues and cells. Overexpression of HSH2D was found to enhance the proliferation and migration capabilities of CRC cells, whereas silencing HSH2D had the opposite effect. Subsequent investigations unveiled that HSH2D upregulated YAP1 expression, and the tumorpromoting influence of HSH2D was, in part, dependent on YAP1. Furthermore, heightened HSH2D expression correlated with increased resistance of CRC cells to cisplatin. Conclusion: This study marks the initial identification of HSH2D upregulation in CRC and its role in advancing the progression and chemoresistance of CRC by modulating YAP1. HSH2D emerges as a promising novel target for CRC treatment, suggesting a potential therapeutic strategy. Future research should delve deeper into the specific interaction mechanisms between HSH2D and YAP1, aiming to effectively target this pathway for enhanced CRC treatment.
C1 [Chen, Xin; Liu, Bo; Zhao, Zengren; He, Meng] Hebei Med Univ, Hosp 1, Dept Gen Surg, Shijiazhuang 050011, Hebei, Peoples R China.
   [Yu, Kuaiyun] Yantaishan Hosp, Dept Gen Surg, Yantai 264001, Shandong, Peoples R China.
C3 Hebei Medical University
RP Yu, KY (corresponding author), Yantaishan Hosp, Dept Gen Surg, Yantai 264001, Shandong, Peoples R China.
EM 13853524166@163.com
RI Li, chunbao/KHD-9616-2024
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NR 33
TC 1
Z9 1
U1 3
U2 3
PU BIOLIFE SAS
PI SILVA MARINA (TE)
PA VIA S STEFANO 39 BIS, 64029 SILVA MARINA (TE), ITALY
SN 0393-974X
EI 1724-6083
J9 J BIOL REG HOMEOS AG
JI J. Biol. Regul. Homeost. Agents
PD MAR
PY 2024
VL 38
IS 3
BP 2307
EP 2318
DI 10.23812/j.biol.regul.homeost.agents.20243803.181
PG 12
WC Endocrinology & Metabolism; Immunology; Medicine, Research &
   Experimental; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Immunology; Research & Experimental
   Medicine; Physiology
GA KT5B9
UT WOS:001182218200001
DA 2025-01-04
ER

PT J
AU Kim, JK
   Byun, MR
   Maeng, CH
   Kim, YR
   Choi, JW
AF Kim, Jun Ki
   Byun, Mi Ran
   Maeng, Chi Hoon
   Kim, Yi Rang
   Choi, Jin Woo
TI Selective Targeting of Cancer Stem Cells (CSCs) Based on Photodynamic
   Therapy (PDT) Penetration Depth Inhibits Colon Polyp Formation in Mice
SO CANCERS
LA English
DT Article
DE cancer stem cells; green fluorescent protein; colon cancer; photodynamic
   therapy; rose bengal photosensitizers
ID ENHANCED PERMEABILITY; ADENOMATOUS POLYPOSIS; IDENTIFICATION; TUMORS;
   RETENTION; MARKER; MODEL; LUNG
AB Targeting cancer stem cells (CSCs) without damaging normal stem cells could contribute to the development of novel radical cancer therapies. Cells expressing leucine-rich repeat-containing G-protein coupled receptor 5 (Lgr5) constitute a cancer-causing population in the colon; therefore, targeting of Lgr5+ cells is expected to provide an opportunity to mitigate colon cancer. However, the expression of Lgr5 in normal stem cells makes it difficult to prove the efficacy of therapies targeted exclusively at Lgr5+ cancer cells. We used a modified photodynamic therapy technique involving cellular radiative transfer between green fluorescent protein (GFP)-expressing cells and a rose bengal photosensitizer. After treatment, tumors containing GFP-Lgr5+ cells were observed to be significantly suppressed or retarded with little effect on GFP-Lgr5+ stem cells at the crypt bottom. Lgr5+ CSCs were specifically eradicated in situ, when localized based on the depth from the colon lumen, revealing the potential preventive efficacy of Lgr5-targeted therapy on tumor growth. This study supports the idea that Lgr5+ cells localized near the colon luminal surface are central to colorectal cancer. With further development, the targeting of localized Lgr5+ cancer stem cells, which this study demonstrates in concept, may be feasible for prevention of colon cancer in high-risk populations.
C1 [Kim, Jun Ki] Asan Med Ctr, Asan Inst Life Sci, Biomed Engn Res Ctr, Seoul 05505, South Korea.
   [Kim, Jun Ki] Univ Ulsan, Dept Convergence Med, Coll Med, Seoul 05505, South Korea.
   [Byun, Mi Ran; Choi, Jin Woo] Kyung Hee Univ, Dept Pharmacol, Coll Pharm, Seoul 02447, South Korea.
   [Maeng, Chi Hoon] Kyung Hee Univ, Dept Hematooncol, Coll Med, Seoul 02447, South Korea.
   [Kim, Yi Rang] Yuseong Sun Hosp, Dept Hematooncol, Daejeon 34084, South Korea.
   [Kim, Yi Rang] Oncocross Ltd, Seoul 04168, South Korea.
C3 University of Ulsan; Kyung Hee University; Kyung Hee University
RP Choi, JW (corresponding author), Kyung Hee Univ, Dept Pharmacol, Coll Pharm, Seoul 02447, South Korea.; Kim, YR (corresponding author), Yuseong Sun Hosp, Dept Hematooncol, Daejeon 34084, South Korea.; Kim, YR (corresponding author), Oncocross Ltd, Seoul 04168, South Korea.
EM kim@amc.seoul.kr; bml1230@naver.com; mchihoon@khu.ac.kr;
   99yirang@gmail.com; jinwoo.ch@khu.ac.kr
RI Kim, Jun/W-5117-2019; Maeng, Chi/AAI-8539-2020
OI MAENG, Chi Hoon/0000-0002-4450-3350; Kim, Yi Rang/0000-0001-9864-5453;
   Kim, Jun Ki/0000-0002-0099-9681
FU Basic Science Research Program through the National Research Foundation
   of Korea (NRF) - Ministry of Science and ICT [NRF-2017R1A5A2014768,
   2016R1D1A1B03930490, 2017R1C1B5017615, 2019R1A2C2084122]; MRC grant
   through the National Research Foundation of Korea (NRF) - Ministry of
   Science and ICT [2017R1A5A2014768, 2018R1A5A2020732]; National R&D
   Program for Cancer Control through the Korea Health Industry Development
   Institute (KHIDI) - Ministry of Health & Welfare, Republic of Korea
   [HA17C0039, HI18C2391]; Korea Health Technology R&D Project through the
   Korea Health Industry Development Institute (KHIDI) - Ministry of Health
   & Welfare, Republic of Korea [HA17C0039, HI18C2391]; Ministry of Trade,
   Industry & Energy (MOTIE) under the Industrial Technology Innovation
   Program [10080726, 20000843]
FX This research was supported by the Basic Science Research Program
   (NRF-2017R1A5A2014768, 2016R1D1A1B03930490, 2017R1C1B5017615,
   2019R1A2C2084122) and an MRC grant (2017R1A5A2014768, 2018R1A5A2020732)
   through the National Research Foundation of Korea (NRF) funded by the
   Ministry of Science and ICT, and a grant from the National R&D Program
   for Cancer Control and Korea Health Technology R&D Project through the
   Korea Health Industry Development Institute (KHIDI), funded by the
   Ministry of Health & Welfare, Republic of Korea (HA17C0039, HI18C2391),
   and by the Ministry of Trade, Industry & Energy (MOTIE) under the
   Industrial Technology Innovation Program (10080726, 20000843).
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NR 42
TC 10
Z9 11
U1 0
U2 17
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JAN
PY 2020
VL 12
IS 1
AR 203
DI 10.3390/cancers12010203
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KQ3KZ
UT WOS:000516826700203
PM 31947553
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Steinhart, Z
   Pavlovic, Z
   Chandrashekhar, M
   Hart, T
   Wang, XW
   Zhang, XY
   Robitaille, M
   Browne, KR
   Jaksani, S
   Overmeer, R
   Boj, SF
   Adams, J
   Pan, J
   Clevers, H
   Sidhu, S
   Moffat, J
   Angers, S
AF Steinhart, Zachary
   Pavlovic, Zvezdan
   Chandrashekhar, Megha
   Hart, Traver
   Wang, Xiaowei
   Zhang, Xiaoyu
   Robitaille, Melanie
   Browne, Kevin R.
   Jaksani, Sridevi
   Overmeer, Rene
   Boj, Sylvia F.
   Adams, Jarrett
   Pan, James
   Clevers, Hans
   Sidhu, Sachdev
   Moffat, Jason
   Angers, Stephane
TI Genome-wide CRISPR screens reveal a Wnt-FZD5 signaling circuit as a
   druggable vulnerability of <i>RNF43</i>-mutant pancreatic tumors
SO NATURE MEDICINE
LA English
DT Article
ID MUTATIONAL LANDSCAPE; ESSENTIAL GENES; HUMAN-CELLS; WNT; CANCER; GROWTH;
   RNF43; INHIBITION; MECHANISMS; RECEPTORS
AB Forward genetic screens with CRISPR-Cas9 genome editing enable high-resolution detection of genetic vulnerabilities in cancer cells. We conducted genome-wide CRISPR-Cas9 screens in RNF43-mutant pancreatic ductal adenocarcinoma (PDAC) cells, which rely on Wnt signaling for proliferation. Through these screens, we discovered a unique requirement for a Wnt signaling circuit: engaging FZD5, one of the ten Frizzled receptors encoded in the human genome. Our results uncover an underappreciated level of context-dependent specificity at the Wnt receptor level. We further derived a panel of recombinant antibodies that reports the expression of nine FZD proteins and confirms that FZD5 functional specificity cannot be explained by protein expression patterns. Additionally, antibodies that specifically bind FZD5 and FZD8 robustly inhibited the growth of RNF43-mutant PDAC cells grown in vitro and as xenografts in vivo, providing orthogonal support for the functional specificity observed genetically. Proliferation of a patient-derived PDAC cell line harboring an RNF43 variant was also selectively inhibited by the FZD5 antibodies, further demonstrating their use as a potential targeted therapy. Tumor organoid cultures from colorectal carcinoma patients that carried RNF43 mutations were also sensitive to the FZD5 antibodies, highlighting the potential generalizability of these findings beyond PDAC. Our results show that CRIPSR-based genetic screens can be leveraged to identify and validate cell surface targets for antibody development and therapy.
C1 [Steinhart, Zachary; Robitaille, Melanie; Angers, Stephane] Univ Toronto, Leslie Dan Fac Pharm, Dept Pharmaceut Sci, Toronto, ON, Canada.
   [Pavlovic, Zvezdan; Chandrashekhar, Megha; Hart, Traver; Wang, Xiaowei; Zhang, Xiaoyu; Browne, Kevin R.; Adams, Jarrett; Pan, James; Sidhu, Sachdev; Moffat, Jason] Univ Toronto, Donnelly Ctr, Toronto, ON, Canada.
   [Chandrashekhar, Megha; Zhang, Xiaoyu; Sidhu, Sachdev; Moffat, Jason] Univ Toronto, Dept Mol Genet, Toronto, ON, Canada.
   [Wang, Xiaowei; Pan, James] Ctr Commercializat Antibodies & Biol, Toronto, ON, Canada.
   [Jaksani, Sridevi; Overmeer, Rene; Clevers, Hans] Univ Med Ctr, Hubrecht Inst Dev Biol & Stem Cell Res, Utrecht, Netherlands.
   [Jaksani, Sridevi; Overmeer, Rene; Clevers, Hans] Fdn Hubrecht Organoid Technol, Utrecht, Netherlands.
   [Moffat, Jason] Canadian Inst Adv Res, Toronto, ON, Canada.
   [Angers, Stephane] Univ Toronto, Dept Biochem, Toronto, ON, Canada.
   [Hart, Traver] Univ Texas MD Anderson Canc Ctr, Dept Bioinformat & Computat Biol, Houston, TX USA.
C3 University of Toronto; University of Toronto; University of Toronto;
   Utrecht University; Utrecht University Medical Center; Royal Netherlands
   Academy of Arts & Sciences; Hubrecht Institute (KNAW); Canadian
   Institute for Advanced Research (CIFAR); University of Toronto;
   University of Texas System; UTMD Anderson Cancer Center
RP Angers, S (corresponding author), Univ Toronto, Leslie Dan Fac Pharm, Dept Pharmaceut Sci, Toronto, ON, Canada.; Sidhu, S; Moffat, J (corresponding author), Univ Toronto, Donnelly Ctr, Toronto, ON, Canada.; Sidhu, S; Moffat, J (corresponding author), Univ Toronto, Dept Mol Genet, Toronto, ON, Canada.; Moffat, J (corresponding author), Canadian Inst Adv Res, Toronto, ON, Canada.; Angers, S (corresponding author), Univ Toronto, Dept Biochem, Toronto, ON, Canada.
EM sachdev.sidhu@utoronto.ca; j.moffat@utoronto.ca;
   stephane.angers@utoronto.ca
RI Wang, Xiaowei/R-3888-2019; xiaoyu, zhang/GQH-0475-2022; Clevers,
   Hans/F-9185-2013; Robitaille, Melanie/ABA-5861-2020; Moffat,
   Jason/AAC-1110-2020; Overmeer, René/E-5698-2011; Angers,
   Stephane/E-1432-2014
OI Moffat, Jason/0000-0002-5663-8586; Sidhu, Sachdev/0000-0001-7755-5918;
   Hart, Traver/0000-0002-1880-3341; Overmeer, Rene/0000-0002-4043-0959;
   Angers, Stephane/0000-0001-7241-9044; Adams, Jarrett
   John/0000-0002-0182-922X; Brown, Kevin/0000-0002-5514-2538; Robitaille,
   Melanie/0000-0001-9354-5162
FU Canadian Institutes for Health Research [CIHR-273548, CIHR-342551];
   Ontario Research Fund; Ontario Research Fund [19442, 30961]; Canadian
   Foundation for Innovation
FX We wish to thank members of the Angers and Moffat labs for discussions.
   We are thankful to D. Hedley (Princess Margaret Hospital, Toronto,
   Canada) and M. Tsao (Ontario Cancer Institute, Toronto, Canada) for
   providing the patient-derived xenograft cells; P. Mero (Moffat lab) for
   help with images. This work was supported from grants funded by the
   Canadian Institutes for Health Research to S.A. (CIHR-273548) and J.M.
   (CIHR-342551) and by the Ontario Research Fund to S.S. J.M. holds a
   Canada Research Chair in Functional Genomics of Cancer and S.A. holds a
   Canada Research Chair in Functional Architecture of Signal Transduction.
   Some of the equipment used in this study was supported by The 3D (Diet,
   Digestive Tract and Disease) Centre funded by the Canadian Foundation
   for Innovation and Ontario Research Fund, project numbers 19442 and
   30961.
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NR 31
TC 216
Z9 249
U1 1
U2 105
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD JAN
PY 2017
VL 23
IS 1
BP 60
EP 68
DI 10.1038/nm.4219
PG 9
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
   Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
   Medicine
GA EH3CN
UT WOS:000391646800014
PM 27869803
DA 2025-01-04
ER

PT J
AU Wang, ZY
   Li, WW
   Wei, YN
   An, L
   Su, SY
   Xi, CL
   Wang, KJ
   Hong, D
   Shi, Y
AF Wang, Zhiyu
   Li, Wenwen
   Wei, Yaning
   An, Lin
   Su, Shenyong
   Xi, Chenglin
   Wang, Kunjie
   Hong, Dan
   Shi, Yan
TI A <i>HER2</i>-mutant patient with late-stage duodenal adenocarcinoma
   benefited from anti-HER2 therapy and PD-1 inhibition: a case report
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Small bowel cancer; duodenal adenocarcinoma; trastuzumab; systemic
   therapy; case report
ID BOWEL; TRASTUZUMAB
AB Duodenal adenocarcinoma (DA) is a subtype of small bowel adenocarcinoma (SBA). Compared with gastrointestinal cancers such as colorectal cancer and gastric cancer, SBA is less common. For patients with advanced and metastatic DA, chemotherapies are usually extrapolated from colorectal cancer and gastric cancer but the therapeutic effects remain undefined. Herein, we reported a 50-year-old female patient whom was diagnosed as stage IV DA with metastasis to both lungs and retroperitoneal lymph nodes. The next generation sequencing (NGS) using a panel consisting of 168 cancer related genes revealed amplification of the HER2/ERBB2 gene which has been a well-recognized therapeutic target among various tumor types. The anti-HER2 targeted therapy trastuzumab was used in combination with XELOX (oxaliplatin and capecitabine) as the first line treatment. The patient achieved partial response (PR) and had progression-free survival (PFS) of six months. After progressive disease (PD), the patient started the second line treatment with trastuzumab and PD1 inhibitors and remained stable disease (SD) with PFS for three months. The use of trastuzumab in neoadjuvant and adjuvant settings have been reported in sporadic cases. To the best of our knowledge, it is the first report to use anti-HER2 therapy and PD-1 inhibition as systemic therapy for advanced DA patients.
C1 [Wang, Zhiyu; Li, Wenwen; Wei, Yaning; An, Lin; Su, Shenyong; Xi, Chenglin; Wang, Kunjie; Hong, Dan; Shi, Yan] Hebei Univ, Dept Med Oncol, Affiliated Hosp, Baoding 071000, Peoples R China.
C3 Hebei University
RP Wang, ZY; Shi, Y (corresponding author), Hebei Univ, Dept Med Oncol, Affiliated Hosp, Baoding 071000, Peoples R China.
EM 18931200826@189.cn; 11651735@qq.com
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TC 5
Z9 5
U1 0
U2 2
PU AME PUBL CO
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD AUG
PY 2021
VL 12
IS 4
BP 1939
EP 1943
DI 10.21037/jgo-21-311
EA JUL 2021
PG 5
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA UK2PH
UT WOS:000683732700001
PM 34532140
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zhou, JH
   Sun, HB
   Zhou, H
   Liu, Y
AF Zhou, Jiehao
   Sun, Haobo
   Zhou, Hang
   Liu, Ying
TI SPAG4 enhances mitochondrial respiration and aerobic glycolysis in
   colorectal cancer cells by activating the PI3K/Akt signaling pathway
SO JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
LA English
DT Article
DE aerobic glycolysis; colorectal cancer; mitochondrial respiration;
   PI3K/Akt signaling; SPAG4
ID GLUCOSE-METABOLISM; TARGETED THERAPY; ANTIGEN 4; PROMOTES; GROWTH;
   5-FLUOROURACIL; RESISTANCE; PROGRESS; PROTEIN
AB Aerobic glycolysis plays a pivotal role in the progression of tumors. Previously, a glycolysis-associated prognostic model in CRC was constructed and the glycolysis-related gene SPAG4 was discovered to be upregulated in CRC and was correlated with adverse prognosis. To date, however, no study has elucidated the specific role of SPAG4 in the development of CRC. In our study, CRC cells were transfected with si-SPAG4 or OE-SPAG4 to evaluate the influence of SPAG4 silencing or overexpression on CRC cell malignant behaviors. CRC cell proliferation and metastasis were detected via CCK-8, colony formation, and Transwell assays. The oxygen consumption rate and extracellular acidification rate of CRC cells were determined by using an XF24 extracellular flux analyzer. The expression of SPAG4, key mitochondrial markers (NDUFA1, SDHB, ATP5A, and PGC-1 alpha), key enzymes involved in glycolysis (GLUT1, HK2, LDHA, PKM2, and PFK1), and PI3K/Akt pathway-molecules and downstream transcription factor HIF-1 alpha was assessed by RT-qPCR and western blot analysis. SPAG4 expression in CRC and normal tissue samples was tested through immunohistochemical staining. Finally, SPAG4-overexpressed CRC cells were treated with LY294002 to validate the inhibition of PI3K/Akt pathway on CRC cell malignant phenotypes. Our results showed that SPAG4 was upregulated in CRC cells and tissues, and high expression SPAG4 predicted shorter overall survival time. SPAG4 knockdown inhibited while SPAG4 overexpression enhanced CRC cell proliferation, migration, invasion, mitochondrial respiration, and aerobic glycolysis. Overexpressing SPAG4 elevated p-PI3K, p-Akt, p-mTOR, and HIF-1 alpha protein levels, which were restored after LY294002 treatment. Furthermore, LY294002 abolished the promotion of SPAG4 overexpression on CRC malignant phenotypes. Collectively, SPAG4 plays an oncogenic role in CRC by promoting mitochondrial respiration and aerobic glycolysis through activating the PI3K/Akt signaling. These findings suggest that inhibition of SPAG4-mediated glucose metabolism may represent a potential strategy for the clinical treatment of CRC.
C1 [Zhou, Jiehao; Sun, Haobo; Zhou, Hang; Liu, Ying] Heilongjiang Univ Chinese Med, Dept Digest Diag & Treatment, Affiliated Hosp 1, Harbin, Heilongjiang, Peoples R China.
C3 Heilongjiang University of Chinese Medicine
RP Liu, Y (corresponding author), Heilongjiang Univ Chinese Med, Affiliated Hosp 1, 26 Heping Rd, Harbin, Heilongjiang, Peoples R China.
EM liiuyying@hotmail.com
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NR 58
TC 0
Z9 0
U1 2
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1095-6670
EI 1099-0461
J9 J BIOCHEM MOL TOXIC
JI J. Biochem. Mol. Toxicol.
PD NOV
PY 2024
VL 38
IS 11
AR e70009
DI 10.1002/jbt.70009
PG 15
WC Biochemistry & Molecular Biology; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Toxicology
GA J3B7Q
UT WOS:001335857800001
PM 39410830
DA 2025-01-04
ER

PT J
AU Comunanza, V
   Bussolino, F
AF Comunanza, Valentina
   Bussolino, Federico
TI Therapy for Cancer: Strategy of Combining Anti-Angiogenic and Target
   Therapies
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE cancer; VEGF; angiogenesis; target therapy; resistance
ID ENDOTHELIAL GROWTH-FACTOR; METASTATIC COLORECTAL-CANCER; CELL
   LUNG-CANCER; VESSEL CO-OPTION; SYNERGISTIC ANTITUMOR-ACTIVITY;
   BEVACIZUMAB PLUS IRINOTECAN; BREAST-CANCER; PHASE-III; FACTOR RECEPTOR;
   ANTIANGIOGENIC THERAPY
AB The concept that blood supply is required and necessary for cancer growth and spreading is intuitive and was firstly formalized by Judah Folkman in 1971, when he demonstrated that cancer cells release molecules able to promote the proliferation of endothelial cells and the formation of new vessels. This seminal result has initiated one of the most fascinating story of the medicine, which is offering a window of opportunity for cancer treatment based on the use of molecules inhibiting tumor angiogenesis and in particular vascular-endothelial growth factor (VEGF), which is the master gene in vasculature formation and is the commonest target of anti-angiogenic regimens. However, the clinical results are far from the remarkable successes obtained in pre-clinical models. The reasons of this discrepancy have been partially understood and well addressed in many reviews (Bergers and Hanahan, 2008; Bottsford-Miller et al., 2012; El-Kenawi and El-Remessy, 2013; Wang et al., 2015; Jayson et al., 2016). At present anti-angiogenic regimens are not used as single treatments but associated with standard chemotherapies. Based on emerging knowledge of the biology of VEGF, here we sustain the hypothesis of the efficacy of a dual approach based on targeting pro-angiogenic pathways and other druggable targets such as mutated oncogenes or the immune system.
C1 [Comunanza, Valentina; Bussolino, Federico] Univ Torino, Dept Oncol, Candiolo, Italy.
   [Comunanza, Valentina; Bussolino, Federico] IRCCS, Candiolo Canc Inst FPO, Candiolo, Italy.
C3 University of Turin; IRCCS Fondazione del Piemonte per l'Oncologia
RP Bussolino, F (corresponding author), Univ Torino, Dept Oncol, Candiolo, Italy.; Bussolino, F (corresponding author), IRCCS, Candiolo Canc Inst FPO, Candiolo, Italy.
EM federico.bussolino@unito.it
RI Bussolino, Federico/AES-3951-2022; Comunanza, Valentina/JBJ-2122-2023;
   Bussolino, Federico/K-2500-2016; Comunanza, Valentina/I-8645-2018
OI Bussolino, Federico/0000-0002-5348-1341; Comunanza,
   Valentina/0000-0002-0695-6420
FU Associazione Italiana per la Ricerca sul Cancro (AIRC) [18652, 12182];
   Fondo investimenti per la Ricerca di Base [RBAP11BYNP]; Fondazione Cassa
   di Risparmio di Torino; University of Torino-Compagnia di San Paolo
FX This work was supported by Associazione Italiana per la Ricerca sul
   Cancro (AIRC) investigator grants IG (18652) and AIRC 5 X 1000 (12182);
   Fondo investimenti per la Ricerca di Base (codes: RBAP11BYNP),
   Fondazione Cassa di Risparmio di Torino and University of
   Torino-Compagnia di San Paolo.
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NR 213
TC 65
Z9 70
U1 0
U2 13
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-634X
J9 FRONT CELL DEV BIOL
JI Front. Cell. Dev. Biol.
PY 2017
VL 5
AR 101
DI 10.3389/fcell.2017.00101
PG 18
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA VH8AQ
UT WOS:000455238900100
PM 29270405
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Priyamvada, P
   Ramaiah, S
AF Priyamvada, P.
   Ramaiah, Sudha
TI Potential Signature Therapeutic Biomarkers TOP2A, MAD2L1, and CDK1 in
   Colorectal Cancer: A Systems Biomedicine-Based Approach
SO BIOCHEMICAL GENETICS
LA English
DT Article
DE PPI network; Differentially expressed genes; Transcription factors;
   Survival analysis; Kinases; miRNAs
ID CYCLIN B1; EXPRESSION; OVEREXPRESSION; PROGRESSION; CARCINOMA; SURVIVAL;
   CELLS
AB Colorectal cancer is the third deadliest and fourth most diagnosed cancer. It is heterogeneously driven by varied mutations and mutagens, and thus, it is challenging for targeted therapy. The rapid advancement of high-throughput technology presents considerable opportunities for discovering new colon cancer biomarkers. In the present study, we have explored and identified the biomarkers based on molecular interactions. We curated cancer datasets that were not micro-dissected and performed gene expression analysis. The protein-protein interactions were curated, and a network was constructed for the up-regulated genes. The hub genes were analyzed using 12 different topological parameters. The correlation analysis selected TOP2A, CDK1, CCNB1, AURKA, and MAD2L1 as hub genes. Further, survival analysis was performed to determine the effectiveness of the hub gene on the patient's survival rate. Our findings explore various transcription factors such as E2F4, FOXM1, E2F6, MAX, and SIN3A, along with kinases CSNK2A1, MAPK14, CDK1, CDK4, and CDK2, as potential molecular signatures and aid researchers in understanding the pathophysiological mechanisms underlying CRC development and thus providing novel therapeutic and diagnostic recourse. Furthermore, investigating miRNAs, we focused on hsa-miR-215-5p, hsa-miR-192-5p, and hsa-miR-193b-3p due to their observed impact on a diverse set of colorectal cancer genes. Thereby, the current approach brings into light CRC- related genes at the RNA and protein levels that can potentially act as novel biomarkers opening doors to diagnostic and treatment purposes.
C1 [Priyamvada, P.; Ramaiah, Sudha] Vellore Inst Technol VIT, Sch Biosci & Technol, Med & Biol Comp Lab, Vellore 632014, Tamil Nadu, India.
   [Priyamvada, P.; Ramaiah, Sudha] Vellore Inst Technol VIT, Sch Bio Sci & Technol, Dept Biosci, Vellore 632014, Tamil Nadu, India.
C3 Vellore Institute of Technology (VIT); VIT Vellore; Vellore Institute of
   Technology (VIT); VIT Vellore
RP Ramaiah, S (corresponding author), Vellore Inst Technol VIT, Sch Biosci & Technol, Med & Biol Comp Lab, Vellore 632014, Tamil Nadu, India.; Ramaiah, S (corresponding author), Vellore Inst Technol VIT, Sch Bio Sci & Technol, Dept Biosci, Vellore 632014, Tamil Nadu, India.
EM priyamvada.a@vit.ac.in; sudhaanand@vit.ac.in
RI Ramaiah, Sudha/T-3682-2019; P, Priyamvada/ITT-9191-2023
OI Priyamvada, P./0000-0003-2426-5188
FU The authors would like to extend heartfelt gratitude to Prof. (Dr.)
   Anand Anbarasu (VIT, Vellore) for his guidance in framing the
   manuscript. The authors would like to thank the management of Vellore
   Institute of Technology (VIT), Vellore, for providing th
FX The authors would like to extend heartfelt gratitude to Prof. (Dr.)
   Anand Anbarasu (VIT, Vellore) for his guidance in framing the
   manuscript. The authors would like to thank the management of Vellore
   Institute of Technology (VIT), Vellore, for providing the necessary
   facilities to carry out this research work.
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NR 69
TC 7
Z9 7
U1 0
U2 1
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0006-2928
EI 1573-4927
J9 BIOCHEM GENET
JI Biochem. Genet.
PD JUN
PY 2024
VL 62
IS 3
BP 2166
EP 2194
DI 10.1007/s10528-023-10544-0
EA OCT 2023
PG 29
WC Biochemistry & Molecular Biology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA UU2I9
UT WOS:001090264500002
PM 37884851
DA 2025-01-04
ER

PT J
AU Chen, YC
   Chang, TK
   Su, WC
   Yeh, YS
   Chen, PJ
   Huang, PJ
   Yang, PH
   Tsai, HL
   Wang, JY
   Huang, CW
AF Chen, Yen-Cheng
   Chang, Tsung-Kun
   Su, Wei-Chih
   Yeh, Yung-Sung
   Chen, Po-Jung
   Huang, Peng-Jen
   Yang, Po-Hsiang
   Tsai, Hsiang-Lin
   Wang, Jaw-Yuan
   Huang, Ching-Wen
TI Impact on survival benefits of asymptomatic primary tumor resection
   after bevacizumab plus FOLFIRI as first-line therapy for patients with
   metastatic colorectal cancer with synchronous unresectable metastasis
SO INTERNATIONAL JOURNAL OF COLORECTAL DISEASE
LA English
DT Article
DE Colorectal cancer; Asymptomatic; Unresectable metastasis; Primary tumor
   resection; First-line bevacizumab plus FOLFIRI
ID FACTORS PREDICTING SURVIVAL; IRINOTECAN DOSE-ESCALATION;
   SURGICAL-TREATMENT; COST-EFFECTIVENESS; CHEMOTHERAPY; POLYMORPHISM;
   CETUXIMAB; DRUG
AB BackgroundMetastatic colorectal cancer (mCRC) poses a clinical challenge and requires a combination of systemic therapy and conversion surgery. Although first-line chemotherapy and targeted therapy are considered the standard treatments for mCRC, the role of primary tumor resection (PTR) in asymptomatic synchronous mCRC with unresectable metastatic lesion after initial therapy remains relatively underexplored.MaterialsA retrospective review was conducted from January 2015 to January 2021, involving 74 patients with synchronous mCRC who received bevacizumab plus FOFIRI as first-line systemic therapy. All 74 patients had unresectable metastatic lesions confirmed through multidisciplinary team discussion. Patient characteristics, PTR data, and radiotherapy (RT) and overall survival (OS) outcomes were analyzed. The patients were categorized into a "PTR" group and a "No PTR" group and then further stratified into "4A," "4B," and "4C" subgroups based on the initial mCRC stage. Additionally, four subgroups-namely "PTR( +)/RT( +)," "PTR( +)/RT( -)," "PTR( -)/RT( +)," and "PTR( -)/RT( -)"-were formed to assess the combined effects of PTR and RT.ResultsThe median OS for all the patients was 23.8 months (20.5-27.1 months). The "PTR" group exhibited a significantly higher median OS of 25.9 months (21.3-30.5 months) compared with 21.4 months (15.8-27.1 months) in the "No PTR" group (p = 0.048). Subgroup analyses revealed a trend of improved survival with PTR in patients with stage IVA and IVB; however, the results were not statistically significant (p = 0.116 and 0.493, respectively). A subgroup analysis of PTR and RT combinations revealed no significant difference in median OS rates.ConclusionFor asymptomatic mCRC with synchronous unresectable distant metastasis, PTR following first-line therapy with bevacizumab plus FOLFIRI may provide a potential survival benefit, particularly in stage IVA/IVB patients compared with stage IVC patients. Additionally, RT for primary tumor did not provide an additional OS benefit in mCRC with unresectable metastasis. A prospective randomized trial with a larger sample size is essential to further elucidate the role of PTR in this context.
C1 [Chen, Yen-Cheng; Chang, Tsung-Kun; Su, Wei-Chih; Chen, Po-Jung; Wang, Jaw-Yuan] Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, Kaohsiung 80708, Taiwan.
   [Chen, Yen-Cheng; Chang, Tsung-Kun; Su, Wei-Chih; Chen, Po-Jung; Huang, Peng-Jen; Yang, Po-Hsiang; Tsai, Hsiang-Lin; Wang, Jaw-Yuan; Huang, Ching-Wen] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Colorectal Surg, 100 Tzyou 1st Rd, Kaohsiung 80708, Taiwan.
   [Chen, Yen-Cheng; Tsai, Hsiang-Lin; Wang, Jaw-Yuan; Huang, Ching-Wen] Kaohsiung Med Univ, Coll Med, Fac Med, Dept Surg, Kaohsiung 80708, Taiwan.
   [Chang, Tsung-Kun; Su, Wei-Chih; Yeh, Yung-Sung] Kaohsiung Med Univ, Coll Med, Fac Postbaccalaureate Med, Dept Surg, Kaohsiung 80708, Taiwan.
   [Yeh, Yung-Sung] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Div Trauma & Surg Crit Care, Dept Surg, Kaohsiung 80708, Taiwan.
   [Yeh, Yung-Sung] Kaohsiung Med Univ, Coll Med, Fac Postbaccalaureate Med, Dept Emergency Med, Kaohsiung 80708, Taiwan.
   [Yeh, Yung-Sung] Taipei Med Univ, Grad Inst Injury Prevent & Control, Coll Publ Hlth, Taipei 11031, Taiwan.
   [Wang, Jaw-Yuan] Kaohsiung Med Univ, Grad Inst Med, Coll Med, Kaohsiung 80708, Taiwan.
   [Wang, Jaw-Yuan] Kaohsiung Med Univ, Ctr Canc Res, Kaohsiung 80708, Taiwan.
   [Wang, Jaw-Yuan] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Kaohsiung, Taiwan.
C3 Kaohsiung Medical University; Kaohsiung Medical University; Kaohsiung
   Medical University Hospital; Kaohsiung Medical University; Kaohsiung
   Medical University; Kaohsiung Medical University; Kaohsiung Medical
   University Hospital; Kaohsiung Medical University; Taipei Medical
   University; Kaohsiung Medical University; Kaohsiung Medical University;
   Kaohsiung Medical University; Kaohsiung Medical University Hospital
RP Huang, CW (corresponding author), Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Colorectal Surg, 100 Tzyou 1st Rd, Kaohsiung 80708, Taiwan.; Huang, CW (corresponding author), Kaohsiung Med Univ, Coll Med, Fac Med, Dept Surg, Kaohsiung 80708, Taiwan.
EM baseball5824@yahoo.com.tw
FU National Science and Technology Council [MOST 111-2314-B-037-070-MY3,
   NSTC 112-2314-B-037-050-MY3, NSTC 113-2321-B-037-006, NSTC
   113-2314-B-037-057]; Ministry of Health and Welfare
   [MOHW113-TDU-B-222-134014]; Health and welfare surcharge of on tobacco
   products; Kaohsiung Medical University Hospital [KMUH112-2R37,
   KMUH112-2R38, KMUH112-2R39, KMUH112-2M27, KMUH112-2M28, KMUH112-2M29,
   KMUH-S11303, KMUH-SH11309]; Kaohsiung Medical University Research Center
   Grant [KMU-TC113A04]; Taiwan Precision Medicine Initiative and Taiwan
   Biobank, Academia Sinica, Taiwan
FX This work was supported by grants through funding from the National
   Science and Technology Council (MOST 111-2314-B-037-070-MY3, NSTC
   112-2314-B-037-050-MY3, NSTC 113-2321-B-037-006, NSTC
   113-2314-B-037-057) and the Ministry of Health and Welfare
   (MOHW113-TDU-B-222-134014) and funded by the health and welfare
   surcharge of on tobacco products, and the Kaohsiung Medical University
   Hospital (KMUH112-2R37, KMUH112-2R38, KMUH112-2R39, KMUH112-2M27,
   KMUH112-2M28, KMUH112-2M29, KMUH-S11303, KMUH-SH11309) and Kaohsiung
   Medical University Research Center Grant (KMU-TC113A04). In addition,
   this study was supported by the Grant of Taiwan Precision Medicine
   Initiative and Taiwan Biobank, Academia Sinica, Taiwan, R.O.C.
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NR 54
TC 0
Z9 0
U1 1
U2 1
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0179-1958
EI 1432-1262
J9 INT J COLORECTAL DIS
JI Int. J. Colorectal Dis.
PD OCT 25
PY 2024
VL 39
IS 1
AR 171
DI 10.1007/s00384-024-04745-1
PG 12
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA K0Z8K
UT WOS:001341262900001
PM 39453531
OA hybrid
DA 2025-01-04
ER

PT J
AU Chang, JR
   Xavier, HW
   Chen, DF
   Liu, YM
   Li, H
   Bian, ZX
AF Chang, Jinrong
   Xavier, Hoileong Wong
   Chen, Dongfeng
   Liu, Yamei
   Li, Hui
   Bian, Zhaoxiang
TI Potential Role of Traditional Chinese Medicines by Wnt/β-Catenin Pathway
   Compared With Targeted Small Molecules in Colorectal Cancer Therapy
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE traditional Chinese medicines; colorectal cancer; Wnt/beta-catenin;
   potential role; small molecules; therapeutic mechanism
ID STEM-CELLS; HUMAN COLON; SIGNALING PATHWAY; DOWN-REGULATION;
   TUMOR-GROWTH; PORCUPINE INHIBITORS; WNT PATHWAY; APC GENE; SUPPRESSES;
   MUTATIONS
AB Colorectal cancer (CRC) has become a global public health problem because of its high incidence and mortality rate worldwide. The previous clinical treatment for CRC mainly involves conventional surgery, chemotherapy, and radiotherapy. With the development of tumor molecular targeted therapy, small molecule inhibitors present a great advantage in improving the survival of patients with advanced CRC. However, various side effects and drug resistance induced by chemotherapy are still the major obstacles to improve the clinical benefit. Thus, it is crucial to find new and alternative drugs for CRC treatment. Traditional Chinese medicines (TCMs) have been proved to have low toxicity and multi-target characteristics. In the last few decades, an increasing number of studies have demonstrated that TCMs exhibit strong anticancer effects in both experimental and clinical models and may serve as alternative chemotherapy agents for CRC treatment. Notably, Wnt/beta-catenin signaling pathway plays a vital role in the initiation and progression of CRC by modulating the stability of beta-catenin in the cytoplasm. Targeting Wnt/beta-catenin pathway is a novel direction for developing therapies for CRC. In this review, we outlined the anti-tumor effects of small molecular inhibitors on CRC through Wnt/beta-catenin pathway. More importantly, we focused on the potential role of TCMs against tumors by targeting Wnt/beta-catenin signaling at different stages of CRC, including precancerous lesions, early stage of CRC and advanced CRC. Furthermore, we also discussed perspectives to develop potential new drugs from TCMs via Wnt/beta-catenin pathway for the treatment of CRC.
C1 [Chang, Jinrong; Chen, Dongfeng; Liu, Yamei; Li, Hui] Guangzhou Univ Chinese Med, Sch Basic Med Sci, Guangzhou, Peoples R China.
   [Xavier, Hoileong Wong; Bian, Zhaoxiang] Hong Kong Baptist Univ, Sch Chinese Med, Hong Kong, Peoples R China.
C3 Guangzhou University of Chinese Medicine; Hong Kong Baptist University
RP Li, H (corresponding author), Guangzhou Univ Chinese Med, Sch Basic Med Sci, Guangzhou, Peoples R China.; Bian, ZX (corresponding author), Hong Kong Baptist Univ, Sch Chinese Med, Hong Kong, Peoples R China.
EM lihui@gzucm.edu.cn; bianzxiang@gmail.com
RI Wong, Hoi/P-1293-2019
OI Wong, Hoi Leong Xavier/0000-0002-2460-4808
FU Guangdong Natural Science Foundation [2017A030312009]
FX Supported by the Guangdong Natural Science Foundation, No.
   2017A030312009.
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NR 110
TC 11
Z9 13
U1 2
U2 30
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD JUL 26
PY 2021
VL 12
AR 690501
DI 10.3389/fphar.2021.690501
PG 12
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA TX1WQ
UT WOS:000682882000001
PM 34381360
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Giannini, V
   Pusceddu, L
   Defeudis, A
   Nicoletti, G
   Cappello, G
   Mazzetti, S
   Sartore-Bianchi, A
   Siena, S
   Vanzulli, A
   Rizzetto, F
   Fenocchio, E
   Lazzari, L
   Bardelli, A
   Marsoni, S
   Regge, D
AF Giannini, Valentina
   Pusceddu, Laura
   Defeudis, Arianna
   Nicoletti, Giulia
   Cappello, Giovanni
   Mazzetti, Simone
   Sartore-Bianchi, Andrea
   Siena, Salvatore
   Vanzulli, Angelo
   Rizzetto, Francesco
   Fenocchio, Elisabetta
   Lazzari, Luca
   Bardelli, Alberto
   Marsoni, Silvia
   Regge, Daniele
TI Delta-Radiomics Predicts Response to First-Line Oxaliplatin-Based
   Chemotherapy in Colorectal Cancer Patients with Liver Metastases
SO CANCERS
LA English
DT Article
DE delta-radiomics; prediction; machine learning; CRC liver metastases;
   response to therapy; artificial intelligence
ID TUMOR HETEROGENEITY; TARGETED THERAPY; FLUOROURACIL; LEUCOVORIN;
   EVOLUTION; SURVIVAL; BLOCKADE
AB Simple Summary Oxaliplatin-based chemotherapy remains the mainstay of first-line therapy in patients with metastatic colorectal cancer (mCRC). Unfortunately, only approximately 60% of treated patients achieve response, and half of responders will experience an early onset of disease progression. Furthermore, some individuals will develop a mixed response due to the emergence of resistant tumor subclones. The ability to predicting which patients will acquire resistance could help them avoid the unnecessary toxicity of oxaliplatin therapies. Furthermore, sorting out lesions that do not respond, in the context of an overall good response, could trigger further investigation into their mutational landscape, providing mechanistic insight towards the planning of a more comprehensive treatment. In this study, we validated a delta-radiomics signature capable of predicting response to oxaliplatin-based first-line treatment of individual liver colorectal cancer metastases. Findings could pave the way to a more personalized treatment of patients with mCRC. The purpose of this paper is to develop and validate a delta-radiomics score to predict the response of individual colorectal cancer liver metastases (lmCRC) to first-line FOLFOX chemotherapy. Three hundred one lmCRC were manually segmented on both CT performed at baseline and after the first cycle of first-line FOLFOX, and 107 radiomics features were computed by subtracting textural features of CT at baseline from those at timepoint 1 (TP1). LmCRC were classified as nonresponders (R-) if they showed progression of disease (PD), according to RECIST1.1, before 8 months, and as responders (R+), otherwise. After feature selection, we developed a decision tree statistical model trained using all lmCRC coming from one hospital. The final output was a delta-radiomics signature subsequently validated on an external dataset. Sensitivity, specificity, positive (PPV), and negative (NPV) predictive values in correctly classifying individual lesions were assessed on both datasets. Per-lesion sensitivity, specificity, PPV, and NPV were 99%, 94%, 95%, 99%, 85%, 92%, 90%, and 87%, respectively, in the training and validation datasets. The delta-radiomics signature was able to reliably predict R- lmCRC, which were wrongly classified by lesion RECIST as R+ at TP1, (93%, averaging training and validation set, versus 67% of RECIST). The delta-radiomics signature developed in this study can reliably predict the response of individual lmCRC to oxaliplatin-based chemotherapy. Lesions forecasted as poor or nonresponders by the signature could be further investigated, potentially paving the way to lesion-specific therapies.
C1 [Giannini, Valentina; Defeudis, Arianna; Nicoletti, Giulia; Mazzetti, Simone; Regge, Daniele] Univ Turin, Dept Surg Sci, I-10124 Turin, Italy.
   [Giannini, Valentina; Pusceddu, Laura; Defeudis, Arianna; Cappello, Giovanni; Mazzetti, Simone; Regge, Daniele] FPO IRCCS, Candiolo Canc Inst, Radiol Unit, I-10060 Candiolo, Italy.
   [Sartore-Bianchi, Andrea; Siena, Salvatore; Vanzulli, Angelo] Univ Milan, Dept Oncol & Hematooncol, I-20122 Milan, Italy.
   [Sartore-Bianchi, Andrea; Siena, Salvatore] Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, I-20162 Milan, Italy.
   [Vanzulli, Angelo; Rizzetto, Francesco] ASST Grande Osped Metropolitano Niguarda, Dept Radiol, I-20162 Milan, Italy.
   [Fenocchio, Elisabetta] FPO IRCCS, Candiolo Canc Inst, Multidisciplinary Outpatient Oncol Clin, I-10060 Candiolo, Italy.
   [Lazzari, Luca; Marsoni, Silvia] IFOM FIRC Inst Mol Oncol, Precis Oncol, I-20139 Milan, Italy.
   [Bardelli, Alberto] IRCCS, Candiolo Canc Inst FPO, I-10060 Candiolo, Italy.
   [Bardelli, Alberto] Univ Torino, Dept Oncol, I-10060 Candiolo, Italy.
C3 University of Turin; IRCCS Fondazione del Piemonte per l'Oncologia;
   University of Milan; IRCCS Fondazione del Piemonte per l'Oncologia; IFOM
   - FIRC Institute of Molecular Oncology; IRCCS Fondazione del Piemonte
   per l'Oncologia; University of Turin
RP Giannini, V (corresponding author), Univ Turin, Dept Surg Sci, I-10124 Turin, Italy.; Giannini, V (corresponding author), FPO IRCCS, Candiolo Canc Inst, Radiol Unit, I-10060 Candiolo, Italy.
EM valentina.giannini@unito.it; laura.pscd@gmail.com;
   arianna.defeudis@unito.it; giulia.nicoletti@unito.it;
   giovanni.cappello@ircc.it; simone.mazzetti@ircc.it;
   andrea.sartorebianchi@unimi.it; salvatore.siena@unimi.it;
   angelo.vanzulli@unimi.it; francesco.rizzetto@unimi.it;
   elisabetta.fenocchio@ircc.it; luca.lazzari@ifom.eu;
   alberto.bardelli@unito.it; silvia.marsoni@ifom.eu; daniele.regge@ircc.it
RI Sartore-Bianchi, Andrea/AAB-9848-2019; Cappello, Giovanni/JJD-7653-2023;
   SIENA, SALVATORE/AAC-5806-2019; Giardina, Giorgio/Y-5513-2019; Regge,
   Daniele/AAC-6816-2022; Defeudis, Arianna/AAC-7329-2022; Nicoletti,
   Giulia/CAA-1445-2022; Vanzulli, Angelo/X-4175-2019; Lazzari,
   Luca/HGA-5930-2022; Rizzetto, Francesco/AAH-1067-2019; Giannini,
   Valentina/M-8365-2019
OI Defeudis, Arianna/0000-0002-1745-3044; Mazzetti,
   Simone/0000-0001-6011-4040; Vanzulli, Angelo/0000-0002-2452-3370;
   Marsoni, Silvia/0000-0002-5361-7122; Sartore-Bianchi,
   Andrea/0000-0003-0780-0409; NICOLETTI, GIULIA/0000-0003-2013-5933;
   Fenocchio, Elisabetta/0000-0001-6679-0955; Lazzari,
   Luca/0000-0001-6841-4240; Rizzetto, Francesco/0000-0003-3451-9874;
   Giannini, Valentina/0000-0001-5052-8231; Regge,
   Daniele/0000-0001-8267-5279; SIENA, SALVATORE/0000-0002-2681-2846
FU FONDAZIONE AIRC under 5 per mille [2018-ID, 21091]
FX The research leading to these results has received funding from
   FONDAZIONE AIRC under 5 per mille 2018-ID. 21091 program-P.I. Bardelli
   Alberto, GLs Daniele Regge, Silvia Marsoni, and Salvatore Siena.
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NR 40
TC 18
Z9 19
U1 1
U2 14
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JAN
PY 2022
VL 14
IS 1
AR 241
DI 10.3390/cancers14010241
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YF3WP
UT WOS:000741741400001
PM 35008405
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Chen, LY
   Wu, DS
   Shen, YA
AF Chen, Liang-Yun
   Wu, Dao-Sian
   Shen, Yao-An
TI Fatty acid synthase inhibitor cerulenin hinders liver cancer stem cell
   properties through FASN/APP axis as novel therapeutic strategies
SO JOURNAL OF LIPID RESEARCH
LA English
DT Article
DE cancer stem cell; liver cancer; fatty acid metabolism; combination
   therapy; amyloid precursor protein
ID DIFFERENTIAL EXPRESSION ANALYSIS; DISEASE ONTOLOGY; LIPID-METABOLISM;
   CARCINOMA-CELLS; COLON-CANCER; R PACKAGE; METASTASIS; PROTEIN;
   IDENTIFICATION; PROLIFERATION
AB Hepatocellular carcinoma (HCC) poses significant treatment challenges due to high postoperative recurrence rates and the limited effectiveness of targeted medications. Researchers have identified the unique metabolic profiles of cancer stem cells (CSCs) as the primary drivers of cancer recurrence, metastasis, and drug resistance. Therefore, to address the therapeutic conundrum, this study focused on rewinding metabolic reprogramming of CSCs as a novel therapeutic strategy. HCC CSCs exhibited elevated fatty acid (FA) metabolism compared with parental cells. To specifically target FA metabolism in CSCs, we utilized cerulenin, a fatty acid synthase (FASN) inhibitor. Surprisingly, cerulenin can diminish CSC-like characteristics, including stemness gene expression, spherogenicity, tumorigenicity, and metastatic potential. In addition, sorafenib, a multikinase inhibitor used as targeted therapy for advanced HCC, was employed in combination with cerulenin, demonstrating a great synergistic effect, particularly in CSCs. Importantly, our RNA sequencing analysis disclosed that the amyloid protein precursor (APP) is a crucial downstream effector of FASN in regulating CSC properties. We found that APP plays a crucial role in CSCs' characteristics that can be inhibited by cerulenin.(jlr) By focusing on FA metabolism, this study identified the FASN/APP axis as a viable target to develop a more potent therapy strategy for advanced HCC.
C1 [Chen, Liang-Yun; Wu, Dao-Sian; Shen, Yao-An] Taipei Med Univ, Coll Med, Sch Med, Dept Pathol, Taipei, Taiwan.
   [Shen, Yao-An] Taipei Med Univ, Grad Inst Clin Med, Coll Med, Taipei, Taiwan.
   [Shen, Yao-An] Taipei Med Univ, Coll Med, Int Master PhD Program Med, Taipei, Taiwan.
C3 Taipei Medical University; Taipei Medical University; Taipei Medical
   University
RP Shen, YA (corresponding author), Taipei Med Univ, Coll Med, Sch Med, Dept Pathol, Taipei, Taiwan.; Shen, YA (corresponding author), Taipei Med Univ, Grad Inst Clin Med, Coll Med, Taipei, Taiwan.; Shen, YA (corresponding author), Taipei Med Univ, Coll Med, Int Master PhD Program Med, Taipei, Taiwan.
EM shen1202@tmu.edu.tw
OI Chen, Liang-Yun/0000-0002-5288-3437; Shen, Yao-An/0000-0002-4393-2794
FU Taipei MedicalUniversity, Taiwan [TMU108-AE1-B12]; Ministry of Science
   and Technology, Taiwan [MOST 109-2314-B-038-021-MY3]; National Science
   andTechnology Council, Taiwan (NSTC) [111-2622-B-038-008]; NSTC
   [113-2628-B-038-012]; Taipei Medical University Hospital, Taiwan
   [113TMU-TMUH-012]
FX This work was supported by a grant from Taipei MedicalUniversity, Taiwan
   (TMU108-AE1-B12) , a grant from theMinistry of Science and Technology,
   Taiwan (MOST 109-2314-B-038-021-MY3) , grants from the National Science
   andTechnology Council, Taiwan (NSTC 111-2622-B-038-008,NSTC
   112-2823-8-038-001, NSTC 112-2314-B038-081, NSTC113-2823-8-038-001, NSTC
   113-2628-B-038-012) , and a grant from Taipei Medical University
   Hospital, Taiwan (113TMU-TMUH-012) .
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NR 92
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0022-2275
EI 1539-7262
J9 J LIPID RES
JI J. Lipid Res.
PD NOV
PY 2024
VL 65
IS 11
AR 100660
DI 10.1016/j.jlr.2024.100660
EA OCT 2024
PG 18
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA K2Y2F
UT WOS:001342577200001
PM 39332525
OA gold
DA 2025-01-04
ER

PT J
AU Zhao, JK
   Xia, K
   He, P
   Wei, G
   Zhou, X
   Zhang, XD
AF Zhao, Jingkun
   Xia, Kai
   He, Peng
   Wei, Gang
   Zhou, Xin
   Zhang, Xiaodong
TI Recent advances of nucleic acid-based cancer biomarkers and biosensors
SO COORDINATION CHEMISTRY REVIEWS
LA English
DT Review
DE Nucleic acids; Biomarkers; Functions; Strategies; Biosensors
ID CIRCULATING TUMOR DNA; CELL-FREE DNA; LABEL-FREE DETECTION;
   BREAST-CANCER; GASTRIC-CANCER; MITOCHONDRIAL-DNA; LUNG-CANCER;
   COLORECTAL-CANCER; ELECTROCHEMICAL DETECTION; ULTRASENSITIVE DETECTION
AB Nucleic acid-based cancer biomarkers (NABCBs) have emerged as a notable and continuously captivating research focal point within the domain of oncology. As a result, NABCBs have garnered sustained and steadfast attention from the realms of scientific inquiry and medical practice alike. This comprehensive review embarks on a systematic exploration, delving into the classifications, properties, and functions of NABCBs. Subsequently, it navigates the expanse of clinical applications, where NABCBs assume roles in cancer diagnosis, prognosis, targeted therapy, and immunotherapy. This underscores their pivotal role in translating biomolecular signatures into tangible diagnostic tools. Moreover, an exploration into the strategies underpinning the development of NABCB-based biosensors, such as coordination, crosslinking, fluorescent labeling, and so on, was discussed in details. This segment accentuates the potential of NABCBs to underpin diagnostic and monitoring paradigms, thereby offering a cutting-edge technological foundation for the realization of real-time assessments of early cancer diagnosis and treatment efficacy. In addition, this review embarks on a thorough exploration of these challenges, contributing to an enriched comprehension of the existing status and limitations of NABCBs within the practical clinical milieu. This outlook underscores the call for continued and dedicated research endeavors, poised to forge the theoretical bedrock requisite for early cancer diagnosis, personalized therapeutic methodologies, and the vigilant monitoring of treatment outcomes.
C1 [Zhao, Jingkun; Xia, Kai; He, Peng; Wei, Gang; Zhou, Xin; Zhang, Xiaodong] Qingdao Univ, Coll Chem & Chem Engn, Qingdao 266071, Peoples R China.
C3 Qingdao University
RP Wei, G; Zhou, X; Zhang, XD (corresponding author), Qingdao Univ, Coll Chem & Chem Engn, Qingdao 266071, Peoples R China.
EM weigroup@qdu.edu.cn; zhouxin@qdu.edu.cn; zxdqd@qdu.edu.cn
RI zhang, xiaodong/HNS-5895-2023; zhou, xin/E-9308-2011
OI zhou, Xin/0000-0002-1820-7830
FU Natural Science Foundation of China [21762045, 21911540466, 51873225];
   Shandong Provincial Natural Science Foundation [ZR2019YQ12]; China
   Postdoctoral Science Foundation [219M652306]; Taishan Scholar Project
   [tsqn201812049, tsqn201909104]
FX The authors acknowledge the financial support from the Natural Science
   Foundation of China (no. 21762045, 21911540466, and 51873225), Shandong
   Provincial Natural Science Foundation (ZR2019YQ12), China Postdoctoral
   Science Foundation (219M652306), and Taishan Scholar Project
   (tsqn201812049 and tsqn201909104).
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NR 347
TC 16
Z9 16
U1 12
U2 41
PU ELSEVIER SCIENCE SA
PI LAUSANNE
PA PO BOX 564, 1001 LAUSANNE, SWITZERLAND
SN 0010-8545
EI 1873-3840
J9 COORDIN CHEM REV
JI Coord. Chem. Rev.
PD DEC 15
PY 2023
VL 497
AR 215456
DI 10.1016/j.ccr.2023.215456
EA SEP 2023
PG 22
WC Chemistry, Inorganic & Nuclear
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA GI7W5
UT WOS:001152114400001
DA 2025-01-04
ER

PT J
AU Shin, MH
   Kim, J
   Lim, SA
   Kim, J
   Lee, KM
AF Shin, Min Hwa
   Kim, Jiyoung
   Lim, Siyoung A.
   Kim, Jeongsoo
   Lee, Kyung-Mi
TI Current Insights into Combination Therapies with MAPK Inhibitors and
   Immune Checkpoint Blockade
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE combination therapy; MAPK targeted therapy; BRAF inhibitor; MEK
   inhibitor; immune checkpoint inhibitor; PD-1; PD-L1; CTLA-4
ID TARGETED THERAPIES; BRAF INHIBITION; OPEN-LABEL; T-CELL; TRAMETINIB
   GSK1120212; METASTATIC MELANOMA; CANCER PROGRESSION; PANCREATIC-CANCER;
   IMPROVED SURVIVAL; HUMAN-LYMPHOCYTES
AB The recent development of high-throughput genomics has revolutionized personalized medicine by identifying key pathways and molecular targets controlling tumor progression and survival. Mitogen-activated protein kinase (MAPK) pathways are examples of such targets, and inhibitors against these pathways have shown promising clinical responses in patients with melanoma, non-small-cell lung cancer, colorectal cancer, pancreatic cancer, and thyroid cancer. Although MAPK pathway-targeted therapies have resulted in significant clinical responses in a large proportion of cancer patients, the rate of tumor recurrence is high due to the development of resistance. Conversely, immunotherapies have shown limited clinical responses, but have led to durable tumor regression in patients, and complete responses. Recent evidence indicates that MAPK-targeted therapies may synergize with immune cells, thus providing rationale for the development of combination therapies. Here, we review the current status of ongoing clinical trials investigating MAPK pathway inhibitors, such as BRAF and MAPK/ERK kinase (MEK) inhibitors, in combination with checkpoint inhibitors targeting programmed death protein 1 (PD-1), programmed death-ligand 1 (PD-L1), and cytotoxic T cell associated antigen-4 (CTLA-4). A better understanding of an individual drug's mechanism of action, patterns of acquired resistance, and the influence on immune cells will be critical for the development of novel combination therapies.
C1 [Shin, Min Hwa; Kim, Jiyoung; Lim, Siyoung A.; Kim, Jeongsoo; Lee, Kyung-Mi] Korea Univ, Coll Med, Dept Biochem & Mol Biol, Seoul 02841, South Korea.
C3 Korea University; Korea University Medicine (KU Medicine)
RP Lee, KM (corresponding author), Korea Univ, Coll Med, Dept Biochem & Mol Biol, Seoul 02841, South Korea.
EM mhshin0423@gmail.com; jjyoung0121@gmail.com; s.abby.lim18@gmail.com;
   kjs5043@gmail.com; kyunglee@korea.ac.kr
OI Kim, Jeongsoo/0000-0002-5638-1960; Lim, Siyoung/0000-0003-4791-4056;
   Lee, Kyung-Mi/0000-0002-5378-9258
FU National Research Foundation of Korea (NRF) [NRF-2017R1A2B3004828,
   NRF-2016M3A9B6948342, NRF-2018M3A9D3079288, NRF-2018M3A9D3079285]; Korea
   Health Industry Development Institute - Korean Government
   [KHIDI-HI14C2640]; National Research Foundation of Korea (NRF) grant
   [NRF-2018R1D1A1B07041442]; Korea University Grant
FX K.-M.L. was supported by the National Research Foundation of Korea (NRF)
   grants, NRF-2017R1A2B3004828, NRF-2016M3A9B6948342,
   NRF-2018M3A9D3079288, and NRF-2018M3A9D3079285. K.-M.L. was also
   supported by the Korea Health Industry Development Institute
   (KHIDI-HI14C2640) grant funded by the Korean Government. M.H.S. was
   supported by the National Research Foundation of Korea (NRF) grant,
   NRF-2018R1D1A1B07041442 and a Korea University Grant.
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NR 78
TC 60
Z9 65
U1 1
U2 17
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD APR
PY 2020
VL 21
IS 7
AR 2531
DI 10.3390/ijms21072531
PG 34
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA LR3DN
UT WOS:000535574200273
PM 32260561
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Cai, ZL
   Zhang, F
   Chen, WJ
   Zhang, JZ
   Li, HJ
AF Cai, Zhonglin
   Zhang, Fa
   Chen, Weijie
   Zhang, Jianzhong
   Li, Hongjun
TI miRNAs: A Promising Target in the Chemoresistance of Bladder Cancer
SO ONCOTARGETS AND THERAPY
LA English
DT Review
DE miRNAs; chemoresistant; bladder cancer; biomarkers; targeted therapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; CELL-PROLIFERATION;
   MULTI-CHEMORESISTANCE; TRANSFORMING GENE-1; TUMOR-SUPPRESSOR;
   DRUG-RESISTANCE; MESSENGER-RNAS; PI3K PATHWAY; STEM-CELLS; EXPRESSION
AB Chemotherapy is an important cancer treatment method. Tumor chemotherapy resistance is one of the main factors leading to tumor progression. Like other malignancies, bladder cancer, especially muscle-invasive bladder cancer, is prone to chemotherapy resistance. Additionally, only approximately 50% of muscle-invasive bladder cancer responds to cisplatin-based chemotherapy. miRNAs are a class of small, endogenous, noncoding RNAs that regulate gene expression at the posttranscriptional level, which results in the inhibition of translation or the degradation of mRNA. In the study of miRNAs and cancer, including gastric cancer, prostate cancer, liver cancer, and colorectal cancer, it has been found that miRNAs can regulate the expression of genes related to tumor resistance, thereby promoting the progression of tumors. In bladder cancer, miRNAs are also closely related to chemotherapy resistance, suggesting that miRNAs can be a new therapeutic target for the chemotherapy resistance of bladder cancer. Therefore, understanding the mechanisms of miRNAs in the chemotherapy resistance of bladder cancer is an important foundation for restoring the chemotherapy sensitivity of bladder cancer and improving the efficacy of chemotherapy and patient survival. In this article, we review the role of miRNAs in the development of chemotherapy-resistant bladder cancer and the various resistance mechanisms that involve apoptosis, the cell cycle, epithelial-mesenchymal transition (EMT), and cancer stem cells (CSCs).
C1 [Cai, Zhonglin; Zhang, Jianzhong; Li, Hongjun] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Peking Union Med Coll, Dept Urol, 1 Shuaifuyuan, Beijing 100730, Peoples R China.
   [Zhang, Fa] Lanzhou Univ, Dept Urol, Hosp 1, Lanzhou, Gansu, Peoples R China.
   [Chen, Weijie] Shanghai Tradit Chinese Med Univ, Shanghai Municipal Hosp Tradit Chinese Med, Dept Urol, Shanghai, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Peking Union Medical College; Peking Union Medical College Hospital;
   Lanzhou University
RP Li, HJ (corresponding author), Chinese Acad Med Sci, Peking Union Med Coll Hosp, Peking Union Med Coll, Dept Urol, 1 Shuaifuyuan, Beijing 100730, Peoples R China.
EM lihongjun@pumch.cn
RI Zhang, Jianzhong/AAM-6179-2021
OI Zhang, Jianzhong/0000-0003-3326-0266
FU National Natural Science Foundation of China [81671448]
FX This work is supported by the grant from National Natural Science
   Foundation of China (Grant No. 81671448).
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NR 107
TC 38
Z9 38
U1 1
U2 16
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6930
J9 ONCOTARGETS THER
JI OncoTargets Ther.
PY 2019
VL 12
BP 1805
EP 1816
DI 10.2147/OTT.S231489
PG 12
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA JZ6IE
UT WOS:000505204300001
PM 32099386
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Rémond, M
   Pachev, A
   Battistella, M
   Gandon, C
   Mourah, S
   Madelaine, I
   Maggiori, L
   Benadon, B
   Hammoudi, N
   Lourenco, N
   Aparicio, T
AF Remond, Maxime
   Pachev, Atanas
   Battistella, Maxime
   Gandon, Camille
   Mourah, Samia
   Madelaine, Isabelle
   Maggiori, Leon
   Benadon, Bethsabee
   Hammoudi, Nassim
   Lourenco, Nelson
   Aparicio, Thomas
TI Metastatic perirectal PEComa treated by checkpoint inhibitor
   immunotherapy and multimodal treatment: case report and review of the
   literature
SO THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
LA English
DT Article
DE immunotherapy; PEComa; perivascular epithelioid cell; selective internal
   radiation therapy; targeted therapy
AB Malignant PEComas are an extremely rare subtype of soft tissue sarcomas. Here, we report the case of a man presenting with a perirectal PEComa and liver metastasis. Since the tumor harbored a tumor mutational burden of 23/Mb and a programmed death-ligand 1 tumor positivity score of 50%, the patient was treated with pembrolizumab as a second line of systemic therapy, in combination with everolimus. This combined therapy led to a near-complete response of the primary tumor and a partial response of the metastasis. Radioembolization of the liver metastasis was performed due to isolated liver progression, and the pelvic tumor was treated by radiotherapy because of pelvic symptoms. The disease is still stable after 13 months of pembrolizumab plus everolimus and multimodal treatment. This case shows that malignant PEComas can display molecular features associated with sensitivity to checkpoint inhibitors. The use of checkpoint inhibitors may be a relevant therapeutic strategy in these patients. It is also the first report on selective internal radiation therapy in PEComas.
   A case of a patient with metastatic PEComa of the rectum, a very rare tumor type, treated by immunotherapy in combination with local treatmentsThis article reports the case of a patient presenting with a very rare tumor type called "PEComa". The tumor originated from the rectum and had disseminated to the liver. Since this tumor is very rare, there is a lack of knowledge on which treatments to use, and every case reporting the use of new treatments in PEComas is helpful. Here, the tumor displayed molecular alterations that suggested that it would respond to immunotherapy, such as a high number of mutations. Therefore, the patient was treated with an immunotherapy called pembrolizumab, in combination with another medication (everolimus). The rectal tumor nearly disappeared under treatment, and the liver metastasis decreased in size. The patient had radiotherapy of the rectum because of rectal bleeding. For the liver metastasis we used another technique called radioembolization, that consists in delivering radioactive compounds directly in the metastasis through the bloodstream. Now, he has received immunotherapy for 13 months and the disease is still under control. This case shows that immunotherapy can be a good treatment option in PEComas. It is also the first time that a medical team reports the using radioembolization to treat a PEComa.
C1 [Pachev, Atanas] Univ Paris Cite, St Louis Hosp, Assistance Publ Hop Paris, Dept Radiol, Paris, France.
   [Battistella, Maxime; Gandon, Camille] Univ Paris Cite, St Louis Hosp, Assistance Publ Hop Paris, Dept Pathol, Paris, France.
   [Mourah, Samia] Univ Paris Cite, St Louis Hosp, Assistance Publ Hop Paris, Dept Tumor Genom & Pharmacol, Paris, France.
   [Madelaine, Isabelle] Univ Paris Cite, St Louis Hosp, Assistance Publ Hop Paris, Dept Pharm, Paris, France.
   [Maggiori, Leon] Univ Paris Cite, St Louis Hosp, Assistance Publ Hop Paris, Dept Surg, Paris, France.
   [Benadon, Bethsabee] Univ Paris Cite, St Louis Hosp, Assistance Publ Hop Paris, Dept Radiotherapy, Paris, France.
   [Remond, Maxime; Hammoudi, Nassim; Lourenco, Nelson; Aparicio, Thomas] Univ Paris Cite, St Louis Hosp, Assistance Publ Hop Paris, Dept Gastroenterol, 1 Ave Claude Vellefaux, F-75010 Paris, France.
   [Hammoudi, Nassim; Aparicio, Thomas] Univ Paris Cite, Inst Rech St Louis, INSERM U1160, Paris, France.
C3 Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Saint-Louis - APHP; Assistance Publique Hopitaux
   Paris (APHP); Universite Paris Cite; Hopital Universitaire Saint-Louis -
   APHP; Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Saint-Louis - APHP; Assistance Publique Hopitaux
   Paris (APHP); Universite Paris Cite; Hopital Universitaire Saint-Louis -
   APHP; Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Saint-Louis - APHP; Assistance Publique Hopitaux
   Paris (APHP); Universite Paris Cite; Hopital Universitaire Saint-Louis -
   APHP; Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Saint-Louis - APHP; Institut National de la Sante
   et de la Recherche Medicale (Inserm); Universite Paris Cite
RP Rémond, M (corresponding author), Univ Paris Cite, St Louis Hosp, Assistance Publ Hop Paris, Dept Gastroenterol, 1 Ave Claude Vellefaux, F-75010 Paris, France.
EM maxime.remond@aphp.fr
RI Battistella, Maxime/K-2949-2012; Remond, Maxime/LJK-0954-2024
OI Remond, Maxime/0000-0001-7147-6936
FX None.
CR Anderson WJ, 2023, AM J SURG PATHOL, V47, P535, DOI 10.1097/PAS.0000000000002028
   Choi J, 2021, P NATL ACAD SCI USA, V118, DOI 10.1073/pnas.2025182118
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NR 14
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1758-8340
EI 1758-8359
J9 THER ADV MED ONCOL
JI Ther. Adv. Med. Oncol.
PY 2024
VL 16
AR 17588359241280541
DI 10.1177/17588359241280541
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA G6N1E
UT WOS:001317772400001
PM 39314916
OA gold
DA 2025-01-04
ER

PT J
AU Li, Y
   Zhang, HB
   Chen, X
   Yang, XB
   Ye, YS
   Bekaii-Saab, T
   Zheng, YJ
   Zhang, YH
AF Li, Yong
   Zhang, Hai-Bo
   Chen, Xian
   Yang, Xiaobing
   Ye, Yongsong
   Bekaii-Saab, Tanios
   Zheng, Yaojie
   Zhang, Yihong
TI A Rare <i>EGFR</i>-<i>SEPT14</i> Fusion in a Patient with Colorectal
   Adenocarcinoma Responding to Erlotinib
SO ONCOLOGIST
LA English
DT Article
ID CELL LUNG-CANCER; LANDSCAPE; GEFITINIB; EGFRVIII
AB Colorectal cancer (CRC) is the second leading cause of cancer death worldwide. Growing evidence supports gene fusions as good candidates for molecularly targeted therapy in CRC. Here we describe a case of a 63-year-old man who had a radical right hemicolectomy procedure 24 months ago. Pathological diagnosis indicated colorectal adenocarcinoma with stage pT4N2bMx. During re-examination in December 2016, positron emission tomography/computed tomography scans indicated relapse with multiple lymph nodes metastasis. Then the patient received a nine-cycle combination treatment of XELOX and bevacizumab and showed progressive disease (PD). Subsequently, the patient was treated with bevacizumab plus FOLFIRI for 2 months before discontinuation because of adverse events. Paraffin sections of postoperative colorectal tissue were subjected to next-generation sequencing, and epidermal growth factor receptor (EGFR) amplification and rare EGFR-SEPT14 fusion were identified. The patient then received erlotinib, an EGFR tyrosine kinase inhibitor (TKI), and achieved a partial response. However, the patient subsequently showed PD, and a new variant, EGFRvIII, appeared in metastasis, which may be involved in erlotinib resistance. We suggest that there is value in treating patients harboring EGFR fusions with EGFR TKI therapy, and EGFR-SEPT14 fusion may be used as a therapeutic target for CRC. Key Points
   To the authors' knowledge, this is the first report of EGFR-SEPT14 fusion in colorectal cancer. The patient achieved a partial response after treatment with the epidermal growth factor receptor tyrosine kinase inhibitor erlotinib. This report expands the list of gene fusions in colorectal cancer and highlights new targets for the therapeutic intervention. EGFRvIII may be involved in erlotinib resistance, which is rare in colorectal cancer.
C1 [Li, Yong; Zhang, Hai-Bo; Chen, Xian; Yang, Xiaobing] Guangdong Prov Hosp Chinese Med, Dept Oncol, 111 Dade Rd, Guangzhou 510120, Guangdong, Peoples R China.
   [Ye, Yongsong] Guangdong Prov Hosp Chinese Med, Dept Image, Guangzhou, Guangdong, Peoples R China.
   [Bekaii-Saab, Tanios] Mayo Clin, Phoenix, AZ USA.
   [Zheng, Yaojie; Zhang, Yihong] OrigiMed, Shanghai, Peoples R China.
C3 Guangzhou University of Chinese Medicine; Guangzhou University of
   Chinese Medicine; Mayo Clinic; Mayo Clinic Phoenix
RP Zhang, HB (corresponding author), Guangdong Prov Hosp Chinese Med, Dept Oncol, 111 Dade Rd, Guangzhou 510120, Guangdong, Peoples R China.
EM haibozh@aliyun.com
RI Bekaii-Saab, Tanios/AGD-6851-2022; Zhang, Haibo/HLP-9266-2023; Yang,
   Xiaobing/HTR-2051-2023
OI Zheng, Yaojie/0000-0003-4244-2475; Bekaii-Saab,
   Tanios/0000-0001-7721-1699
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NR 27
TC 14
Z9 14
U1 0
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PD MAR
PY 2020
VL 25
IS 3
BP 203
EP 207
DI 10.1634/theoncologist.2019-0405
EA OCT 2019
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KT6PE
UT WOS:000494102100001
PM 32162810
OA Bronze, Green Published
DA 2025-01-04
ER

PT J
AU Sun, YW
   Lin, Y
   Liu, Z
   Jiang, WZ
   Chi, P
AF Sun, Yanwu
   Lin, Yu
   Liu, Zhun
   Jiang, Weizhong
   Chi, Pan
TI Combined laparoscopic lymphoadenectomy of lateral pelvic and inguinal
   nodal metastases using indocyanine green fluorescence imaging guidance
   in low rectal cancer after preoperative chemoradiotherapy: a case report
SO BMC GASTROENTEROLOGY
LA English
DT Article
DE Rectal cancer; Laparoscopic surgery; Inguinal lymph node metastasis;
   Lateral pelvic lymph node metastasis; Indocyanine green
ID ADENOCARCINOMA; DISSECTION
AB Background Intraoperative near-infrared fluorescence (NIR) imaging with indocyanine green (ICG) can demonstrate real-time lymphatic drainage and thus improve the accuracy and completeness of lymphadenectomy in colorectal cancer surgery. However, it has not been utilized in the inguinal lymphadenectomy in rectal cancer. This study aimed to describe a case of combined laparoscopic lymphadenectomy of left lateral pelvic and inguinal nodal metastases using NIR imaging with ICG imaging guidance for a rectal cancer patient with left lateral pelvic and inguinal lymph node metastases. Case presentation A 26-year-old man presented rectal cancer located 7 cm from the anal verge and enlarged lymph nodes in the left inguinal area. Pretreatment workup revealed rectal cancer with left lateral pelvic and inguinal lymph node metastases. The patient received preoperative chemoradiotherapy (pCRT), including radiation (total dose of 50.4 Gy in 28 fractions) to the whole pelvis and bilateral inguinal regions together with eight cycles of FOLFOX (oxaliplatin, fluoropyrimidine, and leucovorin) and three cycles of bevacizumab targeted chemotherapy. After pCRT, both colonoscopy and MR scan revealed a significant response of the primary tumor to pCRT, while MR scan revealed enlarged left lateral pelvic and inguinal lymph nodes. After four months from the completion of radiation (2 months after the last course of bevacizumab targeted therapy), the patient underwent laparoscopic-assisted ultra-low anterior resection and lymphadenectomy of left lateral pelvic and inguinal nodal metastases using ICG-NIR fluorescence imaging. The combined procedure was performed successfully without perioperative complication. Total operative time was 480 min and estimated blood loss 50 mL. Totally 34 lymph nodes were retrieved. Conclusions This is the first report of the safety and feasibility of ICG-NIR fluorescence imaging-guided laparoscopic lymphadenectomy of left lateral pelvic and inguinal nodal metastases in managing low rectal cancer with lateral pelvic and inguinal LNs metastases.
C1 [Sun, Yanwu; Lin, Yu; Jiang, Weizhong; Chi, Pan] Fujian Med Univ, Union Hosp, Dept Colorectal Surg & Gen Surg, 29 Xinquan Rd, Fuzhou 350001, Fujian, Peoples R China.
   [Sun, Yanwu; Lin, Yu; Jiang, Weizhong; Chi, Pan] Fujian Med Univ, Minimal Invas Ctr, Union Hosp, Fuzhou, Fujian, Peoples R China.
   [Sun, Yanwu; Lin, Yu; Liu, Zhun; Jiang, Weizhong; Chi, Pan] Fujian Med Univ, Fuzhou, Fujian, Peoples R China.
C3 Fujian Medical University; Fujian Medical University; Fujian Medical
   University
RP Chi, P (corresponding author), Fujian Med Univ, Union Hosp, Dept Colorectal Surg & Gen Surg, 29 Xinquan Rd, Fuzhou 350001, Fujian, Peoples R China.; Chi, P (corresponding author), Fujian Med Univ, Minimal Invas Ctr, Union Hosp, Fuzhou, Fujian, Peoples R China.; Chi, P (corresponding author), Fujian Med Univ, Fuzhou, Fujian, Peoples R China.
EM chipan363@163.com
RI 蒋, 伟忠/GYE-2778-2022
OI Jiang, Weizhong/0000-0002-7683-2247
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NR 17
TC 7
Z9 7
U1 0
U2 6
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-230X
J9 BMC GASTROENTEROL
JI BMC Gastroenterol.
PD MAR 16
PY 2022
VL 22
IS 1
AR 123
DI 10.1186/s12876-022-02193-1
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA ZU7GG
UT WOS:000770007600002
PM 35296259
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Rasic, P
   Jovanovic-Tucovic, M
   Jeremic, M
   Djuricic, SM
   Vasiljevic, ZV
   Milickovic, M
   Savic, D
AF Rasic, Petar
   Jovanovic-Tucovic, Maja
   Jeremic, Marija
   Djuricic, Slavisa M.
   Vasiljevic, Zorica V.
   Milickovic, Maja
   Savic, Djordje
TI B7 homologue 3 as a prognostic biomarker and potential therapeutic
   target in gastrointestinal tumors
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE B7 homologue 3; Gastrointestinal tumors; Colorectal cancer; Gastric
   cancer; Esophageal cancer; Targeted therapy
ID COLORECTAL-CANCER CELLS; REGULATORY T-CELLS; GASTRIC-CANCER; B7-H3
   EXPRESSION; RISK-FACTORS; COSTIMULATORY MOLECULE; BISPECIFIC ANTIBODIES;
   SIGNALING PATHWAY; DNA-DAMAGE; FAMILY
AB The most common digestive system (DS) cancers, including tumors of the gastrointestinal tract (GIT) such as colorectal cancer (CRC), gastric cancer (GC) and esophageal cancer (EC) as well as tumors of DS accessory organs such as pancreatic and liver cancer, are responsible for more than one-third of all cancer-related deaths worldwide, despite the progress that has been achieved in anticancer therapy. Due to these limitations in treatment strategies, oncological research has taken outstanding steps towards a better understanding of cancer cell biological complexity and heterogeneity. These studies led to new molecular target-driven therapeutic approaches. Different in vivo and in vitro studies have revealed significant expression of B7 homologue 3 (B7-H3) among the most common cancers of the GIT, including CRC, GC, and EC, whereas B7-H3 expression in normal healthy tissue of these organs was shown to be absent or minimal. This molecule is able to influence the biological behavior of GIT tumors through the various immunological and nonimmunological molecular mechanisms, and some of them are shown to be the result of B7-H3-related induction of signal transduction pathways, such as Janus kinase 2/signal transducer and activator of transcription 3, phosphatidylinositol 3-kinase/protein kinase B, extracellular signal-regulated kinase, and nuclear factor-kappa B. B7-H3 exerts an important role in progression, metastasis and resistance to anticancer therapy in these tumors. In addition, the results of many studies suggest that B7-H3 stimulates immune evasion in GIT tumors by suppressing antitumor immune response. Accordingly, it was observed that experimental depletion or inhibition of B7-H3 in gastrointestinal cancers improved antitumor immune response, impaired tumor progression, invasion, angiogenesis, and metastasis and decreased resistance to anticancer therapy. Finally, the high expression of B7-H3 in most common cancers of the GIT was shown to be associated with poor prognosis. In this review, we summarize the established data from different GIT cancer-related studies and suggest that the B7-H3 molecule could be a promising prognostic biomarker and therapeutic target for anticancer immunotherapy in these tumors.
C1 [Rasic, Petar; Milickovic, Maja; Savic, Djordje] Mother & Child Hlth Care Inst Serbia Dr Vukan Cup, Dept Abdominal Surg, Radoja Dakica 6-8, Belgrade 11000, Serbia.
   [Jovanovic-Tucovic, Maja; Jeremic, Marija] Univ Belgrade, Sch Med, Inst Med & Clin Biochem, Belgrade 11000, Serbia.
   [Djuricic, Slavisa M.] Mother & Child Hlth Care Inst Serbia Dr Vukan Cup, Dept Clin Pathol, Belgrade 11000, Serbia.
   [Djuricic, Slavisa M.] Univ Banja Luke, Fac Med, Banja Luka 78000, Bosnia & Herceg.
   [Vasiljevic, Zorica V.] Mother & Child Hlth Care Inst Serbia Dr Vukan Cup, Dept Clin Microbiol, Belgrade 11000, Serbia.
   [Milickovic, Maja; Savic, Djordje] Univ Belgrade, Sch Med, Belgrade 11000, Serbia.
C3 University of Belgrade; University of Banja Luka (UNIBL); University of
   Belgrade
RP Rasic, P (corresponding author), Mother & Child Hlth Care Inst Serbia Dr Vukan Cup, Dept Abdominal Surg, Radoja Dakica 6-8, Belgrade 11000, Serbia.
EM petar.rasic@imd.org.rs
RI Djuricic, Slavisa/AAT-1481-2021; Vasiljevic, Zorica/J-8389-2016
OI Milickovic, Maja/0000-0002-1185-5827; Savic, Djorde/0000-0001-7189-1160;
   Rasic, Petar/0000-0003-3696-4381; Jeremic, Marija/0000-0003-4761-4387;
   Djuricic, Slavisa/0000-0003-2041-3251
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NR 155
TC 6
Z9 6
U1 0
U2 5
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD AUG 15
PY 2021
VL 13
IS 8
BP 799
EP 821
DI 10.4251/wjgo.v13.i8.799
PG 23
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA UJ2BP
UT WOS:000691097800003
PM 34457187
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Cheng, JJ
   Cashman, JR
AF Cheng, Jiongjia
   Cashman, John R.
TI PAWI-2: A novel inhibitor for eradication of cancer
SO MEDICINAL CHEMISTRY RESEARCH
LA English
DT Review
DE Colorectal cancer; Breast cancer; Prostate cancer; Pancreatic cancer;
   Targeted therapy; PAWI-2
ID INVASIVE PANCREATIC-CANCER; PROSTATE-CANCER; INCREASED SURVIVAL;
   ANDROGEN RECEPTOR; NAB-PACLITAXEL; BREAST-CANCER; CLINICAL BENEFIT;
   BETA-CATENIN; TUMOR-GROWTH; COLON-CANCER
AB Cancer is a major worldwide public health problem and is still the leading cause of death in the United States. There are many types of cancer treatment but completely successful results are oftentimes not attained. It remains a challenge to develop efficacious clinically useful cancer therapies. Therapies targeting dysregulated signal transduction pathways in cancer can be efficacious anti-cancer therapies with minimal adverse effects. In this study, we focus on novel small molecule p53 Activator Wnt Inhibitor-2 (PAWI-2) that was developed by optimizing potency and pharmaceutical properties. PAWI-2 is a nontoxic DNA-damage pathway inhibitor that shows a broad spectrum of potency and significant efficacy in vitro and in vivo. This study focuses on the application of PAWI-2 to four major types of cancers including colorectal cancer (CRC), breast cancer (BC), prostate cancer (PCa), and pancreatic cancer (PC). PAWI-2 shows a novel mechanism of action (MOA) by modulating two mechanisms of cancer invasion. In cancer with unimpaired p53, PAWI-2 activates DNA-damage checkpoint and mitochondrial p53-dependent apoptotic signaling. Consistently observed in most cancer types, PAWI-2 induces phosphorylation of optineurin (OPTN) to cause G2/M cell cycle arrest. These two mechanisms operate regardless of p53 variants and/or KRAS mutation status and also manipulate the effect of PAWI-2 to overcome tumor stemness and drug resistance in PC stem cells (PCSCs). This study summarizes the development of PAWI-2 as an attractive targeted therapeutic for mechanism-driven anti-cancer drug discovery.
C1 [Cheng, Jiongjia; Cashman, John R.] Human BioMol Res Inst, San Diego, CA 92121 USA.
   [Cheng, Jiongjia; Cashman, John R.] ChemRegen Inc, San Diego, CA 92121 USA.
RP Cheng, JJ (corresponding author), Human BioMol Res Inst, San Diego, CA 92121 USA.; Cheng, JJ (corresponding author), ChemRegen Inc, San Diego, CA 92121 USA.
EM jcheng@hbri.org
RI Cheng, Jiongjia/AAM-9464-2020
FU National Institutes of Health; California Institute for Regenerative
   Medicine (CIRM)
FX We acknowledge all the coworkers and collaborators cited in the
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   financial support of the National Institutes of Health and the
   California Institute for Regenerative Medicine (CIRM).
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NR 92
TC 2
Z9 2
U1 1
U2 4
PU SPRINGER BIRKHAUSER
PI NEW YORK
PA 233 SPRING STREET, 6TH FLOOR, NEW YORK, NY 10013 USA
SN 1054-2523
EI 1554-8120
J9 MED CHEM RES
JI Med. Chem. Res.
PD JUL
PY 2020
VL 29
IS 7
SI SI
BP 1147
EP 1159
DI 10.1007/s00044-020-02575-8
EA JUN 2020
PG 13
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA MC7BP
UT WOS:000538378300002
DA 2025-01-04
ER

PT J
AU Ning, ST
   Lee, SY
   Wei, MF
   Peng, CL
   Lin, SYF
   Tsai, MH
   Lee, PC
   Shih, YH
   Lin, CY
   Luo, TY
   Shieh, MJ
AF Ning, Sin-Tzu
   Lee, Shin-Yu
   Wei, Ming-Feng
   Peng, Cheng-Liang
   Lin, Susan Yun-Fan
   Tsai, Ming-Hsien
   Lee, Pei-Chi
   Shih, Ying-Hsia
   Lin, Chun-Yen
   Luo, Tsai-Yueh
   Shieh, Ming-Jium
TI Targeting Colorectal Cancer Stem-Like Cells with Anti-CD133
   Antibody-Conjugated SN-38 Nanoparticles
SO ACS APPLIED MATERIALS & INTERFACES
LA English
DT Article
DE colorectal cancer; cancer stem-like cells; CD133; SN-38; nanoparticles
ID CD133 EXPRESSION; CHEMOTHERAPY; IDENTIFICATION; DELIVERY; THERAPY;
   MODEL; PHARMACOKINETICS; PRINCIPLES
AB Cancer stem-like cells play a key role in tumor development, and these cells are relevant to the failure of conventional chemotherapy. To achieve favorable therapy for colorectal cancer, PEG-PCL-based nanoparticles, which possess good biological compatibility, were fabricated as nanocarriers for the topoisomerase inhibitor, SN-38. For cancer stem cell therapy, CD133 (prominin-1) is a theoretical cancer stem-like cell (CSLC) marker for colorectal cancer and is a proposed therapeutic target. Cells with CD133 over expression have demonstrated enhanced tumor-initiating ability and tumor relapse probability. To resolve the problem of chemotherapy failure, SN-38-loaded nanoparticles were conjugated with anti-CD133 antibody to target CD133-positive (CD1334) cells. In this study, anti-CD133 antibody-conjugated SN-38-loaded nanoparticles (CD133Ab-NPs-SN-38) efficiently bound to HCT116 cells, which overexpress CD133 glycoprotein. The cytotoxic effect of CD133Ab-NPs-SN-38 was greater than that of nontargeted nanoparticles (NPs-SN-38) in HCT116 cells. Furthermore, CD133Ab-NPs-SN-38 could target CD1334 cells and inhibit colony formation compared with NPs-SN-38. In vivo studies in an HCT116 xenograft model revealed that CD133Ab-NPs-SN-38 suppressed tumor growth and retarded recurrence. A reduction in CD133 expression in HCT116 cells treated with CD133Ab-NPs-SN-38 was also observed in immunohistochemistry results. Therefore, this CD133-targeting nanoparticle delivery system could eliminate CD133-positive cells and is a potential cancer stem cell targeted therapy.
C1 [Ning, Sin-Tzu; Lee, Shin-Yu; Wei, Ming-Feng; Lin, Susan Yun-Fan; Tsai, Ming-Hsien; Lee, Pei-Chi; Shih, Ying-Hsia; Lin, Chun-Yen; Shieh, Ming-Jium] Natl Taiwan Univ, Coll Med, Inst Biomed Engn, Taipei 100, Taiwan.
   [Ning, Sin-Tzu; Lee, Shin-Yu; Wei, Ming-Feng; Lin, Susan Yun-Fan; Tsai, Ming-Hsien; Lee, Pei-Chi; Shih, Ying-Hsia; Lin, Chun-Yen; Shieh, Ming-Jium] Natl Taiwan Univ, Coll Engn, Taipei 100, Taiwan.
   [Peng, Cheng-Liang; Shih, Ying-Hsia; Luo, Tsai-Yueh] Inst Nucl Energy Res, Isotope Applicat Div, Taoyuan 325, Taiwan.
   [Shieh, Ming-Jium] Natl Taiwan Univ Hosp & Coll Med, Dept Oncol, Taipei 100, Taiwan.
C3 National Taiwan University; National Taiwan University; Institute of
   Nuclear Energy Research - Taiwan; National Taiwan University; National
   Taiwan University Hospital
RP Shieh, MJ (corresponding author), Natl Taiwan Univ, Coll Med, Inst Biomed Engn, Taipei 100, Taiwan.; Shieh, MJ (corresponding author), Natl Taiwan Univ, Coll Engn, Taipei 100, Taiwan.; Shieh, MJ (corresponding author), Natl Taiwan Univ Hosp & Coll Med, Dept Oncol, Taipei 100, Taiwan.
EM soloman@ntu.edu.tw
RI Tsai, Ming-Hsien/AAT-8218-2021
OI Lee, Shin-Yu/0000-0003-0292-6176
FU Ministry of Science and Technology, R.O.C. [MOST
   102-2320-B-002-038-MY3]; Ministry of Health and Welfare, R.O.C [MOHW
   103-TDU-N-211-133006]; National Taiwan University Hospital [105-S3009]
FX This work was financially supported by the Ministry of Science and
   Technology, R.O.C. (MOST 102-2320-B-002-038-MY3), the Ministry of Health
   and Welfare, R.O.C (MOHW 103-TDU-N-211-133006), and National Taiwan
   University Hospital (105-S3009).
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NR 51
TC 86
Z9 91
U1 3
U2 55
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1944-8244
EI 1944-8252
J9 ACS APPL MATER INTER
JI ACS Appl. Mater. Interfaces
PD JUL 20
PY 2016
VL 8
IS 28
BP 17793
EP 17804
DI 10.1021/acsami.6b04403
PG 12
WC Nanoscience & Nanotechnology; Materials Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Materials Science
GA DS0PE
UT WOS:000380298400008
PM 27348241
DA 2025-01-04
ER

PT J
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   Mueller, S.
   Lerch, M. M.
   Modest, D. P.
   Kirchner, T.
   Jung, A.
   Heinemann, V.
CA Fire-3 Study Grp
TI CEA response is associated with tumor response and survival in patients
   with KRAS exon 2 wild-type and extended RAS wild-type metastatic
   colorectal cancer receiving first-line FOLFIRI plus cetuximab or
   bevacizumab (FIRE-3 trial)<SUP>aEuro</SUP>
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE CEA; tumor marker; metastatic colorectal cancer; KRAS exon 2 wild-type;
   extended RAS wild-type; FIRE-3 trial
ID CARCINOEMBRYONIC ANTIGEN; EVALUATION CRITERIA; SOLID TUMORS;
   CHEMOTHERAPY; SHRINKAGE; MARKERS; FLUOROURACIL; LEUCOVORIN; MUTATIONS;
   THERAPY
AB Carcinoembryonic antigen (CEA) response may be a surrogate for response and long-term outcome in (K)RAS wild-type mCRC receiving first-line targeted therapy. FOLFIRI and cetuximab induced a greater CEA response than FOLFIRI and bevacizumab. CEA response correlated with longer survival. Hypothesizing that CEA reflects tumor burden, greater CEA response may indicate greater antitumor efficacy.To examine the relation of carcinoembryonic antigen (CEA) response with tumor response and survival in patients with (K)RAS wild-type metastatic colorectal cancer receiving first-line chemotherapy in the FIRE-3 trial comparing FOLFIRI plus cetuximab versus FOLFIRI plus bevacizumab.
   CEA response assessed as the percentage of CEA decrease from baseline to nadir was evaluated for its association with tumor response and survival. Receiver operating characteristic analysis revealed an optimal cut-off value of 75% using the maximum of sensitivity and specificity for CEA response to discriminate CEA responders from non-responders. In addition, the time to CEA nadir was calculated.
   Of 592 patients in the intent-to-treat population, 472 were eligible for analysis of CEA (cetuximab arm: 230 and bevacizumab arm: 242). Maximal relative CEA decrease (%) significantly (P = 0.003) differed between the cetuximab arm (median 83.0%; IQR 40.9%-94.7%) and the bevacizumab arm (median 72.3%; IQR 26.3%-91.0%). In a longitudinal analysis, the CEA decrease occurred faster in the cetuximab arm and was greater than in the bevacizumab arm at all evaluated time points until 56 weeks after treatment start. CEA nadir occurred after 3.3 months (cetuximab arm) and 3.5 months (bevacizumab arm), (P = 0.49). In the cetuximab arm, CEA responders showed a significantly longer progression-free survival [11.8 versus 7.4 months; hazard ratio (HR) 1.53; 95% Cl, 1.15-2.04; P = 0.004] and longer overall survival (36.6 versus 21.3 months; HR 1.73; 95% Cl, 1.24-2.43; P = 0.001) than CEA non-responders. Analysis of extended RAS wild-type patients revealed similar results.
   In the FIRE-3 trial, CEA decrease was significantly faster and greater in the cetuximab arm than in the bevacizumab arm and correlated with the prolonged survival observed in patients receiving FOLFIRI plus cetuximab.
   NCT00433927 (ClinicalTrials.gov); AIO KRK0306 FIRE-3.
C1 [Michl, M.; Stintzing, S.; Modest, D. P.; Heinemann, V.] Univ Munich, Klinikum Grosshadern, Dept Hematol & Med Oncol, Munich, Germany.
   [Michl, M.; Stintzing, S.; Modest, D. P.; Heinemann, V.] Univ Munich, Comprehens Canc Ctr Munich, Munich, Germany.
   [Stintzing, S.; Modest, D. P.; Kirchner, T.; Jung, A.; Heinemann, V.] German Canc Res Ctr, German Canc Consortium DKTK, Heidelberg, Germany.
   [Fischer von Weikersthal, L.] Gesundheitszentrum St Marien, Hematol & Med Oncol, Amberg, Germany.
   [Decker, T.] Onkonet Onkol Ravensburg, Hematol & Med Oncol, Ravensburg, Germany.
   [Kiani, A.] Klin Herzoghohe, Dept Hematol & Med Oncol, Bayreuth, Germany.
   [Al-Batran, S. -E.] Univ Canc Ctr Frankfurt, Krankenhaus Nordwest, Dept Hematol & Med Oncol, Frankfurt, Germany.
   [Heintges, T.] Stadt Klinikum Neuss, Lukaskrankenhaus, Dept Med 2, Dept Gastroenterol & Oncol, Neuss, Germany.
   [Kahl, C.] Klinikum Magdeburg, Dept Hematol & Med Oncol, Magdeburg, Germany.
   [Kullmann, F.] Klinikum Weiden, Dept Gastroenterol Hematol & Med Oncol, Weiden, Germany.
   [Scheithauer, W.] Med Univ Vienna, Dept Hematol & Med Oncol, Vienna, Austria.
   [Hielscher, J.] Klinikum Chemnitz, Dept Surg, Chemnitz, Germany.
   [Scholz, M.] Klinikum Stuttgart, Dept Med, Stuttgart, Germany.
   [Lerch, M. M.] Univ Med Greifswald, Dept Med A, Greifswald, Germany.
   [Kirchner, T.; Jung, A.] Univ Munich, Klinikum Grosshadern, Dept Pathol, Munich, Germany.
C3 University of Munich; University of Munich; Helmholtz Association;
   German Cancer Research Center (DKFZ); Krankenhaus Nordwest; Medical
   University of Vienna; Chemnitz Clinic; Klinikum Stuttgart; Greifswald
   Medical School; University of Munich
RP Michl, M (corresponding author), Univ Munich, Klinikum Grosshadern, Dept Hematol & Med Oncol, Munich, Germany.
EM marlies.michl@med.uni-muenchen.de
RI Modest, Dominik Paul/AAW-9756-2021; Michl, Marlies/M-7969-2019;
   Stintzing, Sebastian/I-4538-2016; Lerch, Markus M./E-2206-2016
OI Stintzing, Sebastian/0000-0002-3297-5801; Lerch, Markus
   M./0000-0002-9643-8263; Decker, Thomas/0000-0003-3814-8775
FU Merck KGaA; Pfizer
FX The FIRE-3 trial was funded by Merck KGaA and Pfizer. However, for the
   present analysis, no funding was received and thus no grant number is
   applicable. The funding sources had no role in the design,
   interpretation or conduct of this evaluation, writing manuscript, or
   decision to submit or publish the data. Merck KGaA and Pfizer reviewed
   the manuscript before journal submission. However, the authors are fully
   responsible for the content of this manuscript, and the views and
   opinions described in the publication reflect solely those of the
   authors. VH has full access to all study data and had final
   responsibility for publication.
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NR 20
TC 26
Z9 27
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
EI 1569-8041
J9 ANN ONCOL
JI Ann. Oncol.
PD AUG
PY 2016
VL 27
IS 8
BP 1565
EP 1572
DI 10.1093/annonc/mdw222
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DV8JH
UT WOS:000383182800026
PM 27234640
OA Bronze
DA 2025-01-04
ER

PT J
AU Martin, SZ
   Wagner, DC
   Hörner, N
   Horst, D
   Lang, HK
   Tagscherer, KE
   Roth, W
AF Martin, Steve Z.
   Wagner, Daniel C.
   Hoerner, Nina
   Horst, David
   Lang, Hauke
   Tagscherer, Katrin E.
   Roth, Wilfried
TI Ex vivo tissue slice culture system to measure drug-response rates of
   hepatic metastatic colorectal cancer
SO BMC CANCER
LA English
DT Article
DE Ex vivo culture; Colorectal liver metastases; CRLM; Predictive
   biomarker; Predictive test system
ID PLUS CETUXIMAB TREATMENT; RAS MUTATIONS; PHASE-II; LIVER METASTASES;
   PD-1 BLOCKADE; SINGLE-AGENT; TUMOR; OXALIPLATIN; CHEMOTHERAPY;
   MICROENVIRONMENT
AB Background: The lack of predictive biomarkers or test systems contributes to high failure rates of systemic therapy in metastasized colorectal carcinoma, accounting for a still unfavorable prognosis. Here, we present an ex vivo functional assay to measure drug-response based on a tissue slice culture approach.
   Methods: Tumor tissue slices of hepatic metastases of nine patients suffering from colorectal carcinoma were cultivated for 72 h and treated with different concentrations of the clinically relevant drugs Oxaliplatin, Cetuximab and Pembrolizumab. Easy to use, objective and automated analysis routines based on the Halo platform were developed to measure changes in proliferative activity and the morphometric make-up of the tumor. Apoptotic indices were assessed semiquantitatively.
   Results: Untreated tumor tissue slices showed high morphological comparability with the original "in vivo"-tumor, preserving proliferation and stromal-tumor interactions. All but one patients showed a dosage dependent susceptibility to treatment with Oxaliplatin, whereas only two patients showed responses to Cetuximab and Pembrolizumab, respectively. Furthermore, we identified possible non-responders to Cetuximab therapy in absence of RAS-mutations.
   Conclusions: This is the first time to demonstrate feasibility of the tissue slice culture approach for metastatic tissue of colorectal carcinoma. An automated readout of proliferation and tumor-morphometry allows for quantification of drug susceptibility. This strongly indicates a potential value of this technique as a patient-specific test-system of targeted therapy in metastatic colorectal cancer. Co-clinical trials are needed to customize for clinical application and to define adequate read-out cut-off values.
C1 [Martin, Steve Z.; Wagner, Daniel C.; Hoerner, Nina; Tagscherer, Katrin E.; Roth, Wilfried] Univ Med Ctr Mainz, Inst Pathol, Langenbeckstr 1, D-55131 Mainz, Germany.
   [Martin, Steve Z.; Horst, David] Charite Univ Med Berlin, Inst Pathol, D-10117 Berlin, Germany.
   [Martin, Steve Z.; Horst, David] Free Univ Berlin, D-10117 Berlin, Germany.
   [Martin, Steve Z.; Horst, David] Humboldt Univ, D-10117 Berlin, Germany.
   [Martin, Steve Z.; Horst, David] Berlin Inst Hlth, Campus Charite Mitte, D-10117 Berlin, Germany.
   [Lang, Hauke] Univ Med Ctr Mainz, Dept Gen Visceral & Transplantat Surg, Langenbeckstr 1, D-55131 Mainz, Germany.
C3 Johannes Gutenberg University of Mainz; Berlin Institute of Health; Free
   University of Berlin; Humboldt University of Berlin; Charite
   Universitatsmedizin Berlin; Free University of Berlin; Humboldt
   University of Berlin; Berlin Institute of Health; Free University of
   Berlin; Humboldt University of Berlin; Charite Universitatsmedizin
   Berlin; Johannes Gutenberg University of Mainz
RP Martin, SZ (corresponding author), Univ Med Ctr Mainz, Inst Pathol, Langenbeckstr 1, D-55131 Mainz, Germany.; Martin, SZ (corresponding author), Charite Univ Med Berlin, Inst Pathol, D-10117 Berlin, Germany.; Martin, SZ (corresponding author), Free Univ Berlin, D-10117 Berlin, Germany.; Martin, SZ (corresponding author), Humboldt Univ, D-10117 Berlin, Germany.; Martin, SZ (corresponding author), Berlin Inst Hlth, Campus Charite Mitte, D-10117 Berlin, Germany.
EM steve.martin@charite.de
RI Wagner, Daniel/IZE-2807-2023; Tagscherer, Katrin/AAS-3809-2021
OI Martin, Steve/0000-0003-0653-6458; Horst, David/0000-0003-4755-5743;
   Wagner, Daniel-Christoph/0000-0001-7516-5860
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NR 54
TC 32
Z9 33
U1 0
U2 2
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD NOV 1
PY 2019
VL 19
IS 1
AR 1030
DI 10.1186/s12885-019-6270-4
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JK4KS
UT WOS:000494813100009
PM 31675944
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yue, TH
   Cai, YL
   Zhu, J
   Liu, YC
   Chen, SW
   Wang, PY
   Rong, L
AF Yue, Taohua
   Cai, Yunlong
   Zhu, Jing
   Liu, Yucun
   Chen, Shanwen
   Wang, Pengyuan
   Rong, Long
TI Autophagy-related IFNG is a prognostic and immunochemotherapeutic
   biomarker of COAD patients
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE colon adenocarcinoma (COAD); autophagy; IFNg; prognosis; immunotherapy;
   cisplatin
ID GAMMA; MACROPHAGES; SERVER; ALPHA
AB BackgroundNumerous studies have shown autophagy affects cellular immune responses. This study aims to explore prognosis and immunotherapeutic biomarkers related to autophagy in colon adenocarcinoma (COAD). MethodsBased on R software, we performed the ssGSEA, differential expression analysis, Kaplan-Meier survival analysis, correlation analysis, and enrichment analysis. For wet experiment, we did qRT-PCR, immunohistochemistry and CCK-8 experiments. ResultsUsing autophagy-related genes (ARGs) and the ssGSEA, COAD patients were divided into low and high autophagy groups. For immune score, stromal score, tumor purity, tumor infiltrating immune cells, co-signaling molecules, tumor mutational burden, microsatellite instability, mismatch repair, immune-related pathways, immune signatures, somatic mutations and subtype analysis, high autophagy group might benefit more from immunotherapy. Among 232 ARGs, IFNG was generally significantly correlated with tumor immunotherapy biomarkers (PD-L1, CD8A and cytotoxic T lymphocytes (CTL)). The disease-free survival of high IFNG group was significantly longer than that of low group. On above-mentioned immune-related research, the high IFNG group reached the same conclusion. The qRT-PCR and IHC analysis confirmed that IFNG was significantly higher expressed in dMMR samples compared to pMMR samples. For chemotherapy, the autophagy and IFNG were significantly negatively related to the chemosensitivity to cisplatin; IFNG inhibitor glucosamine increased cisplatin chemoresistance while IFNG increased cisplatin chemosensitivity; IFNG could reverse glucosamine induced chemoresistance. The functional enrichment analysis of IFNG, PD-L1, CD8A and 20 similar proteins were related to the activation of the immune system. The GSEA and ceRNA network partly described interaction mechanisms of IFNG with PD-L1 and CD8A. ConclusionAutophagy score and IFNG expression were novel immunotherapy predictive biomarkers, which might play predictive effects through the JAK-STAT signaling pathway. IFNG might be a potential targeted therapy for cisplatin resistant colon cancer. Besides, IFNG was also a prognostic indicator.
C1 [Yue, Taohua; Cai, Yunlong; Rong, Long] Peking Univ, Peking Univ First Hosp, Dept Endoscopy Ctr, Beijing, Peoples R China.
   [Zhu, Jing; Liu, Yucun; Chen, Shanwen; Wang, Pengyuan] Peking Univ, Peking Univ First Hosp, Div Gen Surg, Beijing, Peoples R China.
C3 Peking University; Peking University
RP Rong, L (corresponding author), Peking Univ, Peking Univ First Hosp, Dept Endoscopy Ctr, Beijing, Peoples R China.; Wang, PY (corresponding author), Peking Univ, Peking Univ First Hosp, Div Gen Surg, Beijing, Peoples R China.
EM pengyuan_wang_bjmu@163.com; long_rong_bjmu@163.com
RI wang, rui/JAC-6240-2023; Liu, Yucun/AAW-9532-2020; yue,
   taohua/AAH-8434-2021
FU National High Level Hospital Clinical Research Funding (Scientific
   Research Seed Fund of Peking University First Hospital) [2023SF36];
   Capital Health Development Scientific Research Project [2022-2-40710]
FX This research was supported by the National High Level Hospital Clinical
   Research Funding (Scientific Research Seed Fund of Peking University
   First Hospital) (2023SF36) and the Capital Health Development Scientific
   Research Project (No. 2022-2-40710).
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NR 57
TC 5
Z9 5
U1 1
U2 6
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JAN 23
PY 2023
VL 14
AR 1064704
DI 10.3389/fimmu.2023.1064704
PG 18
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 8O9MW
UT WOS:000926156300001
PM 36756126
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhen, ZP
   Tang, W
   Wang, MZ
   Zhou, SY
   Wang, H
   Wu, ZH
   Hao, ZL
   Li, ZB
   Liu, L
   Xie, J
AF Zhen, Zipeng
   Tang, Wei
   Wang, Mengzhe
   Zhou, Shiyi
   Wang, Hui
   Wu, Zhanhong
   Hao, Zhonglin
   Li, Zibo
   Liu, Lin
   Xie, Jin
TI Protein Nanocage Mediated Fibroblast-Activation Protein Targeted
   Photoimmunotherapy To Enhance Cytotoxic T Cell Infiltration and Tumor
   Control
SO NANO LETTERS
LA English
DT Article
DE Photodynamic therapy; immunotherapy; cytotoxic T cells;
   carcinoma-associated fibroblast; fibroblast-activation protein
ID NEAR-INFRARED PHOTOIMMUNOTHERAPY; REACTIVE STROMAL FIBROBLASTS;
   PHOTODYNAMIC THERAPY; MONOCLONAL-ANTIBODY; DRUG-DELIVERY; EPITHELIAL
   CANCERS; SERINE-PROTEASE; COLON-CANCER; IMMUNE; GROWTH
AB Carcinoma-associated fibroblasts (CAFs) are found in many types of cancer and play an important role in tumor growth and metastasis. Fibroblast-activation protein (FAP), which is overexpressed on the surface of CAFs, has been proposed as a universal tumor targeting antigen. However, recent studies show that FAP is also expressed on multipotent bone marrow stem cells. A systematic anti-FAP therapy may lead to severe side effects and even death. Hence, there is an urgent need of a therapy that can selectively kill CAFs without causing systemic toxicity. Herein we report a nanopartide-based photoimmunotherapy (nano-PIT) approach that addresses the need. Specifically, we exploit ferritin, a compact nanopartide protein cage, as a photosensitizer carrier, and we conjugate to the surface of ferritin a FAP-specific single chain variable fragment (scFv). With photoirradiation, the enabled nano-PIT efficiently eliminates CAFs in tumors but causes little damage to healthy tissues due to the localized nature of the treatment. Interestingly, while not directly killing cancer cells, the nano-PIT caused efficient tumor suppression in tumor-bearing immunocompetent mice. Further investigations found that the nano-PIT led to suppressed C-X-C motif chemokine ligand 12 (CXCL12) secretion and extracellular matrix (ECM) deposition, both of which are regulated by CAFs in untreated tumors and mediate T cell exclusion that prevents physical contact between T cells and cancer cells. By selective killing of CAFs, the nano-PIT reversed the effect, leading to significantly enhanced T cell infiltration, followed by efficient tumor suppression. Our study suggests a new and safe CAF-targeted therapy and a novel strategy to modulate tumor microenvironment (TME) for enhanced immunity against cancer.
C1 [Zhen, Zipeng; Liu, Lin] Jilin Univ, China Japan Union Hosp, Dept Radiol, Changchun 130033, Peoples R China.
   [Zhen, Zipeng; Tang, Wei; Zhou, Shiyi; Xie, Jin] Univ Georgia, Bioimaging Res Ctr, Dept Chem, Athens, GA 30602 USA.
   [Wang, Mengzhe; Wang, Hui; Wu, Zhanhong; Li, Zibo] Univ North Carolina Chapel Hill, Dept Radiol, Chapel Hill, NC 27599 USA.
   [Wang, Mengzhe; Wang, Hui; Wu, Zhanhong; Li, Zibo] Univ North Carolina Chapel Hill, Biomed Res Imaging Ctr, Chapel Hill, NC 27599 USA.
   [Hao, Zhonglin] Augusta Univ, Med Coll Georgia, Dept Internal Med, Augusta, GA 30912 USA.
C3 Jilin University; University System of Georgia; University of Georgia;
   University of North Carolina; University of North Carolina Chapel Hill;
   University of North Carolina School of Medicine; University of North
   Carolina School of Medicine; University of North Carolina; University of
   North Carolina Chapel Hill; University System of Georgia; Augusta
   University
RP Liu, L (corresponding author), Jilin Univ, China Japan Union Hosp, Dept Radiol, Changchun 130033, Peoples R China.; Xie, J (corresponding author), Univ Georgia, Bioimaging Res Ctr, Dept Chem, Athens, GA 30602 USA.
EM liulin5413@126.com; jinxie@uga.edu
RI Xie, Jin/E-8193-2010; Tang, Wei/AGX-1319-2022; Zhen,
   Zipeng/IVV-2266-2023; Li, Zi-Jian/IWM-1489-2023
OI Wang, Hui/0000-0002-2346-8621; Wu, Zhanhong/0000-0002-3528-5603; Xie,
   Jin/0000-0002-8915-6233; Tang, Wei/0000-0001-8613-4285; li,
   zibo/0000-0002-1063-0298
FU DoD CDMRP grant [CA140666]; NSF CAREER grant [NSF1552617]; UGA-Augusta
   seed grant; American Cancer Society grant [MSRG-12-034-01-CCE]; Direct
   For Mathematical & Physical Scien; Division Of Materials Research
   [1552617] Funding Source: National Science Foundation; CDMRP [793849,
   CA140666] Funding Source: Federal RePORTER
FX The lung, liver, and kidney tumor slices were a courtesy from professor
   Dexi Liu at the Pharmacy College of UGA. This research was supported by
   a DoD CDMRP grant (CA140666, J.X.), an NSF CAREER grant (NSF1552617,
   J.X.), a UGA-Augusta seed grant (J.X.), and an American Cancer Society
   grant (MSRG-12-034-01-CCE).
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NR 60
TC 168
Z9 180
U1 2
U2 192
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1530-6984
EI 1530-6992
J9 NANO LETT
JI Nano Lett.
PD FEB
PY 2017
VL 17
IS 2
BP 862
EP 869
DI 10.1021/acs.nanolett.6b04150
PG 8
WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience &
   Nanotechnology; Materials Science, Multidisciplinary; Physics, Applied;
   Physics, Condensed Matter
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science;
   Physics
GA EK3SW
UT WOS:000393848800038
PM 28027646
DA 2025-01-04
ER

PT J
AU Yuan, YX
   Guo, MJ
   Gu, CY
   Yang, Y
AF Yuan, Yuxia
   Guo, Mengjie
   Gu, Chunyan
   Yang, Ye
TI The role of Wnt/β-catenin signaling pathway in the pathogenesis and
   treatment of multiple myeloma (review)
SO AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH
LA English
DT Review
DE Multiple myeloma; Wnt/beta-catenin pathway; bone marrow
   microenvironment; osteoblasts; targeted therapy; drugs or small-molecule
   inhibitors
ID CANONICAL WNT PATHWAY; BETA-CATENIN; INHIBITS PROLIFERATION;
   PARATHYROID-HORMONE; COLORECTAL-CANCER; DRUG-RESISTANCE; SCLEROSTIN;
   CELLS; PROMOTES; EXPRESSION
AB Multiple myeloma (MM) is a refractory hematological malignancy characterized by aberrant accumulation of plasma cells. Patients with MM are susceptible to becoming resistant to chemotherapy, eventually leading to relapse. Progression of MM is largely dependent on the bone marrow microenvironment. Stromal cells in the bone marrow microenvironment secrete Wnt ligands to activate Wnt signaling in MM, which is mediated through the transcription regulator beta-catenin. In addition, Wnt/beta-catenin pathway encourages osteoblast differentiation and bone formation, dysregulation of which is responsible for proliferation and drug resistance of MM cells. As a result, direct inhibition or silencing of beta-catenin or associated genes in the Wnt/beta-catenin pathway has been proposed to be an effective therapeutic anti-MM strategy. However, the underlying regulatory mechanism of the Wnt/beta-catenin pathway in MM remains to be fully elucidated. Herein, we summarized research advances on the specific genes and molecular biology process of Wnt/beta-catenin pathway involved in tumorigenesis of MM, as well as the interaction with bone marrow microenvironment. Additionally, comprehensive summaries of drugs or small molecule inhibitors acting on Wnt/beta-catenin pathway and targeting MM were introduced. This review intends to provide an overview of theoretical supports for novel Wnt/beta-catenin pathway based treatment strategies in MM.
C1 [Yuan, Yuxia; Gu, Chunyan; Yang, Ye] Nanjing Univ Chinese Med, Nanjing Hosp Chinese Med, Nanjing 210022, Jiangsu, Peoples R China.
   [Yuan, Yuxia; Guo, Mengjie; Gu, Chunyan; Yang, Ye] Nanjing Univ Chinese Med, Sch Med & Holist Integrat Med, Nanjing 210023, Jiangsu, Peoples R China.
C3 Nanjing University of Chinese Medicine; Nanjing University of Chinese
   Medicine
RP Gu, CY; Yang, Y (corresponding author), Nanjing Univ Chinese Med, 138 Xianlin Rd, Nanjing 210023, Jiangsu, Peoples R China.
EM guchunyan@njucm.edu.cn; yangye876@sina.com
RI yang, yang/GWB-9426-2022; YANG, YE/F-4987-2015
OI YANG, YE/0000-0003-0228-5102
FU National Natural Science Foundation of China [82003832, 81970196,
   81670200]; Priority Academic Program Development of Jiangsu Higher
   Education Institutions (Integration of Chinese and Western Medicine);
   Innovation Team of Six Talent Peaks Project in Jiangsu Province
   [TD-SWYY-015]; Natural Science Foundation of Jiangsu Province for
   Excellent Young Scholars
FX This work was supported by National Natural Science Foundation of China
   82003832, 81970196 and 81670200 (to MG & CG & YY) ; A Project Funded by
   the Priority Academic Program Development of Jiangsu Higher Education
   Institutions (Integration of Chinese and Western Medicine) ; Innovation
   Team of Six Talent Peaks Project in Jiangsu Province (TD-SWYY-015) ;
   Natural Science Foundation of Jiangsu Province for Excellent Young
   Scholars. The authors gratefully appreciate the help of Dr. Miaomiao
   Shao and Dr. Xiaoxuan Yu in the process of editing the manuscript.
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NR 123
TC 9
Z9 10
U1 0
U2 3
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1943-8141
J9 AM J TRANSL RES
JI Am. J. Transl. Res.
PY 2021
VL 13
IS 9
BP 9932
EP 9949
PG 18
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA WC1PK
UT WOS:000704035800002
PM 34650674
DA 2025-01-04
ER

PT J
AU Jiang, CY
   Meng, LX
   Yang, BJ
   Luo, X
AF Jiang, Chunyang
   Meng, Lingxiang
   Yang, Bingjun
   Luo, Xin
TI Application of <i>CRISPR/Cas9</i> gene editing technique in the study of
   cancer treatment
SO CLINICAL GENETICS
LA English
DT Review
DE Cancer; CRISPR; Cas9; gene editing; therapy
ID ONE-STEP GENERATION; CELL LUNG-CANCER; COLORECTAL-CANCER; DNA
   METHYLATION; IN-VITRO; ACQUIRED-RESISTANCE; CHECKPOINT BLOCKADE;
   DRUG-RESISTANCE; PROTEIN-KINASE; BREAST-CANCER
AB In recent years, gene editing, especially that using clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9, has made great progress in the field of gene function. Rapid development of gene editing techniques has contributed to their significance in the field of medicine. Because the CRISPR/Cas9 gene editing tool is not only powerful but also has features such as strong specificity and high efficiency, it can accurately and rapidly screen the whole genome, facilitating the administration of gene therapy for specific diseases. In the field of tumor research, CRISPR/Cas9 can be used to edit genomes to explore the mechanisms of tumor occurrence, development, and metastasis. In these years, this system has been increasingly applied in tumor treatment research. CRISPR/Cas9 can be used to treat tumors by repairing mutations or knocking out specific genes. To date, numerous preliminary studies have been conducted on tumor treatment in related fields. CRISPR/Cas9 holds great promise for gene-level tumor treatment. Personalized and targeted therapy based on CRISPR/Cas9 will possibly shape the development of tumor therapy in the future. In this study, we review the findings of CRISPR/Cas9 for tumor treatment research to provide references for related future studies on the pathogenesis and clinical treatment of tumors.
C1 [Jiang, Chunyang; Yang, Bingjun] Tianjin Union Med Ctr, Dept Thorac Surg, 190 Jieyuan Rd, Tianjin 300121, Peoples R China.
   [Meng, Lingxiang] Tianjin Union Med Ctr, Anorectal Surg Ctr, Dept Anorectal Surg, Tianjin, Peoples R China.
   [Luo, Xin] Second Affiliated Hosp, Gansu Med Coll, Hosp PingLiang City 2, Dept Radiotherapy, Pingliang, Peoples R China.
C3 Gansu Medical College
RP Jiang, CY (corresponding author), Tianjin Union Med Ctr, Dept Thorac Surg, 190 Jieyuan Rd, Tianjin 300121, Peoples R China.
EM chunyangjiang@126.com
RI jiang, chunyang/AEQ-0436-2022
OI , Chunyang/0000-0002-7878-2829
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NR 166
TC 43
Z9 47
U1 9
U2 111
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0009-9163
EI 1399-0004
J9 CLIN GENET
JI Clin. Genet.
PD JAN
PY 2020
VL 97
IS 1
BP 73
EP 88
DI 10.1111/cge.13589
EA JUL 2019
PG 16
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA NE4IZ
UT WOS:000477247900001
PM 31231788
DA 2025-01-04
ER

PT J
AU Pan, P
   Peiffer, DS
   Huang, YW
   Oshima, K
   Stoner, GD
   Wang, LS
AF Pan, Pan
   Peiffer, Daniel S.
   Huang, Yi-Wen
   Oshima, Kiyoko
   Stoner, Gary D.
   Wang, Li-Shu
TI Inhibition of the development of N-nitrosomethylbenzylamine-induced
   esophageal tumors in rats by strawberries and aspirin, alone and in
   combination
SO JOURNAL OF BERRY RESEARCH
LA English
DT Article
DE Esophageal squamous cell carcinoma; strawberries; aspirin; PCNA
ID COLONIC ADENOMA DEVELOPMENT; BLACK-RASPBERRIES; COLORECTAL-CANCER;
   TARGETED THERAPY; GENE-EXPRESSION; CYCLIN D1; RISK; CHEMOPREVENTION;
   ANTHOCYANINS; PREVENTION
AB BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is one of two subtypes of esophageal cancer, with high incidence and mortality rates in developing countries.
   OBJECTIVE: The current study investigated the potential chemoprotective effects of strawberries and aspirin against the development of rat esophageal papillomas, the precursors to ESCC.
   METHODS: Using a prevention model, we administered study diets to rats before, during, and after N-nitrosomethylbenzylamine (NMBA) treatment. The effects of the four diets were evaluated: the control diet, 5% strawberry powder in the control diet, 0.01% aspirin in the drinking water, and the combination of strawberries and aspirin. At week 25, we euthanized all the rats and collected their esophagi to quantify tumor incidence, multiplicity, and burden, as well as for molecular analysis.
   RESULTS: Both strawberries and aspirin significantly decreased esophageal tumor multiplicity, with the combination causing the most robust suppression. Aspirin alone and the combination decreased the total tumor burden in the esophagus. None of the diets had a significant effect on tumor incidence or the expression of COX-1 and COX-2. Strawberries and aspirin, alone and in combination, significantly suppressed squamous epithelial cell proliferation (PCNA).
   CONCLUSIONS: Strawberries, aspirin, and their combination exhibit chemoprotective effects against NMBA-induced esophageal tumors in rats.
C1 [Pan, Pan; Peiffer, Daniel S.; Stoner, Gary D.; Wang, Li-Shu] Med Coll Wisconsin, Dept Med, Div Hematol & Oncol, RM C4930,8701 Watertown Plank Rd, Milwaukee, WI 53226 USA.
   [Peiffer, Daniel S.] Loyola Univ, Stritch Sch Med, Chicago, IL 60611 USA.
   [Huang, Yi-Wen] Med Coll Wisconsin, Dept Obstet & Gynecol, Milwaukee, WI 53226 USA.
   [Oshima, Kiyoko] Med Coll Wisconsin, Dept Pathol, Milwaukee, WI 53226 USA.
   [Oshima, Kiyoko] Johns Hopkins Univ, Dept Pathol, Baltimore, MD USA.
   [Stoner, Gary D.] Med Coll Wisconsin, Dept Med, Milwaukee, WI 53226 USA.
C3 Medical College of Wisconsin; Loyola University Chicago; Medical College
   of Wisconsin; Medical College of Wisconsin; Johns Hopkins University;
   Medical College of Wisconsin
RP Stoner, GD; Wang, LS (corresponding author), Med Coll Wisconsin, Dept Med, Div Hematol & Oncol, RM C4930,8701 Watertown Plank Rd, Milwaukee, WI 53226 USA.
EM gstoner@mcw.edu; liswang@mcw.edu
RI Huang, Yiwen/KPB-2034-2024; PAN, PAN/IWV-1122-2023
FU NIH [5 R01 CA103180, 5 R01 CA148818]; Advancing a Healthier Wisconsin
   grant [5520197]
FX We are grateful for financial support from NIH grants 5 R01 CA103180 (to
   G. Stoner) and 5 R01 CA148818 (to L.-S. Wang) as well as Advancing a
   Healthier Wisconsin grant 5520197.
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NR 58
TC 15
Z9 15
U1 0
U2 7
PU IOS PRESS
PI AMSTERDAM
PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
SN 1878-5093
EI 1878-5123
J9 J BERRY RES
JI J. Berry Res.
PY 2018
VL 8
IS 2
BP 137
EP 146
DI 10.3233/JBR-170291
PG 10
WC Plant Sciences; Food Science & Technology; Horticulture; Nutrition &
   Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Plant Sciences; Food Science & Technology; Agriculture; Nutrition &
   Dietetics
GA GG5OQ
UT WOS:000432746000006
PM 29977412
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Premnath, N
   O'Reilly, EM
AF Premnath, Naveen
   O'Reilly, Eileen M.
TI BReast CAncer (<i>BRCA</i>) gene mutations as an emerging biomarker for
   the treatment of gastrointestinal malignancies
SO CHINESE CLINICAL ONCOLOGY
LA English
DT Review
DE BReast CAncer (BRCA); poly-ADP ribose polymerase inhibitors (PARP
   inhibitors); gastrointestinal cancer; pancreatic cancer; synthetic
   lethality; Pancreas cancer OLaparib Ongoing (POLO)
ID PHASE-II TRIAL; PANCREATIC DUCTAL ADENOCARCINOMA; RIBOSE POLYMERASE
   INHIBITOR; DNA-REPAIR; POLY(ADP-RIBOSE) POLYMERASE; CLINICAL
   CHARACTERISTICS; SYNTHETIC LETHALITY; COLORECTAL-CANCER; OVARIAN-CANCER;
   DOUBLE-BLIND
AB BReast CAncer (BRCA) genes 1 and 2 were discovered in the 1990's by Hall et al. and Wooster et al. respectively. BRCA genes have been shown to be associated with an increased risk of various gastrointestinal (GI) cancers beyond known risk of breast, ovary and prostate cancers. Studies have demonstrated the role of BRCA genes in the DNA repair pathway and modalities to exploit this pathway are being currently explored. Using the concept of synthetic lethality, poly-ADP ribose polymerase inhibitors (PARPi) have significant activity in BRCA deficient cells. Targeted therapy is gaining popularity worldwide and BRCA genes have received much attention since the development and approval of PARPis. Multiple studies have also identified the predictive value of BRCA genes related to platinum and other DNA-damaging cytotoxic agents. BRCA deficient cells are about 5-fold more sensitive to platinum-based agents and almost 1,000-fold more with PARPis. Genomic instability has been established as the hallmark of BRCA deficient tumors and the specific roles of BRCA genes in DNA damage repair is increasingly clear. Herein, we discuss the risks and incidence of individual GI cancers seen with BRCA mutations, highlight tumor biology and provide a comprehensive review of the available preclinical and clinical data and upcoming trials related to this topic. The "POLO" trial in metastatic pancreas cancer establishes a "proof of principle" regarding treatment of BRCA-related cancer and PARPi. In pancreatic cancer routine germline genetic testing is now recommended in most major guidelines. Newer studies are emerging, which will expand the concept of BRCAness and ways to effectively detect this phenotype in GI cancers and impact clinical practice.
C1 [Premnath, Naveen; O'Reilly, Eileen M.] Univ Texas Southwestern Med Ctr Dallas, Dept Internal Med, Dallas, TX 75390 USA.
C3 University of Texas System; University of Texas Southwestern Medical
   Center Dallas
RP O'Reilly, EM (corresponding author), Mem Sloan Kettering Canc Ctr, Med Oncol, 1275 York Ave, New York, NY 10021 USA.; O'Reilly, EM (corresponding author), Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10021 USA.; O'Reilly, EM (corresponding author), Weill Cornell Med Coll, Med, New York, NY 10065 USA.
EM oreillye@mskcc.org
RI Premnath, Naveen/HTT-3035-2023
OI Premnath, Naveen/0000-0001-5183-2657
FU David M. Rubenstein Center for Pancreatic Cancer Research, Reiss Family
   Foundation, Cancer Support Grant [P30 CA008748]
FX David M. Rubenstein Center for Pancreatic Cancer Research, Reiss Family
   Foundation, Cancer Support Grant P30 CA008748.
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NR 137
TC 4
Z9 5
U1 0
U2 6
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2304-3865
EI 2304-3873
J9 CHIN CLIN ONCOL
JI Chin. Clin. Oncol.
PD OCT
PY 2020
VL 9
IS 5
AR 64
DI 10.21037/cco-2019-ddp-05
PG 23
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA OJ3AE
UT WOS:000583836800002
PM 32787343
OA gold
DA 2025-01-04
ER

PT J
AU Ledderhof, NJ
   Caminiti, MF
   Bradley, G
   Lam, DK
AF Ledderhof, Nicholas J.
   Caminiti, Marco F.
   Bradley, Grace
   Lam, David K.
TI Topical 5-Fluorouracil is a Novel Targeted Therapy for the Keratocystic
   Odontogenic Tumor
SO JOURNAL OF ORAL AND MAXILLOFACIAL SURGERY
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMA; THYMIDYLATE SYNTHASE; DIHYDROPYRIMIDINE
   DEHYDROGENASE; CARNOYS SOLUTION; THYMIDINE PHOSPHORYLASE;
   COLORECTAL-CANCER; SIGNALING PATHWAY; DOWN-REGULATION; EXPRESSION;
   ENUCLEATION
AB Purpose: The antimetabolite drug, 5-fluorouracil (5-FU), is used in the treatment of various cancers, including basal cell carcinomas (BCCs). The authors hypothesized that keratocystic odontogenic tumors (KOTs) would respond to 5-FUtreatment because of their similarities to BCCs in molecular etiopathogenesis.
   Materials and Methods: An ambispective cohort study of the treatment efficacy of topical 5-FU on KOTs was conducted. Independent variables included the topical application of 5% 5-FU or modified Carnoy's solution (MC) after enucleation and peripheral ostectomy at the University of Toronto from 2006 through 2014. Outcome variables included time to recurrence and peripheral nerve injury. KOT specimens in these patients were immunostained with p53, Ki-67, thymidylate synthetase (TS), thymidylate phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) antibodies. Semiquantitative staining scores were calculated for all immunohistochemistry sections examined. Descriptive statistics were computed using Fisher exact test and Kaplan-Meier analysis as appropriate with the P value set at .05.
   Results: Thirty-two patients with 32 KOTs were reviewed (41% in women and 59% in men). There were no KOT recurrences in the 5-FU group (n = 11), whereas there were 4 recurrences in the MC group (n = 21; P = .190). There was a significantly lower incidence of inferior alveolar nerve paresthesia with 5-FU treatment (P = .039). Immunohistochemical staining showed upregulation of TP (P < .0001) and DPD (P < .0001) and no change in TS (P > .05) in inflamed KOTs.
   Conclusions: 5-FU effectively treats KOTs with less postoperative morbidity than conventional treatment with MC. Low TS and upregulated TP expressions in inflamed KOTs suggest increased 5-FU efficacy in inflamed KOTs. Topical 5-FU is a novel therapy for KOTs and provides a targeted molecular approach to treatment. (C) 2016 American Association of Oral and Maxillofacial Surgeons.
C1 [Ledderhof, Nicholas J.] Univ Toronto, Fac Dent, Dept Oral & Maxillofacial Surg, Toronto, ON, Canada.
   [Caminiti, Marco F.; Lam, David K.] Univ Toronto, Dept Oral & Maxillofacial Surg, 124 Edward St,Room 143, Toronto, ON M5G 1G6, Canada.
   [Bradley, Grace] Univ Toronto, Fac Dent, Dept Oral Pathol & Oral Med, Toronto, ON, Canada.
C3 University of Toronto; University of Toronto; University of Toronto
RP Lam, DK (corresponding author), Univ Toronto, Dept Oral & Maxillofacial Surg, 124 Edward St,Room 143, Toronto, ON M5G 1G6, Canada.
EM david.lam@utoronto.ca
RI Caminiti, Marco/KCJ-6939-2024
FU Canadian Association of Oral and Maxillofacial Surgeons Research Grant;
   Bertha Rosenstadt Endowment Fund
FX This study was supported by a Canadian Association of Oral and
   Maxillofacial Surgeons Research Grant and the Bertha Rosenstadt
   Endowment Fund.
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NR 49
TC 31
Z9 32
U1 1
U2 10
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0278-2391
EI 1531-5053
J9 J ORAL MAXIL SURG
JI J. Oral Maxillofac. Surg.
PD MAR
PY 2017
VL 75
IS 3
BP 514
EP 524
DI 10.1016/j.joms.2016.09.039
PG 11
WC Dentistry, Oral Surgery & Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dentistry, Oral Surgery & Medicine
GA ES0NL
UT WOS:000399223200014
PM 27789270
DA 2025-01-04
ER

PT J
AU Kanzaki, R
   Fukui, E
   Kanou, T
   Ose, N
   Funaki, S
   Minami, M
   Shintani, Y
   Okumura, M
AF Kanzaki, Ryu
   Fukui, Eriko
   Kanou, Takashi
   Ose, Naoko
   Funaki, Soichiro
   Minami, Masato
   Shintani, Yasushi
   Okumura, Meinoshin
TI Preoperative evaluation and indications for pulmonary metastasectomy
SO JOURNAL OF THORACIC DISEASE
LA English
DT Review
DE Pulmonary metastasectomy (PM); indication; radiological examinations;
   prognostic factor
ID RENAL-CELL CARCINOMA; LYMPH-NODE DISSECTION;
   POSITRON-EMISSION-TOMOGRAPHY; UTERINE MALIGNANCY OUTCOMES; TUMOR
   DOUBLING TIME; LONG-TERM SURVIVAL; COLORECTAL-CANCER; SURGICAL
   RESECTION; PROGNOSTIC-FACTORS; LUNG METASTASECTOMY
AB Pulmonary metastasectomy (PM) is an established treatment that can provide improved long-term survival for patients with metastatic tumor(s) in the lung. In the current era, where treatment options other than PM such as stereotactic body radiation therapy (SBRT), immunotherapy, and molecular-targeted therapy are available, thoracic surgeons should review the approach to the preoperative evaluation and the indications. Preoperative evaluation consists of history and physical examinations, physiological tests, and radiological examinations. Radiological examinations serve to identify the differential diagnosis of the pulmonary nodules, evaluate their precise number, location, and features, and search for extra thoracic metastases. The indication of PM should be considered from both physiological and oncological points of view. The general criteria for PM are as follows; (I) the patient has a good general condition, (II) the primary malignancy is controlled, (III) there is no other extrapulmonary metastases, and (IV) the pulmonary lesion(s) are thought to be completely resectable. In addition to the general eligibility criteria of PM, prognostic factors of each tumor type should be considered when deciding the indication for PM. When patients have multiple poor prognostic factors and/or a short disease-free interval (DFI), thoracic surgeons should not hesitate to observe the patient for a certain period before deciding on the indication for PM. A multidisciplinary discussion is needed in order to decide the indication for PM.
C1 [Kanzaki, Ryu; Fukui, Eriko; Kanou, Takashi; Ose, Naoko; Funaki, Soichiro; Minami, Masato; Shintani, Yasushi; Okumura, Meinoshin] Osaka Univ, Grad Sch Med, Dept Gen Thorac Surg, L5-2-2 Yamadaoka, Suita, Osaka 5650871, Japan.
   [Okumura, Meinoshin] Natl Hosp Org Toneyama Hosp, Dept Gen Thorac Surg, Toyonaka, Osaka, Japan.
C3 Osaka University
RP Kanzaki, R (corresponding author), Osaka Univ, Grad Sch Med, Dept Gen Thorac Surg, L5-2-2 Yamadaoka, Suita, Osaka 5650871, Japan.
EM rkanzaki@tj8.so-net.ne.jp
RI Kanzaki, Ryu/Q-8381-2018
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NR 126
TC 13
Z9 13
U1 0
U2 3
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2072-1439
EI 2077-6624
J9 J THORAC DIS
JI J. Thorac. Dis.
PD APR
PY 2021
VL 13
IS 4
BP 2590
EP 2602
DI 10.21037/jtd-19-3791
PG 13
WC Respiratory System
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Respiratory System
GA TA8LO
UT WOS:000667497200020
PM 34012607
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Takahashi, N
   Hoshi, H
   Higa, A
   Hiyama, G
   Tamura, H
   Ogawa, M
   Takagi, K
   Goda, K
   Okabe, N
   Muto, S
   Suzuki, H
   Shimomura, K
   Watanabe, S
   Takagi, M
AF Takahashi, Nobuhiko
   Hoshi, Hirotaka
   Higa, Arisa
   Hiyama, Gen
   Tamura, Hirosumi
   Ogawa, Mayu
   Takagi, Kosuke
   Goda, Kazuhito
   Okabe, Naoyuki
   Muto, Satoshi
   Suzuki, Hiroyuki
   Shimomura, Kenju
   Watanabe, Shinya
   Takagi, Motoki
TI An In Vitro System for Evaluating Molecular Targeted Drugs Using Lung
   Patient-Derived Tumor Organoids
SO CELLS
LA English
DT Article
DE molecular targeted therapy; cancer immunotherapy; cancer immunity;
   molecular targeted drugs; antibody drug; antibody-drug conjugate; immune
   checkpoint inhibitor; patient-derived tumor organoid; antibody-dependent
   cellular cytotoxicity; 3D cell-analysis system
ID COLORECTAL-CANCER; CULTURE; MODELS; CELLS; SENSITIVITY; NIVOLUMAB;
   EFFICACY
AB Patient-derived tumor organoids (PDOs) represent a promising preclinical cancer model that better replicates disease, compared with traditional cell culture models. We have established PDOs from various human tumors to accurately and efficiently recapitulate the tissue architecture and function. Molecular targeted therapies with remarkable efficacy are currently in use against various tumors. Thus, there is a need for in vitro functional-potency assays that can be used to test the efficacy of molecular targeted drugs and model complex interactions between immune cells and tumor cells to evaluate the potential for cancer immunotherapy. This study represents an in vitro evaluation of different classes of molecular targeted drugs, including small-molecule inhibitors, monoclonal antibodies, and an antibody-drug conjugate, using lung PDOs. We evaluated epidermal growth factor receptor and human epidermal growth factor receptor 2 (HER2) inhibitors using a suitable high-throughput assay system. Next, the antibody-dependent cellular cytotoxicity (ADCC) activity of an anti-HER2 monoclonal antibody was evaluated to visualize the interactions of immune cells with PDOs during ADCC responses. Moreover, an evaluation system was developed for the immune checkpoint inhibitors, nivolumab and pembrolizumab, using PDOs. Our results demonstrate that the in vitro assay systems using PDOs were suitable for evaluating molecular targeted drugs under conditions that better reflect pathological conditions.
C1 [Takahashi, Nobuhiko; Hoshi, Hirotaka; Higa, Arisa; Hiyama, Gen; Tamura, Hirosumi; Watanabe, Shinya; Takagi, Motoki] Fukushima Med Univ, Med Ind Translat Res Ctr, Fukushima 9601295, Japan.
   [Takahashi, Nobuhiko; Shimomura, Kenju] Fukushima Med Univ, Dept Bioregulat & Pharmacol Med, Fukushima 9601295, Japan.
   [Ogawa, Mayu; Goda, Kazuhito] Olympus Corp, Res & Dev, Biol Evaluat Technol 2, Hachioji, Tokyo 1928512, Japan.
   [Takagi, Kosuke] Olympus Corp, Res & Dev, SSD Technol Innovat 3, Hachioji, Tokyo 1928512, Japan.
   [Okabe, Naoyuki; Muto, Satoshi; Suzuki, Hiroyuki] Fukushima Med Univ, Dept Chest Surg, Sch Med, Fukushima 9601295, Japan.
C3 Fukushima Medical University; Fukushima Medical University; Olympus
   Corporation; Olympus Corporation; Fukushima Medical University
RP Takagi, M (corresponding author), Fukushima Med Univ, Med Ind Translat Res Ctr, Fukushima 9601295, Japan.
EM tkhsnbhk@fmu.ac.jp; h-hoshi@fmu.ac.jp; arisaxon1945@gmail.com;
   hiyamag@fmu.ac.jp; tamura@fmu.ac.jp; mayu_ogawa@ot.olympus.co.jp;
   ko_takagi@ot.olympus.co.jp; k_goda@ot.olympus.co.jp; okaben@fmu.ac.jp;
   smutoo@fmu.ac.jp; hiro@fmu.ac.jp; shimomur@fmu.ac.jp;
   swata@mvc.biglobe.ne.jp; m-takagi@fmu.ac.jp
FU Translational Research Programs from Fukushima Prefecture
FX Translational Research Programs from Fukushima Prefecture.
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NR 33
TC 31
Z9 32
U1 2
U2 38
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD MAY
PY 2019
VL 8
IS 5
AR 481
DI 10.3390/cells8050481
PG 18
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA IC5FZ
UT WOS:000470994400101
PM 31137590
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Thein, KZ
   Myat, YM
   Park, BS
   Panigrahi, K
   Kummar, S
AF Thein, Kyaw Z.
   Myat, Yin M.
   Park, Byung S.
   Panigrahi, Kalpana
   Kummar, Shivaani
TI Target-Driven Tissue-Agnostic Drug Approvals-A New Path of Drug
   Development
SO CANCERS
LA English
DT Review
DE tissue-agnostic drug development; pembrolizumab; microsatellite
   instability-high (MSI-H); tumor mutational burden-high (TMB-H);
   dostarlimab-gxly; larotrectinib; entrectinib; neurotrophic tyrosine
   kinase (NTRK); dabrafenib and trametinib; V-Raf murine sarcoma viral
   oncogene homolog B V600E (BRAF(V600E)); selpercatinib; rearranged during
   transfection (RET); precision oncology
ID POSITIVE SOLID TUMORS; PATIENTS PTS; TRASTUZUMAB DERUXTECAN; UMBRELLA
   TRIALS; EFFICACY; SAFETY; BASKET; SELPERCATINIB; LAROTRECTINIB;
   GLIOBLASTOMA
AB The regulatory approvals of tumor-agnostic therapies have led to the re-evaluation of the drug development process. The conventional models of drug development are histology-based. On the other hand, the tumor-agnostic drug development of a new drug (or combination) focuses on targeting a common genomic biomarker in multiple cancers, regardless of histology. The basket-like clinical trials with multiple cohorts allow clinicians to evaluate pan-cancer efficacy and toxicity. There are currently eight tumor agnostic approvals granted by the Food and Drug Administration (FDA). This includes two immune checkpoint inhibitors, and five targeted therapy agents. Pembrolizumab is an anti-programmed cell death protein-1 (PD-1) antibody that was the first FDA-approved tumor-agnostic treatment for unresectable or metastatic microsatellite instability-high (MSI-H) or deficient mismatch repair (dMMR) solid tumors in 2017. It was later approved for tumor mutational burden-high (TMB-H) solid tumors, although the TMB cut-off used is still debated. Subsequently, in 2021, another anti-PD-1 antibody, dostarlimab, was also approved for dMMR solid tumors in the refractory setting. Patients with fusion-positive cancers are typically difficult to treat due to their rare prevalence and distribution. Gene rearrangements or fusions are present in a variety of tumors. Neurotrophic tyrosine kinase (NTRK) fusions are present in a range of pediatric and adult solid tumors in varying frequency. Larotrectinib and entrectinib were approved for neurotrophic tyrosine kinase (NTRK) fusion-positive cancers. Similarly, selpercatinib was approved for rearranged during transfection (RET) fusion-positive solid tumors. The FDA approved the first combination therapy of dabrafenib, a B-Raf proto-oncogene serine/threonine kinase (BRAF) inhibitor, plus trametinib, a mitogen-activated protein kinase (MEK) inhibitor for patients 6 months or older with unresectable or metastatic tumors (except colorectal cancer) carrying a BRAF(V600E) mutation. The most recent FDA tumor-agnostic approval is of fam-trastuzumab deruxtecan-nxki (T-Dxd) for HER2-positive solid tumors. It is important to identify and expeditiously develop drugs that have the potential to provide clinical benefit across tumor types.
C1 [Thein, Kyaw Z.] Comprehens Canc Ctr Nevada Cent Valley, Div Hematol & Med Oncol, 3730 S Eastern Ave, Las Vegas, NV 89169 USA.
   [Thein, Kyaw Z.] Univ Nevada Las Vegas UNLV, Kirk Kerkorian Sch Med, Dept Med, 4505 S,Maryland Pkwy, Las Vegas, NV 89154 USA.
   [Thein, Kyaw Z.] Touro Univ Nevada, Coll Osteopath Med, Touro Coll & Univ Syst, 874 Amer Pacific Dr, Henderson, NV 89014 USA.
   [Myat, Yin M.] Univ Coll Dublin UCD, Sch Med, Belfield Campus, Dublin D04 V1W8, Ireland.
   [Myat, Yin M.; Panigrahi, Kalpana] One Brooklyn Hlth, Interfaith Med Ctr Campus, Dept Internal Med, 1545, Atlantic Ave, Brooklyn, NY 11213 USA.
   [Park, Byung S.] OHSU PSU Sch Publ Hlth, Portland, OR 97201 USA.
   [Park, Byung S.] OHSU Knight Canc Inst, OHSU Sch Med, Biostat Shared Resource, Portland, OR 97239 USA.
   [Kummar, Shivaani] Oregon Hlth & Sci Univ, Knight Canc Inst, Div Hematol & Med Oncol, Ctr Expt Therapeut, 3181 SW Sam Jackson Pk Rd, Portland, OR 97239 USA.
C3 Nevada System of Higher Education (NSHE); University of Nevada Las
   Vegas; University College Dublin; Oregon Health & Science University;
   Oregon Health & Science University
RP Thein, KZ (corresponding author), Comprehens Canc Ctr Nevada Cent Valley, Div Hematol & Med Oncol, 3730 S Eastern Ave, Las Vegas, NV 89169 USA.; Thein, KZ (corresponding author), Univ Nevada Las Vegas UNLV, Kirk Kerkorian Sch Med, Dept Med, 4505 S,Maryland Pkwy, Las Vegas, NV 89154 USA.; Thein, KZ (corresponding author), Touro Univ Nevada, Coll Osteopath Med, Touro Coll & Univ Syst, 874 Amer Pacific Dr, Henderson, NV 89014 USA.
EM kyaw.thein@usoncology.com; ym.myat8@gmail.com; parkb@ohsu.edu;
   kpanigrahi@interfaithmedical.org; kummar@ohsu.edu
OI /0000-0003-3516-7516; Thein, Kyaw/0000-0003-1518-1097
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NR 78
TC 1
Z9 1
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUL
PY 2024
VL 16
IS 14
AR 2529
DI 10.3390/cancers16142529
PG 24
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZW0P4
UT WOS:001278208700001
PM 39061168
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Luchini, C
   Veronese, N
   Solmi, M
   Cho, H
   Kim, JH
   Chou, A
   Gill, AJ
   Faraj, SF
   Chaux, A
   Netto, GJ
   Nakayama, K
   Kyo, S
   Lee, SY
   Kim, DW
   Yousef, GM
   Scorilas, A
   Nelson, GS
   Köbel, M
   Kalloger, SE
   Schaeffer, DF
   Yan, HB
   Liu, F
   Yokoyama, Y
   Zhang, XY
   Pang, D
   Lichner, Z
   Sergi, G
   Manzato, E
   Capelli, P
   Wood, LD
   Scarpa, A
   Correll, CU
AF Luchini, Claudio
   Veronese, Nicola
   Solmi, Marco
   Cho, Hanbyoul
   Kim, Jae-Hoon
   Chou, Angela
   Gill, Anthony J.
   Faraj, Sheila F.
   Chaux, Alcides
   Netto, George J.
   Nakayama, Kentaro
   Kyo, Satoru
   Lee, Soo Young
   Kim, Duck-Woo
   Yousef, George M.
   Scorilas, Andreas
   Nelson, Gregg S.
   Koebel, Martin
   Kalloger, Steve E.
   Schaeffer, David F.
   Yan, Hai-Bo
   Liu, Feng
   Yokoyama, Yoshihito
   Zhang, Xianyu
   Pang, Da
   Lichner, Zsuzsanna
   Sergi, Giuseppe
   Manzato, Enzo
   Capelli, Paola
   Wood, Laura D.
   Scarpa, Aldo
   Correll, Christoph U.
TI Prognostic role and implications of mutation status of tumor suppressor
   gene ARID1A in cancer: a systematic review and meta-analysis
SO ONCOTARGET
LA English
DT Article
DE ARID1A; SWI/SNF; chromatin remodeling; targeted therapy; tumor
   suppressor gene
ID IDENTIFIES FREQUENT MUTATION; CLEAR-CELL; CLINICOPATHOLOGICAL
   SIGNIFICANCE; PROTEIN EXPRESSION; COLORECTAL-CARCINOMA; PATHWAY
   ALTERATIONS; SWI/SNF COMPLEX; POOR-PROGNOSIS; 1A EXPRESSION;
   CHEMORESISTANCE
AB Loss of the tumor suppressor gene AT-rich interactive domain-containing protein 1A (ARID1A) has been demonstrated in several cancers, but its prognostic role is unknown. We aimed to investigate the risk associated with loss of ARID1A (ARID1A-) for all-cause mortality, cancer-specific mortality and recurrence of disease in subjects with cancer. PubMed and SCOPUS search from database inception until 01/31/2015 without language restriction was conducted, contacting authors for unpublished data. Eligible were prospective studies reporting data on prognostic parameters in subjects with cancer, comparing participants with presence of ARID1A (ARID1A+) vs. ARID1A-, assessed either via immunohistochemistry (loss of expression) or with genetic testing (presence of mutation). Data were summarized using risk ratios (RR) for number of deaths/recurrences and hazard ratios (HR) for time-dependent risk related to ARID1A- adjusted for potential confounders. Of 136 hits, 25 studies with 5,651 participants (28 cohorts; ARID1A-: n = 1,701; ARID1A+: n = 3,950), with a mean follow-up period of 4.7 +/- 1.8 years, were meta-analyzed. Compared to ARID1A+, ARID1A- significantly increased cancer-specific mortality (studies = 3; RR = 1.55, 95% confidence interval (CI) = 1.19-2.00, I-2 = 31%). Using HRs adjusted for potential confounders, ARID1A- was associated with a greater risk of cancer-specific mortality (studies = 2; HR = 2.55, 95% CI = 1.19-5.45, I-2 = 19%) and cancer recurrence (studies = 10; HR = 1.93, 95% CI = 1.22-3.05, I-2 = 76%). On the basis of these results, we have demonstrated that loss of ARID1A shortened time to cancer-specific mortality, and to recurrence of cancer when adjusting for potential confounders. For its role, this gene should be considered as an important potential target for personalized medicine in cancer treatment.
C1 [Luchini, Claudio; Capelli, Paola; Scarpa, Aldo] Univ & Hosp Trust Verona, Dept Pathol & Diagnost, Verona, Italy.
   [Luchini, Claudio; Faraj, Sheila F.; Chaux, Alcides; Netto, George J.; Wood, Laura D.] Johns Hopkins Univ, Dept Pathol, Baltimore, MD USA.
   [Veronese, Nicola; Sergi, Giuseppe; Manzato, Enzo] Univ Padua, Dept Med, Div Geriatr, Padua, Italy.
   [Solmi, Marco] Univ Padua, Dept Neurosci, Padua, Italy.
   [Cho, Hanbyoul; Kim, Jae-Hoon] Yonsei Univ, Coll Med, Gangnam Severance Hosp, Dept Obstet & Gynecol, Seoul, South Korea.
   [Chou, Angela; Gill, Anthony J.] Royal N Shore Hosp, Kolling Inst Med Res, Canc Diag & Pathol Grp, St Leonards, NSW 2065, Australia.
   [Chou, Angela; Gill, Anthony J.] Sydney Vital Translat Res Ctr, St Leonards, NSW, Australia.
   [Chou, Angela; Gill, Anthony J.] Univ Sydney, Sydney, NSW 2006, Australia.
   [Chou, Angela] SYDPATH St Vincents Hosp, Dept Anat Pathol, Sydney, NSW, Australia.
   [Chaux, Alcides] CEDIC, Asuncion, Paraguay.
   [Nakayama, Kentaro; Kyo, Satoru] Shimane Univ, Sch Med, Dept Obstet & Gynecol, Shimane, Japan.
   [Lee, Soo Young] Gachon Univ, Lee Gil Ya Canc & Diabet Inst, Inchon, South Korea.
   [Kim, Duck-Woo] Seoul Natl Univ, Bundang Hosp, Dept Surg, Songnam, South Korea.
   [Yousef, George M.] St Michaels Hosp, Li Ka Shing Knowledge Inst, Dept Lab Med, Toronto, ON M5B 1W8, Canada.
   [Yousef, George M.] St Michaels Hosp, Li Ka Shing Knowledge Inst, Keenan Res Ctr, Toronto, ON M5B 1W8, Canada.
   [Scorilas, Andreas] Univ Athens, Fac Biol, Dept Biochem & Mol Biol, Athens, Greece.
   [Nelson, Gregg S.] Tom Baker Canc Clin, Dept Gynecol Oncol, Calgary, AB, Canada.
   [Koebel, Martin] Univ Calgary, Dept Pathol & Lab Med, Calgary, AB, Canada.
   [Kalloger, Steve E.; Schaeffer, David F.] Univ British Columbia, Dept Pathol & Lab Med, Vancouver, BC V5Z 1M9, Canada.
   [Yan, Hai-Bo; Liu, Feng] Fudan Univ, Sch Basic Med Sci, Dept Syst Biol Med, Shanghai 200433, Peoples R China.
   [Yan, Hai-Bo; Liu, Feng] Fudan Univ, Inst Biomed Sci, Shanghai 200433, Peoples R China.
   [Yokoyama, Yoshihito] Hirosaki Univ, Grad Sch Med, Dept Obstet & Gynecol, Hirosaki, Aomori, Japan.
   [Zhang, Xianyu; Pang, Da] Harbin Med Univ, Canc Hosp, Dept Breast Surg, Harbin, Peoples R China.
   [Lichner, Zsuzsanna] St Michaels Hosp, Dept Lab Med, Toronto, ON M5B 1W8, Canada.
   [Lichner, Zsuzsanna] St Michaels Hosp, Li Ka Shing Knowledge Inst, Keenan Res Ctr, Toronto, ON M5B 1W8, Canada.
   [Correll, Christoph U.] North Shore Long Isl Jewish Hlth Syst, Psychiat Res, Zucker Hillside Hosp, Glen Oaks, NY USA.
   [Correll, Christoph U.] Hofstra North Shore LIJ Sch Med, Hempstead, NY USA.
   [Correll, Christoph U.] Feinstein Inst Med Res, Manhasset, NY USA.
   [Correll, Christoph U.] Albert Einstein Coll Med, Bronx, NY USA.
C3 University of Verona; Azienda Ospedaliera Universitaria Integrata
   Verona; Johns Hopkins University; University of Padua; University of
   Padua; Yonsei University; Yonsei University Health System; Royal North
   Shore Hospital; University of Sydney; Kolling Institute of Medical
   Research; University of Sydney; Shimane University; Gachon University;
   Seoul National University (SNU); University of Toronto; Saint Michaels
   Hospital Toronto; Li Ka Shing Knowledge Institute; University of
   Toronto; Li Ka Shing Knowledge Institute; Saint Michaels Hospital
   Toronto; National & Kapodistrian University of Athens; University of
   Calgary; Tom Baker Cancer Clinic; University of Calgary; University of
   British Columbia; Fudan University; Fudan University; Hirosaki
   University; Harbin Medical University; University of Toronto; Saint
   Michaels Hospital Toronto; University of Toronto; Saint Michaels
   Hospital Toronto; Li Ka Shing Knowledge Institute; Northwell Health;
   Northwell Health; Hofstra University; Northwell Health; Montefiore
   Medical Center; Albert Einstein College of Medicine; Yeshiva University
RP Luchini, C (corresponding author), Univ & Hosp Trust Verona, Dept Pathol & Diagnost, Verona, Italy.
EM claudio.luchini@katamail.com
RI Nelson, Gregg/HCH-9224-2022; Kim, Jee/J-5441-2012; Cho, Hwa
   Jin/AFA-1420-2022; Kim, Sang/AAI-5704-2020; Köbel, Martin/A-7373-2011;
   solmi, marco/K-3906-2018; Correll, Christoph/D-3530-2011; Wood,
   Laura/ABF-1531-2020; SERGI, GIUSEPPE/J-9396-2018; Faraj,
   Sheila/I-9725-2016; Scarpa, Aldo/K-6832-2016; Veronese,
   Nicola/K-4343-2018; Gill, Anthony/D-4215-2015; Chaux,
   Alcides/H-4656-2019; Luchini, Claudio/Q-4922-2016
OI Chou, Angela/0000-0001-9212-6927; Scorilas, Andreas/0000-0003-2427-4949;
   Kim, Jae-Hoon/0000-0001-6599-7065; Scarpa, Aldo/0000-0003-1678-739X;
   Netto, George/0000-0003-3915-9134; Kobel, Martin/0000-0002-6615-2037;
   Veronese, Nicola/0000-0002-9328-289X; Gill, Anthony/0000-0002-9447-1967;
   Nelson, Gregg/0000-0002-8177-1098; solmi, marco/0000-0003-4877-7233;
   Chaux, Alcides/0000-0002-5824-9867; Luchini,
   Claudio/0000-0003-4901-4908; SERGI, GIUSEPPE/0000-0001-9757-856X; Cho,
   Hanbyoul/0000-0002-6177-1648
FU BMS; Feinstein Institute for Medical Research; Janssen/J J; National
   Institute of Mental Health (NIMH); National Alliance for Research in
   Schizophrenia and Depression (NARSAD); Otsuka; Takeda; AIRC [12182]
FX Dr. Correll has been a consultant and/or advisor to or has received
   honoraria from: AbbVie, Actavis, Actelion, Alexza, Bristol-Myers Squibb,
   Cephalon, Eli Lilly, Genentech, GersonLehrman Group, IntraCellular
   Therapies, Lundbeck, Medavante, Medscape, Merck, National Institute of
   Mental Health, Janssen/J & J, Otsuka, Pfizer, ProPhase, Reviva, Roche,
   Sunovion, Takeda, Teva, and Vanda. He has received grant support from
   BMS, Feinstein Institute for Medical Research, Janssen/J & J, National
   Institute of Mental Health (NIMH), National Alliance for Research in
   Schizophrenia and Depression (NARSAD), Otsuka and Takeda. Prof. Scarpa
   is supported by AIRC (grant 12182).
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NR 51
TC 61
Z9 68
U1 0
U2 10
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD NOV 17
PY 2015
VL 6
IS 36
BP 39088
EP 39097
DI 10.18632/oncotarget.5142
PG 10
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA CY0RS
UT WOS:000366114000050
PM 26384299
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Wedden, S
   Miller, K
   Frayling, IM
   Thomas, T
   Chefani, A
   Miller, K
   Hamblin, A
   Taylor, JC
   D'Arrigo, C
AF Wedden, Sarah
   Miller, Keith
   Frayling, Ian M.
   Thomas, Teresa
   Chefani, Alina
   Miller, Karolina
   Hamblin, Angela
   Taylor, Jenny C.
   D'Arrigo, Corrado
TI Colorectal Cancer Stratification in the Routine Clinical Pathway: A
   District General Hospital Experience
SO APPLIED IMMUNOHISTOCHEMISTRY & MOLECULAR MORPHOLOGY
LA English
DT Article
DE colorectal cancer; Lynch syndrome; mismatch repair proteins;
   personalized medicine; targeted therapy
ID MISMATCH-REPAIR; EFFICACY; KRAS; PANITUMUMAB; STRATEGIES; CETUXIMAB;
   HER2; BRAF; MET
AB Colorectal cancer (CRC) has many subtypes with different prognoses and response to treatment. Patients must be characterized to access the most appropriate treatment and improve outcomes. An increasing number of biomarkers are required for characterization but are not in routine use. We investigated whether CRC can be stratified routinely within a small district general hospital to inform clinical decision making at local multidisciplinary team meeting/tumor board level. We evaluated mismatch repair (MMR) and EGFR signaling pathways using predominantly in-house immunohistochemical (IHC) tests (MSH2, MSH6, MLH1, PMS2, BRAF-V600E, Her2, PTEN, cMET) as well as send away PCR/NGS tests (NRAS, KRAS, and BRAF). We demonstrated that many of the tests required for personalized treatment of CRC can be done locally and timely. Send away tests need to be requested shortly after cut-up and this needs to be firmly established in the tissue pathways for the results to be considered at multidisciplinary team meeting/tumor board. We have shown that MMR IHC combined with BRAFV600E IHC is practical and easy to perform in a small district general hospital, has full concordance with DNA-based tests and satisfies the latest NICE requirements for the identification of potential Lynch syndrome patients. We provide a framework for the interpretation and presentation of test results. It is a practical classification that clinical pathologists can use to communicate effectively with the clinical team. It is broadly based on molecular subtyping, firmly focused on treatment decisions and dependent on the panel of molecular tests currently available.
C1 [Wedden, Sarah; Miller, Keith; D'Arrigo, Corrado] Poundbury Canc Inst, CADQAS CIC, Newborough House,3 Queen Mother Sq, Dorchester DT1 3BJ, Dorset, England.
   [Miller, Keith] UK NEQAS Immunocytochem & In Situ Hybridisat, London, England.
   [Frayling, Ian M.] Cardiff Univ, Inst Canc & Genet, Cardiff, S Glam, Wales.
   [Thomas, Teresa; Chefani, Alina; Miller, Karolina] Dorset Cty Hosp Fdn Trust, Dorchester, England.
   [Hamblin, Angela] Oxford Univ Hosp NHS Fdn Trust, Oxford BRC Haematol Theme, Mol Diagnost Ctr, Oxford, England.
   [Taylor, Jenny C.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
   [Taylor, Jenny C.] Oxford NIHR Biomed Res Ctr, Oxford, England.
C3 Cardiff University; Oxford University Hospitals NHS Foundation Trust;
   University of Oxford; Wellcome Centre for Human Genetics; University of
   Oxford
RP Wedden, S (corresponding author), Poundbury Canc Inst, CADQAS CIC, Newborough House,3 Queen Mother Sq, Dorchester DT1 3BJ, Dorset, England.
EM sarah@cadqas.org
OI Taylor, Jenny/0000-0003-3602-5704; Frayling, Ian/0000-0002-3420-0794
FU Roche Tissue Diagnostics; Technology Strategy Board
FX The authors acknowledge the support of Roche Tissue Diagnostics for
   funding this work and the Technology Strategy Board for funding the NGS
   panel. We are indebted to the following for advice, discussion and help
   with manuscript preparation: Anne Waydelich, Gilles Erb, Uwe Schalles,
   Paula Toro, Joakim Jagorstrand and Chris Hudson.
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NR 37
TC 9
Z9 9
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1541-2016
EI 1533-4058
J9 APPL IMMUNOHISTO M M
JI Appl. Immunohistochem.
PD JUL
PY 2019
VL 27
IS 6
BP E54
EP E62
DI 10.1097/PAI.0000000000000631
PG 9
WC Anatomy & Morphology; Medical Laboratory Technology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Anatomy & Morphology; Medical Laboratory Technology; Pathology
GA IO1BH
UT WOS:000479114600001
PM 29985199
OA hybrid, Green Accepted, Green Published
DA 2025-01-04
ER

PT J
AU Guo, SC
   Yan, HY
   Wang, LQ
   Liu, Y
   Yu, B
AF Guo, Sicheng
   Yan, Hanyu
   Wang, Liqin
   Liu, Yue
   Yu, Bo
TI GlyH-101 and CaCCinh-A01 Inhibited HT-29 Proliferation by Activating the
   Mitochondrial Apoptosis Pathway and Arresting the Cell Cycle
SO ANTICANCER RESEARCH
LA English
DT Article
DE GlyH-101; CaCCinh-A01; apoptosis; cell cycle; HT-29
AB Background/Aim: GlyH-101 and CaCCinh-A01 are effective blockers of cystic fibrosis transmembrane conductance regulator (CFTR) and Ca2+-activated chloride channels (CaCCs), respectively. Available evidence suggests that GlyH-101 and CaCCinh-A01 can suppress cell proliferation, block invasion and metastasis, and cause several cancer cell types to undergo apoptosis, demonstrating their anti-tumor properties. The aim of this study was to investigate the effect of GlyH-101 and CaCCinh-A01 on HT 29 cell activity and to suggest the possible molecular mechanisms by which inhibitors of CFTR and CaCCs inhibit HT-29 cell activity. Materials and Methods: Human colon HT-29 cancer cells were treated with GlyH-101 or CaCCinh- A01 or GlyH-101 plus CaCCinh-A01 complex. Cell viability was determined by MTT assay, the apoptosis and cell cycle were determined by flow cytometry, and reactive oxygen species (ROS) leves were determined by 2',7'Dichlorodihydrofluorescein diacetate staining. The expression of proteins related to apoptosis and cell cycle regulation was measured by western blotting. Results: The proliferative ability of HT-29 cells was dose-and time-dependently reduced by GlyH-101 and CaCCinh-A01. Treatment with GlyH-101 and CaCCinh-A01 resulted in cell necrosis and apoptosis, up-regulated ROS levels, activated the mitochondrial apoptosis pathway, prompted arrest of the cell cycle in S phase, and increased the levels of proteins related to the cell cycle. Additionally, the combination of these two inhibitors had a stronger regulatory effect on HT-29 cell proliferation than either GlyH-101 or CaCCinh-A01 treated alone. Conclusion: GlyH-101 and CaCCinh-A01 inhibited cell proliferation through cell cycle arrest and mitochondrialrelated pathways in vitro. The combination of these inhibitors could further enhance their anti-proliferative effects. Our findings propose new lead compounds with anti-colon cancer activity, and also provide new evidence for the effectiveness of chloride channels-targeted therapy in anticancer therapy.
C1 [Guo, Sicheng; Yan, Hanyu; Wang, Liqin; Liu, Yue; Yu, Bo] Liaoning Normal Univ, Sch Life Sci, Liaoning Prov Key Lab Biotechnol & Drug Discovery, Dalian, Peoples R China.
C3 Liaoning Normal University
RP Yu, B (corresponding author), Liaoning Normal Univ, Sch Life Sci, Liaoning Prov Key Lab Biotechnol & Drug Discovery, Dalian 110167, Peoples R China.
EM yubo821208@163.com
RI Guo, Sicheng/JGM-2558-2023
FU Scientific Research Project of Liaoning Province Education Department
   [LJKMZ2022143]; (Liaoning, P.R. China)
FX Funding This work was supported by Scientific Research Project of
   Liaoning Province Education Department (No. LJKMZ2022143, Liaoning, P.R.
   China) .
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NR 26
TC 0
Z9 0
U1 0
U2 1
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
   ATHENS 19014, GREECE
SN 0250-7005
EI 1791-7530
J9 ANTICANCER RES
JI Anticancer Res.
PD AUG
PY 2023
VL 43
IS 8
BP 3471
EP 3477
DI 10.21873/anticanres.16523
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA P8WD4
UT WOS:001053412600010
PM 37500166
DA 2025-01-04
ER

PT J
AU Wang, J
   Nishiyama, A
   Matsuyama, M
   Wang, ZY
   Yuan, Y
AF Wang, Juan
   Nishiyama, Akira
   Matsuyama, Makoto
   Wang, Zhiyu
   Yuan, Ying
TI The (pro)renin receptor: a novel biomarker and potential therapeutic
   target for various cancers
SO CELL COMMUNICATION AND SIGNALING
LA English
DT Review
DE (Pro) renin receptor; Cancer; Wnt/beta-catenin signaling pathway; RAS;
   Biomarker; Cancer targeted therapy
ID RENIN-ANGIOTENSIN SYSTEM; VACUOLAR H+-ATPASE; WNT/BETA-CATENIN;
   BETA-CATENIN; INCREASED EXPRESSION; COLON-CANCER; PRORENIN; CELLS;
   IDENTIFICATION; SECRETION
AB Background The (pro) renin receptor ((P)RR) plays important roles in various pathways, such as the Wnt/beta-catenin, renin-angiotensin system (RAS), MAPK/ERK and PI3K/AKT/mTOR pathways, that are involved in a wide range of physiological and pathological processes incorporating the tumorigenesis. However, our knowledge about (P) RR was mostly limited to its roles in cardiovascular and renal physiological functions and diseases. In the past 5 years, however, compelling evidence has revealed that (P) RR is aberrantly expressed in and contributes to the development of various cancers by different means. For instance, (P) RR was recently demonstrated to induce the oncogenesis of pancreatic, colorectal and brain cancers via the Wnt signaling, while promote the endometrial cancer and glioblastoma through the RAS. Methods Combining with the deep analysis of big data from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases, this review updates and summarizes the recent studies about the newly recognized roles of (P) RR in the pathophysiological processes of cancer development and its detailed functions through related pathways, as well as the novel research progress of (P) RR in related fields including the development and application of soluble (P) RR detection kit and monoclonal (P) RR antibody. Results This review provides an overview of the essential roles of (P) RR in the tumorigenesis and progression of various cancers and offers a translational outlook for the future research and clinical practices. Conclusion (P) RR in the tumor tissues and/or body fluids of patients may be a novel and promising biomarker and potential therapeutic target for diagnosis, treatment and prognosis prediction in various cancers.
C1 [Wang, Juan; Yuan, Ying] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Dept Med Oncol, Hangzhou, Peoples R China.
   [Wang, Juan; Yuan, Ying] Zhejiang Univ, Sch Med, Affiliated Hosp 2,China Natl Minist Educ, Canc Inst,Key Lab Canc Prevent & Intervent, 88 Jiefang Rd, Hangzhou 310009, Peoples R China.
   [Nishiyama, Akira] Kagawa Univ, Dept Pharmacol, Fac Med, Takamatsu, Kagawa, Japan.
   [Matsuyama, Makoto] Shigei Med Res Inst, Div Mol Genet, Okayama, Japan.
   [Wang, Zhiyu] Hebei Med Univ, Affiliated Hosp 4, Dept Immunooncol, Shijiazhuang, Hebei, Peoples R China.
C3 Zhejiang University; Zhejiang University; Kagawa University; Hebei
   Medical University
RP Wang, J; Yuan, Y (corresponding author), Zhejiang Univ, Sch Med, Affiliated Hosp 2, Dept Med Oncol, Hangzhou, Peoples R China.; Wang, J; Yuan, Y (corresponding author), Zhejiang Univ, Sch Med, Affiliated Hosp 2,China Natl Minist Educ, Canc Inst,Key Lab Canc Prevent & Intervent, 88 Jiefang Rd, Hangzhou 310009, Peoples R China.
EM wangjuan2@zju.edu.cn; yuanying1999@zju.edu.cn
OI Ying, Yuan/0000-0002-3922-9553; Wang, Juan/0000-0002-8476-407X; wang,
   zhiyu/0000-0002-0606-318X; Matsuyama, Makoto/0000-0003-2606-059X;
   Nishiyama, Akira/0000-0001-5971-820X
FU Japanese Society for the Promotion of Science; Hoansha Foundation of
   Japan; Fundamental Research Funds for the Central Universities of China;
   National Natural Science Foundation of China; Japanese Society for the
   Promotion of Science [KAKENHI: 18H03191]; Fundamental Research Funds for
   the Central Universities of China [2019FZJD009]; National Natural
   Science Foundation of China [81902956, 81872481, 81872101]
FX We sincerely acknowledge the generous support by the Japanese Society
   for the Promotion of Science Grants-in-Aid for Scientific Research,
   Hoansha Foundation of Japan, Fundamental Research Funds for the Central
   Universities of China and National Natural Science Foundation of China.
   This study was partially supported by the Japanese Society for the
   Promotion of Science Grants-in-Aid for Scientific Research (KAKENHI:
   18H03191 to A. N.) and Hoansha Foundation of Japan (to A. N.). This work
   was also supported by Fundamental Research Funds for the Central
   Universities of China (No. 2019FZJD009 to J. W.) and grants from the
   National Natural Science Foundation of China (No. 81902956 to J. W., No.
   81872481 to Y. Y. and No. 81872101 to Z. W.).
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NR 56
TC 29
Z9 31
U1 1
U2 12
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1478-811X
J9 CELL COMMUN SIGNAL
JI Cell Commun. Signal.
PD MAR 6
PY 2020
VL 18
IS 1
AR 39
DI 10.1186/s12964-020-0531-3
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA KT5LM
UT WOS:000519055900003
PM 32143717
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Bui, VMH
   Mettling, C
   Jou, J
   Sun, HS
AF Vo-Minh-Hoang Bui
   Mettling, Clement
   Jou, Jonathan
   Sun, H. Sunny
TI Genomic amplification of chromosome 20q13.33 is the early biomarker for
   the development of sporadic colorectal carcinoma
SO BMC MEDICAL GENOMICS
LA English
DT Article; Proceedings Paper
CT 18th Asia Pacific Bioinformatics Conference (APBC) - Medical Genomics
CY AUG 18-20, 2020
CL Seoul, SOUTH KOREA
DE Chromosome instability; Microsatellite instability; Biomarker; Sporadic
   CRC; Adenoma - carcinoma process
ID MICROSATELLITE INSTABILITY; CANCER; ABERRATIONS; GENETICS; DELETION;
   ADENOMA; CELL; 20Q
AB BackgroundColorectal carcinoma (CRC) is the third most common cancer in the world and also the third leading cause of cancer-related mortality in Taiwan. CRC tumorigenesis is a multistep process, starting from mutations causing loss of function of tumor suppressor genes, canonically demonstrated in adenomatous polyposis coli pathogenesis. Although many genes or chromosomal alterations have been shown to be involved in this process, there are still unrecognized molecular events within CRC tumorigenesis. Elucidating these mechanisms may help improve the management and treatment.MethodsIn this study, we aimed to identify copy number alteration of the smallest chromosomal regions that is significantly associated with sporadic CRC tumorigenesis using high-resolution array-based Comparative Genomic Hybridization (aCGH) and quantitative Polymerase chain reaction (qPCR). In addition, microsatellite instability assay and sequencing-based mutation assay were performed to illustrate the initiation event of CRC tumorigenesis.ResultsA total of 571 CRC patients were recruited and 377 paired CRC tissues from sporadic CRC cases were used to define the smallest regions with chromosome copy number changes. In addition, 198 colorectal polyps from 160 patients were also used to study the role of 20q13.33 gain in CRC tumorigenesis. We found that gain in 20q13.33 is the main chromosomal abnormalities in this patient population and counts 50.9 and 62.8% in CRC and colon polyps, respectively. Furthermore, APC and KRAS gene mutations were profiled simultaneously and co-analyzed with microsatellite instability and 20q13.33 gain in CRC patients. Our study showed that the frequency of 20q13.33 copy number gain was highest among all reported CRC mutations.ConclusionAs APC or KRAS mutations are currently identified as the most important targets for CRC therapy, this study proposes that 20q13.33 copy number gain and the associated chromosomal genes function as promising biomarkers for both early stage detection and targeted therapy of sporadic CRCs in the future.
C1 [Vo-Minh-Hoang Bui; Sun, H. Sunny] Natl Cheng Kung Univ, Coll Med, Inst Basic Med, Tainan 701, Taiwan.
   [Vo-Minh-Hoang Bui] Univ Med & Pharm Ho Chi Minh City, Dept Histol Embryol & Pathol, Ho Chi Minh City, Vietnam.
   [Mettling, Clement] CNRS, Inst Genet Humaine, Unite Propre Rech 1142, F-34396 Montpellier 5, France.
   [Jou, Jonathan] Univ Illinois, Coll Med, Champaign, IL 61820 USA.
   [Sun, H. Sunny] Natl Cheng Kung Univ, Coll Med, Inst Mol Med, 1 Univ Rd, Tainan 70101, Taiwan.
C3 National Cheng Kung University; Hochiminh City University of Medicine &
   Pharmacy; Centre National de la Recherche Scientifique (CNRS);
   Universite de Montpellier; University of Illinois System; University of
   Illinois Urbana-Champaign; National Cheng Kung University
RP Sun, HS (corresponding author), Natl Cheng Kung Univ, Coll Med, Inst Basic Med, Tainan 701, Taiwan.; Sun, HS (corresponding author), Natl Cheng Kung Univ, Coll Med, Inst Mol Med, 1 Univ Rd, Tainan 70101, Taiwan.
EM hssun@mail.ncku.edu.tw
FU Ministry of Science and Technology, Taiwan [MOST 104-2320-B-006-042 -]
FX Research and publication costs are funded y the grant from the Ministry
   of Science and Technology, Taiwan (MOST 104-2320-B-006-042 -) to HSS.
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NR 35
TC 8
Z9 9
U1 0
U2 1
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1755-8794
J9 BMC MED GENOMICS
JI BMC Med. Genomics
PD OCT 22
PY 2020
VL 13
SU 10
SI SI
AR 149
DI 10.1186/s12920-020-00776-z
PG 11
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Genetics & Heredity
GA OM0ZR
UT WOS:000585759600002
PM 33087131
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Xu, Y
   Guo, QL
   Wei, LB
AF Xu, Ye
   Guo, Qinglong
   Wei, Libin
TI The Emerging Influences of Alpha-Fetoprotein in the Tumorigenesis and
   Progression of Hepatocellular Carcinoma
SO CANCERS
LA English
DT Review
DE hepatocellular carcinoma; alpha-fetoprotein; different functions in
   serum and cytoplasm
ID GAMMA-CARBOXY PROTHROMBIN; FINGER PROTEIN ZBTB20; EARLY-DIAGNOSIS;
   EXTRAHEPATIC METASTASIS; TUMOR-CELLS; TRANSARTERIAL CHEMOEMBOLIZATION;
   MOLECULAR-MECHANISMS; ANTITUMOR-ACTIVITY; HEPATOMA-CELLS; GROWTH-FACTORS
AB Simple Summary:& nbsp;Hepatocellular carcinoma is characterized by aggressive invasion, rapid progress and poor prognosis. Since hepatocellular carcinoma is a highly heterogeneous cancer, both at the molecular and histological level, the precision medicine for patients is not very effective and the systematic targeted therapies remain unsatisfactory. The identification of new targets and molecular pathways is urgently needed for drug treatment of hepatocellular carcinoma. Alpha-fetoprotein acts as the most common tumor marker used for hepatocellular carcinoma diagnosis. Alpha-fetoprotein in serum and cytoplasm shows very different influences in the tumorigenesis and progression of hepatocellular carcinoma. The aim of this review is to summarize the current knowledge of the role of alpha-fetoprotein in hepatocellular carcinoma.</p>
   <br></p>
   Hepatocellular carcinoma (HCC) is the sixth most common cancer worldwide, and its mortality rate is the third-highest, after lung cancer and colorectal cancer. Currently, systematic targeted therapies for HCC mainly include multiple kinase inhibitors and immunotherapy. However, these drugs carry a black-box warning about the potential for inducing severe toxicity, and they do not significantly prolong the survival period of patients due to the highly heterogeneous characteristics of HCC etiology. In order to improve the prediction, effective treatment and prognosis of HCC, the tools and different biomarkers in clinical practices are recommended. Alpha-fetoprotein (AFP) is the earliest and the most widely used serum marker in the detection of HCC. Interestingly, serum AFP and cytoplasmic AFP show different, even opposite, roles in the cancer progression of HCC. This review focuses on biological characteristics, regulatory mechanisms for gene expression, emerging influences of AFP in HCC and its possible implications in HCC-targeted therapy.</p>
C1 [Xu, Ye; Guo, Qinglong; Wei, Libin] China Pharmaceut Univ, Sch Basic Med Sci & Clin Pharm, Jiangsu Key Lab Carcinogenesis & Intervent, State Key Lab Nat Med, 24 Tongjiaxiang, Nanjing 210009, Peoples R China.
C3 China Pharmaceutical University
RP Wei, LB (corresponding author), China Pharmaceut Univ, Sch Basic Med Sci & Clin Pharm, Jiangsu Key Lab Carcinogenesis & Intervent, State Key Lab Nat Med, 24 Tongjiaxiang, Nanjing 210009, Peoples R China.
EM 219091310@stu.cpu.edu.cn; 1019840800@cpu.edu.cn; 1020142410@cpu.edu.cn
OI Xu, Ye/0000-0001-8052-9147
FU National Natural Science Foundation of China [82174027]; Social
   Development Project of Jiangsu Provincial Key Research and Development
   Program [BE2021782]
FX FundingThis work was supported by the National Natural Science
   Foundation of China (no. 82174027) and the Social Development Project of
   Jiangsu Provincial Key Research and Development Program (BE2021782).
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NR 119
TC 19
Z9 20
U1 4
U2 27
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD OCT
PY 2021
VL 13
IS 20
AR 5096
DI 10.3390/cancers13205096
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA WQ4GV
UT WOS:000713777700001
PM 34680245
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ekmekciu, I
   Zucha, DM
   Christmann, J
   Wisser, S
   Heuer, V
   Sargin, B
   Hollerbach, S
   Lamberti, C
   Müller, L
   Lugnier, C
   Verdoodt, B
   Denz, R
   Terzer, T
   Feder, I
   Reinacher-Schick, A
   Tannapfel, A
   Tischoff, I
AF Ekmekciu, Ira
   Zucha, Doreen Maria
   Christmann, Jens
   Wisser, Sarah
   Heuer, Vera
   Sargin, Buelent
   Hollerbach, Stephan
   Lamberti, Christof
   Mueller, Lothar
   Lugnier, Celine
   Verdoodt, Berlinda
   Denz, Robin
   Terzer, Tobias
   Feder, Inke
   Reinacher-Schick, Anke
   Tannapfel, Andrea
   Tischoff, Iris
TI Exploring the molecular profile of localized colon cancer: insights from
   the AIO Colopredict Plus registry
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colon cancer; localized; real world data; microsatellite instability;
   RAS; BRAF
ID METASTATIC COLORECTAL-CANCER; MICROSATELLITE INSTABILITY; ADJUVANT
   CHEMOTHERAPY; POOLED ANALYSIS; RAS MUTATIONS; BRAF-MUTATION; STAGE-II;
   KRAS; CETUXIMAB; SURVIVAL
AB Introduction Understanding the mutational landscape of colon cancer (CC) is crucial for targeted therapy development. Microsatellite instability (MSI-H), rat sarcoma (RAS), and B-Raf proto-oncogene, serine/threonine kinase (BRAF) mutations (MT) are pivotal markers. Further investigation into clinicopathological features of RAS and BRAF MT in microsatellite stable (MSS) and MSI-H tumors is warranted. Methods A retrospective analysis of 4883 localized CC patients (pts.) was conducted. Molecular profiling assessed MSI, KRAS, NRAS, and BRAF MT. Correlation with clinicopathological data employed ANOVA and Chi-square tests. Disease-free survival (DFS) and overall survival (OS) were analyzed adjusting for age, gender, sidedness, UICC stage, Charlson Comorbidity Index (CCI). A Cox model incorporated all variables as covariates. Results This analysis included 4883 pts. (2302 female/2572 male, 3865 (79.2%) MSS, 1018 (20.8%) MSI-H). MSS pts. had more All-Wild Type (WT), KRAS MT, and NRAS MT tumors vs. MSI-H pts. (42.1% vs. 21.1%; 39.8% vs. 15.4%; 3.6% vs. 0.7%; p<0.001 for each). BRAF MT tumors (95.5% BRAF V600E MT) were more prevalent in MSI-H individuals (62.8% vs. 8.1%, p<0.001). KRAS and BRAF MT tumors were more frequently right-sided, while BRAF MT tumors were associated with female gender, advanced disease stage, lymph node positivity, and poorer differentiation in the MSS subset (p<0.001). Common KRAS mutations included p.G12D (30.44%) and p.G12V (21.3%) in MSS and p.G13D (28.9%) and p.G12D (22.37%) in MSI-H. NRAS MT tumors were dominated by codon 61 mutations (51.7%). Survival analysis revealed worst prognosis in BRAF MT MSS tumors (DFS: HR 1.74 (95% CI 1.15-2.62, p=0.009; OS: HR 1.61 (95% CI 0.99-2.6), p=0.055). The 3-years DFS and 5-years OS rates were lowest in this subset (61.6% and 57.7% respectively). Discussion These findings highlight the complex interplay between molecular subtypes, clinicopathological features, and survival outcomes in early CC. Further research is needed to elucidate underlying mechanisms and develop personalized treatment strategies.
C1 [Ekmekciu, Ira; Heuer, Vera; Lugnier, Celine; Terzer, Tobias; Reinacher-Schick, Anke] Ruhr Univ, St Josef Hosp, Dept Hematol & Oncol Palliat Care, Bochum, Germany.
   [Zucha, Doreen Maria; Christmann, Jens; Wisser, Sarah; Verdoodt, Berlinda; Feder, Inke; Tannapfel, Andrea; Tischoff, Iris] Ruhr Univ, Inst Pathol, Bochum, Germany.
   [Sargin, Buelent] St Marien Hosp Lunen, Hematol & Med Oncol, Lunen, Germany.
   [Hollerbach, Stephan] Allgemeines Krankenhaus AKH Celle, Dept Gastroenterol, Celle, Germany.
   [Lamberti, Christof] Regiomed Hosp Grp, Hematol & Oncol, Coburg, Germany.
   [Mueller, Lothar] Onkol UnterEms, Leer, Germany.
   [Denz, Robin] Ruhr Univ Bochum, Dept Med Informat Biometr & Epidemiol, Bochum, Germany.
C3 Ruhr University Bochum; Ruhr University Bochum; St. Marien Hospital;
   Ruhr University Bochum
RP Ekmekciu, I (corresponding author), Ruhr Univ, St Josef Hosp, Dept Hematol & Oncol Palliat Care, Bochum, Germany.
EM ira.ekmekciu@rub.de
FU Protein Research Unit Ruhr within Europe (PURE) - Ministry of
   Innovation, Science and Research (MIWF) of North-Rhine Westphalia,
   Germany [233-1.08.03.03-031-68079]; Roche Pharma AG
FX The author(s) declare financial support was received for the research,
   authorship, and/or publication of this article. This research was
   supported by the Protein Research Unit Ruhr within Europe (PURE), funded
   by the Ministry of Innovation, Science and Research (MIWF) of
   North-Rhine Westphalia, Germany (grant number: 233-1.08.03.03-031-68079)
   and by Roche Pharma AG from 2016-2018. The funder was not involved in
   the study design, collection, analysis, interpretation of data, the
   writing of this article, or the decision to submit it for publication.
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NR 49
TC 0
Z9 0
U1 0
U2 0
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD NOV 19
PY 2024
VL 14
AR 1434791
DI 10.3389/fonc.2024.1434791
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA O1Y3D
UT WOS:001369163000001
PM 39628993
OA gold
DA 2025-01-04
ER

PT J
AU Song, JR
   Song, ZM
   Zhang, JP
   Gong, YL
AF Song, Junrong
   Song, Zhiming
   Zhang, Jinpeng
   Gong, Yuanli
TI Privacy-Preserving Identification of Cancer Subtype-Specific Driver
   Genes Based on Multigenomics Data with Privatedriver
SO JOURNAL OF COMPUTATIONAL BIOLOGY
LA English
DT Article
DE data integration; federated learning; privacy-preserving study;
   subtype-specific driver gene identification
ID HEALTH; PATHWAYS
AB Identifying cancer subtype-specific driver genes from a large number of irrelevant passengers is crucial for targeted therapy in cancer treatment. Recently, the rapid accumulation of large-scale cancer genomics data from multiple institutions has presented remarkable opportunities for identification of cancer subtype-specific driver genes. However, the insufficient subtype samples, privacy issues, and heterogenous of aberration events pose great challenges in precisely identifying cancer subtype-specific driver genes.To address this, we introduce privatedriver, the first model for identifying subtype-specific driver genes that integrates genomics data from multiple institutions in a data privacy-preserving collaboration manner. The process of identifying subtype-specific cancer driver genes using privatedriver involves the following two steps: genomics data integration and collaborative training. In the integration process, the aberration events from multiple genomics data sources are combined for each institution using the forward and backward propagation method of NetICS. In the collaborative training process, each institution utilizes the federated learning framework to upload encrypted model parameters instead of raw data of all institutions to train a global model by using the non-negative matrix factorization algorithm.We applied privatedriver on head and neck squamous cell and colon cancer from The Cancer Genome Atlas website and evaluated it with two benchmarks using macro-Fscore. The comparison analysis demonstrates that privatedriver achieves comparable results to centralized learning models and outperforms most other nonprivacy preserving models, all while ensuring the confidentiality of patient information. We also demonstrate that, for varying predicted driver gene distributions in subtype, our model fully considers the heterogeneity of subtype and identifies subtype-specific driver genes corresponding to the given prognosis and therapeutic effect. The success of privatedriver reveals the feasibility and effectiveness of identifying cancer subtype-specific driver genes in a data protection manner, providing new insights for future privacy-preserving driver gene identification studies.
C1 [Song, Junrong; Song, Zhiming; Zhang, Jinpeng; Gong, Yuanli] Yunnan Univ Finance & Econ, Sch Informat, Kunming 650221, Peoples R China.
   [Song, Junrong; Song, Zhiming; Zhang, Jinpeng] Yunnan Univ Finance & Econ, Yunnan Key Lab Serv Comp, Kunming, Peoples R China.
   [Zhang, Jinpeng] Yunnan Univ, Sch Comp Sci & Engn, Kunming 650091, Yunnan, Peoples R China.
C3 Yunnan University of Finance & Economics; Yunnan University of Finance &
   Economics; Yunnan University
RP Song, JR (corresponding author), Yunnan Univ Finance & Econ, Sch Informat, Kunming 650221, Peoples R China.
EM sjunrong1990@163.com
OI Song, Junrong/0009-0000-6716-5975
FU National Natural Science Foundation of China [62202415]; Natural Science
   Foundation of Yunnan Province of China [202201AU070115]; Scientific
   Research Foundation of Yunnan University of Finance and Economics
   [20220002]; Yunnan Fundamental Research Projects [202201AU070116];
   Talent introduction project of Yunnan University of Finance and
   Economics [2022D08]
FX This work was supported, in part, by the National Natural Science
   Foundation of China (Grant No.62202415), the Natural Science Foundation
   of Yunnan Province of China (Grant No. 202201AU070115), the Scientific
   Research Foundation of Yunnan University of Finance and Economics (Grant
   No. 20220002),the Yunnan Fundamental Research Projects (Grant No.
   202201AU070116), and the Talent introduction project of Yunnan
   University of Finance and Economics (Grant No. 2022D08).
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NR 70
TC 0
Z9 0
U1 4
U2 7
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1066-5277
EI 1557-8666
J9 J COMPUT BIOL
JI J. Comput. Biol.
PD FEB 1
PY 2024
VL 31
IS 2
BP 99
EP 116
DI 10.1089/cmb.2023.0115
EA JAN 2024
PG 18
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
   Computer Science, Interdisciplinary Applications; Mathematical &
   Computational Biology; Statistics & Probability
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Computer Science; Mathematical & Computational Biology; Mathematics
GA HJ7Y8
UT WOS:001150816600002
PM 38271572
DA 2025-01-04
ER

PT J
AU Smith, AD
   Gray, MR
   del Campo, SM
   Shlapak, D
   Ganeshan, B
   Zhang, X
   Carson, WE
AF Smith, Andrew D.
   Gray, Mark R.
   del Campo, Sara Martin
   Shlapak, Darya
   Ganeshan, Balaji
   Zhang, Xu
   Carson, William E., III
TI Predicting Overall Survival in Patients With Metastatic Melanoma on
   Antiangiogenic Therapy and RECIST Stable Disease on Initial Posttherapy
   Images Using CT Texture Analysis
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Article
DE antiangiogenic therapy; biomarker; CT texture analysis; metastatic
   melanoma
ID RENAL-CELL CARCINOMA; GUIDELINE VERSION 1.1; TUMOR HETEROGENEITY;
   TARGETED THERAPY; PHASE-2 TRIAL; DOSE INTERFERON-ALPHA-2B;
   COMPUTED-TOMOGRAPHY; RESPONSE EVALUATION; COLORECTAL-CANCER; POTENTIAL
   MARKER
AB OBJECTIVE. The purpose of this study was to use CT texture analysis to predict overall survival (OS) in patients with metastatic melanoma and stable disease (SD) according to the Response Evaluation Criteria in Solid Tumors (RECIST) on initial posttherapy CT images.
   MATERIALS AND METHODS. This retrospective study included 42 patients with metastatic melanoma who received bevacizumab therapy in the context of a randomized prospective phase II clinical trial. Target lesions on the baseline and initial posttherapy contrast-enhanced CT examinations were evaluated by CT texture analysis using TexRAD software before and after image filtering in patients with RECIST SD on initial posttherapy images. Cox proportional hazards models were used to assess the associations of CT texture analysis measurements and of other patient factors with OS. The AUC was used to evaluate predictive accuracy.
   RESULTS. In multivariate analysis (in 23 patients with RECIST SD; median OS, 1.51 years), absolute change in mean positive pixels at spatial scaling filter of 4 mm, change in tumor size, and baseline serum lactate dehydrogenase (LDH) level were predictors of OS (hazard ratio [HR] = 5.05 for decrease in mean positive pixels at spatial scaling filter of 4 mm vs increase, p = 0.007; HR = 4.14 for > 5% increase in tumor size vs otherwise, p = 0.025; and HR = 1.29 for every 100 IU/L increase in baseline LDH level, p = 0.068). A prognostic index containing these three factors was highly accurate for predicting OS at 18 months (AUC = 0.917).
   CONCLUSION. In patients with metastatic melanoma and RECIST SD on initial posttherapy CT images, a model incorporating CT texture analysis of target lesions, tumor size changes, and baseline LDH levels was highly accurate in predicting OS.
C1 [Smith, Andrew D.; Gray, Mark R.; Shlapak, Darya; Zhang, Xu] Univ Mississippi, Med Ctr, Dept Radiol, Jackson, MS 39216 USA.
   [del Campo, Sara Martin; Carson, William E., III] Ohio State Univ, Dept Surg, Ctr Comprehens Canc, Columbus, OH 43210 USA.
   [Ganeshan, Balaji] UCL, Dept Biomed Engn, London, England.
C3 University of Mississippi; University of Mississippi Medical Center;
   James Cancer Hospital & Solove Research Institute; University System of
   Ohio; Ohio State University; University of London; University College
   London
RP Smith, AD (corresponding author), Univ Mississippi, Med Ctr, Dept Radiol, 2500 N State St, Jackson, MS 39216 USA.
EM asmith4@umc.edu
RI Smith, Andrew/KQU-0358-2024; Carson, William/E-2846-2011
OI Carson, III, William E./0000-0001-7024-7533; Martin del Campo,
   Sara/0000-0002-8821-3208
FU Pfizer
FX A. D. Smith was supported by an investigator-initiated grant from
   Pfizer.
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U2 5
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
EI 1546-3141
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD SEP
PY 2015
VL 205
IS 3
BP W283
EP W293
DI 10.2214/AJR.15.14315
PG 11
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA CP6KW
UT WOS:000359997100007
PM 26295664
DA 2025-01-04
ER

PT J
AU Fumet, JD
   Isambert, N
   Hervieu, A
   Zanetta, S
   Guion, JF
   Hennequin, A
   Rederstorff, E
   Bertaut, A
   Ghiringhelli, F
AF Fumet, Jean-David
   Isambert, Nicolas
   Hervieu, Alice
   Zanetta, Sylvie
   Guion, Jean-Florian
   Hennequin, Audrey
   Rederstorff, Emilie
   Bertaut, Aurelie
   Ghiringhelli, Francois
TI Phase Ib/II trial evaluating the safety, tolerability and immunological
   activity of durvalumab (MEDI4736) (anti-PD-L1) plus tremelimumab
   (anti-CTLA-4) combined with FOLFOX in patients with metastatic
   colorectal cancer
SO ESMO OPEN
LA English
DT Article
ID CHEMOTHERAPY; BEVACIZUMAB; NIVOLUMAB; CELLS; MULTICENTER; OXALIPLATIN;
   COMBINATION; CETUXIMAB; BLOCKADE; SURVIVAL
AB Background 5-Fluorouracil plus irinotecan or oxaliplatin alone or in association with target therapy are standard first-line therapy for metastatic colorectal cancer (mCRC). Checkpoint inhibitors targeting PD-1/PD-L1 demonstrated efficacy on mCRC with microsatellite instability but remain ineffective alone in microsatellite stable tumour. 5-Fluorouracil and oxaliplatin were known to present immunogenic properties. Durvalumab (D) is a human monoclonal antibody (mAb) that inhibits binding of programmed cell death ligand 1 (PD-L1) to its receptor. Tremelimumab (T) is a mAb directed against the cytotoxic T-lymphocyte-associated protein 4 (CTLA-4). This study is designed to evaluate whether the addition of PD-L1 and CTLA-4 inhibition to oxaliplatin, fluorouracil and leucovorin (FOLFOX) increases treatment efficacy.
   Methods This phase II study (ClinicalTrials.gov NCT03202758) will assess the efficacy and safety of FOLFOX/D/T association in patients with mCRC (n=48). Good performance status patients (Eastern Cooperative Oncology Group <2) with untreated, RAS mutational status mCRC will be eligible. Prior adjuvant therapy is allowed provided recurrence is >6 months postcompletion. There is a safety lead in nine patients receiving FOLFOX/D/T. Assuming no safety concerns the study will go on to include 39 additional patients. Patients will receive folinic acid (400 mg/m(2))/5-fluorouracil (400 mg/m(2) as bolus followed by 2400 mg/m(2) as a 46-hour infusion)/oxaliplatin (85 mg/m(2)) every 14 days with D (750 mg) D1 every 14 days and T (75 mg) D1 every 28 days. After six cycles of FOLFOX only D/T will continue until disease progression, death, intolerable toxicity, or patient/investigator decision to stop. Primary endpoint is safety and efficacy according to progression-free survival (PFS); secondary endpoints include overall response rate and quality of life. Hypothesis is that a PFS of 50% at 6 months is insufficient and a PFS of 70.7% is expected (with alpha=10%, beta=10%). Blood, plasma and tumour tissue will be collected and assessed for potential prognostic and predictive biomarkers.
C1 [Fumet, Jean-David; Isambert, Nicolas; Hervieu, Alice; Zanetta, Sylvie; Guion, Jean-Florian; Hennequin, Audrey; Ghiringhelli, Francois] Ctr Georges Francois Leclerc, Dept Med Oncol, Dijon, France.
   [Fumet, Jean-David; Ghiringhelli, Francois] Georges Francois Leclerc Ctr, Res Platform Biol Oncol, Dijon, France.
   [Fumet, Jean-David; Ghiringhelli, Francois] Univ Burgundy Franche Comte, Dijon, France.
   [Rederstorff, Emilie; Bertaut, Aurelie] Georges Francois Leclerc Ctr, Dept Epidemiol & Biostat, Dijon, France.
   [Ghiringhelli, Francois] INSERM, UMR1231, Dijon, France.
   [Ghiringhelli, Francois] GIMI Genet & Immunol Med Inst, Dijon, France.
C3 UNICANCER; Centre Georges-Francois Leclerc; UNICANCER; Centre
   Georges-Francois Leclerc; UNICANCER; Centre Georges-Francois Leclerc;
   Institut Agro; AgroSup Dijon; Institut National de la Sante et de la
   Recherche Medicale (Inserm); Universite de Bourgogne
RP Fumet, JD (corresponding author), Ctr Georges Francois Leclerc, Dept Med Oncol, Dijon, France.; Fumet, JD (corresponding author), Georges Francois Leclerc Ctr, Res Platform Biol Oncol, Dijon, France.; Fumet, JD (corresponding author), Univ Burgundy Franche Comte, Dijon, France.
EM jd.fumet@gmail.com
RI Isambert, Nicolas/C-5041-2009
OI ghiringhelli, francois/0000-0002-5465-8305
FU AstraZeneca
FX The study was funded in total by AstraZeneca.
CR Antonia SJ, 2017, NEW ENGL J MED, V377, P1919, DOI 10.1056/NEJMoa1709937
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   Wolchok JD, 2017, NEW ENGL J MED, V377, P1345, DOI 10.1056/NEJMoa1709684
NR 32
TC 42
Z9 49
U1 0
U2 8
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2059-7029
J9 ESMO OPEN
JI ESMO Open
PD MAY
PY 2018
VL 3
IS 4
AR UNSP e000375
DI 10.1136/esmoopen-2018-000375
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JM3VN
UT WOS:000496146300005
PM 29942666
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Snyder, M
   Bottiglieri, S
   Almhanna, K
AF Snyder, Matthew
   Bottiglieri, Sal
   Almhanna, Khaldoun
TI Impact of Primary Tumor Location on First-line Bevacizumab or Cetuxi-mab
   in Metastatic Colorectal Cancer
SO REVIEWS ON RECENT CLINICAL TRIALS
LA English
DT Article
DE Bevacizumab; cetuximab; left-sided tumors; metastatic colorectal cancer;
   primary tumor location; right-sided tumors; targeted therapy
ID FLUOROURACIL; CHEMOTHERAPY; OXALIPLATIN; PROGRESSION; LEUCOVORIN; FIRE-3
AB Background: Colorectal cancer is one of the most common malignancies in the United States, with a large proportion of patients presenting with metastatic disease or developing a recurrence. Systemic chemotherapy is the mainstay of therapy in this setting. There is a clear benefit in the addition of bevacizumab or cetuximab (for rat sarcoma [RAS] wild type tumors) to oxaliplatin- and irinotecan-based regimens which can be considered for first-line therapy. However, many significant questions remain as to which agent reflects best practice.
   Objective: Our review aimed to elucidate the benefit of adding bevacizumab and cetuximab to initial therapy for metastatic colorectal cancer based on primary tumor location and a variety of other disease- and patient-related factors, addressing the paucity of evidence that currently exists in this area and contributing to current literature and clinical practices.
   Methods: The primary endpoints of the study were first Progression-Free Survival (PFS) and Overall Survival (OS). Secondary endpoints included best response to first- and second-line therapies, Treatment-Related Adverse Events (TRAEs), second PFS, cost of therapy, and an assessment of other patient- and disease-related factors affecting PFS and OS.
   Results: While there were trends towards improved OS in patients with left-sided primary tumors (n=57) compared to those with right-sided disease (n=23), there were no significant differences between the two groups in either primary endpoint. While no differences were found for patients with left- or right- sided tumors stratified by add-on agent, these analyses were limited by the small number of patients receiving cetuximab with first-line therapy (n=4). However, the bevacizumab cohort (n=76) was sizable enough to provide ample data and produce clinically relevant results. Add-on therapy with bevacizumab in our study achieved impressive survival outcomes in both left-sided (median first PFS = 13 months, 95% CI 11-15 months; median OS = 37 months, 95% CI 21-53 months) and right-sided (median first PFS = 13 months, 95% CI 9-17 months; median OS = 37 months, 95% CI 22-52 months) disease.
   Conclusion: These results raised questions regarding the true significance of primary tumor location when selecting bevacizumab or cetuximab for first-line therapy, particularly the current thought of using cetuximab for left-sided tumors. While the superiority of bevacizumab over cetuximab in right-sided disease remained evident upon comparison of our analysis with historical controls, survival outcomes with the agent in our analysis appeared to be similar to that of cetuximab in CRYSTAL, FIRE-3, and CALGB/SWOG 80405 in left-sided disease. Further study is required to determine if bevacizumab truly does produce similar outcomes to cetuximab in left-sided primary tumors.
C1 [Snyder, Matthew; Bottiglieri, Sal] H Lee Moffitt Canc Ctr & Res Inst, Dept Pharm, Tampa, FL 33612 USA.
   [Almhanna, Khaldoun] Brown Univ, Oncol Grp, Providence, RI 02912 USA.
C3 H Lee Moffitt Cancer Center & Research Institute; Brown University
RP Snyder, M (corresponding author), H Lee Moffitt Canc Ctr & Res Inst, Dept Pharm, Tampa, FL 33612 USA.
EM Matthew.Snyder@moffitt.org
CR [Anonymous], J CLIN ONCOL S
   [Anonymous], COL CANC NCCN CLIN P
   [Anonymous], RECT CANC NCCN CLIN
   Bennouna J, 2013, LANCET ONCOL, V14, P29, DOI 10.1016/S1470-2045(12)70477-1
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NR 18
TC 18
Z9 19
U1 0
U2 0
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1574-8871
EI 1876-1038
J9 REV RECENT CLIN TRIA
JI Rev. Recent Clin. Trials
PY 2018
VL 13
IS 2
BP 139
EP 149
DI 10.2174/1574887113666180328104109
PG 11
WC Pharmacology & Pharmacy
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA GK3ZX
UT WOS:000436093000008
PM 29595113
DA 2025-01-04
ER

PT J
AU Gao, LL
   Tang, L
   Hu, ZX
   Peng, JQ
   Li, XQ
   Liu, B
AF Gao, Loulu
   Tang, Lin
   Hu, Zixuan
   Peng, Jieqiong
   Li, Xiaoqian
   Liu, Bo
TI Comparison of the efficacy and safety of third-line treatments for
   metastatic colorectal cancer: a systematic review and network
   meta-analysis
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE colorectal cancer; third-line; neoplasm metastasis; network
   meta-analysis (NMA); treatment
ID DOUBLE-BLIND; OPEN-LABEL; TAS-102 MONOTHERAPY; ANTITUMOR-ACTIVITY; ASIAN
   PATIENTS; PLACEBO; BEVACIZUMAB; MULTICENTER; ANTIMETABOLITE; INHIBITION
AB <bold>Background:</bold> Many options for third-line treatment of advanced gastric cancer (GC) or gastroesophageal junction carcinoma (GEJC) have been developed. Therapies including immunotherapy (nivolumab), chemotherapy (irinotecan, FTD/TPI), targeted therapy (apatinib), and antibody drug conjugates (ADC) have shown to increase the survival rates in patients, but few studies have compared the relative efficacy of these treatments. Here, we compared the efficacies of these regimens using network meta-analysis (NMA) to provide guides in selecting the best regimen and formulating a precise individualized treatment plan.<bold>Methods:</bold> The published RCTs of phase II/III in PubMed, the Cochrane Central Register of Controlled Trials, and Embase were searched. The median overall survival (mOS) was the primary outcome of NMA, and the other outcomes were median progression-free survival (mPFS), disease control rate (DCR) (proportion of patients with confirmed CR, PR, or stable disease (SD)) and incidence of grade 3 or above adverse events (>= 3AEs).<bold>Results:</bold> Five phase II/III RCTs involving 1674 patients and 7 treatment regimens were analyzed. It showed that Trastuzumab Deruxtecan (DS-8201) prolonged the OS of patients significantly comparing with chemotherapy (HR: 0.59; 95% CI: 0.39-0.89) for the overall population. DS-8201 (HR: 0.27; 95% CI: 0.17-0.42) and chemotherapy (HR: 0.57; 95% CI: 0.47-0.7) improved the PFS significantly over nivolumab. Apatinib (RR: 3.04; 95% CI: 1.65-5.95) and DS-8201 (RR: 2.67; 95% CI: 1.51-4.83) were more effective than nivolumab in improving DCR. DS-8201 achieved greater OS benefits compared to chemotherapy (HR: 0.59; 95% CI: 0.39-0.88) for patients who were HER2-positive. We ranked the Bayesian surface under the cumulative ranking curve according to OS benefit, and showed that ADC ranked first for the general patient population and for patients with a HER2-positive diagnosis, intestinal histopathology, previous gastrectomy history, gastric origination cancer, ages over 65 and ECOG PS=0/1, followed by nivolumab and apatinib. For patients with GEJC, nivolumab ranked first.<bold>Conclusions:</bold> Nivolumab, apatinib, chemotherapy, and ADC all improved the OS of GC/GEJC patients significantly. ADC may be the best option for the overall population of GC, as well as for patients with HER2-overexpression, intestinal histopathology, previous gastrectomy history, gastric origination cancer, ages over 65 and ECOG PS=0/1, followed by nivolumab and apatinib. Nivolumab may be the first treatment option for GEJC patients.
C1 [Gao, Loulu; Hu, Zixuan] Weifang Med Univ, Sch Clin Med, Weifang, Peoples R China.
   [Gao, Loulu; Tang, Lin; Peng, Jieqiong; Li, Xiaoqian; Liu, Bo] Shandong First Med Univ & Shandong Acad Med Sci, Shandong Canc Hosp & Inst, Dept Oncol, Jinan, Peoples R China.
   [Tang, Lin] Shandong First Med Univ & Shandong Acad Med Sci, Dept Oncol, Jinan, Peoples R China.
C3 Shandong Second Medical University; Shandong First Medical University &
   Shandong Academy of Medical Sciences; Shandong First Medical University
   & Shandong Academy of Medical Sciences
RP Liu, B (corresponding author), Shandong First Med Univ & Shandong Acad Med Sci, Shandong Canc Hosp & Inst, Dept Oncol, Jinan, Peoples R China.
EM liubosdsz@163.com
RI Peng, Jie qiong/JDW-2960-2023; Hu, Zixuan/JGE-0032-2023
FU The author(s) declare that no financial support was received for the
   research, authorship, and/or publication of this article.
FX The author(s) declare that no financial support was received for the
   research, authorship, and/or publication of this article.
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NR 40
TC 2
Z9 2
U1 2
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD SEP 21
PY 2023
VL 13
AR 1269203
DI 10.3389/fonc.2023.1269203
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA T5FF9
UT WOS:001078235700001
PM 37810981
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Nakayama, I
   Hirota, T
   Shinozaki, E
AF Nakayama, Izuma
   Hirota, Toru
   Shinozaki, Eiji
TI <i>BRAF</i> Mutation in Colorectal Cancers: From Prognostic Marker to
   Targetable Mutation
SO CANCERS
LA English
DT Review
DE RAF&#8211; MEK&#8211; ERK signaling pathway; BRAF inhibitor; cancer
   precision medicine
ID III COLON-CANCER; CETUXIMAB PLUS IRINOTECAN; ISLAND METHYLATOR
   PHENOTYPE; EGFR MONOCLONAL-ANTIBODIES; CONSENSUS MOLECULAR SUBTYPES;
   MISMATCH REPAIR STATUS; K-RAS MUTATIONS; KRAS WILD-TYPE; MICROSATELLITE
   INSTABILITY; 1ST-LINE TREATMENT
AB Simple Summary
   Colorectal cancer with a mutation in an oncogene BRAF has paid much attention, as it comprises a population with dismal prognosis since two decades ago. A series of research since then has successfully changed this malignancy to be treatable with specific treatment. Here we thoroughly overviewed the basic, translational and clinical studies on colorectal cancer with BRAF mutation from a physician's viewpoint. Accumulating lines of evidence suggest that intervention of the trunk cellular growth signal transduction pathway, namely EGFR-RAS-RAF-MEK-ERK pathway, is a clue to controlling this disease. However, it is not so straightforward. Recent studies unveil the diverse and plastic nature of this signal transduction pathway. We will introduce our endeavor to conquer this condition, based on newly arriving datasets, and discuss how we could open the door to future development of CRC treatment.
   The Raf murine sarcoma viral oncogene homolog B (BRAF) mutation is detected in 8-12% of metastatic colorectal cancers (mCRCs) and is strongly correlated with poor prognosis. The recent success of the BEACON CRC study and the development of targeted therapy have led to the determination of BRAF-mutated mCRCs as an independent category. For nearly two decades, a growing body of evidence has established the significance of the BRAF mutation in the development of CRC. Herein, we overview both basic and clinical data relevant to BRAF-mutated CRC, mainly focusing on the development of treatment strategies. This review is organized into eight sections, including clinicopathological features, molecular features, prognosis, the predictive value of anti-epidermal growth factor receptor (EGFR) therapy, resistant mechanisms for BRAF-targeting treatment, the heterogeneity of the BRAF mutation, future perspectives, and conclusions. A characterization of the canonical mitogen-activated protein kinase (MAPK) pathway is essential for controlling this malignancy, and the optimal combination of multiple interventions for treatments remains a point of debate.
C1 [Nakayama, Izuma; Shinozaki, Eiji] Japanese Fdn Canc Res JFCR, Canc Inst Hosp, Dept Gastroenterol Chemotherapy, Tokyo 1358550, Japan.
   [Hirota, Toru] Japanese Fdn Canc Res JFCR, Canc Inst, Dept Expt Pathol, Tokyo 1358550, Japan.
C3 Japanese Foundation for Cancer Research; Japanese Foundation for Cancer
   Research
RP Nakayama, I; Shinozaki, E (corresponding author), Japanese Fdn Canc Res JFCR, Canc Inst Hosp, Dept Gastroenterol Chemotherapy, Tokyo 1358550, Japan.
EM izuma.nakayama@jfcr.or.jp; thirota@jfcr.or.jp; eiji.shinozaki@jfcr.or.jp
OI Nakayama, Izuma/0000-0003-4987-1934
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NR 202
TC 28
Z9 29
U1 1
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD NOV
PY 2020
VL 12
IS 11
AR 3236
DI 10.3390/cancers12113236
PG 29
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OX4BZ
UT WOS:000593513400001
PM 33152998
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Hosseini, NF
   Amini, R
   Ramezani, M
   Saidijam, M
   Hashemi, SM
   Najafi, R
AF Hosseini, Nashmin Fayazi
   Amini, Razieh
   Ramezani, Mohammad
   Saidijam, Massoud
   Hashemi, Seyed Mahmoud
   Najafi, Rezvan
TI AS1411 aptamer-functionalized exosomes in the targeted delivery of
   doxorubicin in fighting colorectal cancer
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Doxorubicin; Colorectal cancer; Exosome; AS1411; Nucleolin
ID NANODRUG
AB Severe side effects of chemotherapy agents on vital organs are the major causes of cancer-related mortality, not merely cancer disease. Encapsulating chemotherapeutic molecules in nanocarriers is a justifiable solution in decreasing the risk of their side effects and boosting the efficiency of treatment. The present study has developed the doxorubicin (DOX)-loaded AS1411 (anti-nucleolin) aptamer surface-functionalized exosome (DOX-Apt-Exo) to treat colorectal cancer in both in-vitro and in-vivo experimental models. HEK293-derived exosomes were loaded with DOX through the incubation method with a nearly 13% encapsulation efficiency. Afterwards, the 5 -terminal carboxyl group of AS1411-aptamer was converted into amine-reactive NHS esters with EDC/NHS amide coupling chemistry before being conjugated to the amine groups on the exosome surface. DLS and TEM estimated the designed formulation (DOX-Apt-Exo) size of about 200 nm. Aptamer-binding affinity and cellular uptake of DOX-Apt-Exo by nucleolin-overexpressing cancer cells were depicted through fluorescence microscopy. Comparing the in-vitro cytotoxicity impact of DOX-loaded exosomes, either targeted or non-targeted by MTT assay, clearly verified a high effectiveness of ligand-receptor mediated target therapy. Subsequently, in-vivo experiments which were conducted on four groups of ectopic mouse models of colon cancer (5 in each group) demonstrated the tumor growth suppression through professional long-term accumulation and retention of DOX-Apt-Exo at the tumor site by ligand-receptor interaction. The results suggested that AS1411 aptamer-functionalized exosomes can be recommended as a safe and effective system to site-specific drug delivery in possible clinical applications of colon cancer.
C1 [Hosseini, Nashmin Fayazi; Amini, Razieh; Saidijam, Massoud; Najafi, Rezvan] Hamadan Univ Med Sci, Res Ctr Mol Med, Hamadan, Iran.
   [Ramezani, Mohammad] Mashhad Univ Med Sci, Sch Pharm, Dept Pharmaceut Biotechnol, Mashhad, Iran.
   [Hashemi, Seyed Mahmoud] Shahid Beheshti Univ Med Sci, Sch Med, Dept Immunol, Tehran, Iran.
C3 Hamadan University of Medical Sciences; Mashhad University of Medical
   Sciences; Shahid Beheshti University Medical Sciences
RP Najafi, R (corresponding author), Hamadan Univ Med Sci, Res Ctr Mol Med, Hamadan, Iran.
EM re.najafi@umsha.ac.ir
RI Najafi, Rezvan/U-8110-2017; Hashemi, Seyed Mahmoud/F-1221-2010; Hashemi,
   Seyed Mahmoud/P-8771-2018
OI Fayazi Hosseini, Nashmin/0000-0001-7346-2749; Hashemi, Seyed
   Mahmoud/0000-0003-1389-5803
FU Hamadan University of Medical Sciences; Iran National Science
   Foundation: INSF;  [9811018212];  [98010907]
FX Funding The present study was supported by the Hamadan University of
   Medical Sciences (9811018212) and Iran National Science Foundation: INSF
   (98010907) .
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NR 41
TC 54
Z9 54
U1 8
U2 44
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD NOV
PY 2022
VL 155
AR 113690
DI 10.1016/j.biopha.2022.113690
EA SEP 2022
PG 10
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 5A4YL
UT WOS:000862894600003
PM 36099793
OA gold
DA 2025-01-04
ER

PT J
AU Niu, WN
   Chen, F
   Wang, J
   Qian, J
   Yan, SS
AF Niu, Weining
   Chen, Fei
   Wang, Jun
   Qian, Jing
   Yan, Shasha
TI Antitumor effect of sikokianin C, a selective cystathionine β-synthase
   inhibitor, against human colon cancer <i>in vitro</i> and <i>in vivo</i>
SO MEDCHEMCOMM
LA English
DT Article
ID HYDROGEN-SULFIDE; REACTION-MECHANISM; H2S; ASSAY
AB Cystathionine beta-synthase (CBS) overexpression is related to the proliferation and migration of human colon cancers. Targeted therapy that inhibits CBS has achieved promising effects in colon cancer treatments, but no selective inhibitor of CBS is available. In our previous study, a natural biflavonoid compound, sikokianin C, was identified as a potent and selective inhibitor of CBS. However, the mode of action of this compound and its antitumor efficacy in vivo remain unknown. In the present study, we have demonstrated that sikokianin C selectively inhibits CBS activity in a competitive manner, and the five key residues involved in the binding of sikokianin C to the substrate channel of CBS protein were identified via a combination of molecular docking and site-directed mutagenesis. Additionally, we analyzed the antitumor efficacy of sikokianin C against human colon cancer cells in vitro and in vivo. Sikokianin C greatly suppressed the proliferation of HT29 colon cancer cells with an IC50 value of 1.6 mu M, and CBS is the target of sikokianin C in mammalian cells, as evidenced by CBS knockdown analyses. Moreover, sikokianin C induced the apoptosis of HT29 cancer cells in a dose dependent manner. Treating mice with sikokianin C dramatically reduced the tumor volume and the weight of the colon cancer xenograft in vivo. These results indicate that the selective CBS inhibitor sikokianin C can potentially be used for the treatment of colon cancer.
C1 [Niu, Weining; Chen, Fei; Wang, Jun; Qian, Jing; Yan, Shasha] Northwestern Polytech Univ, Sch Life Sci, Xian 710072, Shaanxi, Peoples R China.
C3 Northwestern Polytechnical University
RP Niu, WN (corresponding author), Northwestern Polytech Univ, Sch Life Sci, Xian 710072, Shaanxi, Peoples R China.
EM niuweining@nwpu.edu.cn
OI Wang, Jun/0000-0002-7597-6927
FU National Natural Science Foundation of China [31471086]; Key Science and
   Technology Program of Shaanxi Province, China [2017GY-143]; Fundamental
   Research Funds for the Central Universities of China [G2017KY0001]; Seed
   Foundation of Innovation and Creation for Graduate Students in
   Northwestern Polytechnical University [Z2017233]
FX This work was supported by the National Natural Science Foundation of
   China (Grant Number 31471086), the Key Science and Technology Program of
   Shaanxi Province, China (Grant Number 2017GY-143), the Fundamental
   Research Funds for the Central Universities of China (Grant Number:
   G2017KY0001) and the Seed Foundation of Innovation and Creation for
   Graduate Students in Northwestern Polytechnical University (Grant Number
   Z2017233).
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NR 35
TC 15
Z9 17
U1 1
U2 14
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 2040-2503
EI 2040-2511
J9 MEDCHEMCOMM
JI MedChemComm
PD JAN
PY 2018
VL 9
IS 1
BP 113
EP 120
DI 10.1039/c7md00484b
PG 8
WC Biochemistry & Molecular Biology; Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA FT9IN
UT WOS:000423465800011
PM 30108905
OA Green Published
DA 2025-01-04
ER

PT J
AU Song, MQ
   Yoon, G
   Choi, JS
   Kim, E
   Liu, XJ
   Oh, H
   Chae, JI
   Lee, MH
   Shim, JH
AF Song, Mengqiu
   Yoon, Goo
   Choi, Joon-Seok
   Kim, Eunae
   Liu, Xuejiao
   Oh, Ha-Na
   Chae, Jung-Il
   Lee, Mee-Hyun
   Shim, Jung-Hyun
TI Janus kinase 2 inhibition by Licochalcone B suppresses esophageal
   squamous cell carcinoma growth
SO PHYTOTHERAPY RESEARCH
LA English
DT Article
DE esophageal squamous cell carcinoma; JAK2 inhibitor; Licochalcone B
ID IN-VITRO; COLORECTAL-CANCER; CYCLE PROGRESSION; JAK INHIBITOR;
   APOPTOSIS; AZD1480; SURVIVAL; STAT3; AUTOPHAGY; ACCURACY
AB Esophageal cancer (EC) is one of the leading causes to cancer death in the worldwide and major population of EC is esophageal squamous cell carcinoma (ESCC). Still, ESCC-targeted therapy has not been covered yet. In the present study we have identified that Licochalcone B (Lico B) inhibited the ESCC growth by directly blocking the Janus kinase (JAK) 2 activity and its downstream signaling pathway. Lico B suppressed KYSE450 and KYSE510 ESCC cell growth, arrested cell cycle at G2/M phase and induced apoptosis. Direct target of Lico B was identified by kinase assay and verified with in vitro and ex vivo binding. Computational docking model predicted for Lico B interaction to ATP-binding pocket of JAK2. Furthermore, treatment of JAK2 clinical medicine AZD1480 to ESCC cells showed similar tendency with Lico B. Thus, JAK2 downstream signaling proteins phosphorylation of STAT3 at Y705 and S727 as well as STAT3 target protein Mcl-1 expression was decreased with treatment of Lico B. Our results suggest that Lico B inhibits ESCC cell growth, arrests cell cycle and induces apoptosis, revealing the underlying mechanism involved in JAK2/STAT3 signaling pathways after Lico B treatment. It might provide potential role of Lico B in the treatment of ESCC.
C1 [Song, Mengqiu; Liu, Xuejiao; Lee, Mee-Hyun] Zhengzhou Univ, Sch Basic Med Sci, Dept Pathophysiol, Zhengzhou, Peoples R China.
   [Song, Mengqiu; Liu, Xuejiao; Lee, Mee-Hyun] China US Henan Hormel Canc Inst, 127 Dongming Rd, Zhengzhou 450008, Henan, Peoples R China.
   [Yoon, Goo; Oh, Ha-Na; Shim, Jung-Hyun] Mokpo Natl Univ, Coll Pharm, Dept Pharm, Muan Gun 58554, Jeonnam, South Korea.
   [Choi, Joon-Seok] Daegu Catholic Univ, Coll Pharm, Gyongsan, South Korea.
   [Kim, Eunae] Chosun Univ, Coll Pharm, Gwangju, South Korea.
   [Chae, Jung-Il] Jeonbuk Natl Univ, BK21 Plus, Sch Dent, Dept Dent Pharmacol, Jeonju, South Korea.
   [Lee, Mee-Hyun] Dongshin Univ, Coll Korean Med, 85 Geonjae Ro, Naju Si 58245, Jeollanam Do, South Korea.
C3 Zhengzhou University; Mokpo National University; Catholic University of
   Daegu; Chosun University; Jeonbuk National University; Dongshin
   University
RP Lee, MH (corresponding author), China US Henan Hormel Canc Inst, 127 Dongming Rd, Zhengzhou 450008, Henan, Peoples R China.; Shim, JH (corresponding author), Mokpo Natl Univ, Coll Pharm, Dept Pharm, Muan Gun 58554, Jeonnam, South Korea.; Lee, MH (corresponding author), Dongshin Univ, Coll Korean Med, 85 Geonjae Ro, Naju Si 58245, Jeollanam Do, South Korea.
EM mhlee@hci-cn.org; s1004jh@gmail.com
RI Song, Choo-choo/AAT-2126-2020
OI Liu, Xuejiao/0009-0005-7045-6323; Lee, Mee-Hyun/0000-0002-1216-0218;
   Shim, Jung-Hyun/0000-0002-4062-4016; Song, Mengqiu/0000-0003-1249-9876
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NR 47
TC 19
Z9 20
U1 0
U2 12
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0951-418X
EI 1099-1573
J9 PHYTOTHER RES
JI Phytother. Res.
PD AUG
PY 2020
VL 34
IS 8
BP 2032
EP 2043
DI 10.1002/ptr.6661
PG 12
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA MV8PF
UT WOS:000556612000021
PM 32144852
DA 2025-01-04
ER

PT J
AU Pagès, A
   Foulon, S
   Zou, ZM
   Lacroix, L
   Lemare, F
   de Baère, T
   Massard, C
   Soria, JC
   Bonastre, J
AF Pages, Arnaud
   Foulon, Stephanie
   Zou, Zhaomin
   Lacroix, Ludovic
   Lemare, Francois
   de Baere, Thierry
   Massard, Christophe
   Soria, Jean-Charles
   Bonastre, Julia
TI The cost of molecular-guided therapy in oncology: a prospective cost
   study alongside the MOSCATO trial
SO GENETICS IN MEDICINE
LA English
DT Article
DE economic evaluation; genetics; genomics; molecular medicine;
   molecular-guided therapy targeted therapies
ID METASTATIC COLORECTAL-CANCER; PERSONALIZED MEDICINE; UNITED-STATES;
   KRAS; TECHNOLOGIES; PERSPECTIVE; MUTATIONS; GENOMICS; ISSUES; READY
AB Aim: There is increasing use of molecular technologies to guide cancer treatments, but few cost data are available. Our objective was to assess the costs of molecular-guided therapy for patients with advanced solid tumors alongside the Molecular Screening for Cancer Treatment and Optimization (MOSCATO) trial.
   Materials and methods: The study population consisted of 529 patients. The molecular diagnosis included seven steps from tumor biopsy to the multidisciplinary molecular tumor board. The cost of a complete molecular diagnosis was assessed by micro-costing. Direct costs incurred from enrollment until progression were assessed from the French National Health Insurance perspective.
   Results: The patients' mean age was 54 years (range: 3-82) and the mean follow-up period was 145 days (range: 1-707 days). A complete molecular diagnosis cost (sic)2,396. There were 220 patients with an actionable target (42%), among whom 105 (20%) actually received a targeted therapy. The cost of molecular-guided therapy per patient was (sic)31,269. The main cost drivers were anticancer drugs (54%) and hospitalizations (35%).
   Conclusion: This prospective cost analysis showed that molecular diagnosis accounts for only 6% of the cost of molecular-guided therapy per patient. The costs of drugs and hospitalizations are the main cost drivers.
C1 [Pages, Arnaud; Foulon, Stephanie; Zou, Zhaomin; Bonastre, Julia] Gustave Roussy, Serv Biostat & Epidemiol, Villejuif, France.
   [Foulon, Stephanie; Zou, Zhaomin; Bonastre, Julia] Paris Sud Univ, INSERM U1018, CESP Ctr Res Epidemiol & Populat Hlth, Villejuif, France.
   [Lacroix, Ludovic] Gustave Roussy, Dept Biol & Pathol Med, Villejuif, France.
   [Lacroix, Ludovic; de Baere, Thierry; Soria, Jean-Charles] Univ Paris 11, Orsay, France.
   [Lacroix, Ludovic] Gustave Roussy, Lab Rech Translat, Villejuif, France.
   [Lacroix, Ludovic] Gustave Roussy, Ctr Ressources Biol, AMMICA, INSERM CNRS UMS3655 US23, Villejuif, France.
   [Lemare, Francois] Gustave Roussy, Dept Pharm Clin, Villejuif, France.
   [Lemare, Francois] Univ Sorbonne Paris Cite, Fac Sci Pharmaceut & Biol, Paris, France.
   [de Baere, Thierry] Gustave Roussy, Dept Radiol Intervent, Villejuif, France.
   [Massard, Christophe; Soria, Jean-Charles] Gustave Roussy, Dept Innovat Therapeut & Essais Precoces, Villejuif, France.
C3 UNICANCER; Gustave Roussy; Universite Paris Saclay; Institut National de
   la Sante et de la Recherche Medicale (Inserm); UNICANCER; Gustave
   Roussy; Universite Paris Saclay; UNICANCER; Gustave Roussy; UNICANCER;
   Gustave Roussy; Centre National de la Recherche Scientifique (CNRS);
   CNRS - National Institute for Biology (INSB); Universite Paris Saclay;
   UNICANCER; Gustave Roussy; Universite Paris Cite; UNICANCER; Gustave
   Roussy; UNICANCER; Gustave Roussy
RP Bonastre, J (corresponding author), Gustave Roussy, Serv Biostat & Epidemiol, Villejuif, France.; Bonastre, J (corresponding author), Paris Sud Univ, INSERM U1018, CESP Ctr Res Epidemiol & Populat Hlth, Villejuif, France.
EM julia.bonastre@gustaveroussy.fr
RI Soria, Jean-Charles/F-3619-2014; massard, christophe/HTQ-3843-2023;
   PAGES, Arnaud/L-4444-2016
OI LEMARE, Francois/0000-0001-8196-970X; bonastre,
   julia/0000-0001-9884-0072; Foulon, Stephanie/0000-0002-0213-0736; PAGES,
   Arnaud/0000-0002-2337-8693
FU French National Agency for Research [ANR-10-IBHU-0001]; Gustave Roussy;
   SANOFI-Aventis; Genentech; Agence Nationale de la Recherche (ANR)
   [ANR-10-IBHU-0001] Funding Source: Agence Nationale de la Recherche
   (ANR)
FX This cost study received financial support from the French National
   Agency for Research (ANR-10-IBHU-0001). The MOSCATO trial was sponsored
   by Gustave Roussy and received financial support from SANOFI-Aventis and
   Genentech.
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NR 36
TC 25
Z9 26
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
EI 1530-0366
J9 GENET MED
JI Genet. Med.
PD JUN
PY 2017
VL 19
IS 6
BP 683
EP 690
DI 10.1038/gim.2016.174
PG 8
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA EW5AK
UT WOS:000402517400011
PM 27906201
OA Bronze
DA 2025-01-04
ER

PT J
AU Gentile, C
   Martorana, A
   Lauria, A
   Bonsignore, R
AF Gentile, Carla
   Martorana, Annamaria
   Lauria, Antonino
   Bonsignore, Riccardo
TI Kinase Inhibitors in Multitargeted Cancer Therapy
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
DE Multitargeted drugs; anticancer agents; polypharmacology; tyrosine
   kinase receptors; oncogene addiction; tumor microenvironment;
   FDA-approved drugs
ID GROWTH-FACTOR-RECEPTOR; CELL LUNG-CANCER; GASTROINTESTINAL STROMAL
   TUMORS; CHRONIC MYELOGENOUS LEUKEMIA; REGORAFENIB BAY 73-4506; BCR-ABL
   INHIBITOR; TYROSINE KINASE; PHILADELPHIA-CHROMOSOME; COLORECTAL-CANCER;
   TARGETED-THERAPY
AB The old-fashioned anticancer approaches, aiming at arresting cancer cell proliferation interfering with non-specific targets (e.g. DNA), have been replaced, in the last decades, by more specific target oriented ones. Nonetheless, single-target approaches have not always led to optimal outcomes because, for its complexity, cancer needs to be tackled at various levels by modulation of several targets. Although at present, combinations of individual single target drugs represent the most clinically practiced therapeutic approaches, the modulation of multiple proteins by a single drug, in accordance with the polypharmacological strategy, has become more and more appealing. In the perspective of a multi-target approach, the closely related evolutionary members of the tyrosine kinase family are ideal candidates. Indeed, tyrosine kinase activities are not only critical in tumor phenotype maintenance, but also modulate several functions in the tumor microenvironment. Consequently, several multikinase inhibitors were approved in the last decade, and many new molecules are currently in preclinical or clinical development. In the present review we report on the most widely FDA-approved multitargeted drugs, discussing about their mechanism of action and outlining the clinical trials that have brought them to approval.
C1 [Gentile, Carla; Martorana, Annamaria; Lauria, Antonino; Bonsignore, Riccardo] Univ Palermo, Dipartimento Sci & Tecnol Biol Chim & Framaceut S, Viale Sci Ed 17, I-90128 Palermo, Italy.
C3 University of Palermo
RP Lauria, A (corresponding author), Univ Palermo, Dipartimento Sci & Tecnol Biol Chim & Framaceut S, Viale Sci Ed 17, I-90128 Palermo, Italy.
EM antonino.lauria@unipa.it
RI Bonsignore, Riccardo/H-5028-2019; Gentile, Carla/AAB-1540-2020; Lauria,
   Antonino/I-3412-2013
OI GENTILE, Carla/0000-0001-5861-3342; MARTORANA,
   Annamaria/0000-0002-9560-1882; Bonsignore, Riccardo/0000-0003-2699-4384
FU FFR - University of Palermo grant [CUP:B78C120003-80001]
FX This work was in part supported by an FFR2012 - University of Palermo
   grant (CUP:B78C120003-80001).
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NR 124
TC 30
Z9 33
U1 2
U2 21
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 0929-8673
EI 1875-533X
J9 CURR MED CHEM
JI Curr. Med. Chem.
PY 2017
VL 24
IS 16
BP 1671
EP 1686
DI 10.2174/0929867324666170112112734
PG 16
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
   Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA EZ8ON
UT WOS:000404986000004
PM 28078996
DA 2025-01-04
ER

PT J
AU Huang, CR
   Lee, CT
   Chang, KY
   Chang, WC
   Liu, YW
   Lee, JC
   Chen, BK
AF Huang, Chi-Ruei
   Lee, Chung-Ta
   Chang, Kwang-Yu
   Chang, Wen-Chang
   Liu, Yao-Wen
   Lee, Jenq-Chang
   Chen, Ben-Kuen
TI Down-regulation of ARNT promotes cancer metastasis by activating the
   fibronectin/integrin β1/FAK axis
SO ONCOTARGET
LA English
DT Article
DE metastasis; ARNT; oncogene; ROS
ID ARYL-HYDROCARBON-RECEPTOR; ENDOTHELIAL GROWTH-FACTOR; NUCLEAR
   TRANSLOCATOR; GENE-EXPRESSION; CELLS; OVEREXPRESSION; ASSOCIATION;
   INHIBITION; FAMILY; HIF-1
AB The aryl hydrocarbon receptor nuclear translocator (ARNT) is broadly involved in regulating tumorigenesis by inducing genes that are involved in tumor growth and angiogenesis. Tumorigenesis usually involves normoxic conditions. However, the role of ARNT in tumor metastasis during normoxia remains unclear. Here, we demonstrate that ARNT protein levels were decreased in late-stage human colorectal cancer using immunohistochemical analysis. Down-regulation of ARNT protein promoted cancer cell migration and invasion, which was mediated by activation of the fibronectin/integrin beta 1/FAK signaling axis. In addition, the enhancement of migration and invasion in ANRT knockdown cells was blocked when ARNT was restored in the cells. In xenografts in severe combined immunodeficiency mice, tumor growth was significantly inhibited in the ARNT-knockdown condition. However, the tail-vein injection animal model revealed that the depletion of ARNT-induced metastatic lung colonies was further enhanced when ARNT expression was recovered post-injection. Interestingly, chemotherapeutic drugs inhibited ARNT expression and promoted the invasion of residual tumor cells. These results suggest that ARNT may play a positive role during tumor growth (either in early-stage tumor growth or in organ metastases), but plays a negative role in tumor migration and invasion. Therefore, the efficiency of ARNT-targeted therapy during different cancer stages should be carefully evaluated.
C1 [Huang, Chi-Ruei; Chen, Ben-Kuen] Natl Cheng Kung Univ, Inst Bioinformat & Biosignal Transduct, Coll Biosci & Biotechnol, Tainan 70101, Taiwan.
   [Huang, Chi-Ruei; Chang, Wen-Chang] Taipei Med Univ, Grad Inst Med Sci, Coll Med, Taipei, Taiwan.
   [Lee, Chung-Ta] Natl Cheng Kung Univ Hosp, Dept Pathol, Tainan, Taiwan.
   [Chang, Kwang-Yu] Natl Hlth Res Inst, Natl Inst Canc Res, Zhunan Township, Miaoli County, Taiwan.
   [Chang, Kwang-Yu] Natl Cheng Kung Univ, Div Hematol Oncol, Dept Internal Med, Tainan 70101, Taiwan.
   [Chang, Kwang-Yu] Natl Cheng Kung Univ, Natl Cheng Kung Univ Hosp, Coll Med, Tainan 70101, Taiwan.
   [Liu, Yao-Wen] Kuo Gen Hosp, Dept Pathol, Tainan, Taiwan.
   [Lee, Jenq-Chang] Natl Cheng Kung Univ Hosp, Dept Surg, Tainan, Taiwan.
   [Chen, Ben-Kuen] Natl Cheng Kung Univ, Coll Med, Dept Pharmacol, Tainan 70101, Taiwan.
   [Chen, Ben-Kuen] Taipei Med Univ, Coll Med Sci & Technol, Inst Canc Biol & Drug Discovery, Taipei, Taiwan.
C3 National Cheng Kung University; Taipei Medical University; National
   Cheng Kung University; National Cheng Kung University Hospital; National
   Health Research Institutes - Taiwan; National Cheng Kung University;
   National Cheng Kung University; National Cheng Kung University Hospital;
   National Cheng Kung University; National Cheng Kung University Hospital;
   National Cheng Kung University; Taipei Medical University
RP Chen, BK (corresponding author), Natl Cheng Kung Univ, Inst Bioinformat & Biosignal Transduct, Coll Biosci & Biotechnol, Tainan 70101, Taiwan.
EM bkchen58@mail.ncku.edu.tw
RI Chang, Kwang-Yu/G-9161-2011; li, zy/HZM-1892-2023
OI Huang, Chi-Ruei/0000-0001-9646-8852
FU Ministry of Science and Technology of Taiwan [NSC
   102-2628-B-006-011-MY3, 102-2320-B-038 -046 -MY3]; National Cheng Kung
   University [the Headquarters of University Advancement]
FX This work was supported by the Ministry of Science and Technology of
   Taiwan [Grant NSC 102-2628-B-006-011-MY3 and 102-2320-B-038 -046 -MY3];
   and National Cheng Kung University [the Headquarters of University
   Advancement]. We thank Dr. Trai-Ming Yeh for providing the HMEC-1 cell
   line. We thank Dr. Chi-Wu Chiang for critical review for the manuscript.
   We thank Dr. Shih-Hsien Hsu and Dr. Liang-Yi Hung for the gift of the
   shAhR and pAhR-EGFP plasmids, and the aurora C promoter construct,
   respectively.
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NR 53
TC 35
Z9 40
U1 2
U2 11
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD MAY 10
PY 2015
VL 6
IS 13
BP 11530
EP 11546
DI 10.18632/oncotarget.3448
PG 17
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA CO2SH
UT WOS:000359006400066
PM 25839165
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Good, JT
   Rollins, DR
   Kolakowski, CA
   Stevens, AD
   Denson, JL
   Martin, RJ
AF Good, James T., Jr.
   Rollins, Donald R.
   Kolakowski, Christena A.
   Stevens, Allen D.
   Denson, Joshua L.
   Martin, Richard J.
TI New insights in the diagnosis of chronic refractory cough
SO RESPIRATORY MEDICINE
LA English
DT Article
DE Asthma; Bronchiectasis; Chronic cough; Gastroesophageal reflux;
   Obstructive sleep apnea; Tracheobronchomalacia
ID POSITIVE AIRWAY PRESSURE; QUALITY-OF-LIFE; GASTROESOPHAGEAL REFLUX;
   APNEA SYNDROME; TRACHEOBRONCHOMALACIA; TRACHEOMALACIA; PREVALENCE;
   INFLAMMATION; ASSOCIATION; GUIDELINES
AB Background: Chronic Refractory Cough (CRC) is a common condition that significantly impairs patients' quality of life. Unfortunately, in many situations patients continue to experience CRC in spite of following published guidelines for diagnosis and treatment.
   Methods: 99 patients were referred to National Jewish Health (NJH), a specialty respiratory center for evaluation of CRC (cough= 8 weeks duration). Study duration occurred over 18 months. Intake evaluation for all patients included history, physical examination, spirometry and fiberoptic laryngoscopy. Testing to confirm causes of CRC were performed. Specific therapy for each potential cause was provided. A visual analog cough scale measured cough response.
   Results: Ten final diagnostic categories were found in the cohort of 99 patients with CRC: Obstructive sleep apnea (apnea/hypoxia index= 5), rhinosinusitis, Tracheobronchomalacia (= 65% collapse of airway with dynamic expiratory imaging), esophageal dysmotility, gastroesophageal reflux, abnormal swallowing with laryngeal penetration, asthma, COPD, bronchiectasis and paradoxical vocal cord movement. In these patients there were 42 incorrect intake diagnoses and 101 new diagnoses established. Patients with CRC have had multiple diagnoses (3.8 +/- 1.6) associated with chronic cough. With directed therapy 71/76 (93%) patients had resolution or improvement in cough symptoms.
   Conclusions: Among patients referred to a specialty respiratory center with CRC multiple concomitant diagnoses for cough were common. Certain diagnoses such as OSA and TBM have not been reported in cough guidelines but in this study are commonly associated diagnoses. Targeted therapy for each recognized diagnosis improves patient response.
C1 [Good, James T., Jr.; Rollins, Donald R.; Kolakowski, Christena A.; Stevens, Allen D.; Denson, Joshua L.; Martin, Richard J.] Natl Jewish Hlth, Dept Med, 1400 Jackson St, Denver, CO 80206 USA.
C3 National Jewish Health
RP Good, JT (corresponding author), Natl Jewish Hlth, Dept Med, 1400 Jackson St, Denver, CO 80206 USA.
EM GoodJ@NJHealth.org; RollinsD@NJHealth.org; KolakowskiC@NJHealth.org;
   StevensA@NJHealth.org; DensonJ@NJHealth.org; MartinR@NJHealth.org
OI /0009-0009-7921-7248; Denson, Joshua/0000-0002-8654-7765
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NR 36
TC 23
Z9 23
U1 0
U2 7
PU W B SAUNDERS CO LTD
PI LONDON
PA 32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND
SN 0954-6111
EI 1532-3064
J9 RESP MED
JI Respir. Med.
PD AUG
PY 2018
VL 141
BP 103
EP 110
DI 10.1016/j.rmed.2018.06.024
PG 8
WC Cardiac & Cardiovascular Systems; Respiratory System
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology; Respiratory System
GA GO1KI
UT WOS:000439709700016
PM 30053955
OA Bronze
DA 2025-01-04
ER

PT J
AU Chen, HF
   Yao, JM
   Bao, RJ
   Dong, Y
   Zhang, T
   Du, YH
   Wang, GY
   Ni, D
   Xun, ZZ
   Niu, XY
   Ye, YQ
   Li, HB
AF Chen, Huifang
   Yao, Jiameng
   Bao, Rujuan
   Dong, Yu
   Zhang, Ting
   Du, Yanhua
   Wang, Gaoyang
   Ni, Duan
   Xun, Zhenzhen
   Niu, Xiaoyin
   Ye, Youqiong
   Li, Hua-Bing
TI Cross-talk of four types of RNA modification writers defines tumor
   microenvironment and pharmacogenomic landscape in colorectal cancer
SO MOLECULAR CANCER
LA English
DT Article
DE RNA modification "writer"; Colorectal cancer; Tumor microenvironment;
   WM_Score; Drug sensitivity; Immunotherapy
AB BackgroundThe four major RNA adenosine modifications, i.e., m(6)A, m(1)A, alternative polyadenylation, and adenosine-to-inosine RNA editing, are mediated mostly by the "writer" enzymes and constitute critical mechanisms of epigenetic regulation in immune response and tumorigenesis. However, the cross-talk and potential roles of these "writers" in the tumor microenvironment (TME), drug sensitivity, and immunotherapy remain unknown.MethodsWe systematically characterized mRNA expression and genetic alterations of 26 RNA modification "writers" in colorectal cancer (CRC), and evaluated their expression pattern in 1697 CRC samples from 8 datasets. We used an unsupervised clustering method to assign the samples into two patterns of expression of RNA modification "writers". Subsequently, we constructed the RNA modification "writer" Score (WM_Score) model based on differentially expressed genes (DEGs) responsible for the RNA modification patterns to quantify the RNA modification-related subtypes of individual tumors. Furthermore, we performed association analysis for WM_Score and characteristics of TME, consensus molecular subtypes (CMSs), clinical features, transcriptional and post-transcriptional regulation, drug response, and the efficacy of immunotherapy.ResultsWe demonstrated that multi-layer alterations of RNA modification "writer" are associated with patient survival and TME cell-infiltrating characteristics. We identified two distinct RNA modification patterns, characterized by a high and a low WM_Score. The WM_Score-high group was associated with worse patient overall survival and with the infiltration of inhibitory immune cells, such as M2 macrophages, EMT activation, and metastasis, while the WM_Score-low group was associated with a survival advantage, apoptosis, and cell cycle signaling pathways. WM_Score correlated highly with the regulation of transcription and post-transcriptional events contributing to the development of CRC. ?In response to anti-cancer drugs, WM_Score highly negatively correlated (drug sensitive) with drugs which targeted oncogenic related pathways, such as MAPK, EGFR, and mTOR signaling pathways, positively correlated (drug resistance) with drugs which targeted in apoptosis and cell cycle. Importantly, the WM_Score was associated with the therapeutic efficacy of PD-L1 blockade, suggesting that the development of potential drugs targeting these "writers" to aid the clinical benefits of immunotherapy.ConclusionsOur study is the first to ?provide a comprehensive analysis of four RNA modifications in CRC. We revealed the potential function of these writers in TME, transcriptional and post-transcriptional events, and identified their therapeutic liability in targeted therapy and immunotherapy. This work highlights the cross-talk and potential clinical utility of RNA modification "writers" in cancer therapy.
C1 [Chen, Huifang; Yao, Jiameng; Bao, Rujuan; Dong, Yu; Zhang, Ting; Du, Yanhua; Wang, Gaoyang; Xun, Zhenzhen; Niu, Xiaoyin; Ye, Youqiong; Li, Hua-Bing] Shanghai Jiao Tong Univ, Shanghai Inst Immunol, Dept Immunol & Microbiol, Sch Med, Shanghai 200025, Peoples R China.
   [Ni, Duan] Univ Sydney, Charles Perkins Ctr, Sydney, NSW 2006, Australia.
   [Li, Hua-Bing] Shanghai Jiao Tong Univ, Sch Med, Yale Inst Immune Metab, Shanghai 200025, Peoples R China.
   [Li, Hua-Bing] Shanghai Jiao Tong Univ, Sch Med, Dept Liver Surg, State Key Lab Oncogenes & Related Genes,Renji Hos, Shanghai 200127, Peoples R China.
C3 Shanghai Jiao Tong University; Chinese Academy of Sciences; University
   of Sydney; Shanghai Jiao Tong University; Shanghai Jiao Tong University
RP Ye, YQ; Li, HB (corresponding author), Shanghai Jiao Tong Univ, Shanghai Inst Immunol, Dept Immunol & Microbiol, Sch Med, Shanghai 200025, Peoples R China.; Li, HB (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Yale Inst Immune Metab, Shanghai 200025, Peoples R China.; Li, HB (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Dept Liver Surg, State Key Lab Oncogenes & Related Genes,Renji Hos, Shanghai 200127, Peoples R China.
EM youqiong.ye@shsmu.edu.cn; huabing.li@shsmu.edu.cn
RI chen, huifang/JPX-4934-2023; Ni, Duan/L-7062-2019; ZHANG,
   Ting/HQZ-7212-2023; Xun, Zhenzhen/JPK-4059-2023; Li, Huabing/M-5390-2013
OI wang, gaoyang/0000-0001-6941-7363; Li, Huabing/0000-0003-3573-6803
FU National Natural Science Foundation of China [82073145,
   82030042/32070917/91753141]; Shanghai Science and Technology Committee
   [20ZR1472900, 20JC1417400/201409005500]; Shanghai Science and Technology
   Commission [20JC1410100]; Shanghai Pujiang Program [20PJ1412800]
FX This study was supported by the National Natural Science Foundation of
   China (grant no.82073145 to Y.Y., 82030042/32070917/91753141 to HBL),
   Shanghai Science and Technology Committee (grant no.20ZR1472900 to Y.Y.,
   20JC1417400/201409005500 to HBL), Shanghai Science and Technology
   Commission (20JC1410100), Shanghai Pujiang Program (grant no.
   20PJ1412800 to Y.Y.)
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NR 91
TC 150
Z9 152
U1 2
U2 49
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD FEB 8
PY 2021
VL 20
IS 1
AR 29
DI 10.1186/s12943-021-01322-w
PG 21
WC Biochemistry & Molecular Biology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA QG5MW
UT WOS:000617630200001
PM 33557837
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU McHugh, KE
   Dermawan, JK
   Cheng, YW
   Cruise, M
   Sohal, DPS
   Reynolds, JP
AF McHugh, Kelsey E.
   Dermawan, Josephine K.
   Cheng, Yu-Wei
   Cruise, Michael
   Sohal, Davendra P. S.
   Reynolds, Jordan P.
TI Molecular testing in metastatic colorectal adenocarcinoma cytology cell
   pellets
SO DIAGNOSTIC CYTOPATHOLOGY
LA English
DT Article
DE colorectal carcinoma; cytology; fine-needle aspiration; molecular
   diagnostic technique; targeted molecular therapy
ID GROWTH-FACTOR RECEPTOR; MUTATIONAL ANALYSIS; AMERICAN SOCIETY; PREDICT
   RESPONSE; KRAS; CANCER; CARCINOMA; PANITUMUMAB; CHALLENGES; RESISTANCE
AB Background Mutational status for KRAS, NRAS, and BRAF genes should be performed on all colorectal carcinoma (CRC) specimens in order to guide targeted therapy selection for metastatic disease. Mutations are typically assessed via polymerase chain reaction and/or next generation sequencing (NGS) on formalin-fixed paraffin-embedded tissues. With minimally invasive diagnostic methodologies, the cytology cell pellet obtained by fine-needle aspiration (FNA) can serve as an alternative source of tumor deoxyribonucleic acid. Methods An electronic record review of the cytopathology files (CoPathPlus, Cerner Corp., North Kansas City, Missouri) from September 1, 2015 through December 31, 2018 was conducted. All cytology specimens obtained via FNA and diagnosed as metastatic CRC on which NGS was performed were included. NGS for KRAS, NRAS, and BRAF mutations using the AmpliSeq Cancer Hotspot Panel v2.0 kit (Thermo Fisher Scientific, Waltham, Massachusetts) was performed on cytology cell pellets. Results Forty-eight cases were identified. Forty-six of 48 specimens (96%) were adequate for molecular testing. Of those adequate specimens, proportion of malignant cells in the sample ranged from 5% to 95% (mean 46%). Twenty-seven of 48 cases (56%) were positive for clinically relevant mutations. Twenty-four of 27 cases (89%) were positive for KRAS mutations, with exon 2 most frequently involved (22/24 cases, 92%). Two of 27 cases (7%) were positive for NRAS mutations and one case (1/27, 4%) was positive for a BRAF mutation involving codon 594. Conclusion Mutational analysis performed on cytology cell pellets serves as a useful means of gathering clinically actionable information on tumor mutation status in metastatic CRC.
C1 [McHugh, Kelsey E.; Dermawan, Josephine K.; Cheng, Yu-Wei; Cruise, Michael; Reynolds, Jordan P.] Cleveland Clin, Robert J Tomsich Pathol & Lab Med Inst, 9500 Euclid Ave,L25, Cleveland, OH 44195 USA.
   [Sohal, Davendra P. S.] Cleveland Clin, Dept Hematol & Med Oncol, Taussig Canc Inst, Cleveland, OH 44195 USA.
C3 Cleveland Clinic Foundation; Cleveland Clinic Foundation
RP McHugh, KE (corresponding author), Cleveland Clin, Robert J Tomsich Pathol & Lab Med Inst, 9500 Euclid Ave,L25, Cleveland, OH 44195 USA.
EM mchughk3@ccf.org
RI McHugh, Kelsey/AAH-9060-2020; Dermawan, Josephine/AAD-2077-2019;
   Reynolds, Jordan/AFN-4150-2022
OI Dermawan, Josephine Kam Tai/0000-0002-1139-2914; Reynolds,
   Jordan/0000-0001-7455-6122; McHugh, Kelsey/0000-0002-2389-9851
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NR 34
TC 2
Z9 2
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 8755-1039
EI 1097-0339
J9 DIAGN CYTOPATHOL
JI Diagn. Cytopathol.
PD NOV
PY 2019
VL 47
IS 11
BP 1132
EP 1137
DI 10.1002/dc.24275
EA JUL 2019
PG 6
WC Medical Laboratory Technology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology; Pathology
GA JG7QO
UT WOS:000477440100001
PM 31290252
DA 2025-01-04
ER

PT J
AU Ogawa, T
   Hirohashi, Y
   Murai, A
   Nishidate, T
   Okita, K
   Wang, LM
   Ikehara, Y
   Satoyoshi, T
   Usui, A
   Kubo, T
   Nakastugawa, M
   Kanaseki, T
   Tsukahara, T
   Kutomi, G
   Furuhata, T
   Hirata, K
   Sato, N
   Mizuguchi, T
   Takemasa, I
   Torigoe, T
AF Ogawa, Tadashi
   Hirohashi, Yoshihiko
   Murai, Aiko
   Nishidate, Toshihiko
   Okita, Kenji
   Wang, Liming
   Ikehara, Yuzuru
   Satoyoshi, Tetsuta
   Usui, Akihiro
   Kubo, Terufumi
   Nakastugawa, Munehide
   Kanaseki, Takayuki
   Tsukahara, Tomohide
   Kutomi, Goro
   Furuhata, Tomohisa
   Hirata, Koichi
   Sato, Noriyuki
   Mizuguchi, Toru
   Takemasa, Ichiro
   Torigoe, Toshihiko
TI ST6GALNAC1 plays important roles in enhancing cancer stem phenotypes of
   colorectal cancer via the Akt pathway
SO ONCOTARGET
LA English
DT Article
DE colorectal cancer; cancer stem cell; ST6GALNAC1; STn antigen; Akt
   pathway
ID ANTIGEN SIALYL-TN; INDEPENDENT PREDICTOR; SIALOSYL-TN; KLH VACCINE;
   EXPRESSION; CELLS; GLYCOSYLATION; PROGNOSIS; SURVIVAL; MARKER
AB Colorectal cancer (CRC) is a mortal disease due to treatment resistance, recurrence and distant metastasis. Emerging evidence has revealed that a small sub-population of cancer cells termed cancer stem cells (CSCs)/cancer-initiating cells (CICs) is endowed with high levels of tumor-initiating ability, self-renewal ability and differentiation ability and is responsible for treatment resistance, recurrence and distant metastasis. Eradication of CSCs/CICs is essential to improve current treatments. However, the molecular mechanisms by which CSCs/CICs are maintained are still elusive. In this study, we aimed to determine the molecular mechanisms by which colorectal (CR)-CSCs/CICs in are maintained human primary CRC cells. CR-CSCs/CICs were isolated by sphere-culture and the ALDEFLUOR assay, and transcriptome analysis revealed that the gene ST6 N-Acetylgalactosaminide Alpha2,6-Sialyltransferase 1 (ST6GALNAC1) was expressed at high levels in CR-CSCs/CICs. Overexpression of ST6GALNAC1 enhanced the expression of sialyl-Tn (STn) antigen, which is carried by the CSC marker CD44, and increased the sphere-forming ability and resistance to a chemotherapeutic reagent. The opposite phenomena were observed by gene knockdown using siRNA. Furthermore, the Akt pathway was activated in ST6GANAC1-overexpressed cells, and activation of the pathway was cancelled by gene knockdown of galectin-3. The results indicate that ST6GALNAC1 has a role in the maintenance of CR-CSCs/CICs by activating the Akt pathway in cooperation with galectin-3 and that ST6GalNAC1 (or STn antigen) might be a reasonable molecule for CSC/CIC-targeting therapy.
C1 [Ogawa, Tadashi; Hirohashi, Yoshihiko; Murai, Aiko; Wang, Liming; Satoyoshi, Tetsuta; Usui, Akihiro; Kubo, Terufumi; Nakastugawa, Munehide; Kanaseki, Takayuki; Tsukahara, Tomohide; Sato, Noriyuki; Torigoe, Toshihiko] Sapporo Med Univ, Sch Med, Dept Pathol, Chuo Ku, Sapporo, Hokkaido 0608556, Japan.
   [Ogawa, Tadashi; Nishidate, Toshihiko; Okita, Kenji; Satoyoshi, Tetsuta; Usui, Akihiro; Kutomi, Goro; Furuhata, Tomohisa; Hirata, Koichi; Mizuguchi, Toru; Takemasa, Ichiro] Sapporo Med Univ, Sch Med, Dept Surg, Chuo Ku, Sapporo, Hokkaido 0608556, Japan.
   [Ikehara, Yuzuru] Natl Inst Adv Ind Sci & Technol, Res Ctr Med Glycosci, Mol Med Team, Tsukuba, Ibaraki 3058568, Japan.
C3 Sapporo Medical University; Sapporo Medical University; National
   Institute of Advanced Industrial Science & Technology (AIST)
RP Hirohashi, Y; Torigoe, T (corresponding author), Sapporo Med Univ, Sch Med, Dept Pathol, Chuo Ku, Sapporo, Hokkaido 0608556, Japan.
EM hirohash@sapmed.ac.jp; torigoe@sapmed.ac.jp
RI Nishidate, Toshihiko/AFP-4588-2022; Wang, Liming/N-9512-2015; Hirohashi,
   Yoshihiko/AFQ-4227-2022; Ikehara, yuzuru/R-2239-2019; Kanaseki,
   Takayuki/LKK-0993-2024; Ikehara, Yuzuru/L-7696-2018
OI Ikehara, Yuzuru/0000-0002-1915-9172; Kanaseki,
   Takayuki/0000-0001-7294-6880; Torigoe, Toshihiko/0000-0002-9463-5917
FU KAKENHI [15H04722, 17H01540]; Japan Agency for Medical Research and
   Development, AMED; Grants-in-Aid for Scientific Research [15K08413,
   15H04722, 17H01540, 26462013] Funding Source: KAKEN
FX This work was supported by KAKENHI (15H04722 and 17H01540) (to Y.H and
   T.T.) and the project for Development of Innovative Research on Cancer
   Therapeutics from the Japan Agency for Medical Research and Development,
   AMED.
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NR 46
TC 42
Z9 45
U1 0
U2 6
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD DEC 22
PY 2017
VL 8
IS 68
BP 112550
EP 112564
DI 10.18632/oncotarget.22545
PG 15
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FS1WP
UT WOS:000419569800033
PM 29348846
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Lim, SH
   Lee, SY
   Hong, JY
   Lee, J
   Kim, ST
AF Lim, Sung Hee
   Lee, Song-Yi
   Hong, Jung Yong
   Lee, Jeeyun
   Kim, Seung Tae
TI CDK4/6 inhibition to resensitize BRAF/EGFR inhibitor in patient-derived
   BRAF/PTEN-mutant colon cancer cells
SO TRANSLATIONAL CANCER RESEARCH
LA English
DT Article
DE BRAF mutation; colon cancer; PTEN mutation; CDK4/6 inhibitor; BRAF/EGFR
   inhibitor
ID BRAF MUTATION; PTEN LOSS; CETUXIMAB; RESISTANCE; EXPRESSION; RAF;
   ENCORAFENIB; PHOSPHATASE; ACTIVATION; BLOCKADE
AB Background: In v-raf murine sarcoma viral oncogene homolog B1 (BRAF)-mutant colorectal cancer (CRC), encorafenib-cetuximab has been established as standard second-line therapy, but not all patients respond and the duration of response is relatively short. Overcoming intrinsic or acquired resistance to BRAF/EGFR inhibitors is crucial for enhancing treatment outcomes in metastatic BRAF-mutated CRC. The aim of the study is to investigate the resistance mechanisms in BRAF-mutant CRC patient refractory to BRAF/EGFR targeted therapy. Methods: We established patient-derived cells (PDCs) from a patient with BRAF/PTEN-mutant metastatic colon cancer who progressed rapidly on encorafenib plus cetuximab. To explore potential treatment options for inherent resistance caused by simultaneous PTEN mutation in BRAF-mutated CRC, we conducted cell viability assays using PDCs treated with encorafenib-cetuximab in combination with a cyclin-dependent kinase-4 and 6 (CDK4/6) inhibitor. Results: The patient's tumor had concurrent PTEN loss-of-function alteration at diagnosis and PDCs were generated from ascites after resistance to the BRAF/EGFR inhibitor. The PDCs were resistant to the encorafenib-cetuximab combination even at a high concentration of cetuximab (up to 500 mu g/mL). Adding the CDK4/6 inhibitor, ribociclib, to encorafenib-cetuximab showed a synergistic effect in a proliferation assay. Ribociclib plus encorafenib-cetuximab represented a significantly lower expression of Ki-67 compared to the dual combination alone. An MTS assay showed that triplet therapy with ribociclib, encorafenib, and cetuximab suppressed cell viability more efficiently than the two-drug combinations. Investigating the combined effect of triplet therapy using the calculated combination index (CI) showed that ribociclib had a synergistic effect with encorafenib-cetuximab when applied to PDCs with a concurrent BRAF/PTEN mutation. Conclusions: Our results suggest that combining the CDK4/6 inhibitor with the BRAF/EGFR inhibitor might be a novel treatment strategy for concomitant BRAF and PTEN-mutant CRC.
C1 [Lim, Sung Hee; Lee, Song-Yi; Hong, Jung Yong; Lee, Jeeyun; Kim, Seung Tae] Sungkyunkwan Univ, Samsung Med Ctr, Dept Med, Div Hematol Oncol, Seoul, South Korea.
C3 Sungkyunkwan University (SKKU); Samsung Medical Center
RP Kim, ST (corresponding author), Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Div Hematol Oncol,Dept Med, 81 Irwon Ro, Seoul 06351, South Korea.
EM seungtae1.kim@samsung.com
RI kim, st/O-5928-2014; Kim, Jong/I-3135-2019
FU Bio & Medical Technology Development Program of the National Research
   Foundation (NRF) - Korean government (MSIT) [RS-2023-00222838]
FX Funding: The study was supported by the Bio & Medical Technology
   Development Program of the National Research Foundation (NRF) funded by
   the Korean government (MSIT) (No. RS-2023-00222838) .
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NR 39
TC 1
Z9 1
U1 0
U2 0
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2218-676X
EI 2219-6803
J9 TRANSL CANCER RES
JI Transl. Cancer Res.
PD JUL 31
PY 2024
VL 13
IS 7
DI 10.21037/tcr-24-20
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA D4I2Y
UT WOS:001295830200007
PM 39145064
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Borie, F
   Dubray, V
   Tretarre, B
AF Borie, Frederic
   Dubray, Vincent
   Tretarre, Brigitte
TI Impact of recommendations and new therapies on the prognosis of colon
   cancer with synchronous liver metastasis
SO CLINICS AND RESEARCH IN HEPATOLOGY AND GASTROENTEROLOGY
LA English
DT Article
DE Recommendations; Prognosis; Colon; Cancer; Liver; Metastasis
ID PHASE-III TRIAL; COLORECTAL-CANCER; 1ST-LINE TREATMENT; INFUSIONAL
   FLUOROURACIL; RAS MUTATIONS; RECTAL-CANCER; CHEMOTHERAPY; FOLFOXIRI;
   CETUXIMAB; BEVACIZUMAB
AB Summary Objective: To assess the prognostic impact of the new therapies recommended over the past twenty years for colonic cancers with synchronous hepatic metastasis (hmCC). Methods: From 1995 to 2016, 802 hmCC were identified in a tumor registry. An univariate and multivariate analysis looked for the impact of the different recommendations over three periods: chemotherapy without targeted therapy (p1CH), chemotherapy with targeted agent in 2nd line (p2TA2), chemotherapy with TA in 1st line (p3TA1) depending on anatomoclinical criteria and therapeutic sequences: chemotherapy then resection of the primary tumor (CR) (n = 100), resection of the primary tumor then chemotherapy (RC) (n = 541), chemotherapy alone with or without TC (onlyCH) (n = 161). Results: The rates of onlyCH, CR and RC had varied respectively during these 3 periods from 12% to 26%, 6% to 21% and from 82% to 53% (p = 0.001). The medians of p1CH, p2TA2 and p3TA1 survival were 20.2, 22.7 and 23.6 months, respectively (p = 0.12). The independent factors of poor prognosis were age > 75 years (1.6 [1.35; 1.9] p = 0.0001), chemotherapy only 2.3 [1.6; 3.5] p = 0.0001), p1CH 1.7 [1.4; 2.1] p<0.0001), p2TA2 1.2 [1.02;1.6] p = 0.04. The p2TA2 period had a worse prognosis than p3TA1 (1.25 [1.01; 1.5] p = 0.03). Conclusion: In public health point of view, the recommendation of first-line TA improved survival and increased rate of primary tumor resection after chemotherapy. (c) 2021 Elsevier Masson SAS. All rights reserved.
C1 [Borie, Frederic; Dubray, Vincent; Tretarre, Brigitte] Registre Tumeurs, 208 Rue Apothicaires, F-34298 Montpellier, France.
   [Borie, Frederic] Univ Montpellier, Res Unit, INSERM, IDESP Inst Desbrest Epidemiol & Publ Hlth, Montpellier, France.
   [Borie, Frederic] CHU Caremeau, Dept Digest Surg, Pl Pr Debre, F-30090 Nimes, France.
C3 Universite de Montpellier; Institut National de la Sante et de la
   Recherche Medicale (Inserm); Universite de Montpellier; CHU de Nimes
RP Borie, F (corresponding author), CHU Carerneau, Chirurg Digest, Pl Pr Debre, F-30029 Nimes, France.
EM frederic.borie@chu-nimes.fr
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NR 22
TC 1
Z9 1
U1 0
U2 1
PU ELSEVIER MASSON, CORP OFF
PI PARIS
PA 65 CAMILLE DESMOULINS CS50083 ISSY-LES-MOULINEAUX, 92442 PARIS, FRANCE
SN 2210-7401
EI 2210-741X
J9 CLIN RES HEPATOL GAS
JI Clin. Res. Hepatol. Gastroenterol.
PD MAR
PY 2022
VL 46
IS 3
AR 101856
DI 10.1016/j.clinre.2021.101856
EA FEB 2022
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 1Y0KM
UT WOS:000807835300001
PM 34963650
OA Bronze, Green Published
DA 2025-01-04
ER

PT J
AU Ye, SB
   Cheng, YK
   Hu, JC
   Gao, F
   Lan, P
AF Ye, Shu-Biao
   Cheng, Yi-Kan
   Hu, Jian-Cong
   Gao, Feng
   Lan, Ping
TI Development and validation of an individualized gene expression-based
   signature to predict overall survival in metastatic colorectal cancer
SO ANNALS OF TRANSLATIONAL MEDICINE
LA English
DT Article
DE Metastatic colorectal cancer (mCRC); TCGA; gene signature; prognostic
ID CONSENSUS MOLECULAR SUBTYPES; CIRCULATING TUMOR-CELLS; BEVACIZUMAB;
   DEFINES; COLON
AB Background: Metastatic colorectal cancer (mCRC) is a heterogeneous disease. Predictive biomarkers are in great demand to optimize patient selection at high risk for death and to provide a novel insight into potential targeted therapy.
   Methods: The present study retrospectively analyzed the gene expression profiles of tumor tissue samples from 4 public CRC cohorts, including 1 RNA-Seq data set from The Cancer Genome Atlas (TCGA) CRC cohort and 3 microarray data sets from GEO. Prognostic analysis was performed to test the predictive value of prognostic gene signature.
   Results: Of 192 patients, 108 patients (56.3%) were men and median age was 65 years. A prognostic gene signature that consisted of 15 unique genes was generated in the discovery cohort. In the meta-validation cohorts, the signature significantly classified patients into high-risk and low-risk groups with regard to overall survival (OS) in mCRC patients with advanced stage disease and remained as an independent prognostic marker in multivariable analysis (1.57; 95% CI: 1.16-2.11; P=0.003) after adjusting for clinical parameters and molecular types. Gene Set Enrichment Analysis showed that several biological processes, including angiogenesis (P<0.001), epithelial mesenchymal transit (P<0.001) and inflammatory response (P=0.001), were enriched among this prognostic gene signature.
   Conclusions: The proposed prognostic gene signature is a promising prognostic tool to estimate OS in mCRC. Prospective larger studies to examine the clinical utility of the biomarkers to guide individualized treatment of mCRC are warranted.
C1 [Ye, Shu-Biao; Hu, Jian-Cong; Gao, Feng; Lan, Ping] Sun Yat Sen Univ, Affiliated Hosp 6, Dept Colorectal Surg, Guangzhou 510655, Peoples R China.
   [Ye, Shu-Biao; Hu, Jian-Cong; Gao, Feng; Lan, Ping] Guangdong Inst Gastroenterol, Guangdong Prov Key Lab Colorectal & Pelv Floor Di, Guangzhou 510655, Peoples R China.
   [Cheng, Yi-Kan] Sun Yat Sen Univ, Affiliated Hosp 6, Dept Radiat Oncol, Guangzhou 510655, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University
RP Gao, F; Lan, P (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 6, Dept Colorectal Surg, Guangzhou 510655, Peoples R China.; Gao, F; Lan, P (corresponding author), Guangdong Prov Key Laboratoryof Colorectal & Pelv, Guangzhou 510655, Peoples R China.
EM gaof57@mail.sysu.edu.cn; lanping@mail.sysu.edu.cn
RI Hu, Jiancong/HLW-0576-2023; lan, ping/T-1708-2017; ye,
   shubiao/GZM-4506-2022
FU National Natural Science Foundation of China [81703060, 81802441];
   Natural Science Foundation of Guangdong Province [2017A030310644]; China
   Postdoctoral Science Foundation [2018T110911, 2019B020229002]; National
   Key Research and Development Program of China [2017YFC1308800]; Science
   and Technology Planning Project of Guangdong Province [20160916,
   2014SC111, 201902020009]; National Key Clinical Discipline
FX This work was supported by National Natural Science Foundation of China
   (Grant No. 81703060, 81802441), Natural Science Foundation of Guangdong
   Province (Grant No. 2017A030310644), China Postdoctoral Science
   Foundation funded project (Grant No. 2018T110911, 2019B020229002), the
   National Key Research and Development Program of China
   (N0.2017YFC1308800), Science and Technology Planning Project of
   Guangdong Province (No. 20160916, 2014SC111, 201902020009), and National
   Key Clinical Discipline.
CR [Anonymous], PLOS ONE
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NR 30
TC 5
Z9 5
U1 1
U2 8
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2305-5839
EI 2305-5847
J9 ANN TRANSL MED
JI ANN. TRANSL. MED.
PD FEB
PY 2020
VL 8
IS 4
AR 96
DI 10.21037/atm.2019.12.112
PG 9
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA KS6IG
UT WOS:000518410000048
PM 32175389
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wen, S
   Li, M
   Liu, ZM
   Liu, LS
   Tian, C
   Shao, XQ
   Lv, S
AF Wen, Shuang
   Li, Mei
   Liu, Zhi-Min
   Liu, Li-Sha
   Tian, Can
   Shao, Xiao-Qing
   Lv, Shen
TI EGFR, KRAS and BRAF mutations in Chinese patients with clear cell renal
   cell carcinoma
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
LA English
DT Article
DE Clear cell renal cell carcinoma; EGFR; KRAS; BRAF; mutation
ID LUNG-CANCER; COLORECTAL-CANCER; PIK3CA MUTATIONS; GASTRIC-CANCER;
   PROGNOSIS; GENE; ADENOCARCINOMAS; EXPRESSION; SUBTYPES; THERAPY
AB The EGFR-KRAS-BRAF-MEK-ERK (MAPK) pathway plays an important role in most cancers with close association of EGFR, KRAS or BRAF mutations with carcinogenesis and drug resistance. EGFR have been developed for molecular targeted therapy of various cancers. However, it remains to be determined whether aberration of this pathway is essential for the survival of clear cell renal cell carcinoma (CCRCC) and whether EGFR tyrosine kinases inhibitors (TKIs) could benefit CCRCC patients. In this study, we detect EGFR, KRAS and BRAF mutations in CCRCC, investigate the potential of EGFR TKIs for the treatment of CCRCC patients, and summarize clinicopathological characteristics of CCRCC carrying EGFR, KRAS and BRAF mutations. EGFR, KRAS and BRAF mutation in 100 CCRCC from China were detected by high resolution melting analysis. Positive mutations were confirmed using direct sequencing. The cases with EGFR, KRAS and BRAF mutations were further assessed by immunohistochemistry (IHC). The diagnosis of CCRCC was confirmed by IHC staining of CK (Pan), EMA, Vimentin, CD10, Desmin and SMA, and the activation of MAPK pathway was assessed by IHC staining of EGFR, KRAS, BRAF and p-BRAF. One KRAS while no EGFR or BRAF mutations were identified in these 100 CCRCC patients. The case with KRAS mutation was histologic grade G4, tumor stage III and TNM stage III (T3NOMO). Lung metastasis was found four months after surgery and the patient died two and a half months after metastasis. The tumor with KRAS mutation was positive for CK (Pan), EMA, Vimentin, CD10, but negative for desmin and SMA, and positive for KRAS, BRAF, and p-BRAF, but negative for EGFR. To conclude, our results support EGFR, KRAS and BRAF mutations are rare in CCRCC, EGFR TKIs may be not suitable for the majority of CCRCC patients and CCRCC patients with the tumor carrying KRAS mutation might have poor prognosis.
C1 [Wen, Shuang; Li, Mei; Liu, Li-Sha; Tian, Can; Shao, Xiao-Qing; Lv, Shen] Dalian Med Univ, Lab Ctr, Affiliated Hosp 2, Zhongshan Rd, Dalian 116027, Liaoning, Peoples R China.
   [Wen, Shuang; Liu, Zhi-Min] Friendship Hosp Dalian, Dept Pathol, Dalian, Liaoning, Peoples R China.
   [Lv, Shen] Dalian Med Univ, Dept Pathol, Dalian, Liaoning, Peoples R China.
C3 Dalian Medical University; Dalian Medical University
RP Lv, S (corresponding author), Dalian Med Univ, Lab Ctr, Affiliated Hosp 2, Zhongshan Rd, Dalian 116027, Liaoning, Peoples R China.
EM lu.shen@aliyun.com
FU National Natural Science Foundation of China [81572919]
FX This work was supported by the National Natural Science Foundation of
   China (81572919).
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NR 39
TC 0
Z9 0
U1 0
U2 5
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1936-2625
J9 INT J CLIN EXP PATHO
JI Int. J. Clin. Exp. Pathol.
PY 2017
VL 10
IS 1
BP 578
EP 586
PG 9
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA EH8DO
UT WOS:000392002100067
DA 2025-01-04
ER

PT J
AU Danielli, M
   Thomas, RC
   Quinn, LM
   Tan, BK
AF Danielli, Marianna
   Thomas, Roisin Clare
   Quinn, Lauren Marie
   Tan, Bee Kang
TI Vascular adhesion protein-1 (VAP-1) in vascular inflammatory diseases A
   narrative review
SO VASA-EUROPEAN JOURNAL OF VASCULAR MEDICINE
LA English
DT Review
DE Vascular adhesion protein-1; semicarbazide-sensitive amine oxidase;
   amine oxidase; copper 3; inflammation; cardiovascular; biomarker
ID SENSITIVE AMINE OXIDASE; DEPENDENT DIABETES-MELLITUS; MEDIATED
   DEAMINATION; GLUCOSE-TRANSPORT; P-SELECTIN; EXPRESSION; INHIBITION;
   RISK; PHOSPHORYLATION; INVOLVEMENT
AB Vascular adhesion protein-1 (VAP-1) also known as amino oxidase copper containing 3 (AOC3) is a pro-inflammatory and versatile molecule with adhesive and enzymatic properties. VAP-1 is a primary amine oxidase belonging to the semicarbazide-sensitive amine oxidase (SSAO) family, which catalyzes the oxidation of primary amines leading to the production of ammonium, formaldehyde, methylglyoxal, and hydrogen peroxide. VAP-1 is mainly expressed by endothelial cells, smooth muscle cells, adipocytes and pericytes. It is involved in a repertoire of biological functions, e.g., immune cell extravasation, angiogenesis, and vascularization. Research into VAP-1 has intensified within the last decade on its role as a novel clinical biomarker and as a potential therapeutic target of vascular inflammatory disorders such as atherosclerosis, stroke, diabetes, neurovascular disorders (e.g., Alzheimer's Disease), hepatic disease (e.g., non-alcoholic steatohepatitis), and skin conditions (e.g., psoriasis). This is the most up-to-date and comprehensive review on VAP-1 focusing on the translational aspects of VAP-1. Compared to recent reviews, our review provides novel insights on VAP-1 and heart failure, stroke and frailty, diabetes, endometriosis, osteoarthritis, COVID-19, conjunctivitis associated systemic lupus erythematosus, hematopoietic stem cells, gliomas, treatment of colorectal cancer with a novel VAP-1 inhibitor (U-V269), promoting recovery of motor functions and habit learning with a novel VAP-1 inhibitor (PXS-4681A), and 68Ga-DOTA-Siglec-9, a labelled peptide of Siglec-9 (a VAP-1 ligand), which appears to be a safe PET tracer for inflammation in rheumatoid arthritis. Finally, we present the emerging role of VAP-1 in pregnancy as a gatekeeper of immune cells, which are critical for spiral arterial remodeling, the deficiency of which could lead to vascular disorders of pregnancy such as preeclampsia. Future research should prioritize clinical trials on VAP-1 small-molecule inhibitors and monoclonal antibodies, thus, maximizing the potential of VAP-1 targeted therapy as well as research into sVAP-1 as a clinical biomarker of diseases and its prognosis.
C1 [Danielli, Marianna; Thomas, Roisin Clare; Tan, Bee Kang] Univ Leicester, Cardiovasc Sci, Leicester, Leics, England.
   [Quinn, Lauren Marie] Univ Birmingham, Inst Immunol & Immunotherapy, Birmingham, W Midlands, England.
   [Tan, Bee Kang] Leicester Gen Hosp, Diabet Res Ctr, Leicester, Leics, England.
C3 University of Leicester; University of Birmingham; University Hospitals
   of Leicester NHS Trust; Leicester General Hospital
RP Tan, BK (corresponding author), Univ Leicester, Dept Cardiovasc Sci & Diabet, Res Ctr, Univ Rd, Leicester LE1 7RH, Leics, England.
EM bee.k.tan@leicester.ac.uk
OI Thomas, Roisin/0000-0002-8987-1720; Danielli,
   Marianna/0000-0002-7848-5189
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NR 76
TC 12
Z9 13
U1 1
U2 8
PU HOGREFE AG-HOGREFE AG SUISSE
PI BERN
PA LANGGASS STRASSE 76, BERN, SWITZERLAND
SN 0301-1526
EI 1664-2872
J9 VASA
JI Vasa
PD NOV
PY 2022
VL 51
IS 6
BP 341
EP 350
DI 10.1024/0301-1526/a001031
PG 10
WC Peripheral Vascular Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology
GA 7T1MV
UT WOS:000911212800003
PM 36200383
DA 2025-01-04
ER

PT J
AU Barault, L
   Amatu, A
   Siravegna, G
   Ponzetti, A
   Moran, S
   Cassingena, A
   Mussolin, B
   Falcomatà, C
   Binder, AM
   Cristiano, C
   Oddo, D
   Guarrera, S
   Cancelliere, C
   Bustreo, S
   Bencardino, K
   Maden, S
   Vanzati, A
   Zavattari, P
   Matullo, G
   Truini, M
   Grady, WM
   Racca, P
   Michels, KB
   Siena, S
   Esteller, M
   Bardelli, A
   Sartore-Bianchi, A
   Di Nicolantonio, F
AF Barault, Ludovic
   Amatu, Alessio
   Siravegna, Giulia
   Ponzetti, Agostino
   Moran, Sebastian
   Cassingena, Andrea
   Mussolin, Benedetta
   Falcomata, Chiara
   Binder, Alexandra M.
   Cristiano, Carmen
   Oddo, Daniele
   Guarrera, Simonetta
   Cancelliere, Carlotta
   Bustreo, Sara
   Bencardino, Katia
   Maden, Sean
   Vanzati, Alice
   Zavattari, Patrizia
   Matullo, Giuseppe
   Truini, Mauro
   Grady, William M.
   Racca, Patrizia
   Michels, Karin B.
   Siena, Salvatore
   Esteller, Manel
   Bardelli, Alberto
   Sartore-Bianchi, Andrea
   Di Nicolantonio, Federica
TI Discovery of methylated circulating DNA biomarkers for comprehensive
   non-invasive monitoring of treatment response in metastatic colorectal
   cancer
SO GUT
LA English
DT Article
ID EARLY TUMOR SHRINKAGE; DIGITAL PCR; PHASE-II; HYPERMETHYLATION;
   QUANTIFICATION; RESISTANCE; MUTATIONS; PLASMA; TISSUE; TRIAL
AB Objective Mutations in cell-free circulating DNA (cfDNA) have been studied for tracking disease relapse in colorectal cancer (CRC). This approach requires personalised assay design due to the lack of universally mutated genes. In contrast, early methylation alterations are restricted to defined genomic loci allowing comprehensive assay design for population studies. Our objective was to identify cancer-specific methylated biomarkers which could be measured longitudinally in cfDNA (liquid biopsy) to monitor therapeutic outcome in patients with metastatic CRC (mCRC).
   Design G enome-wide methylation microarrays of CRC cell lines (n=149) identified five cancer-specific methylated loci (EYA4, GRIA4, ITGA4, MAP3K14-AS1, MSC). Digital PCR assays were employed to measure methylation of these genes in tumour tissue DNA (n=82) and cfDNA from patients with mCRC (n=182). Plasma longitudinal assessment was performed in a patient subset treated with chemotherapy or targeted therapy.
   Results Methylation in at least one marker was detected in all tumour tissue samples and in 156 mCRC patient cfDNA samples (85.7%). Plasma marker prevalence was 71.4% for EYA4, 68.5% for GRIA4, 69.7% for ITGA4, 69.1% for MAP3K14-AS1% and 65.1% for MSC. Dynamics of methylation markers was not affected by treatment type and correlated with objective tumour response and progression-free survival.
   Conclusion T his five-gene methylation panel can be used to circumvent the absence of patient-specific mutations for monitoring tumour burden dynamics in liquid biopsy under different therapeutic regimens. This method might be proposed for assessing pharmacodynamics in clinical trials or when conventional imaging has limitations.
C1 [Barault, Ludovic; Siravegna, Giulia; Falcomata, Chiara; Oddo, Daniele; Bardelli, Alberto; Di Nicolantonio, Federica] Univ Torino, Dept Oncol, Turin, Italy.
   [Barault, Ludovic; Siravegna, Giulia; Mussolin, Benedetta; Falcomata, Chiara; Oddo, Daniele; Cancelliere, Carlotta; Bardelli, Alberto; Di Nicolantonio, Federica] IRCCS, Candiolo Canc Inst FPO, Candiolo, Italy.
   [Amatu, Alessio; Cassingena, Andrea; Bencardino, Katia; Truini, Mauro; Siena, Salvatore; Sartore-Bianchi, Andrea] Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, Milan, Italy.
   [Siravegna, Giulia; Vanzati, Alice] FIRC Inst Mol Oncol IFOM, Milan, Italy.
   [Ponzetti, Agostino; Cristiano, Carmen; Bustreo, Sara; Racca, Patrizia] San Giovanni Battista Hosp, AOU Citta Salute & Sci, Med Oncol Div 1, Colorectal Canc Unit, Turin, Italy.
   [Moran, Sebastian; Esteller, Manel] Bellvitge Biomed Res Inst, Canc Epigenet & Biol Program, Barcelona, Spain.
   [Binder, Alexandra M.; Michels, Karin B.] Univ Calif Los Angeles, Fielding Sch Publ Hlth, Dept Epidemiol, Los Angeles, CA USA.
   [Guarrera, Simonetta; Matullo, Giuseppe] Univ Torino, Italian Inst Genom Med IIGM HuGeF, Dept Med Sci, Turin, Italy.
   [Maden, Sean; Grady, William M.] Fred Hutchinson Canc Res Ctr, Div Clin Res, 1124 Columbia St, Seattle, WA 98104 USA.
   [Zavattari, Patrizia] Univ Cagliari, Unit Biol & Genet, Dept Biomed Sci, Cagliari, Italy.
   [Grady, William M.] Univ Washington, Sch Med, Dept Med, Seattle, WA 98195 USA.
   [Siena, Salvatore] Univ Milan, Dept Oncol & Hematooncol, Milan, Italy.
   [Esteller, Manel] Univ Barcelona, Sch Med, Dept Physiol Sci 2, Barcelona, Catalonia, Spain.
   [Esteller, Manel] Inst Catalana Recerca & Estudis Avancats, Barcelona, Catalonia, Spain.
C3 University of Turin; IRCCS Fondazione del Piemonte per l'Oncologia; IFOM
   - FIRC Institute of Molecular Oncology; A.O.U. Citta della Salute e
   della Scienza di Torino; AOU San Giovanni Battista-Molinette; Institut
   d'Investigacio Biomedica de Bellvitge (IDIBELL); University of
   California System; University of California Los Angeles; Italian
   Institute for Genomic Medicine (IIGM); University of Turin; Fred
   Hutchinson Cancer Center; University of Cagliari; University of
   Washington; University of Washington Seattle; University of Milan;
   University of Barcelona; ICREA
RP Barault, L; Di Nicolantonio, F (corresponding author), Univ Torino, Dept Oncol, Turin, Italy.; Barault, L; Di Nicolantonio, F (corresponding author), IRCCS, Candiolo Canc Inst FPO, Candiolo, Italy.
EM ludovic.barault@unito.it; federica.dinicolantonio@unito.it
RI Cassingena, Andrea/AGD-7137-2022; Sartore-Bianchi, Andrea/AAB-9848-2019;
   Guarrera, Simonetta/AAB-8482-2022; Binder, Alexandra/JCP-1962-2023;
   Siravegna, Giulia/Z-2826-2019; SIENA, SALVATORE/AAC-5806-2019;
   Falcomatà, Chiara/GQZ-8018-2022; Moran, Sebastian/G-5293-2013; MATULLO,
   Giuseppe/K-6383-2016; bisconti, alessandro/I-8016-2018; Di Nicolantonio,
   Federica/A-2503-2011; Barault, Ludovic/J-2472-2016; BARDELLI,
   Alberto/J-9721-2018; Esteller, Manel/L-5956-2014
OI MUSSOLIN, BENEDETTA/0000-0001-5723-5685; Cassingena,
   Andrea/0000-0003-4116-3992; Sartore-Bianchi, Andrea/0000-0003-0780-0409;
   MATULLO, Giuseppe/0000-0003-0674-7757; bisconti,
   alessandro/0000-0002-8474-5733; Guarrera, Simonetta/0000-0003-4400-1817;
   Di Nicolantonio, Federica/0000-0001-9618-2010; Maden,
   Sean/0000-0002-2212-4894; Barault, Ludovic/0000-0001-5227-5047; ODDO,
   DANIELE/0000-0001-6179-1668; Falcomata, Chiara/0000-0001-9269-2582;
   BARDELLI, Alberto/0000-0003-1647-5070; SIENA,
   SALVATORE/0000-0002-2681-2846; Esteller, Manel/0000-0003-4490-6093
FU AIRC IG [17707, 16788]; Fondo per la Ricerca Locale, Universita di
   Torino,; Fondazione Piemontese per la Ricerca sul Cancro-ONLUS
   Farmacogenomica 5 per mille 2009 MIUR (FDN); European Community [602901
   MErCuRIC, 635342-2 MoTriColor, 115749 CANCER-ID]; Fondazione Piemontese
   per la Ricerca sul Cancro-ONLUS 5 per mille 2011 Ministero della Salute;
   Fondazione Piemontese per la Ricerca sul Cancro-ONLUS 5 per mille 2014
   Ministero della Salute; Terapia Molecolare dei Tumori; Dynamic of Tumor
   Evolution & Therapy (AS-B) from Fondazione Oncologia Niguarda Onlus;
   Associazione Italiana per la Ricerca sul Cancro (AIRC) 2010 Special
   Program Molecular Clinical Oncology 5x1000 [9970]; Fondazione Banco di
   Sardegna; Regione Autonoma della Sardegna [CRP-79303]; NIH
   [1R01CA194663, 1R01CA189184, U01CA152756, P30CA15704]; Fondazione
   Umberto Veronesi; 'Assegno di Ricerca' from the University of Torino
FX Research in the authors' laboratory was supported by grants AIRC IG n.
   17707 (FDN); AIRC IG n. 16788 (AB); Fondo per la Ricerca Locale (ex
   60%), Universita di Torino, 2014 and 2017 (FDN); grant Fondazione
   Piemontese per la Ricerca sul Cancro-ONLUS Farmacogenomica 5 per mille
   2009 MIUR (FDN), grant Fondazione Piemontese per la Ricerca sul
   Cancro-ONLUS 5 per mille 2011 Ministero della Salute (AB and FDN);
   European Community's Seventh Framework Programme under grant agreement
   no. 602901 MErCuRIC (AB and FDN); H2020 grant agreement no. 635342-2
   MoTriColor (AB); IMI contract n. 115749 CANCER-ID (AB); Fondazione
   Piemontese per la Ricerca sul Cancro-ONLUS 5 per mille 2014 Ministero
   della Salute (AB). Investigators at Niguarda Cancer Centers are
   supported by the following grants: Terapia Molecolare dei Tumori (AS-B
   and SS) and Dynamic of Tumor Evolution & Therapy (AS-B) from Fondazione
   Oncologia Niguarda Onlus; Associazione Italiana per la Ricerca sul
   Cancro (AIRC) 2010 Special Program Molecular Clinical Oncology 5x1000,
   project 9970 (SS and AB). PZ is partly funded by Fondazione Banco di
   Sardegna (2012) and Regione Autonoma della Sardegna (CRP-79303). Partly
   supported also by NIH grants 1R01CA194663, 1R01CA189184, U01CA152756 and
   P30CA15704 to WMG. Ludovic Barault was the recipient of a postdoctoral
   fellowship from Fondazione Umberto Veronesi in 2013 and 2015, and of
   'Assegno di Ricerca' from the University of Torino in 2016.
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NR 53
TC 175
Z9 180
U1 1
U2 99
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0017-5749
EI 1468-3288
J9 GUT
JI Gut
PD NOV
PY 2018
VL 67
IS 11
BP 1995
EP 2005
DI 10.1136/gutjnl-2016-313372
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GY4GP
UT WOS:000448519800013
PM 28982739
OA Green Submitted, Green Accepted
DA 2025-01-04
ER

PT J
AU Alcaide, J
   Delgado, M
   Legerén, M
   Jurado, JM
   Blancas, I
   Pereda, T
   López, J
   Garrido, M
   Sánchez, MJ
   García, JL
   Rueda, A
AF Alcaide, Julia
   Delgado, Mayte
   Legeren, Marta
   Jurado, Jose Miguel
   Blancas, Isabel
   Pereda, Teresa
   Lopez, Jorge
   Garrido, Margarita
   Sanchez, Maria J.
   Garcia, Jose L.
   Rueda, Antonio
TI Efficacy and safety of aflibercept in metastatic colorectal cancer
   pretreated with bevacizumab: A report of five cases
SO ONCOLOGY LETTERS
LA English
DT Article
DE metastatic colorectal cancer; aflibercept; angiogenesis; targeted
   therapy; VEGF; VEGFR
ID RAS MUTATIONS; XENOGRAFT MODELS; 1ST PROGRESSION; CHEMOTHERAPY;
   FLUOROURACIL; IRINOTECAN; LEUCOVORIN; ASSOCIATION; COMBINATION;
   GUIDELINES
AB Aflibercept is a recombinant fusion protein that acts by inhibiting tumoural angiogenesis. Efficacy data obtained in the VELOUR randomised study has contributed to the approval of aflibercept as a second-line metastatic colorectal cancer (mCRC) treatment following an oxaliplatin-based regimen. The present study reports a case series of five patients with mCRC, who were treated in two centres since 2011 in the Compassionate Use Program for aflibercept. All patients had a KRAS mutation and previously received palliative fluoropyrimidine-oxaliplatin-based chemotherapy with bevacizumab. A doublet with irinotecan combined with aflibercept was administered until progression of disease. The majority of patients received a greater number of aflibercept cycles than the median reported in the VELOUR study (12 vs. 7 cycles), with manageable and reversible toxicity. The most frequent adverse events observed were diarrhoea, neutropenia, fatigue, proteinuria and hypertension. Most cases obtained a progression-free survival greater than the median reported in the VELOUR study (11 vs. 6.9 months) and, in a subgroup of patients previously treated with bevacizumab, and a median survival time of similar to 47 months was reached from the initial treatment of the disease. The present study contrasts the efficacy and safety results obtained from the pivotal VELOUR trial, and confirms that aflibercept, used in routine clinical practice outside of the clinical trial environment, is active and well-tolerated following bevacizumab treatment.
C1 [Alcaide, Julia; Rueda, Antonio] Costa Sol Hosp, Dept Oncol, Malaga 29603, Spain.
   [Delgado, Mayte; Legeren, Marta; Jurado, Jose Miguel; Blancas, Isabel; Sanchez, Maria J.; Garcia, Jose L.] San Cecilio Clin Hosp, Dept Oncol, Dr Oloriz Ave, Granada 18014, Andalucia, Spain.
   [Pereda, Teresa; Lopez, Jorge] Costa Sol Hosp, Dept Pathol, Malaga 29603, Spain.
   [Garrido, Margarita] Costa Sol Hosp, Pharm & Nutr Dept, Malaga 29603, Spain.
C3 Hospital Universitario San Cecilio
RP Delgado, M (corresponding author), San Cecilio Clin Hosp, Dept Oncol, Dr Oloriz Ave, Granada 18014, Andalucia, Spain.
EM maitechu22@hotmail.com
RI Sánchez, María/HOC-7747-2023; Blancas, Isabel/H-4130-2012; García,
   José/AAB-3048-2019; SANCHEZ-PEREZ, MARIA JOSE/D-1087-2011
OI Alcaide Garcia, Julia/0000-0002-9301-1387; Jurado Garcia, Jose
   Miguel/0000-0003-3083-3751; Blancas, Isabel/0000-0002-5867-6615;
   SANCHEZ-PEREZ, MARIA JOSE/0000-0003-4817-0757
FU Sanofi Spain (Barcelona, Spain)
FX Medical writing assistance, supported financially by Sanofi Spain
   (Barcelona, Spain), was provided by Mrs. A. Del Campo (Pivotal S.L.,
   Madrid, Spain).
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NR 28
TC 2
Z9 2
U1 0
U2 5
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD NOV
PY 2016
VL 12
IS 5
BP 3127
EP 3134
DI 10.3892/ol.2016.5068
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ED4RR
UT WOS:000388838900014
PM 27899972
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Sawaid, IO
   Samson, AO
   Al-Ramahi, R
AF Sawaid, Ibrahim O.
   Samson, Abraham O.
   Al-Ramahi, Rowa
TI Evaluation of Stages, Treatment Protocols, and Outcomes of Colorectal
   Cancer among West Bank Patients
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Article
DE colorectal cancer; colon cancer; rectal cancer; healthcare; West Bank
ID RISK-FACTORS; EPIDEMIOLOGY; POPULATION; CARE
AB Background: Colorectal cancer (CRC) is the second most widespread cancer among Palestinian patients. As cancer care improves in hospitals across the West Bank, services like palliative care, targeted therapy, bone marrow transplantation, and individualized therapy are still limited. This study aimed to assess the CRC stages, treatment protocols, and survival rates of patients in the West Bank. Methodology: This retrospective study collected data from the medical records of Al-Najah University Hospital (NUH), which specializes in the care of cancer patients. Patients with confirmed CRC (stages I-IV) undergoing surgical or medical treatment were included in the study. Data collection was standardized by using a data collection form to gather information from the medical records included in the study. All statistical analyses were performed using SPSS (version v27), and survival was assessed using a regression analysis of the number of days from the time of diagnosis to the most recent visit against the type of treatment (e.g., surgery, chemotherapy, radiotherapy). Results: A sample of 252 patients with CRC from NUH was collected, including 143 males and 109 females aged between 27 and 86 years, with the average age being 60.6 +/- 11.4 years. The sample included 183 patients (72.6%) diagnosed with colon cancer only, 29 patients (11.5%) diagnosed with rectal cancer only, and 40 patients (15.9%) diagnosed with both. Diagnosis took place at CRC stage I for 3 patients (1.2%), stage II for 33 patients (13.1%), stage III for 57 patients (22.6%), and stage IV for 159 patients (63.1%). Surgery was the most prevailing mode of treatment for 230 patients (91.3%), while 227 patients (90.1%) received chemotherapy treatment, and 38 patients (15.1%) received radiotherapy. Of the 252 patients, 40 patients (15.8%) received FOLFOX (i.e., folinic acid, fluorouracil, oxaliplatin), and 25 patients (9.9%) received FOLFIRI (i.e., folinic acid, fluorouracil, irinotecan), while the 187 remaining patients (74.2%) were treated with capecitabine, oxaliplatin, bevacizumab, cetuximab, regorafenib, cisplatin, etoposide, gemcitabine, or a combination thereof. The sample was categorized into six outcomes: (1) death, (2) cure, (3) disease progression, (4) disease recurrence, (5) under-treatment, and (6) unknown. Mortality was high, with 104 patients (41.3%) dying within a short time after diagnosis, and may have been attributable to delayed diagnosis. Surgical treatment had a positive impact on increasing the survival years, and it was significant (p = 0.033). Conclusions: A high percentage of patients were diagnosed in advanced CRC stages. The treatment modes were adopted from general international guidelines; however, the cure rates were low, and mortality was high. More studies need to be undertaken to investigate the actual application of chemotherapy protocols, and survival would benefit from the involvement of clinical pharmacists in the chemotherapy protocol selection, dosing, frequency, and follow-up. The present study advocates for greater public awareness of CRC and attests to the merits of screening by primary care professionals, which can help to avoid this serious illness and to promote a better prognosis.
C1 [Sawaid, Ibrahim O.; Samson, Abraham O.] Bar Ilan Univ, Azrieli Fac Med, IL-1311502 Safed, Israel.
   [Sawaid, Ibrahim O.; Al-Ramahi, Rowa] An Najah Natl Univ, Fac Grad Studies, P-400 Nablus, Palestinian Ter, Palestine.
C3 Bar Ilan University
RP Sawaid, IO (corresponding author), Bar Ilan Univ, Azrieli Fac Med, IL-1311502 Safed, Israel.; Sawaid, IO (corresponding author), An Najah Natl Univ, Fac Grad Studies, P-400 Nablus, Palestinian Ter, Palestine.
EM ibrahim.sawaid@biu.ac.il; avraham.samson@biu.ac.il; rowa@naja.ac.pl
OI Samson, Abraham O./0000-0001-7436-3515
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NR 30
TC 1
Z9 1
U1 0
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD APR
PY 2024
VL 13
IS 8
AR 2284
DI 10.3390/jcm13082284
PG 13
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA OV1U1
UT WOS:001209971300001
PM 38673557
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Huang, ZY
   Hu, HF
AF Huang, Zhiying
   Hu, Haifeng
TI Arginine Deiminase Induces Immunogenic Cell Death and Is Enhanced by
   <i>N</i>-acetylcysteine in Murine MC38 Colorectal Cancer Cells and
   MDA-MB-231 Human Breast Cancer Cells In Vitro
SO MOLECULES
LA English
DT Article
DE arginine deiminase; N-acetylcysteine; cell cycle arrest; mitochondrial
   membrane potential; immunogenic cell death; BMDC phagocytosis
AB The use of arginine deiminase (ADI) for arginine depletion therapy is an attractive anticancer approach. Combination strategies are needed to overcome the resistance of severe types of cancer cells to this monotherapy. In the current study, we report, for the first time, that the antioxidant N-acetylcysteine (NAC), which has been used in therapeutic practices for several decades, is a potent enhancer for targeted therapy that utilizes arginine deiminase. We demonstrated that pegylated arginine deiminase (ADI-PEG 20) induces apoptosis and G0/G1 phase arrest in murine MC38 colorectal cancer cells; ADI-PEG 20 induces Ca2+ overload and decreases the mitochondrial membrane potential in MC38 cells. ADI-PEG 20 induced the most important immunogenic cell death (ICD)-associated feature: cell surface exposure of calreticulin (CRT). The antioxidant NAC enhanced the antitumor activity of ADI-PEG 20 and strengthened its ICD-associated features including the secretion of high mobility group box 1 (HMGB1) and adenosine triphosphate (ATP). In addition, these regimens resulted in phagocytosis of treated MC38 cancer cells by bone marrow-derived dendritic cells (BMDCs). In conclusion, we describe, for the first time, that NAC in combination with ADI-PEG 20 not only possesses unique cytotoxic anticancer properties but also triggers the hallmarks of immunogenic cell death. Hence, ADI-PEG 20 in combination with NAC may represent a promising approach to treat ADI-sensitive tumors while preventing relapse and metastasis.
C1 [Huang, Zhiying] Shanghai Jiao Tong Univ, Sch Pharm, Shanghai 200240, Peoples R China.
   [Huang, Zhiying; Hu, Haifeng] China State Inst Pharmaceut Ind, Shanghai Inst Pharmaceut Ind, Shanghai 201203, Peoples R China.
C3 Shanghai Jiao Tong University
RP Hu, HF (corresponding author), China State Inst Pharmaceut Ind, Shanghai Inst Pharmaceut Ind, Shanghai 201203, Peoples R China.
EM decrest@sjtu.edu.cn; haifenghu66@163.com
RI Huang, Zhiying/IVH-4880-2023
FU Key Projects of Shanghai in Biomedicine [14431904500]
FX This work was funded by the Key Projects of Shanghai in Biomedicine (no.
   14431904500).
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TC 7
Z9 7
U1 1
U2 26
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD JAN
PY 2021
VL 26
IS 2
AR 511
DI 10.3390/molecules26020511
PG 16
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA PX6RX
UT WOS:000611482600001
PM 33478072
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Arcaroli, JJ
   Tai, WM
   McWilliams, R
   Bagby, S
   Blatchford, PJ
   Varella-Garcia, M
   Purkey, A
   Quackenbush, KS
   Song, EK
   Pitts, TM
   Gao, DX
   Lieu, C
   McManus, M
   Tan, AC
   Zheng, XX
   Zhang, Q
   Ozeck, M
   Olson, P
   Jiang, ZQ
   Kopetz, S
   Jimeno, A
   Keysar, S
   Eckhardt, G
   Messersmith, WA
AF Arcaroli, John J.
   Tai, W. M.
   McWilliams, Ryan
   Bagby, Stacey
   Blatchford, Patrick J.
   Varella-Garcia, Marileila
   Purkey, Alicia
   Quackenbush, Kevin S.
   Song, Eun-Kee
   Pitts, Todd M.
   Gao, Dexiang
   Lieu, Chris
   McManus, Martine
   Tan, Aik Choon
   Zheng, Xianxian
   Zhang, Qin
   Ozeck, Mark
   Olson, Peter
   Jiang, Zhi-Qin
   Kopetz, Scott
   Jimeno, Antonio
   Keysar, Stephen
   Eckhardt, Gail
   Messersmith, Wells A.
TI A <i>NOTCH1</i> gene copy number gain is a prognostic indicator of worse
   survival and a predictive biomarker to a Notch1 targeting antibody in
   colorectal cancer
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE colorectal cancer; Notch1; biomarker
ID GAMMA-SECRETASE INHIBITOR; TUMOR-INITIATING CELLS; COLON-CANCER;
   ANTITUMOR-ACTIVITY; EXPLANT MODEL; STEM-CELLS; XENOGRAFTS; PATHWAY;
   GROWTH; WNT
AB Dysregulation of the Notch1 receptor has been shown to facilitate the development and progression of colorectal cancer (CRC) and has been identified as an independent predictor of disease progression and worse survival. Although mutations in the NOTCH1 receptor have not been described in CRC, we have previously discovered a NOTCH1 gene copy number gain in a portion of CRC tumor samples. Here, we demonstrated that a NOTCH1 gene copy number gain is significantly associated with worse survival and a high percentage of gene duplication in a cohort of patients with advanced CRC. In our CRC patient-derived tumor xenograft (PDTX) model, tumors harboring a NOTCH1 gain exhibited significant elevation of the Notch1 receptor, JAG1 ligand and cleaved Notch1 activity. In addition, a significant association was identified between a gain in NOTCH1 gene copy number and sensitivity to a Notch1-targeting antibody. These findings suggest that patients with metastatic CRC that harbor a gain in NOTCH1 gene copy number have worse survival and that targeting this patient population with a Notch1 antibody may yield improved outcomes.
   What's new? There is mounting evidence that the Notch1 receptor is important in modulating tumor growth and an independent predictor of survival in colorectal cancer (CRC). While mutations in the NOTCH1 receptor have not yet been described in CRC, this study shows that a gain in NOTCH1 gene copy number is associated with worse survival. Targeting cells with a specific Notch1 antibody resulted in potent antitumor growth in a CRC patient-derived tumor xenograft model. A NOTCH1 gene copy number gain may thus be a prognostic marker for disease recurrence as well as a predictive biomarker of sensitivity to a Notch1 targeted therapy.
C1 [Arcaroli, John J.; Tai, W. M.; McWilliams, Ryan; Bagby, Stacey; Varella-Garcia, Marileila; Purkey, Alicia; Quackenbush, Kevin S.; Song, Eun-Kee; Pitts, Todd M.; Lieu, Chris; McManus, Martine; Tan, Aik Choon; Jimeno, Antonio; Keysar, Stephen; Eckhardt, Gail; Messersmith, Wells A.] Univ Colorado Denver Anschutz Med Campus, Div Med Oncol, Aurora, CO USA.
   [Arcaroli, John J.; Tai, W. M.; McWilliams, Ryan; Bagby, Stacey; Blatchford, Patrick J.; Varella-Garcia, Marileila; Purkey, Alicia; Quackenbush, Kevin S.; Song, Eun-Kee; Pitts, Todd M.; Gao, Dexiang; Lieu, Chris; McManus, Martine; Tan, Aik Choon; Jimeno, Antonio; Keysar, Stephen; Eckhardt, Gail; Messersmith, Wells A.] Univ Colorado, Ctr Canc, Aurora, CO USA.
   [Blatchford, Patrick J.; Gao, Dexiang] Univ Colorado Denver Anschutz Med Campus, Dept Biostat & Informat, Aurora, CO USA.
   [Zheng, Xianxian; Zhang, Qin; Ozeck, Mark; Olson, Peter] Pfizer, Pfizer Oncol Res Unit, Translat Res, La Jolla, CA USA.
   [Jiang, Zhi-Qin; Kopetz, Scott] Univ Texas MD Anderson Canc Ctr, Texas Med Ctr, Houston, TX 77030 USA.
C3 University of Colorado System; University of Colorado Anschutz Medical
   Campus; University of Colorado System; University of Colorado Anschutz
   Medical Campus; University of Colorado System; University of Colorado
   Anschutz Medical Campus; Pfizer; Baylor College of Medicine; Baylor
   College Medical Hospital; University of Texas System; UTMD Anderson
   Cancer Center
RP Messersmith, WA (corresponding author), 12801 E 17th Ave,MS 8117, Aurora, CO 80045 USA.
EM wells.messersmith@ucdenver.edu
RI Gao, Dexiang/ABC-8930-2020; Jiang, Zhi-Qin/O-8999-2014; Kopetz,
   Scott/AAC-1387-2019; Tan, Aik Choon/A-3135-2011
OI Tan, Aik Choon/0000-0003-2955-8369; Purkey, Alicia/0000-0002-1865-1421;
   Kopetz, Scott/0000-0001-9647-3416
FU NCATS NIH HHS [UL1 TR000371] Funding Source: Medline; NCI NIH HHS [P30
   CA016672, P30 CA046934] Funding Source: Medline
CR Anderson RT, 2013, MOL CANCER THER, V12, P1994, DOI 10.1158/1535-7163.MCT-13-0206
   Arcaroli JJ, 2013, BRIT J CANCER, V109, P667, DOI 10.1038/bjc.2013.361
   Arcaroli JJ, 2012, MOL ONCOL, V6, P370, DOI 10.1016/j.molonc.2012.03.004
   Arcaroli JJ, 2010, CLIN CANCER RES, V16, P4165, DOI 10.1158/1078-0432.CCR-10-0066
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NR 34
TC 36
Z9 40
U1 1
U2 24
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD JAN 1
PY 2016
VL 138
IS 1
BP 195
EP 205
DI 10.1002/ijc.29676
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CU0JY
UT WOS:000363203600024
PM 26152787
OA Bronze, Green Accepted
DA 2025-01-04
ER

PT J
AU Ge, P
   Han, CY
   Reyila, A
   Liu, DY
   Hong, WY
   Liu, JX
   Zhang, JZ
   Han, X
   Li, XL
   Huang, MJ
   Fan, SY
   Kaierdebieke, A
   Wu, XY
   Huang, XL
   Guo, WR
   Liu, SY
   Bian, Y
AF Ge, Pu
   Han, Chunyan
   Reyila, Abudurousuli
   Liu, Diyue
   Hong, Wenying
   Liu, Jiaxin
   Zhang, Jinzi
   Han, Xiao
   Li, Xialei
   Huang, Mengjie
   Fan, Siyuan
   Kaierdebieke, Ayidana
   Wu, Xiaoyu
   Huang, Xiaolu
   Guo, Weirui
   Liu, Siyu
   Bian, Ying
TI Risk of antiangiogenic adverse events in metastatic colorectal cancer
   patients receiving aflibercept in combination with chemotherapy: A
   meta-analysis
SO MEDICINE
LA English
DT Review
DE adverse events; aflibercept; antiangiogenesis; meta-analysis; metastatic
   colorectal cancer; safety; systematic review
ID GROWTH-FACTOR VEGF; PHASE-II; 1ST-LINE TREATMENT; TARGETED THERAPY;
   DOUBLE-BLIND; TRAP; BEVACIZUMAB; ANGIOGENESIS; OXALIPLATIN; PERFORATION
AB Background:Aflibercept has been approved for the treatment of metastatic colorectal cancer for more than a decade, but its antiangiogenesis adverse effect profile during treatment remains unclear. This study is conducted to systematically review the risk of antiangiogenic adverse events in patients with metastatic colorectal cancer receiving aflibercept plus chemotherapy.Methods:We searched databases, including PubMed, Embase and the Cochrane Library up to September 9, 2021. Relevant randomized controlled trials (RCTs) and single-arm studies were included in the review. Statistical analyses were performed using R to calculate the summary incidence rate of antiangiogenic-related adverse events, odds ratios and 95% CIs. Heterogeneity among the included studies was assessed by subgroup analysis. Publication bias analysis and sensitivity analysis were performed to confirm the reliability of the results.Results:A total of 2889 patients from 10 studies met the inclusion criteria. The quality of the included studies was evaluated as qualified for further quantitative synthesis. In part of single-arm studies, the occurrence rates were 44.2% (95%CI, 39.7-48.7%) for hypertension, 31.3% (95% CI, 19.3-43.3%) for proteinuria, 27.3% (95%CI, 21.2-33.4%) for epistaxis, 22.5% (95%CI, 7.8-37.3%) for hemorrhage events, 8.0% (95%CI, 2.0-14 .0%) for venous thromboembolic event in all grades and 22.6% (95%CI, 19.1-26.2%) for grade III/IV hypertension, 7.4% (95%CI, 6.2-8.5%) for grade III/IV proteinuria. In part of RCT, compared to its counterpart, aflibercept containing arm was associated with the increased incidence rate in hypertension (OR:6.30, 95%CI: 3.49-11.36), proteinuria (OR:4.12, 95%CI: 1.25-13.61), epistaxis (OR:3.71, 95%CI: 2.84-4.85), III/IV hypertension (OR:7.20, 95%CI: 5.23-9.92), III/IV proteinuria (OR:5.13, 95%CI: 3.13-8.41). The funnel plot, Begg test and Egger test were carried out on the primary endpoints, III/IV hypertension rate and III/IV proteinuria rate, the result of which detected no obvious publication bias. No significant difference was observed in subgroup analysis in the primary endpoint between the subgroups stratified by treatment line (firstline or non-firstline), chemotherapy regime (FOLFIRI or others) and study design (RCTs or single-arm trials).Conclusion:The available evidence suggests that using aflibercept is associated with an increased risk of antiangiogenic adverse events compared with controls. Further studies are needed to investigate this association. In the appropriate clinical scenario, the use of aflibercept in its approved indications remains justified. However, the results of this study should be interpreted with caution, as some of the evidence comes from single-arm clinical trials.
C1 [Ge, Pu; Bian, Ying] Univ Macau, Inst Chinese Med Sci, Macau, Peoples R China.
   [Ge, Pu; Bian, Ying] Univ Macau, State Key Lab Qual Res Chinese Med, Macau, Peoples R China.
   [Ge, Pu; Bian, Ying] Univ Macau, Fac Hlth Sci, Dept Publ Hlth & Med Adm, Macau, Peoples R China.
   [Han, Chunyan] Shandong Univ, Sch Polit Sci & Publ Adm, Qingdao, Peoples R China.
   [Reyila, Abudurousuli] Air Force Med Univ, Xijing Hosp, Xian, Peoples R China.
   [Liu, Diyue] Hainan Med Univ, Int Sch Publ Hlth & One Hlth, Haikou, Peoples R China.
   [Hong, Wenying] Univ Macau, Fac Hlth Sci, Macau, Peoples R China.
   [Liu, Jiaxin] Cent South Univ, Xiangya Sch Nursing, Changsha, Peoples R China.
   [Zhang, Jinzi] Harbin Med Univ, Sch Humanities & Social Sci, Harbin, Peoples R China.
   [Han, Xiao] Sun Yat Sen Univ, Affiliated Hosp 5, Zhuhai, Peoples R China.
   [Li, Xialei; Wu, Xiaoyu] Shandong Univ, Sch Pharmaceut Sci, Jinan, Peoples R China.
   [Huang, Mengjie] Shandong Univ, Sch Publ Hlth, Jinan, Peoples R China.
   [Fan, Siyuan] Capital Med Univ, Yanjing Med Coll, Dept Prevent Med, Beijing, Peoples R China.
   [Kaierdebieke, Ayidana] Xi An Jiao Tong Univ, Sch Publ Hlth, Xian, Peoples R China.
   [Huang, Xiaolu] China Med Univ, Clinically Series 3, Shenyang, Peoples R China.
   [Guo, Weirui] Jining Med Univ, Sch Clin Med, Jining, Peoples R China.
   [Liu, Siyu] Shandong Univ, Stomatol Coll, Jinan, Peoples R China.
C3 University of Macau; University of Macau; University of Macau; Shandong
   University; Air Force Military Medical University; Hainan Medical
   University; University of Macau; Central South University; Harbin
   Medical University; Sun Yat Sen University; Shandong University;
   Shandong University; Capital Medical University; Xi'an Jiaotong
   University; China Medical University; Jining Medical University;
   Shandong University
RP Bian, Y (corresponding author), Univ Macau, Inst Chinese Med Sci, Macau, Peoples R China.
EM bianying@um.edu.mo
RI Guo, Weirui/G-2868-2015; Liu, Siyu/GYV-4856-2022; pu, ge/JTV-2070-2023;
   wu, xiaoyu/GWM-9019-2022; wang, wei/JYP-7819-2024; zhang,
   ying/HJB-1230-2022
OI Fan, Siyuan/0000-0003-3247-115X; Ge, Pu/0000-0002-9295-6389
FU University of Macau Foundation [MYRG106 (Y1-L3)-ICMS13-BY,
   MYRG2015-00190-ICMS-QRCM]; University of Macau [MYRG2022-00257-ICMS]
FX This study was supported by the University of Macau Foundation (MYRG106
   (Y1-L3)-ICMS13-BY), University of Macau Foundation
   (MYRG2015-00190-ICMS-QRCM) and Funding from University of Macau,
   (MYRG2022-00257-ICMS).
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NR 54
TC 0
Z9 0
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD SEP 1
PY 2023
VL 102
IS 35
AR e34793
DI 10.1097/MD.0000000000034793
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA Q8JQ7
UT WOS:001059934400009
PM 37657052
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Suh, SS
   Hong, JM
   Kim, EJ
   Jung, SW
   Kim, SM
   Kim, JE
   Kim, IC
   Kim, S
AF Suh, Sung-Suk
   Hong, Ju-Mi
   Kim, Eun Jae
   Jung, Seung Won
   Kim, Sun-Mi
   Kim, Jung Eun
   Kim, Il-Chan
   Kim, Sanghee
TI Anti-inflammation and Anti-Cancer Activity of Ethanol Extract of
   Antarctic Freshwater Microalga, <i>Micractinium</i> sp.
SO INTERNATIONAL JOURNAL OF MEDICAL SCIENCES
LA English
DT Article
DE Inflammation; cancer; Micractinium sp.; proinflammatory cytokines;
   HCT116
ID NF-KAPPA-B; DISEASE; HOMEOSTASIS; EXPRESSION; CYTOKINES; CANCER
AB Inflammation mediated by the innate immune system is an organism's protective mechanism against infectious environmental risk factors. It is also a driver of the pathogeneses of various human diseases, including cancer development and progression. Microalgae are increasingly being focused on as sources of bioactive molecules with therapeutic potential against various diseases. Furthermore, the antioxidant, anti-inflammatory, and anticancer potentials of microalgae and their secondary metabolites have been widely reported. However, the underlying mechanisms remain to be elucidated. Therefore, in this study, we investigated the molecular mechanisms underlying the anti-inflammatory and anticancer activities of the ethanol extract of the Antarctic freshwater microalga Micractinium sp. (ETMI) by several in vitro assays using RAW 264.7 macrophages and HCTI 16 human colon cancer cells. ETMI exerted its anti-inflammatory activity by modulating the main inflammatory indicators such as cyclooxygenase (COX)-2, interleukin (IL)-6, inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF)-alpha, and nitric oxide (NO) in a dose-dependent manner. In addition, ETMI exerted cytotoxic activity against HCTI 16 cells in a dose-dependent manner, leading to significantly reduced cancer cell proliferation. Further, it induced cell cycle arrest in the G 1 phase through the regulation of hallmark genes of the G I/S phase transition, including CDKN IA, and cyclin-dependent kinase 4 and 6 (CDK4 and CDK6, respectively). At the transcriptional level, the expression of CDKN I A gradually increased in response to ETMI treatment while that of CDK4 and CDK6 decreased. Taken together, our findings suggest that the anti-inflammatory and anticancer activities of the Antarctic freshwater microalga, Micractinium sp., and ETMI may provide a new clue for understanding the molecular link between inflammation and cancer and that ETMI may be a potential anticancer agent for targeted therapy of colorectal cancer.
C1 [Suh, Sung-Suk] Mokpo Natl Univ, Dept Biosci, Muan 58554, South Korea.
   [Hong, Ju-Mi; Kim, Eun Jae; Kim, Sun-Mi; Kim, Jung Eun; Kim, Il-Chan; Kim, Sanghee] Korea Polar Res Inst, Dept Polar Life Sci, Incheon 21990, South Korea.
   [Jung, Seung Won] Korea Inst Ocean Sci & Technol, South Sea Environm Res Dept, Geoje 656830, South Korea.
   [Kim, Eun Jae; Kim, Jung Eun; Kim, Il-Chan; Kim, Sanghee] Univ Sci & Technol, Dept Polar Sci, Incheon 21990, South Korea.
C3 Mokpo National University; Korea Polar Research Institute (KOPRI); Korea
   Institute of Ocean Science & Technology (KIOST)
RP Suh, SS (corresponding author), Mokpo Natl Univ, Dept Biosci, Muan 58554, South Korea.; Hong, JM (corresponding author), Korea Polar Res Inst, Dept Polar Life Sci, Incheon 21990, South Korea.
EM sangheekim@kopri.re.kr
FU Korea Polar Research Institute, Republic of Korea [PE17180]
FX This research was supported by the research projects (PE17180) of Korea
   Polar Research Institute, Republic of Korea.
CR Cekici A, 2014, PERIODONTOL 2000, V64, P57, DOI 10.1111/prd.12002
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NR 28
TC 32
Z9 33
U1 0
U2 15
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1449-1907
J9 INT J MED SCI
JI Int. J. Med. Sci.
PY 2018
VL 15
IS 9
BP 929
EP 936
DI 10.7150/ijms.26410
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA GM6IH
UT WOS:000438268100009
PM 30008606
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Baran, B
   Ozupek, NM
   Tetik, NY
   Acar, E
   Bekcioglu, O
   Baskin, Y
AF Baran, Burcin
   Ozupek, Nazli Mert
   Tetik, Nihal Yerli
   Acar, Emine
   Bekcioglu, Omer
   Baskin, Yasemin
TI Difference Between Left-Sided and Right-Sided Colorectal Cancer: A
   Focused Review of Literature
SO GASTROENTEROLOGY RESEARCH
LA English
DT Review
DE Colorectal cancer; Right side; Left side; Epidemiology; Molecular
   mechanism; Adjuvant chemotherapies; Targeted therapies; Immunotherapies
ID IMMUNE CHECKPOINT BLOCKADE; PRIMARY TUMOR LOCATION; KIRSTEN RAS
   MUTATIONS; COLON-CANCER; MICROSATELLITE-INSTABILITY; STAGE-II; ADJUVANT
   CHEMOTHERAPY; TARGETED THERAPY; SURVIVAL; KRAS
AB Colorectal cancer is the third most common cancer worldwide with a high mortality rate at the advanced stages. However, colorectal cancer is not a single type of tumor; its pathogenesis depends on the anatomical location of the tumor and differs between right side and left side of the colon. Tumors in the proximal colon (right side) and distal colon (left side) exhibit different molecular characteristics and histology. In the right-sided tumors, mutations in the DNA mismatch repair pathway are commonly observed; and these tumors generally have a flat histology. In the left-sided tumors, chromosomal instability pathway-related mutations, such as KRAS, APC, PIK3CA, p53 mutations are observed and these tumors demonstrate polypoid-like morphology. Therapy responses are totally different between these tumor entities. Left-sided colorectal cancer (LCRC) patients benefit more from adjuvant chemotherapies such as 5-fluorouracil (5-FU)-based regimes, and targeted therapies such as anti-epidermal growth factor receptor (EGFR) therapy, and have a better prognosis. Right-sided colorectal cancer (RCRC) patients do not respond well to conventional chemotherapies, but demonstrate more promising results with immunotherapies because these tumors have high antigenic load. For the development of effective therapy regimes and better treatment options, it is essential to evaluate right-sided and left-sided tumors as separate entities, and design the therapy regime considering the differences between these tumors.
C1 [Baran, Burcin; Ozupek, Nazli Mert; Tetik, Nihal Yerli; Bekcioglu, Omer; Baskin, Yasemin] Dokuz Eylul Univ, Inst Oncol, Dept Basic Oncol, Izmir, Turkey.
   [Acar, Emine] Dokuz Eylul Univ, Dept Translat Oncol, Izmir, Turkey.
   [Acar, Emine] Katip Celebi Univ, Dept Nucl Med, Izmir, Turkey.
   [Baskin, Yasemin] Dokuz Eylul Univ, Personalized Med & Pharmacogen Res Ctr, Izmir, Turkey.
C3 Dokuz Eylul University; Dokuz Eylul University; Izmir Katip Celebi
   University; Dokuz Eylul University
RP Baran, B; Baskin, Y (corresponding author), Dokuz Eylul Univ, Inst Oncol, Dept Basic Oncol, TR-35340 Izmir, Turkey.
EM burcinbrn@gmail.com; yasemin.baskin@deu.edu.tr
RI basbinar, yasemin/P-1137-2019; MERT-OZUPEK, NAZLI/ABB-2691-2020; Baran,
   Burcin/JEO-8145-2023; acar, emine/ABB-2581-2020; BEKCİOĞLU,
   ÖMER/IWD-6455-2023
OI Acar, Emine/0000-0002-6861-8814; Mert Ozupek, Nazli/0000-0002-1627-1548
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NR 104
TC 319
Z9 342
U1 1
U2 19
PU ELMER PRESS INC
PI QUEBEC
PA 9160 BOUL LEDUC, BUREAU 410, BROSSARD, QUEBEC, J4Y 0E3, CANADA
SN 1918-2805
EI 1918-2813
J9 GASTROENTEROL RES
JI Gasteroenterol. Res.
PD AUG
PY 2018
VL 11
IS 4
BP 264
EP 273
DI 10.14740/gr1062w
PG 10
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA GP1SD
UT WOS:000440596200002
PM 30116425
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Chiadini, E
   Scarpi, E
   Passardi, A
   Calistri, D
   Valgiusti, M
   Saragoni, L
   Zoli, W
   Amadori, D
   Ulivi, P
AF Chiadini, Elisa
   Scarpi, Emanuela
   Passardi, Alessandro
   Calistri, Daniele
   Valgiusti, Martina
   Saragoni, Luca
   Zoli, Wainer
   Amadori, Dino
   Ulivi, Paola
TI <i>EGFR</i> methylation and outcome of patients with advanced colorectal
   cancer treated with cetuximab
SO ONCOLOGY LETTERS
LA English
DT Article
DE methylation; colorectal cancer; epidermal growth factor receptor;
   cetuximab
ID BRAF MUTATION; COLON-CANCER; PLUS IRINOTECAN; EXPRESSION; KRAS;
   PANITUMUMAB; EFFICACY; THERAPY; PTEN
AB Targeted therapy of metastatic colorectal cancer (mCRC) with monoclonal antibody anti-epidermal growth factor receptor (EGFR) agents, such as cetuximab (CTX) or panitumumab, is the treatment strategy of choice in patients characterised by a wild-type (wt) RAS gene status. However, despite selection based on RAS status, a high proportion of patients do not respond to therapy. EGFR methylation has been reported to have a role in predicting the response to anti-EGFR agents. The present study aimed to evaluate the role of EGFR methylation in association with the clinical outcome of patients with mCRC treated with CTX. In total, 64 patients with mCRC were assessed in the present study. Genomic DNA was extracted from tumoral tissue and EGFR methylation and mutation of the KRAS,BRAF and PIK3CA genes were analysed by pyrosequencing. EGFR expression was assessed by immunohistochemistry. The various alterations were analysed by assessing the objective response rate (ORR), progression free survival (PFS) and overall survival (OS) rates. In total, 42 cases (66%) exhibited >10% EGFR methylation and there was no correlation with EGFR expression. Mean EGFR methylation of 41 and 9% was observed in KRAS-mutated and -wt patients, respectively (P=0.05). Conversely, a high EGFR methylation was observed in BRAF-wt patients with compared with patients possessing the mutated gene (18 vs. 3%, respectively; P=0.07). EGFR methylation was significantly correlated with the OS rate [hazard ratio, 0.98; 95% confidence interval (CI), 0.96-1.00; P=0.019], but not PFS rate. In patients with a methylation rate <10 and >10%, the median OS rate was 7.5 months (95% CI, 4.4-9.4 months) and 12.0 months (95% CI, 8.7-13.9 months), respectively (P=0.034). In conclusion, the present study revealed a correlation between EGFR methylation and improved OS rate in patients treated. with CTX-based chemotherapy. The presence of EGFR methylation is inversely correlated with BRAF and PIK3CA mutations, indicating that the prognostic value of gene methylation may be worth verifying in further studies.
C1 [Chiadini, Elisa; Calistri, Daniele; Zoli, Wainer; Ulivi, Paola] Ist Sci Romagnolo Studio & Cura Tumori IRST IRCCS, Biosci Lab, I-47014 Meldola, FC, Italy.
   [Scarpi, Emanuela] Ist Sci Romagnolo Studio & Cura Tumori IRST IRCCS, Unit Biostat & Clin Trials, I-47014 Meldola, FC, Italy.
   [Passardi, Alessandro; Valgiusti, Martina; Amadori, Dino] Ist Sci Romagnolo Studio & Cura Tumori IRST IRCCS, Dept Med Oncol, I-47014 Meldola, FC, Italy.
   [Saragoni, Luca] Morgagni Pierantoni Hosp, Pathol Unit, Forli, Italy.
C3 IRCCS Meldola (IRST); IRCCS Meldola (IRST); IRCCS Meldola (IRST)
RP Ulivi, P (corresponding author), Ist Sci Romagnolo Studio & Cura Tumori IRST IRCCS, Biosci Lab, 40 Via Maroncelli, I-47014 Meldola, FC, Italy.
EM paola.ulivi@irst.emr.it
RI Chiadini, Elisa/AAC-3742-2022; Calistri, Daniele/K-5788-2016; passardi,
   alessandro/AAH-4786-2019; Scarpi, Emanuela/AAD-7036-2019
OI Ulivi, Paola/0000-0002-4334-9662; Calistri, Daniele/0000-0002-5064-2023;
   passardi, alessandro/0000-0002-7099-240X; chiadini,
   elisa/0000-0001-5373-3636; Scarpi, Emanuela/0000-0001-7230-9267
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NR 27
TC 2
Z9 2
U1 0
U2 5
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD MAR
PY 2015
VL 9
IS 3
BP 1432
EP 1438
DI 10.3892/ol.2015.2876
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CD2OE
UT WOS:000350918100078
PM 25663927
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Sun, Y
   Wang, D
   Yuan, C
   Lang, XJ
   Fu, SB
AF Sun, Yue
   Wang, Dan
   Yuan, Chen
   Lang, Xiujuan
   Fu, Songbo
TI Lapatinib: A Potential Therapeutic Agent for Colon Cancer Targeting
   Ferroptosis
SO ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
LA English
DT Article
DE Lapatinib; colon cancer; GPX4; ferroptosis; targeted therapy; ROS
ID BREAST-CANCER; HER2 STATUS; RECEPTOR; EXPRESSION; ESOPHAGEAL; SORAFENIB;
   FAMILY; GROWTH; FORM
AB Background Colon cancer poses a significant threat to the lives of several patients, impacting their quality of life, thus necessitating its urgent treatment. Lapatinib, a new generation of targeted anti-tumor drugs for clinical application, has yet to be studied for its molecular mechanisms in treating colon cancer.Objectives This study aimed to uncover the underlying molecular mechanisms through which lapatinib exerts its therapeutic effects in colon cancer treatment.Methods We accessed pertinent data on patients with colon cancer from the Cancer Genome Atlas (TCGA) database and performed bioinformatics analysis to derive valuable insights. The cell counting kit-8 (CCK8) assay was employed to assess whether lapatinib has a potential inhibitory effect on the growth and proliferation of HT-29 cells. Additionally, we employed western blot and real-time quantitative polymerase chain reaction methods to investigate whether lapatinib regulates the expression of the ferroptosis-associated protein GPX4 in HT-29 cells. Furthermore, we utilized specific assay kits to measure the levels of reactive oxygen species (ROS) and malondialdehyde in HT-29 cells treated with lapatinib, aiming to elucidate the precise pattern of cell damage induced by this compound.Results GPX4 exhibited high expression levels in tissues from patients with colon cancer and was significantly associated with patient prognosis and diagnosis. Lapatinib inhibited the growth and proliferation of the colon cancer cell line HT-29. Additionally, lapatinib suppressed the expression of GPX4 in HT-29 cells, while the ferroptosis inhibitor ferrostatin-1 (Fer-1) partially restored its expression. Lapatinib induced an increase in intracellular ROS levels and malondialdehyde content in HT-29 cells, with Fer-1 partially restoring these levels.Conclusion Our findings demonstrated that lapatinib could effectively suppress the mRNA and protein expression of GPX4 in colon cancer cells, which elevates intracellular levels of ROS and malondialdehyde, ultimately inducing ferroptosis in these cells. This mechanism underscores the potential of lapatinib as a therapeutic strategy for targeting tumors.
C1 [Sun, Yue; Wang, Dan; Fu, Songbo] Harbin Med Univ, Ctr Endem Dis Control, Chinese Ctr Dis Control & Prevent, Key Lab Etiol & Epidemiol Educ Bur Heilongjiang Pr, Harbin 150081, Heilongjiang, Peoples R China.
   [Sun, Yue; Wang, Dan; Fu, Songbo] Harbin Med Univ, NHC Key Lab Etiol & Epidemiol, Harbin 150086, Heilongjiang, Peoples R China.
   [Yuan, Chen] Harbin Med Univ, Basic Med Coll, Harbin 150086, Heilongjiang, Peoples R China.
   [Lang, Xiujuan] Harbin Med Univ, Dept Neurobiol, Heilongjiang Prov Key Lab Neurobiol, Harbin 150081, Heilongjiang, Peoples R China.
C3 Chinese Center for Disease Control & Prevention; Harbin Medical
   University; Harbin Medical University; Harbin Medical University; Harbin
   Medical University
RP Fu, SB (corresponding author), Harbin Med Univ, Ctr Endem Dis Control, Chinese Ctr Dis Control & Prevent, Key Lab Etiol & Epidemiol Educ Bur Heilongjiang Pr, Harbin 150081, Heilongjiang, Peoples R China.; Lang, XJ (corresponding author), Harbin Med Univ, Dept Neurobiol, Heilongjiang Prov Key Lab Neurobiol, Harbin 150081, Heilongjiang, Peoples R China.
EM fusongbo@hrbmu.edu.cn; langxiujuan11@163.com
RI Yuan, CHEN/JDD-1642-2023
FU National Natural Science Foundation of China [82200304]; China
   Postdoctoral Science Foundation [2022M710985]; Heilongjiang Province
   Postdoctoral Science Foundation [LBH-Z22212]; Scientific research
   project on the basic research business fee of Heilongjiang Provincial
   Higher Education Institutions in 2022 [2022-KYYWF-0260]
FX This investigation was supported by the National Natural Science
   Foundation of China (grant number: 82200304), the China Postdoctoral
   Science Foundation (grant number: 2022M710985), the Heilongjiang
   Province Postdoctoral Science Foundation (grant number: LBH-Z22212), and
   the scientific research project on the basic research business fee of
   Heilongjiang Provincial Higher Education Institutions in 2022
   (2022-KYYWF-0260).
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NR 77
TC 0
Z9 0
U1 5
U2 5
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1871-5206
EI 1875-5992
J9 ANTI-CANCER AGENT ME
JI Anti-Cancer Agents Med. Chem.
PY 2025
VL 25
IS 2
BP 114
EP 123
DI 10.2174/0118715206327756240830062531
EA SEP 2024
PG 10
WC Oncology; Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA O6V4J
UT WOS:001312752600001
PM 39238394
DA 2025-01-04
ER

PT J
AU Fawzy, MS
   Ibrahiem, AT
   Abu Alsel, BT
   Alghamdi, SA
   Toraih, EA
AF Fawzy, Manal S.
   Ibrahiem, Afaf T.
   Abu Alsel, Baraah T.
   Alghamdi, Saleh A.
   Toraih, Eman A.
TI Analysis of microRNA-34a expression profile and rs2666433 variant in
   colorectal cancer: a pilot study
SO SCIENTIFIC REPORTS
LA English
DT Article
ID NEGATIVE BREAST-CANCER; GENE-EXPRESSION; COLON-CANCER; MIR-34A;
   POLYMORPHISM; METASTASIS; INVASION; MIRNAS; IMPACT; CERNAS
AB MicroRNAs (miRNAs) are implicated in every stage of carcinogenesis and play an essential role as genetic biomarkers of cancer. We aimed to evaluate microRNA-34a gene (MIR34A) expression in colorectal cancer (CRC) tissues compared with non-cancer one and to preliminarily explore the association of one related variant to CRC risk. A total of 116 paraffin-embedded colon specimens were enrolled. MiR-34a was quantified by qPCR, and rs2666433 (A/G) genotyping was performed by TaqMan Real-Time PCR. Also, the somatic mutation burden was assessed. MIR34A expression in the CRC specimens was significantly upregulated (median = 21.50, IQR: 7.0-209.2; P = 0.001) relative to the non-cancer tissues. Allele (A) was highly prevalent in CRC tissues represented 0.56 (P < 0.001). AA/AG genotype carriers were 5.7 and 2.8 more likely to develop cancer than GG carriers. Tumor-normal tissue paired analysis revealed genotype concordance in 33 out of 58 tissue samples. Approximately 43% of the specimens showed a tendency for G to A shift. Additionally, a higher frequency of somatic mutation (92%) was observed in adenocarcinoma (P = 0.006). MIR34A expression and gene variant did not show associations with the clinicopathological data. However, G>A somatic mutation carriers had more prolonged DFS and OS. Bioinformatics analysis revealed miR-34a could target 30 genes that are implied in all steps of CRC tumorigenesis. In conclusion, this study confirms MIR34A upregulation in CRC tissues, and its rs2666433 (A/G) variant showed association with CRC and a high somatic mutation rate in cancer tissues. MiR-34a could provide a novel targeted therapy after validation in large-scale studies.
C1 [Fawzy, Manal S.] Northern Border Univ, Dept Biochem, Fac Med, Ar Ar 1321, Saudi Arabia.
   [Ibrahiem, Afaf T.] Northern Border Univ, Dept Pathol, Fac Med, Ar Ar 1321, Saudi Arabia.
   [Abu Alsel, Baraah T.] Northern Border Univ, Dept Microbiol, Fac Med, Ar Ar 1321, Saudi Arabia.
   [Alghamdi, Saleh A.] Taif Univ, Coll Appl Med Sci, Clin Lab Dept, Med Genet, At Taif 21944, Saudi Arabia.
   [Fawzy, Manal S.] Suez Canal Univ, Dept Med Biochem & Mol Biol, Fac Med, Ismailia 41522, Egypt.
   [Ibrahiem, Afaf T.] Mansoura Univ, Dept Pathol, Fac Med, Mansoura 35516, Egypt.
   [Toraih, Eman A.] Tulane Univ, Sch Med, Dept Surg, New Orleans, LA 70112 USA.
   [Toraih, Eman A.] Suez Canal Univ, Dept Histol & Cell Biol, Genet Unit, Fac Med, Ismailia 41522, Egypt.
C3 Northern Border University; Northern Border University; Northern Border
   University; Taif University; Egyptian Knowledge Bank (EKB); Suez Canal
   University; Egyptian Knowledge Bank (EKB); Mansoura University; Tulane
   University; Egyptian Knowledge Bank (EKB); Suez Canal University
RP Fawzy, MS (corresponding author), Northern Border Univ, Dept Biochem, Fac Med, Ar Ar 1321, Saudi Arabia.; Fawzy, MS (corresponding author), Suez Canal Univ, Dept Med Biochem & Mol Biol, Fac Med, Ismailia 41522, Egypt.
EM manal_mohamed@med.suez.edu.eg
RI Toraih, Eman/I-3024-2019; Ibrahiem, Afaf/AEJ-2582-2022; ABU ALSEL,
   BARAAH/KCY-2181-2024; Fawzy, Manal Said/L-1516-2016
OI Fawzy, Manal Said/0000-0003-1252-8403; toraih, Eman/0000-0001-9267-3787
FU Deanship of Scientific Research, Northern Border University (NBU), Arar,
   Saudi Arabia [MED-2018-39-F-7825]; Taif University Researchers, Taif,
   Saudi Arabia [TURSP-2020/108]
FX This study was supported by research funding from the Deanship of
   Scientific Research (grant no. MED-2018-39-F-7825), Northern Border
   University (NBU), Arar, Saudi Arabia, and Taif University Researchers
   supporting project number (TURSP-2020/108), Taif, Saudi Arabia.
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NR 56
TC 14
Z9 14
U1 0
U2 3
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD OCT 9
PY 2020
VL 10
IS 1
AR 16940
DI 10.1038/s41598-020-73951-y
PG 12
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA QD2SC
UT WOS:000615373800010
PM 33037254
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Bai, L
   Wang, F
   Li, ZZ
   Ren, C
   Zhang, DS
   Zhao, Q
   Lu, YX
   Wang, DS
   Ju, HQ
   Qiu, MZ
   Wang, ZQ
   Wang, FH
   Xu, RH
AF Bai, Long
   Wang, Feng
   Li, Zhe-zhen
   Ren, Chao
   Zhang, Dong-sheng
   Zhao, Qi
   Lu, Yun-xin
   Wang, De-shen
   Ju, Huai-qiang
   Qiu, Miao-zhen
   Wang, Zhi-qiang
   Wang, Feng-hua
   Xu, Rui-hua
TI Chemotherapy plus bevacizumab versus chemotherapy plus cetuximab as
   first-line treatment for patients with metastatic colorectal cancer
SO MEDICINE
LA English
DT Article
DE bevacizumab; cetuximab; Chinese population; first-line treatment;
   metastatic colorectal cancer; peritoneal metastasis
ID ENDOTHELIAL GROWTH-FACTOR; RANDOMIZED PHASE-III; PERITONEAL
   CARCINOMATOSIS; MALIGNANT ASCITES; TARGETED THERAPY; MUTATION STATUS;
   POOLED ANALYSIS; OVARIAN-CANCER; K-RAS; TRIAL
AB The present observational cohort study was designed to elucidate the efficacy and safety profile of bevacizumab or cetuximab with chemotherapy as the first-line treatment in Chinese patients with metastatic colorectal cancer (mCRC). Clinical data were collected from a single-center registry study where mCRC patients received first-line fluoropyrimidine-based chemotherapy combined with either bevacizumab (188 patients with KRAS wild-type or mutated tumors) or cetuximab (101 patients with KRAS wild-type tumors) between January 2009 and December 2013. The Kaplan-Meier method was used for survival analysis. Cox proportional hazards model was used for estimating the prognostic and predictive values of clinicopathological characteristics. No statistically significant difference was observed between the bevacizumab and cetuximab groups in terms of median progression-free survival (PFS) (10.6 vs 8.7 months, P=0.317), median overall survival (OS) (27.7 vs 28.3 months, P=0.525), or overall response rate (43.1% vs 53.5%, P=0.108). For the subset of patients with peritoneal dissemination, bevacizumab-based triplet appears to be superior to cetuximab-based triplet as measured by PFS (9.6 vs 6.1 months) and OS (26.3 vs 12.7 months), but not for patients without peritoneal dissemination (PFS, 10.6 vs 9.1 months; OS, 27.9 vs 30.7 months) (all unadjusted and adjusted interaction P<0.05). Our study suggests that bevacizumab- or cetuximab-based regimens have similar effectiveness as first-line treatment of mCRC in Chinese population. Patients with peritoneal dissemination were likely to gain more benefit from bevacizumab than cetuximab treatment. Future prospective studies are required to further confirm these results.
C1 [Bai, Long; Wang, Feng; Li, Zhe-zhen; Ren, Chao; Zhang, Dong-sheng; Lu, Yun-xin; Wang, De-shen; Ju, Huai-qiang; Qiu, Miao-zhen; Wang, Zhi-qiang; Wang, Feng-hua; Xu, Rui-hua] Sun Yat Sen Univ, Ctr Canc, Dept Med Oncol, 651 Dongfeng Rd East, Guangzhou 510060, Guangdong, Peoples R China.
   [Bai, Long; Wang, Feng; Li, Zhe-zhen; Ren, Chao; Zhang, Dong-sheng; Lu, Yun-xin; Wang, De-shen; Ju, Huai-qiang; Qiu, Miao-zhen; Wang, Zhi-qiang; Wang, Feng-hua; Xu, Rui-hua] Sun Yat Sen Univ, Ctr Canc, State Key Lab Oncol South China, Guangzhou, Guangdong, Peoples R China.
   [Bai, Long; Wang, Feng; Li, Zhe-zhen; Ren, Chao; Zhang, Dong-sheng; Lu, Yun-xin; Wang, De-shen; Ju, Huai-qiang; Qiu, Miao-zhen; Wang, Zhi-qiang; Wang, Feng-hua; Xu, Rui-hua] Collaborat Innovat Ctr Canc Med, Guangzhou, Guangdong, Peoples R China.
   [Zhao, Qi] Sun Yat Sen Univ, Sch Life Sci, State Key Lab Biocontrol, Guangzhou, Guangdong, Peoples R China.
C3 Sun Yat Sen University; State Key Lab Oncology South China; Sun Yat Sen
   University; Sun Yat Sen University
RP Xu, RH (corresponding author), Sun Yat Sen Univ, Ctr Canc, Dept Med Oncol, 651 Dongfeng Rd East, Guangzhou 510060, Guangdong, Peoples R China.
EM xurh@sysucc.org.cn
RI Zhao, Qi/X-7899-2019; REN, CHAO/KRO-9616-2024; Dongsheng,
   ZHANG/AAL-6913-2020; Xu, Rui-Hua/AAW-4766-2021; Zhao, Qi/M-4830-2016;
   Wang, De-shen/JBR-7938-2023
OI Xu, Rui-Hua/0000-0001-9771-8534; Zhao, Qi/0000-0002-8683-6145; Wang,
   De-shen/0000-0001-9657-4380; , REN CHAO/0009-0006-5629-9947
FU National High Technology Research and Development Program of China (863
   Program), China [2015AA020103]; National Natural Science Foundation of
   China [81372570, 81572392]; Natural Science Foundation of Guangdong
   Province [2014A030312015]; Science and Technology Program of Guangzhou
   [15570006, 158100066]
FX Project supported by the National High Technology Research and
   Development Program of China (863 Program), China (No. 2015AA020103),
   the National Natural Science Foundation of China (No. 81372570,
   81572392), the Natural Science Foundation of Guangdong Province (No.
   2014A030312015), and the Science and Technology Program of Guangzhou
   (No. 15570006, 158100066).
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NR 59
TC 13
Z9 13
U1 3
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD DEC
PY 2016
VL 95
IS 51
AR e4531
DI 10.1097/MD.0000000000004531
PG 9
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA EH2UG
UT WOS:000391623300001
PM 28002313
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Lengyel, CG
   Habeeb, B
   Khan, SZ
   El Bairi, K
   Altuna, SC
   Hussain, S
   Mazher, SA
   Trapani, D
   Petrillo, A
AF Lengyel, Csongor G.
   Habeeb, Baker
   Khan, Shah Z.
   El Bairi, Khalid
   Altuna, Sara C.
   Hussain, Sadaqat
   Mazher, Syed Ayub
   Trapani, Dario
   Petrillo, Angelica
TI Role of Her-2 in Gastrointestinal Tumours beyond Gastric Cancer: A Tool
   for Precision Medicine
SO GASTROINTESTINAL DISORDERS
LA English
DT Review
DE biliary cancer; colorectal cancer; cholangiocarcinoma; prognostic
   factor; predictive; GIST; precision medicine; target therapy; metastatic
   cancer
ID GROWTH-FACTOR-RECEPTOR; PHASE-II TRIAL; BREAST-CANCER; BILIARY-TRACT;
   PANCREATIC-CANCER; LAPATINIB GW572016; PATIENTS PTS; RHUMAB 2C4;
   TRASTUZUMAB; ANTIBODY
AB Gastrointestinal (GI) tumors account for a quarter of all the cancer burden and a third of the global cancer-related mortality. Among them, some cancers retain a dismal prognosis; therefore, newer and innovative therapies are urgently needed in priority disease areas of high-unmet medical need. In this context, HER2 could be a relevant prognostic and predictive biomarker acting as a target for specific drugs. However, if the role of HER2 has been object of investigation for several years in gastric cancer, it is not well established in other GI malignancies. The aim of this narrative review was to portray the current landscape of the potential role of HER2 as a predictive biomarker for GI tumors beyond gastric cancer. In colon cancer, the benefit from anti-HER2 therapies is less clear than in gastric neoplasms for the lack of controlled studies. Pancreatic, biliary tract adenocarcinomas and hepatocarcinoma may derive a less clear clinical benefit by using anti-HER2 agents in HER2 positive tumors. Overall, the results are promising and seem to suggest that the integration of multiple modalities of therapies can optimize the cancer care. However, further prospective trials are needed to validate the use of personalized targeted therapies in this field.
C1 [Lengyel, Csongor G.] Natl Inst Oncol, Head & Neck Surg, H-1122 Budapest, Hungary.
   [Habeeb, Baker] Shaqlawa Teaching Hosp, Med Oncol Dept, Erbil 44001, Iraq.
   [Khan, Shah Z.] BINOR Canc Hosp, Dept Clin Oncol, Bannu 28100, Pakistan.
   [El Bairi, Khalid] Canc Biomarkers Working Grp, Oujda 60000, Morocco.
   [Altuna, Sara C.] Oncomedica CA, Caracas 1060, Venezuela.
   [Hussain, Sadaqat] Western Hlth & Social Care Trust, Altnagelvin Hosp, Northwest Canc Ctr, Derry BT47 6SB, Londonderry, North Ireland.
   [Mazher, Syed Ayub] UT Southwestern Clements Univ Hosp, Dallas, TX 75390 USA.
   [Trapani, Dario] IRCCS, European Inst Oncol, I-20141 Milan, Italy.
   [Petrillo, Angelica] Osped Mare, Med Oncol Unit, I-80147 Naples, Italy.
   [Petrillo, Angelica] Univ Campania L Vanvitelli, Sch Med, Dept Precis Med, Div Med Oncol, I-81100 Caserta, Italy.
C3 National Institute of Oncology Hungary; IRCCS European Institute of
   Oncology (IEO); Universita della Campania Vanvitelli
RP Petrillo, A (corresponding author), Osped Mare, Med Oncol Unit, I-80147 Naples, Italy.; Petrillo, A (corresponding author), Univ Campania L Vanvitelli, Sch Med, Dept Precis Med, Div Med Oncol, I-81100 Caserta, Italy.
EM lengyel.csongor@gmail.com; bakershalal@gmail.com;
   skhanizhere0@gmail.com; k.elbairi@ump.ac.ma; altunamujica.md@gmail.com;
   oncologysh@gmail.com; ayub.mazher@yahoo.com; dario.trapani@ieo.it;
   angelic.petrillo@gmail.com
RI ALTUNA, SARA/JPX-9724-2023; tra, Dar/ABF-2184-2022; Khan,
   Shah/AAL-3859-2020; Habeeb, Baker/JBR-9011-2023; Petrillo,
   Angelica/JFS-3719-2023; El Bairi, Khalid/G-4005-2015
OI Petrillo, Angelica/0000-0001-5489-5733; Lengyel, Csongor
   Gyorgy/0000-0001-7767-516X; hussain, sadaqat/0000-0002-6082-180X;
   Habeeb, Baker/0000-0001-8070-8532; Zeb Khan, Shah/0000-0002-3692-6150;
   Altuna Mujica, Sara Cecilia/0000-0002-7054-691X; El Bairi,
   Khalid/0000-0002-8414-4145
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NR 116
TC 7
Z9 7
U1 0
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2624-5647
J9 GASTROINTEST DISORD
JI Gastrointest. Disord.
PD MAR
PY 2021
VL 3
IS 1
BP 1
EP 22
DI 10.3390/gidisord3010001
PG 22
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA TM4AY
UT WOS:000675494800001
OA gold
DA 2025-01-04
ER

PT J
AU Herr, R
   Halbach, S
   Heizmann, M
   Busch, H
   Boerries, M
   Brummer, T
AF Herr, Ricarda
   Halbach, Sebastian
   Heizmann, Miriam
   Busch, Hauke
   Boerries, Melanie
   Brummer, Tilman
TI BRAF inhibition upregulates a variety of receptor tyrosine kinases and
   their downstream effector Gab2 in colorectal cancer cell lines
SO ONCOGENE
LA English
DT Article
ID MAMMARY EPITHELIAL-CELLS; ACQUIRED-RESISTANCE; MOLECULAR LANDSCAPE;
   FEEDBACK INHIBITION; PROGNOSTIC-FACTOR; GENE-EXPRESSION; MEK INHIBITORS;
   RAF INHIBITION; TUMOR-GROWTH; COLON-CANCER
AB BRAF mutations occur in similar to 10% of colorectal cancer (CRC) and are associated with poor prognosis. Inhibitors selective for the BRAF(V600E) oncoprotein, the most common BRAF mutant, elicit only poor response rates in BRAF-mutant CRC as single agents. This unresponsiveness was mechanistically attributed to the loss of negative feedbacks on the epidermal growth factor receptor (EGFR) and initiated clinical trials that combine BRAF (and MEK) inhibitors, either singly or in combination, with the anti-EGFR antibodies cetuximab or panitumumab. First results of these combinatorial studies demonstrated improved efficacy, however, the response rates still were heterogeneous. Here, we show that BRAF inhibition leads to the upregulation of a variety of receptor tyrosine kinases (RTKs) in CRC cell lines, including not only the EGFR, but also human epidermal growth factor receptor (HER) 2 and HER3. Importantly, combination of the BRAF inhibitors (BRAFi) vemurafenib (PLX4032), dabrafenib, or encorafenib with inhibitors dually targeting the EGFR and HER2 (such as lapatinib, canertinib, and afatinib) significantly reduced the metabolic activity and proliferative potential of CRC cells. This re-sensitization was also observed after genetic depletion of HER2 or HER3. Interestingly, BRAF inhibitors did not only upregulate RTKs, but also increased the abundance of the GRB2-associated binders (Gab) 1 and Gab2, two important amplifiers of RTK signaling. An allele-specific shRNA-mediated knockdown of BRAF(V600E) revealed that Gab2 upregulation was directly dependent on the loss of the oncoprotein and was not caused by an "off-target" effect of these kinase inhibitors. Furthermore, Gab2 and Gab2-mediated Shp2 signaling were shown to be functionally important in BRAFi resistance. These findings highlight potential new escape mechanisms to these targeted therapies and indicate that a broad suppression of RTK signaling might be beneficial and should be taken into account in future research addressing targeted therapy in BRAF-mutant CRC.
C1 [Herr, Ricarda; Halbach, Sebastian; Heizmann, Miriam; Brummer, Tilman] Univ Freiburg, Inst Mol Med & Cell Res IMMZ, Signal Transduct Tumour Dev & Drug Resistance Grp, Fac Med, Freiburg, Germany.
   [Heizmann, Miriam] Univ Freiburg, Fac Biol, Freiburg, Germany.
   [Busch, Hauke; Boerries, Melanie] Univ Freiburg, Syst Biol Cellular Microenvironm, IMMZ, Fac Med, Freiburg, Germany.
   [Busch, Hauke] Univ Lubeck, Inst Expt Dermatol, Lubeck, Germany.
   [Busch, Hauke] Univ Lubeck, Inst Cardiogenet, Lubeck, Germany.
   [Boerries, Melanie; Brummer, Tilman] German Canc Res Ctr, German Canc Consortium DKTK Partner Site Freiburg, Partner Site Freiburg, Heidelberg, Germany.
   [Boerries, Melanie; Brummer, Tilman] Univ Freiburg, CCCF, Freiburg, Germany.
   [Brummer, Tilman] Univ Freiburg, Ctr Biol Signalling Studies BIOSS, Freiburg, Germany.
C3 University of Freiburg; University of Freiburg; University of Freiburg;
   University of Lubeck; University of Lubeck; Helmholtz Association;
   German Cancer Research Center (DKFZ); University of Freiburg; University
   of Freiburg
RP Herr, R; Brummer, T (corresponding author), Univ Freiburg, Inst Mol Med & Cell Res IMMZ, Signal Transduct Tumour Dev & Drug Resistance Grp, Fac Med, Freiburg, Germany.; Brummer, T (corresponding author), German Canc Res Ctr, German Canc Consortium DKTK Partner Site Freiburg, Partner Site Freiburg, Heidelberg, Germany.; Brummer, T (corresponding author), Univ Freiburg, CCCF, Freiburg, Germany.; Brummer, T (corresponding author), Univ Freiburg, Ctr Biol Signalling Studies BIOSS, Freiburg, Germany.
EM ricarda.herr@mol-med.uni-freiburg.de; tilman.brummer@zbsa.de
RI Boerries, Melanie/AAM-2602-2021; Halbach, Sebastian/G-4021-2012; Busch,
   Hauke/R-6452-2016; Brummer, Tilman/B-6218-2016
OI Halbach, Sebastian/0000-0002-6827-8178; Busch,
   Hauke/0000-0003-4763-4521; Griffin, Ricarda/0000-0003-1368-2832;
   Brummer, Tilman/0000-0003-4387-7905
FU German Research Foundation (DFG) [SFB 850]; Heisenberg professorship
   [EXC 294 BIOSS]; BMBF [e:Bio 0316184D]; e:Med research and funding
   concept, DeCaRe [FKZ 01ZX1409B]
FX We thank Martin Kohler for valuable discussions, Roland Rad for sharing
   MouseT1 cells, and Silke Kowar for expert technical assistance. This
   work was supported by the German Research Foundation (DFG) through SFB
   850, projects B4 (TB) and Z1 (HB and MB), a Heisenberg professorship to
   TB, EXC 294 BIOSS and the BMBF through e:Bio 0316184D, and MB within the
   framework of the e:Med research and funding concept, DeCaRe (FKZ
   01ZX1409B).
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NR 91
TC 35
Z9 37
U1 0
U2 12
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD MAR
PY 2018
VL 37
IS 12
BP 1576
EP 1593
DI 10.1038/s41388-017-0063-5
PG 18
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
GA GA8YC
UT WOS:000428626700003
PM 29326440
DA 2025-01-04
ER

PT J
AU Pietsch, FL
   Haag, F
   Ayx, I
   Grawe, F
   Vellala, AK
   Schoenberg, SO
   Froelich, MF
   Tharmaseelan, H
AF Pietsch, Friedrich L.
   Haag, Florian
   Ayx, Isabelle
   Grawe, Freba
   Vellala, Abhinay K.
   Schoenberg, Stefan O.
   Froelich, Matthias F.
   Tharmaseelan, Hishan
TI Textural heterogeneity of liver lesions in CT imaging - comparison of
   colorectal and pancreatic metastases
SO ABDOMINAL RADIOLOGY
LA English
DT Article
DE Tumoral Heterogeneity; Radiomics; Colorectum; Pancreas; Tumor/Oncology;
   Computed tomography
ID TUMOR HETEROGENEITY; RADIOMICS; CANCER; IMAGES; SYSTEM
AB Purpose Tumoral heterogeneity poses a challenge for personalized cancer treatments. Especially in metastasized cancer, it remains a major limitation for successful targeted therapy, often leading to drug resistance due to tumoral escape mechanisms. This work explores a non-invasive radiomics-based approach to capture textural heterogeneity in liver lesions and compare it between colorectal cancer (CRC) and pancreatic cancer (PDAC). Materials and methods In this retrospective single-center study 73 subjects (42 CRC, 31 PDAC) with 1291 liver metastases (430 CRC, 861 PDAC) were segmented fully automated on contrast-enhanced CT images by a UNet for medical images. Radiomics features were extracted using the Python package Pyradiomics. The mean coefficient of variation (CV) was calculated patient-wise for each feature to quantify the heterogeneity. An unpaired t-test identified features with significant differences in feature variability between CRC and PDAC metastases. Results In both colorectal and pancreatic liver metastases, interlesional heterogeneity in imaging can be observed using quantitative imaging features. 75 second-order features were extracted to compare the varying textural characteristics. In total, 18 radiomics features showed a significant difference (p < 0.05) in their expression between the two malignancies. Out of these, 16 features showed higher levels of variability within the cohort of pancreatic metastases, which, as illustrated in a radar plot, suggests greater textural heterogeneity for this entity. Conclusions Radiomics has the potential to identify the interlesional heterogeneity of CT texture among individual liver metastases. In this proof-of-concept study for the quantification and comparison of imaging-related heterogeneity in liver metastases a variation in the extent of heterogeneity levels in CRC and PDAC liver metastases was shown.
C1 [Pietsch, Friedrich L.; Haag, Florian; Ayx, Isabelle; Grawe, Freba; Vellala, Abhinay K.; Schoenberg, Stefan O.; Froelich, Matthias F.; Tharmaseelan, Hishan] Heidelberg Univ, Univ Med Ctr Mannheim, Dept Radiol & Nucl Med, Theodor Kutzer Ufer 1-3, D-68167 Mannheim, Germany.
   [Grawe, Freba] Univ Med Ctr Mannheim, DKFZ Hector Canc Inst, Neuenheimer Feld 280, D-68167 Heidelberg, Germany.
C3 Ruprecht Karls University Heidelberg; Ruprecht Karls University
   Heidelberg
RP Froelich, MF (corresponding author), Heidelberg Univ, Univ Med Ctr Mannheim, Dept Radiol & Nucl Med, Theodor Kutzer Ufer 1-3, D-68167 Mannheim, Germany.
EM matthias.froelich@medma.uni-heidelberg.de
RI Froelich, Matthias/AAG-9109-2020; Haag, Florian/AAB-4800-2022
OI Froelich, Matthias/0000-0001-8501-2147
FU Projekt DEAL; Hector Foundation
FX Open Access funding enabled and organized by Projekt DEAL. This project
   was supported by funding from the Hector Foundation.
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NR 52
TC 0
Z9 0
U1 3
U2 3
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 2366-004X
EI 2366-0058
J9 ABDOM RADIOL
JI Abdom. Radiol.
PD DEC
PY 2024
VL 49
IS 12
BP 4295
EP 4306
DI 10.1007/s00261-024-04511-5
EA AUG 2024
PG 12
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA K6H1M
UT WOS:001287409900001
PM 39115682
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Wang, MD
   Wang, X
   Li, YW
   Li, QG
   Cai, SJ
   Li, XX
   Ma, MG
AF Wang, Mingdian
   Wang, Xiang
   Li, Yiwei
   Li, Qingguo
   Cai, Sanjun
   Li, Xinxiang
   Ma, Maoguang
TI HER2 status is positively associated with vessel invasion of colorectal
   cancer: a retrospective large cohort study
SO INTERNATIONAL JOURNAL OF COLORECTAL DISEASE
LA English
DT Article
DE Colorectal cancer; HER2; Immunohistochemistry; Vessel invasion
AB Purpose HER2-positive colorectal cancer was drawn increasing attention in recent years. Accumulating evidence showed HER2-positive metastatic colorectal cancer could benefit from HER2-targeted therapy. While HER2 expression and the relationship between HER2 status and clinicopathological characteristics of overall colorectal cancer remains largely unknown. The aim of this study was to evaluate HER2 expression in colorectal cancer and compare the clinicopathological features between HER2-positive and HER2-negative colorectal cancer. Methods We retrospectively analyzed 3910 primary colorectal cancer patients treated in our institution from January 2016 to December 2019. Medical records and pathology reports after surgery were collected to provide information about HER2 status and other clinicopathological characteristics. Results We identified 3347 HER2-negative and 79 HER2-positive colorectal cancer patients in our cohort. The chi-square test showed that vessel invasion was significantly more common in HER2-positive colorectal cancer patients. Crude analysis showed HER2 positive was associated with vessel invasion in colorectal cancer [OR and 95% CI 0.534 (0.341, 0.835), p = 0.006]. After adjusting for N stage, a significant association was still observed between HER2 status and vessel invasion in colorectal cancer [OR and 95% CI 0.550 (0.322, 0.941), p = 0.029]. Survival analysis showed that there was no significant difference in 3-year overall survival rate between HER2 positive and HER2 negative group (p = 0.603). Conclusion Our findings indicate that the rate of HER2 positivity in colorectal cancer was relatively low, and HER2 status was strongly associated with vessel invasion while having no significant influence on the 3-year overall survival rate in colorectal cancer patients.
C1 [Li, Yiwei; Li, Qingguo; Cai, Sanjun; Li, Xinxiang; Ma, Maoguang] Fudan Univ, Dept Colorectal Surg, Shanghai Canc Ctr, Shanghai, Peoples R China.
   [Li, Yiwei; Li, Qingguo; Cai, Sanjun; Li, Xinxiang] Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai, Peoples R China.
   [Wang, Mingdian] Sun Yat Sen Univ, Collaborat Innovat Ctr Canc Med, Dept Pathol, Canc Ctr, Guangzhou, Guangdong, Peoples R China.
   [Wang, Xiang] Anhui Med Univ, Peoples Hosp Hefei 2, Dept Gen Surg, Hefei Hosp, Hefei, Anhui, Peoples R China.
C3 Fudan University; Fudan University; Sun Yat Sen University; Anhui
   Medical University
RP Li, XX; Ma, MG (corresponding author), Fudan Univ, Dept Colorectal Surg, Shanghai Canc Ctr, Shanghai, Peoples R China.; Li, XX (corresponding author), Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai, Peoples R China.
EM xinxiangli@fudan.edu.cn; mamaoguang@shca.org.cn
RI Cai, Jun/GLS-4538-2022; Ma, Maoguang/GQQ-1402-2022
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NR 26
TC 3
Z9 3
U1 4
U2 15
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0179-1958
EI 1432-1262
J9 INT J COLORECTAL DIS
JI Int. J. Colorectal Dis.
PD SEP
PY 2022
VL 37
IS 9
BP 2061
EP 2067
DI 10.1007/s00384-022-04243-2
EA AUG 2022
PG 7
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA 4F8HE
UT WOS:000844506400001
PM 36006442
OA Green Submitted, Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Unseld, M
   Filip, M
   Seiri, S
   Gleiss, A
   Bianconi, D
   Kieler, M
   Demyanets, S
   Scheithauer, W
   Zielinski, C
   Prager, G
AF Unseld, M.
   Filip, M.
   Seiri, S.
   Gleiss, A.
   Bianconi, D.
   Kieler, M.
   Demyanets, S.
   Scheithauer, W.
   Zielinski, C.
   Prager, G.
TI Regorafenib therapy in metastatic colorectal cancer patients: markers
   and outcome in an actual clinical setting
SO NEOPLASMA
LA English
DT Article
DE colon cancer; chemotherapy; regorafenib
ID PHASE-3 TRIAL; DOUBLE-BLIND; MONOTHERAPY; MULTICENTER
AB The oral multikinase inhibitor regorafenib had beneficial effects in randomized clinical phase III trials compared to the placebo in patients with metastatic colorectal cancer (mCRC) who progressed on standard therapies. The factors which influence regorafenib response and therapy sequence during treatment history are still highly discussed, and herein we analyzed the therapy algorithm, outcome and clinical markers following regorafenib application in a single center register study. Clinical data for 48 metastatic colorectal cancer patients were collected from 01.01.2013 to 31.12.2016. Treatment effects according to various patient and tumor characteristics were evaluated using univariate and multivariate Cox proportional hazard regression models. The 48 patients comprised 14 (29%) females and 34 (71%) males, with mean age 64.2 +/- 9 and ECOG 0-1. Progression free survival under regorafenib therapy was 2.9 months (quartiles 2.2; 4.4) and the overall response rate was 2 (4%) and disease control rate was 19 (40%). Overall survival (OS) and progression free survival (PFS) were investigated under regorafenib in the chemotherapy regimen given immediately before and afterthis treatment. Variables including tumor localization, Ras status, CEA and CA 19-9 plasma levels were analyzed for their impact on PFS, and the regorafenib-related adverse events were also observed. Our study confirms the efficacy of regorafenib in a real-life setting. We established that response rate and PFS in regorafenib treatment are independent of tumor localization, Ras status or biomarkers such as CEA and CA 19-9. Trifluridin/tripacil application or re-induction of chemotherapy +/- target therapy was effective following regorafenib therapy.
C1 [Unseld, M.; Filip, M.; Seiri, S.; Bianconi, D.; Kieler, M.; Scheithauer, W.; Zielinski, C.; Prager, G.] Med Univ Vienna, Dept Med 1, Clin Div Oncol, Vienna, Austria.
   [Unseld, M.; Filip, M.; Seiri, S.; Bianconi, D.; Kieler, M.; Scheithauer, W.; Zielinski, C.; Prager, G.] Med Univ Vienna, Comprehens Canc Ctr, Vienna, Austria.
   [Gleiss, A.] Med Univ Vienna, Ctr Med Stat Informat & Intelligent Syst, Vienna, Austria.
   [Demyanets, S.] Med Univ Vienna, Dept Lab Med, Vienna, Austria.
C3 Medical University of Vienna; Medical University of Vienna; Medical
   University of Vienna; Medical University of Vienna
RP Prager, G (corresponding author), Med Univ Vienna, Dept Med 1, Clin Div Oncol, Vienna, Austria.; Prager, G (corresponding author), Med Univ Vienna, Comprehens Canc Ctr, Vienna, Austria.
EM gerald.prager@meduniwien.ac.at
RI Kieler, Markus/AAF-4612-2020; Prager, Gerald/AAS-8674-2021
OI Kieler, Markus/0000-0002-4082-5731; Prager, M.D.,
   Gerald/0000-0002-7854-7781
FU Comprehensive Cancer Center Vienna at the Medical University of Vienna;
   Bayer Austria
FX This work was supported by the Comprehensive Cancer Center Vienna at the
   Medical University of Vienna. Bayer Austria has supported this
   publication with an independent research grant. Bayer had no editorial
   control of this publication.
CR Avallone A, 2016, BMC CANCER, V16, DOI 10.1186/s12885-016-2102-y
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NR 15
TC 5
Z9 5
U1 0
U2 1
PU AEPRESS SRO
PI BRATISLAVA
PA BAJZOVA 7, BRATISLAVA, 821 08, SLOVAKIA
SN 0028-2685
EI 1338-4317
J9 NEOPLASMA
JI Neoplasma
PY 2018
VL 65
IS 4
BP 599
EP 603
DI 10.4149/neo_2018_170727N506
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GO6PZ
UT WOS:000440172400014
PM 29940763
OA Bronze
DA 2025-01-04
ER

PT J
AU Napolitano, S
   Matrone, N
   Muddassir, AL
   Martini, G
   Sorokin, A
   De Falco, V
   Giunta, EF
   Ciardiello, D
   Martinelli, E
   Belli, V
   Furia, M
   Kopetz, S
   Morgillo, F
   Ciardiello, F
   Troiani, T
AF Napolitano, S.
   Matrone, N.
   Muddassir, A. L.
   Martini, G.
   Sorokin, A.
   De Falco, V.
   Giunta, E. F.
   Ciardiello, D.
   Martinelli, E.
   Belli, V.
   Furia, M.
   Kopetz, S.
   Morgillo, F.
   Ciardiello, F.
   Troiani, T.
TI Triple blockade of EGFR, MEK and PD-L1 has antitumor activity in
   colorectal cancer models with constitutive activation of MAPK signaling
   and PD-L1 overexpression
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Article
DE Colorectal cancer; MEK inhibitor resistance; PD-L1 inhibitors
ID CONSENSUS MOLECULAR SUBTYPES; ACQUIRED-RESISTANCE; TARGETED-THERAPY;
   IMMUNE ESCAPE; COLON-CANCER; CETUXIMAB; EFFICACY; PATHWAY;
   CLASSIFICATION; HETEROGENEITY
AB Background: Molecular mechanisms driving acquired resistance to anti-EGFR therapies in metastatic colorectal cancer (mCRC) are complex but generally involve the activation of the downstream RAS-RAF-MEK-MAPK pathway. Nevertheless, even if inhibition of EGFR and MEK could be a strategy for overcoming anti-EGFR resistance, its use is limited by the development of MEK inhibitor (MEKi) resistance.
   Methods: We have generated in vitro and in vivo different CRC models in order to underline the mechanisms of MEKi resistance.
   Results: The three different in vitro MEKi resistant models, two generated by human CRC cells quadruple wild type for KRAS, NRAS, BRAF, PI3KCA genes (SW48-MR and LIM1215-MR) and one by human CRC cells harboring KRAS mutation (HCT116-MR) showed features related to the gene signature of colorectal cancer CMS4 with up-regulation of immune pathway as confirmed by microarray and western blot analysis. In particular, the MEKi phenotype was associated with the loss of epithelial features and acquisition of mesenchymal markers and morphology. The change in morphology was accompanied by up-regulation of PD-L1 expression and activation of EGFR and its downstream pathway, independently to RAS mutation status. To extend these in vitro findings, we have obtained mouse colon cancer MC38- and CT26-MEKi resistant syngeneic models (MC38-MR and CT26-MR). Combined treatment with MEKi, EGFR inhibitor (EGFRi) and PD-L1 inhibitor (PD-L1i) resulted in a marked inhibition of tumor growth in both models.
   Conclusions: These results suggest a strategy to potentially improve the efficacy of MEK inhibition by co-treatment with EGFR and PD-L1 inhibitors via modulation of host immune responses.
C1 [Napolitano, S.; Matrone, N.; Martini, G.; De Falco, V.; Giunta, E. F.; Ciardiello, D.; Martinelli, E.; Belli, V.; Morgillo, F.; Ciardiello, F.; Troiani, T.] Univ Campania Luigi Vanvitelli, Med Oncol Dept Precis Med, I-80100 Naples, Italy.
   [Napolitano, S.; Muddassir, A. L.; Sorokin, A.; Kopetz, S.] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Div Canc Med 0065, 1515 Holcombe Blvd, Houston, TX 77030 USA.
   [Matrone, N.] Med Univ Vienna, Inst Canc Res, Borschkegasse 8A, A-1090 Vienna, Austria.
   [Martini, G.] Vall DHebron Inst Oncol VHIO, Gastrointestinal & Neuroendocrine Tumor Grp, C Natzaret 115-117, Barcelona 08035, Spain.
   [Furia, M.] Univ Naples Federico II, Dept Biol, I-80126 Naples, Italy.
C3 Universita della Campania Vanvitelli; University of Texas System; UTMD
   Anderson Cancer Center; Medical University of Vienna; Vall d'Hebron
   Institut d'Oncologia (VHIO); University of Naples Federico II
RP Troiani, T (corresponding author), Univ Campania Luigi Vanvitelli, Med Oncol Dept Precis Med, I-80100 Naples, Italy.
EM teresa.troiani@unicampania.it
RI Martini, Giulia/AIB-8246-2022; Furia, maria/AHD-7483-2022; Giunta,
   Emilio/AAC-3434-2022; Ciardiello, Davide/AAC-4613-2022; Napolitano,
   Stefania/AAM-6696-2020; De Falco, Vincenzo/AAP-5495-2021; Matrone,
   Nunzia/ABA-8014-2021; Kopetz, Scott/AAC-1387-2019
OI De Falco, Vincenzo/0000-0003-0261-0382; FURIA,
   Maria/0000-0002-9603-7689; Giunta, Emilio Francesco/0000-0002-5383-4469;
   Napolitano, Stefania/0000-0003-3504-8349; belli,
   valentina/0000-0002-7774-3764; MARTINI, Giulia/0000-0003-4093-2681
FU Associazione Italiana per la Ricerca sul Cancro (AIRC) [AIRC IG 18972];
   Regione Campania Cancer Research Campaign I-CURE grant
FX This research has been supported by a grant from Associazione Italiana
   per la Ricerca sul Cancro (AIRC) to FC (AIRC IG 18972) and and Regione
   Campania Cancer Research Campaign I-CURE grant to FC.
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NR 46
TC 28
Z9 28
U1 1
U2 10
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1756-9966
J9 J EXP CLIN CANC RES
JI J. Exp. Clin. Cancer Res.
PD DEC 16
PY 2019
VL 38
IS 1
AR 492
DI 10.1186/s13046-019-1497-0
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KH4TK
UT WOS:000510641700001
PM 31842958
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Greimelmaier, K
   Klopp, N
   Mairinger, E
   Wessolly, M
   Borchert, S
   Steinborn, J
   Schmid, KW
   Wohlschlaeger, J
   Mairinger, FD
AF Greimelmaier, K.
   Klopp, N.
   Mairinger, E.
   Wessolly, M.
   Borchert, S.
   Steinborn, J.
   Schmid, K. W.
   Wohlschlaeger, J.
   Mairinger, F. D.
TI Fibroblast activation protein-a expression in fibroblasts is common in
   the tumor microenvironment of colorectal cancer and may serve as a
   therapeutic target
SO PATHOLOGY & ONCOLOGY RESEARCH
LA English
DT Article
DE colorectal cancer; tumor microenvironment; cancer-associated
   fibroblasts; fibroblast-activation protein; radioligand therapy
ID PATIENT; PET/CT; FAP
AB Background: Colorectal cancer (CRC) is still one of the leading causes of cancer death worldwide, emphasizing the need for further diagnostic and therapeutic approaches. Cancer invasion and metastasis are affected by the tumor microenvironment (TME), with cancer-associated fibroblasts (CAF) being the predominant cellular component. An important marker for CAF is fibroblast activation protein-alpha (FAP) which has been evaluated as therapeutic target for, e.g., radioligand therapy. The aim of this study was to examine CRC regarding the FAP expression as a candidate for targeted therapy.
   Methods: 67 CRC, 24 adenomas, 18 tissue samples of inflammation sites and 28 non-neoplastic, non-inflammatory tissue samples of colonic mucosa were evaluated for immunohistochemical FAP expression of CAF in tissue microarrays. The results were correlated with clinicopathological data, tumor biology and concurrent expression of additional immunohistochemical parameters.
   Results: 53/67 (79%) CRC and 6/18 (33%) inflammatory tissue specimens showed expression of FAP. However, FAP was only present in 1/24 (4%) adenomas and absent in normal mucosa (0/28). Thus, FAP expression in CRC was significantly higher than in the other investigated groups. Within the CRC cohort, expression of FAP did not correlate with tumor stage, grading or the MSI status. However, it was observed that tumors exhibiting high immunohistochemical expression of Ki-67, CD3, p53, and beta-Catenin showed a significantly higher incidence of FAP expression.
   Conclusion: In the crosstalk between tumor cells and TME, CAF play a key role in carcinogenesis and metastatic spread. Expression of FAP was detectable in the majority of CRC but nearly absent in precursor lesions and non-neoplastic, non-inflammatory tissue. This finding indicates that FAP has the potential to emerge as a target for new diagnostic and therapeutic concepts in CRC. Additionally, the association between FAP expression and other immunohistochemical parameters displays the interaction between different components of the TME and demands further investigation.
C1 [Greimelmaier, K.; Wohlschlaeger, J.] Diakonissenkrankenhaus Flensburg, Inst Pathol, Flensburg, Germany.
   [Klopp, N.; Mairinger, E.; Wessolly, M.; Borchert, S.; Steinborn, J.; Schmid, K. W.; Mairinger, F. D.] Univ Klinikum Essen, Inst Pathol, Essen, Germany.
C3 University of Duisburg Essen
RP Greimelmaier, K (corresponding author), Diakonissenkrankenhaus Flensburg, Inst Pathol, Flensburg, Germany.
EM greimelmaierkr@diako.de
RI Mairinger, Fabian Dominik/IST-1621-2023; Wessolly, Michael/ACS-2732-2022
OI Wessolly, Michael/0000-0002-4399-8646; Klopp, Nick
   Alexander/0009-0002-2341-0574
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NR 46
TC 5
Z9 5
U1 0
U2 2
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1219-4956
EI 1532-2807
J9 PATHOL ONCOL RES
JI Pathol. Oncol. Res.
PD AUG 8
PY 2023
VL 29
AR 1611163
DI 10.3389/pore.2023.1611163
PG 9
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA P7IA7
UT WOS:001052362300001
PM 37614665
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Seppänen, AV
   Daniel, F
   Houzard, S
   Le Bihan, C
   Coldefy, M
   Gandré, C
AF Seppaenen, A-V.
   Daniel, F.
   Houzard, S.
   Le Bihan, C.
   Coldefy, M.
   Gandre, C.
TI The double burden of severe mental illness and cancer: a
   population-based study on colorectal cancer care pathways from screening
   to end-of-life care
SO EPIDEMIOLOGY AND PSYCHIATRIC SCIENCES
LA English
DT Article
DE care pathways; colorectal cancer; mental health; oncology; quality
   indicators; quality of care; severe mental illness
ID MORTALITY; PEOPLE; SCHIZOPHRENIA; METAANALYSIS; DISPARITIES;
   INDIVIDUALS; DISORDERS; DISEASE
AB Aims. Cancer is one of the main causes of death in persons with severe mental illness (SMI). Although their cancer incidence is similar, or sometimes even potentially lower compared to the general population, their cancer mortality remains higher. The role of healthcare provision and care equity in this mortality is increasingly being addressed in research, but available studies are limited in their scope. In this context, our aim was to compare colorectal cancer (CRC) care pathways from screening to end-of-life care in patients with and without pre-existing SMI on a national scale.
   Methods. This research leverages real-world data from the French national health claims database, covering the entire population, to assess cancer screening, diagnosis, treatment and post-treatment follow-up as well as quality of care (QOC) pathways among patients with incident CRC in 2015-2018, considering whether they had pre-existing SMI. We matched patients with SMI with three patients without - on age, sex, region of residence, year of cancer incidence and cancer type and location at presentation - as well as nationally established quality of CRC care indicators and regression models adjusting for relevant socio-economic, clinical and care provider-related covariates.
   Results. Among patients with incident CRC, 1,532 individuals with pre-existing SMI were matched with individuals without SMI. After adjusting for covariates, both colon and rectal cancer patients with SMI were less likely to participate in the national CRC screening programme and to receive advanced diagnostic examinations (e.g., colonoscopies and several complementary diagnostic examinations). They also had lower odds of receiving combined treatments (e.g., neoadjuvant chemotherapy, radiotherapy and excision) and of having access to targeted therapy or capecitabine but higher odds for invasive care (e.g., stoma). Colon cancer patients with SMI were also more likely to have no treatment at all, and rectal cancer patients with SMI were less likely to receive post-treatment follow-up. Suboptimal QOC was observed for both groups of patients, but to a higher extent for patients with SMI, with statistically significant differences for indicators focusing on diagnosis and post-treatment follow-up.
   Conclusions. Our findings reveal discrepancies across the care continuum of CRC between individuals with and without SMI and provide initial avenues on where to focus future efforts to address them, notably at the entry and exit stages of cancer care pathways, while calling for further research on the mechanisms preventing equity of physical healthcare for individuals with SMI.
C1 [Seppaenen, A-V.; Daniel, F.; Coldefy, M.; Gandre, C.] Inst Res & Informat Hlth Econ IRDES, Inst Rech & Documentat Econ Sante, Paris, France.
   [Houzard, S.; Le Bihan, C.] French Natl Canc Inst INCa, Inst Natl Canc, Boulogne Billancourt, France.
   [Gandre, C.] Robert Debre Univ Hosp, AP HP, Paris, France.
C3 Institut National du Cancer (INCA) France; Assistance Publique Hopitaux
   Paris (APHP); Universite Paris Cite; Hopital Universitaire Robert-Debre
   - APHP
RP Seppänen, AV (corresponding author), Inst Res & Informat Hlth Econ IRDES, Inst Rech & Documentat Econ Sante, Paris, France.
EM seppanen@irdes.fr
OI Seppanen, Anna-Veera/0000-0001-5615-0639
FU French National Cancer Institute [SHSESP19-028]
FX This research was funded by the French National Cancer Institute, grant
   number SHSESP19-028.
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NR 45
TC 0
Z9 0
U1 0
U2 1
PU CAMBRIDGE UNIV PRESS
PI CAMBRIDGE
PA EDINBURGH BLDG, SHAFTESBURY RD, CB2 8RU CAMBRIDGE, ENGLAND
SN 2045-7960
EI 2045-7979
J9 EPIDEMIOL PSYCH SCI
JI Epidemiol. Psychiatr. Sci.
PD MAY 15
PY 2024
VL 33
AR e27
DI 10.1017/S2045796024000234
PG 14
WC Psychiatry
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Psychiatry
GA J6U4Y
UT WOS:001338397200001
PM 38747198
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Shen, T
   Cai, LD
   Liu, YH
   Li, S
   Gan, WJ
   Li, XM
   Wang, JR
   Guo, PD
   Zhou, Q
   Lu, XX
   Sun, LN
   Li, JM
AF Shen, Tong
   Cai, Ling-Dong
   Liu, Yu-Hong
   Li, Shi
   Gan, Wen-Juan
   Li, Xiu-Ming
   Wang, Jing-Ru
   Guo, Peng-Da
   Zhou, Qun
   Lu, Xing-Xing
   Sun, Li-Na
   Li, Jian-Ming
TI Ube2v1-mediated ubiquitination and degradation of Sirt1 promotes
   metastasis of colorectal cancer by epigenetically suppressing autophagy
SO JOURNAL OF HEMATOLOGY & ONCOLOGY
LA English
DT Article
DE Ubiquitin-conjugating E2 enzyme; Autophagy; Epithelial mesenchymal
   transition; Metastasis; Colorectal cancer
ID EPITHELIAL-MESENCHYMAL TRANSITION; HUMAN BREAST-CANCER; SELECTIVE
   AUTOPHAGY; CONJUGATING ENZYME; ACTIVATION; PROTEIN; TUMORIGENESIS;
   CELLS; KINASE; INHIBITION
AB Background: Ubiquitination is a basic post-translational modification for cellular homeostasis, and members of the conjugating enzyme (E2) family are the key components of the ubiquitin-proteasome system. However, the role of E2 family in colorectal cancer (CRC) is largely unknown. Our study aimed to investigate the role of Ube2v1, one of the ubiquitin-conjugating E2 enzyme variant proteins (Ube2v) but without the conserved cysteine residue required for the catalytic activity of E2s, in CRC.
   Methods: Immunohistochemistry and real-time RT-PCR were used to study the expressions of Ube2v1 at protein and mRNA levels in CRC, respectively. Western blotting and immunofluorescence, transmission electron microscopy, and in vivo rescue experiments were used to study the functional effects of Ube2v1 on autophagy and EMT program. Quantitative mass spectrometry, immunoprecipitation, ubiquitination assay, western blotting, and real-time RT-PCR were used to analyze the effects of Ube2v1 on histone H4 lysine 16 acetylation, interaction with Sirt1, ubiquitination of Sirt1, and autophagy-related gene expression.
   Results: Ube2v1 was elevated in CRC samples, and its increased expression was correlated with poorer survival of CRC patients. Ube2v1 promoted migration and invasion of CRC cells in vitro and tumor growth and metastasis of CRC cells in vivo. Interestingly, Ube2v1suppressed autophagy program and promoted epithelial mesenchymal transition (EMT) and metastasis of CRC cells in an autophagy-dependent pattern in vitro and in vivo. Moreover, both rapamycin and trehalose attenuated the enhanced Ube2v1-mediated lung metastasis by inducing the autophagy pathway in an orthotropic mouse xenograft model of lung metastasis. Mechanistically, Ube2v1 promoted Ubc13-mediated ubiquitination and degradation of Sirt1 and inhibited histone H4 lysine 16 acetylation, and finally epigenetically suppressed autophagy gene expression in CRC.
   Conclusions: Our study functionally links Ube2v1, an E2 member in the ubiquitin-proteasome system, to autophagy program, thereby shedding light on developing Ube2v1 targeted therapy for CRC patients.
C1 [Shen, Tong; Cai, Ling-Dong; Li, Shi; Gan, Wen-Juan; Li, Xiu-Ming; Wang, Jing-Ru; Guo, Peng-Da; Zhou, Qun; Lu, Xing-Xing; Sun, Li-Na; Li, Jian-Ming] Soochow Univ, Med Sch, Dept Pathol, Suzhou 215123, Peoples R China.
   [Liu, Yu-Hong] Southern Med Univ, Baoan Hosp, Dept Pathol, Shenzhen 518101, Peoples R China.
C3 Soochow University - China; Southern Medical University - China
RP Li, JM (corresponding author), Soochow Univ, Med Sch, Dept Pathol, Suzhou 215123, Peoples R China.
EM jianmingli@suda.edu.cn
RI wang, jing/HJA-5384-2022
FU National Nature Science Foundation of China [81525020, 81502033,
   81272300, 31570753]; Postdoctoral Science Foundation of Jiangsu Province
   [1302029B]; Science and Technology Foundation of Suzhou [SYS201412]
FX This work was supported by the National Nature Science Foundation of
   China (Grants81525020, 81502033, 81272300, and 31570753), the
   Postdoctoral Science Foundation (1302029B) of Jiangsu Province, and
   Science and Technology Foundation of Suzhou (SYS201412).
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NR 51
TC 70
Z9 74
U1 0
U2 19
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1756-8722
J9 J HEMATOL ONCOL
JI J. Hematol. Oncol.
PD JUL 17
PY 2018
VL 11
AR 95
DI 10.1186/s13045-018-0638-9
PG 16
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA GN6YE
UT WOS:000439249700001
PM 30016968
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Yang, WT
   Zou, JL
   Li, Y
   Liu, RJ
   Yan, ZQ
   Chen, SQ
   Zhao, XY
   Guo, WJ
   Huang, MZ
   Li, WH
   Zhu, XD
   Chen, ZY
AF Yang, Wentao
   Zou, Jianling
   Li, Ye
   Liu, Rujiao
   Yan, Zhengqing
   Chen, Shiqing
   Zhao, Xiaoying
   Guo, Weijian
   Huang, Mingzhu
   Li, Wenhua
   Zhu, Xiaodong
   Chen, Zhiyu
TI Longitudinal Circulating Tumor DNA Profiling in Metastatic Colorectal
   Cancer During Anti-EGFR Therapy
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colorectal cancer; next-generation sequencing; circulating tumor DNA;
   dynamic monitoring; prognosis
ID ACQUIRED-RESISTANCE; CETUXIMAB; MUTATIONS
AB BackgroundMetastatic colorectal cancer (mCRC) is a heterogenous disease with limited precision medicine and targeted therapy options. Monoclonal antibodies against epidermal growth factor receptor (EGFR) have been a crucial treatment option for mCRC. However, proper biomarkers for predicting therapeutic response remain unknown. As a non-invasive test, circulating tumor DNA (ctDNA) is appropriately positioned to reveal tumor heterogeneity and evolution, as it can be used in real-time genomic profiling. To evaluate the significance of ctDNA in monitoring the dynamic therapeutic response and prognosis of mCRC, we detected the baseline and dynamic changes of ctDNA in mCRC patients receiving anti-EGFR therapies. MethodsA single-center study was conducted retrospectively. Plasma samples from mCRC patients who received anti-EGFR therapies were collected at baseline and continuous treatment points. The ctDNA was extracted and sequenced with a target panel of tumor-related genes via next-generation sequencing (NGS). Clinical information was also collected and analyzed. ResultsWe conducted dynamic sampling of 22 mCRC patients, analyzed 130 plasma samples, obtained a baseline genomic mutation profile of the patients. In total, 54 variations were detected in 22 plasma samples, with a positive rate of 77.3% (17/22). TP53 was the most mutated gene (59.1%, 13/22), followed by APC (18.2%, 4/22). There was a high concordance rate of genomic characteristics between the tumor tissue test by polymerase chain reaction and ctDNA test by NGS. The mutation discrepancy increased with an extended course of treatment. During remission TP53 and APC were the most frequently decreased clonal mutations and KRAS, NRAS, ERBB2 and PIK3CA were the most decreased subclonal mutations. Both mutation types were increased during progression. The ctDNA decreased earlier than did the responses of computed tomography and traditional tumor markers (carbohydrate antigen 19-9 and carcinoembryonic antigen [CEA]). Lactate dehydrogenase level (P = 0.041), CEA level (P = 0.038), and primary lesion site (P = 0.038) were independent risk factors that influenced overall survival. Moreover, patients with RAS mutations tended to have a worse prognosis (P = 0.072). ConclusionsThis study demonstrates that ctDNA is a promising biomarker for monitoring the dynamic response to treatment and determining the prognosis of mCRC.
C1 [Yang, Wentao; Zou, Jianling; Liu, Rujiao; Zhao, Xiaoying; Guo, Weijian; Huang, Mingzhu; Li, Wenhua; Zhu, Xiaodong; Chen, Zhiyu] Fudan Univ, Shanghai Canc Ctr, Dept Gastrointestinal Med Oncol, Shanghai, Peoples R China.
   [Yang, Wentao; Zou, Jianling; Li, Ye; Liu, Rujiao; Zhao, Xiaoying; Guo, Weijian; Huang, Mingzhu; Li, Wenhua; Zhu, Xiaodong; Chen, Zhiyu] Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai, Peoples R China.
   [Li, Ye] Fudan Univ, Shanghai Canc Ctr, Dept Integrat Oncol, Shanghai, Peoples R China.
   [Yan, Zhengqing; Chen, Shiqing] 3D Med Inc, Dept Med, Shanghai, Peoples R China.
C3 Fudan University; Fudan University; Fudan University
RP Chen, ZY (corresponding author), Fudan Univ, Shanghai Canc Ctr, Dept Gastrointestinal Med Oncol, Shanghai, Peoples R China.; Chen, ZY (corresponding author), Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai, Peoples R China.
EM chanhj75@aliyun.com
RI Zhu, Xiao-Dong/A-8197-2010; Yang, Xueli/AAW-4792-2021; Chen,
   Wenyan/V-7000-2019
OI yang, wen tao/0009-0007-6837-1130
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NR 38
TC 8
Z9 11
U1 0
U2 5
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD FEB 24
PY 2022
VL 12
AR 830816
DI 10.3389/fonc.2022.830816
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZQ1LM
UT WOS:000766873900001
PM 35280779
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Qi, CS
   Liu, DQ
   Liu, C
   Wei, XF
   Ma, MY
   Lu, XN
   Tao, M
   Zhang, C
   Wang, XC
   He, T
   Li, J
   Dai, F
   Ding, YP
   Shen, L
AF Qi, Changsong
   Liu, Dongqun
   Liu, Chang
   Wei, Xiaofei
   Ma, Mingyang
   Lu, Xinan
   Tao, Min
   Zhang, Cheng
   Wang, Xicheng
   He, Ting
   Li, Jian
   Dai, Fei
   Ding, Yanping
   Shen, Lin
TI Antigen-independent activation is critical for the durable antitumor
   effect of GUCY2C-targeted CAR-T cells
SO JOURNAL FOR IMMUNOTHERAPY OF CANCER
LA English
DT Article
DE Colorectal Cancer; Adoptive cell therapy - ACT; Chimeric antigen
   receptor - CAR
ID GUANYLYL CYCLASE-C; RECEPTORS; REGIONS; DESIGN; MARKER; TARGET; TUMORS
AB Background Chimeric antigen receptor (CAR)-T cells face many obstacles in solid tumor therapy, including heterogeneous antigen expression and inefficient T cell persistence. Guanylyl cyclase C (GUCY2C) has been identified as a suitable tumor antigen for targeted therapy due to its intestinal-restricted expression pattern in normal tissues and steady overexpression in gastrointestinal tumors, especially colorectal cancer. An antigen-sensitive and long-lasting CAR-T cell targeting GUCY2C was investigated in this study.Methods Using constructed tumor cell lines with various GUCY2C expression densities, we screened out an antigen-sensitive single chain variable fragment (scFv) that enabled CAR-T cells to efficiently eradicate the GUCY2C lowly expressed tumor cells. CAR-T cells with different compositions of the hinge, transmembrane and costimulatory domains were also constructed for selection of the long-lasting CAR-T format with durable antitumor efficacy in vitro and in tumor-bearing mice. The underlying mechanism was further investigated based on mutation of the hinge and transmembrane domains.Results We found that the composition of the antigen-sensitive scFv, CD8 alpha hinge, CD8 alpha transmembrane, and CD28 costimulatory domains boosted CAR-T cells to rapidly kill tumors, maintain high expansion capacity, and long-term efficacy in various colorectal cancer models. The durable antitumor function was attributed to the optimal CAR tonic signaling that conferred CAR-T cells with autonomous activation, proliferation, survival and cytokine release in the absence of antigen stimulation. The tonic signaling was associated with the length and the cysteine residues in the CD8 alpha hinge and transmembrane domains.Conclusions This study demonstrated a potent GUCY2C-targeted CAR-T cell for gastrointestinal tumor therapy and highlights the importance of adequate tonic signaling for effective CAR-T cell therapy against solid tumors.
C1 [Qi, Changsong] Peking Univ, Dept Early Drug Dev Ctr, State Key Lab Holist Integrat Management Gastroint, Beijing Key Lab Carcinogenesis & Translat Res,Canc, Beijing, Peoples R China.
   [Liu, Dongqun; Wei, Xiaofei; Lu, Xinan; He, Ting; Dai, Fei; Ding, Yanping] Beijing Imunopharm Technol Co Ltd, Beijing, Peoples R China.
   [Liu, Chang] Peking Univ, Dept Early Drug Dev Ctr, Key Lab Carcinogenesis & Translat Res, Minist Educ Beijing,Canc Hosp, Beijing, Peoples R China.
   [Ma, Mingyang; Tao, Min; Wang, Xicheng] Peking Univ, Dept Gastrointestinal Oncol, Key Lab Carcinogenesis & Translat Res, Minist Educ Beijing,Canc Hosp, Beijing, Peoples R China.
   [Zhang, Cheng; Li, Jian; Shen, Lin] Peking Univ, Dept Gastrointestinal Oncol, State Key Lab Holist Integrat Management Gastroint, Beijing Key Lab Carcinogenesis & Translat Res,Canc, Beijing, Peoples R China.
C3 Peking University; Peking University; Peking University; Peking
   University
RP Qi, CS (corresponding author), Peking Univ, Dept Early Drug Dev Ctr, State Key Lab Holist Integrat Management Gastroint, Beijing Key Lab Carcinogenesis & Translat Res,Canc, Beijing, Peoples R China.; Ding, YP (corresponding author), Beijing Imunopharm Technol Co Ltd, Beijing, Peoples R China.; Shen, L (corresponding author), Peking Univ, Dept Gastrointestinal Oncol, State Key Lab Holist Integrat Management Gastroint, Beijing Key Lab Carcinogenesis & Translat Res,Canc, Beijing, Peoples R China.
EM changsongqi@bjmu.edu.cn; liudongqun@imunopharm.com; lc21715@163.com;
   weixiaofei@imunopharm.com; mamingyang.love@163.com;
   luxinan@imunopharm.com; taom@bjmu.edu.cn; qenya_z@bjmu.edu.cn;
   xicheng.wang@gmail.com; heting@imunopharm.com; oncogene@163.com;
   daifei@imunopharm.com; dingyanping@imunopharm.com; shenlin@bjmu.edu.cn
RI 齐, 长松/KHV-6581-2024; wang, xicheng/IXX-0974-2023
OI Qi, Changsong/0000-0001-9157-3768
FU Beijing Natural Science Foundation [L232080]; Open Competition to Select
   the Best Candidates" Key Technology Program for Cell Therapies of NCTIB
   [NCTIB2023XB01008]; National Key R&D Program of China, Stem Cell
   Research and Organ Repair [2022YFA1106500]; Beijing Hospitals Authority
   Youth Program [QMS20201101]; Science Foundation of Peking University
   Cancer Hospital [JC202303, JC202406]; Clinical Medicine Plus X - Young
   Scholars Project of Peking University; Peking University Clinical
   Scientist Training Program; Fundamental Research Funds for the Central
   Universities; Beijing Engineering Research Center of Research and
   Development of New Antitumor Drugs and New Technologies
FX This study was supported by Beijing Natural Science Foundation
   (L232080), "Open Competition to Select the Best Candidates" Key
   Technology Program for Cell Therapies of NCTIB (NCTIB2023XB01008),
   National Key R&D Program of China, Stem Cell Research and Organ Repair
   (2022YFA1106500), Beijing Hospitals Authority Youth Program
   (QMS20201101), Science Foundation of Peking University Cancer Hospital
   (JC202303, JC202406), Clinical Medicine Plus X - Young Scholars Project
   of Peking University, Peking University Clinical Scientist Training
   Program, the Fundamental Research Funds for the Central Universities,
   and Beijing Engineering Research Center of Research and Development of
   New Antitumor Drugs and New Technologies.
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NR 42
TC 0
Z9 0
U1 3
U2 3
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
EI 2051-1426
J9 J IMMUNOTHER CANCER
JI J. Immunother. Cancer
PD OCT 4
PY 2024
VL 12
IS 10
AR e009960
DI 10.1136/jitc-2024-009960
PG 15
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA I2J8P
UT WOS:001328580100001
PM 39366753
OA gold
DA 2025-01-04
ER

PT J
AU Marques, RP
   Heudtlass, P
   Pais, HL
   Quintela, A
   Martins, AP
AF Marques, Rui Pedro
   Heudtlass, Peter
   Pais, Helena Luna
   Quintela, Antonio
   Martins, Ana Paula
TI Patient-reported outcomes and health-related quality of life for
   cetuximab versus bevacizumab in metastatic colorectal cancer: a
   prospective cohort study
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Article
DE Patient-reported outcome measures; Quality of life; Targeted therapy;
   Cetuximab; Bevacizumab; Metastatic colorectal cancer
ID FOLFIRI PLUS BEVACIZUMAB; 1ST-LINE TREATMENT; END-POINTS; OPEN-LABEL;
   CHEMOTHERAPY; OXALIPLATIN; GUIDELINES; FOLFOXIRI; SURVIVAL; SOCIETY
AB PurposeUncertainty exists regarding Patient-Reported Outcomes (PROs) and Health-Related Quality of Life (HRQoL) of patients with metastatic colorectal cancer (mCRC) treated with cetuximab or bevacizumab. We conducted a prospective cohort study comparing PROs and HRQoL from both therapies.MethodsWe assessed PROs and HRQoL from patients treated with cetuximab or bevacizumab using QLQ-C30 and QLQ-CR29 questionnaires at three sequential time points, including baseline. Global Health Status (GHS), functional and symptom scales, and Overall Treatment Utility (derived from clinical and patient-reported outcomes) were compared for the two treatment strategies.ResultsBetween January 2017 and April 2018, 44 patients were allocated to cetuximab (n=19) or bevacizumab (n=25). Except for RAS mutation status, patient baseline characteristics were generally well balanced across treatment groups. A higher proportion of patients experienced a deterioration in GHS (10%) in cetuximab arm-53.8% (95% CI 25.1-80.8%) at 6weeks and 66.7% (95% CI 29.9-92.5%) at 12weekscomparing to bevacizumab cohort: 18.2% (95% CI 5.2-40.3%) at 6weeks and 12.5% (95% CI:1.6-38.3%) at 12weeks. Treatment utility rates at 6 and 12weeks were, respectively, 88.6% and 69.8% for bevacizumab, compared to 49% and 19.1% for cetuximab (p=0.004), a difference confirmed in subset analyses.ConclusionsIn patients with mCRC, cetuximab-containing regimens led to a progressive negative impact on PROs and global HRQoL, when compared to baseline and bevacizumab. Future research is needed to confirm these results. Our findings demonstrate the value of PROs when assessing comparative effectiveness of different treatment regimens.
C1 [Marques, Rui Pedro; Martins, Ana Paula] Univ Lisbon, Fac Pharm, Res Inst Med iMed ULisboa, Ave Prof Gama Pinto, P-1649003 Lisbon, Portugal.
   [Marques, Rui Pedro; Pais, Helena Luna; Quintela, Antonio] Ctr Hosp Univ Lisboa Norte CHULN, Hosp Santa Maria, Lisbon, Portugal.
   [Heudtlass, Peter] Portuguese Pharm Assoc ANF, Ctr Hlth Evaluat & Res CEFAR, Lisbon, Portugal.
C3 Universidade de Lisboa; Universidade de Lisboa; Hospital Santa Maria
RP Marques, RP (corresponding author), Univ Lisbon, Fac Pharm, Res Inst Med iMed ULisboa, Ave Prof Gama Pinto, P-1649003 Lisbon, Portugal.; Marques, RP (corresponding author), Ctr Hosp Univ Lisboa Norte CHULN, Hosp Santa Maria, Lisbon, Portugal.
EM rui.p.marques@chln.min-saude.pt
RI Correia, Ana/D-9049-2014
OI Marques, Rui/0000-0002-7880-4506
CR [Anonymous], QUAL LIFE RES
   [Anonymous], ANN ONCOL
   [Anonymous], EORTC QLQ C30 QUAL L
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NR 39
TC 8
Z9 8
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0171-5216
EI 1432-1335
J9 J CANCER RES CLIN
JI J. Cancer Res. Clin. Oncol.
PD JUL
PY 2019
VL 145
IS 7
BP 1719
EP 1728
DI 10.1007/s00432-019-02924-0
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ID4KN
UT WOS:000471645800005
PM 31037398
DA 2025-01-04
ER

PT J
AU Krishnamurthy, N
   Kurzrock, R
AF Krishnamurthy, Nithya
   Kurzrock, Razelle
TI Targeting the Wnt/beta-catenin pathway in cancer: Update on effectors
   and inhibitors
SO CANCER TREATMENT REVIEWS
LA English
DT Review
DE Wnt; Beta-catenin; Colorectal cancers; Gamma secretase; Hedgehog;
   Targeted therapy
ID GAMMA-SECRETASE INHIBITOR; BETA-CATENIN; MONOCLONAL-ANTIBODY;
   COLON-CANCER; STEM-CELLS; PHASE-I; SIGNALING PATHWAY; TUMOR-SUPPRESSOR;
   GASTRIC-CANCER; PDZ DOMAIN
AB The Wnt/beta-catenin pathway is a family of proteins that is implicated in many vital cellular functions such as stem cell regeneration and organogenesis. Several intra-cellular signal transduction pathways are induced by Wnt, notably the Wnt/beta-catenin dependent pathway or canonical pathway and the non canonical or beta-catenin-independent pathway; the latter includes the Wnt/Ca2+ and Planar Cell Polarity pathway (PCP). Wnt activation occurs at the intestinal crypt floor, and is critical to optimal maintenance of stem cells. Colorectal cancers show evidence of Wnt signaling pathway activation and this is associated with loss of function of the tumor regulator APC. Wnt activation has been observed in breast, lung, and hematopoietic malignancies and contributes to tumor recurrence. The Wnt pathway cross talks with the Notch and Sonic Hedgehog pathways, which has implications for therapeutic interventions in cancers. There are significant challenges in targeting the Wnt pathway, including finding agents that are efficacious without damaging the system of normal somatic stem cell function in cellular repair and tissue homeostasis. Here, we comprehensively review the Wnt pathway and its interactions with the Notch and Sonic Hedgehog pathways. We present the state of the field in effectors and inhibitors of Wnt signaling, including updates on clinical trials in various cancers with inhibitors of Wnt, Notch, and Sonic Hedgehog. (C) 2017 Elsevier Ltd. All rights reserved.
C1 [Krishnamurthy, Nithya; Kurzrock, Razelle] Univ Calif San Diego, Ctr Personalized Canc Therapy, UCSD Moores Canc Ctr, La Jolla, CA 92093 USA.
   [Kurzrock, Razelle] Univ Calif San Diego, Div Hematol Oncol, La Jolla, CA 92093 USA.
C3 University of California System; University of California San Diego;
   University of California System; University of California San Diego
RP Krishnamurthy, N (corresponding author), Univ Calif San Diego, Moores Canc Ctr, Ctr Personalized Canc Therapy, 3855 Hlth Sci Dr,MC 0658, La Jolla, CA 92093 USA.
EM nithyamurthy9@gmail.com
RI Kurzrock, Razelle/AAU-9782-2020
OI Krishnamurthy, Nithya/0009-0009-9091-1927
FU National Cancer Institute [P30 CA016672]; Joan and Irwin Jacobs Fund
   philanthropic fund
FX Funded in part by National Cancer Institute grant P30 CA016672 and the
   Joan and Irwin Jacobs Fund philanthropic fund.
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NR 100
TC 770
Z9 869
U1 17
U2 322
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0305-7372
EI 1532-1967
J9 CANCER TREAT REV
JI Cancer Treat. Rev.
PD JAN
PY 2018
VL 62
BP 50
EP 60
DI 10.1016/j.ctrv.2017.11.002
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FU7ZI
UT WOS:000424071000006
PM 29169144
OA Green Accepted, Bronze
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Yangnok, K
   Innajak, S
   Sawasjirakij, R
   Mahabusarakam, W
   Watanapokasin, R
AF Yangnok, Kanyaluck
   Innajak, Sukanda
   Sawasjirakij, Ratchawin
   Mahabusarakam, Wilawan
   Watanapokasin, Ramida
TI Effects of Artonin E on Cell Growth Inhibition and Apoptosis Induction
   in Colon Cancer LoVo and HCT116 Cells
SO MOLECULES
LA English
DT Article
DE colon cancer; artonin E; apoptosis; MAPK
ID MOLECULAR-MECHANISMS; UP-REGULATION; ACTIVATION; CETUXIMAB; DEATH; CYCLE
AB Today, colon cancer is the leading cause of cancer death. In Thailand, colon cancer is the third most common cancer in men and the second in women. Currently, the treatments for colon cancer include surgery, chemotherapy, radiation therapy, immunotherapy, hormone therapy, targeted drug therapy, and stem cell therapy. However, some treatments have side effects for cancer patients, causing unwanted symptoms. In addition, targeted therapy comes with a high cost for patients. Therefore, bioactive compounds might be a good choice for colon cancer treatment. In this study, we investigated the effect of artonin E on apoptosis induction in colon cancer LoVo and HCT116 cells. The concentration ranges of artonin E at 3, 5, 10, and 30 mu g/mL in LoVo cells and 1, 1.5, 2, and 3 mu g/mL in HCT116 cells were examined. The results implied that artonin E decreased cell viability and increased apoptotic cells in a dose-dependent manner. In addition, artonin E stimulated mitochondrial membrane potential (Delta psi m) changes associated with apoptosis by increasing the sub-G1 population analyzed by flow cytometry. Western blotting showed that artonin E increased the proapoptotic protein, Bax, and decreased anti-apoptotic proteins' (Bcl-2 and Bcl-x) expression. Moreover, artonin E also increased cleaved caspase-7 and cleaved-PARP expression in both LoVo and HCT116 cells. Interestingly, artonin E induced apoptosis through p-ERK1/2, p-p38/p38, and p-c-Jun expression in both cells. Our results suggested that artonin E induced apoptosis via caspase activation associated with the MAPKs signaling pathway. Therefore, artonin E might be used as a potential anticancer drug for colon cancer in the future.
C1 [Yangnok, Kanyaluck; Innajak, Sukanda; Watanapokasin, Ramida] Srinakharinwirot Univ, Dept Biochem, Fac Med, Bangkok 10110, Thailand.
   [Sawasjirakij, Ratchawin] Med Univ Lublin, Fac Med, Aleje Raclawickie 1, PL-20059 Lublin, Poland.
   [Mahabusarakam, Wilawan] Prince Songkla Univ, Dept Chem, Fac Sci, Hat Yai 90112, Thailand.
C3 Srinakharinwirot University; Medical University of Lublin; Prince of
   Songkla University
RP Watanapokasin, R (corresponding author), Srinakharinwirot Univ, Dept Biochem, Fac Med, Bangkok 10110, Thailand.
EM kanyaluck.yangnok@g.swu.ac.th; suinnajak@gmail.com; tigatrbl@gmail.com;
   wilawan.m@psu.ac.th; ramidabc@gmail.com
OI Watanapokasin, Ramida/0000-0001-8333-3238
FU Research Division, Faculty of Medicine, Srinakharinwirot University,
   Thailand [391/2563]
FX This research was funded by the Research Division, Faculty of Medicine,
   Srinakharinwirot University, Thailand. Grant number 391/2563.
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PD APR
PY 2022
VL 27
IS 7
AR 2095
DI 10.3390/molecules27072095
PG 11
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 0M3TP
UT WOS:000782081100001
PM 35408492
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Lapeyre-Prost, A
   Pernot, S
   Sigrand, J
   Le Malicot, K
   Mary, F
   Aparicio, T
   Dahan, L
   Caroli-Bosc, FX
   Lecomte, T
   Doat, S
   Marthey, L
   Desrame, J
   Lepage, C
   Taieb, J
AF Lapeyre-Prost, Alexandra
   Pernot, Simon
   Sigrand, Julie
   Le Malicot, Karine
   Mary, Florence
   Aparicio, Thomas
   Dahan, Laetitia
   Caroli-Bosc, Francois-Xavier
   Lecomte, Thierry
   Doat, Solene
   Marthey, Lysianne
   Desrame, Jerome
   Lepage, Come
   Taieb, Julien
TI Aflibercept in Combination With FOLFIRI as First-line Chemotherapy in
   Patients With Metastatic Colorectal Cancer (mCRC): A Phase II Study
   (FFCD 1302)
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE Antiangiogenic therapy; Antineoplasic drug; Colon cancer; Metastases;
   Targeted therapy
ID PLUS BEVACIZUMAB; OPEN-LABEL; OXALIPLATIN; FLUOROURACIL; LEUCOVORIN;
   THERAPY; MULTICENTER; IRINOTECAN; SURVIVAL; PLACEBO
AB Chemotherapy with FOLFIRI (irinotecan, 5-fluorouracil, and leucovorin) + aflibercept improves survival in patients with previously treated metastatic colorectal cancer (mCRC). Our phase II study evaluated efficacy and tolerability of this treatment in non-pretreated patients with mCRC. Though the primary endpoint was not met, results showed that first line FOLFIRI + aflibercept for mCRC leads to survival close to those reported with standard first-line treatments, but with significant toxicities.
   Background: FOLFIRI (irinotecan, 5-fluorouracil, and leucovorin) + aflibercept improves median overall survival (OS) and progression-free survival (PFS) in patients with previously treated metastatic colorectal cancer (mCRC). Our aim was to investigate efficacy and tolerability of this combination in the first line. Patients and Methods: Patients with untreated documented mCRC received aflibercept plus FOLFIRI every 14 days until progression or unacceptable toxicity in an open, phase II single-arm, multicenter trial. The primary endpoint was the 6-month PFS rate. Secondary endpoints were OS and tolerability. A 2-step Simon design was used with H-0: 55% and H-1 = 75%. Data were analyzed in intention to treat. Results: Forty-one patients were included, and 40 were analyzed (1 consent withdrawal) in 9 French centers between October 2014 and February 2017. The median age was 65 years (range, 46-81 years), 55% had > 2 metastatic sites, and 50% and 15% had RAS and BRAF mutations, respectively. Twenty-two (54.5%; 95% confidence interval, 38.9%-68.5%) patients were alive and non-progressive at 6 months. FOLFIRI + aflibercept was considered ineffective, resulting in the cessation of inclusions. The median follow-up was 34 months. The overall response rate was 55%, and the disease control rate was 80%. The median duration of treatment was 5.3 months; the median PFS and OS were 8.2 and 18.6 months, respectively. Grade 3 to 4 adverse events were mainly gastrointestinal (47.5%) and vascular (32.5%). Of the patients, 87.5% had at least 1 dose modification. Conclusion: Although the primary objective was not met, first-line FOLFIRI + aflibercept for mCRC leads to median PFS and OS close to those reported with classical doublet and targeted agents, but with significant toxicities needing dose reduction. (C) 2020 Published by Elsevier Inc.
C1 [Lapeyre-Prost, Alexandra; Pernot, Simon; Taieb, Julien] Hop European George Pompidou, Dept Gastroenterol & Digest Oncol, Paris, France.
   [Sigrand, Julie; Dahan, Laetitia] CHU La Timone, HepatoGastroenterol & Digest Oncol Dept, Marseille, France.
   [Le Malicot, Karine] Univ Burgundy & Franche Comte, FFCD, Biostat, EPICAD INSERM LNC UMR1231, Dijon, France.
   [Mary, Florence; Aparicio, Thomas] Avicenne Hosp, HepatoGastroenterol Dept, Bobigny, France.
   [Aparicio, Thomas] St Louis Hosp, HepatoGastroenterol Dept, Paris, France.
   [Caroli-Bosc, Francois-Xavier] CHU Angers, Gastroenterol Dept, Angers, France.
   [Lecomte, Thierry] Trousseau Hosp, HepatoGastroenterol Dept, Tours, France.
   [Doat, Solene] Hop La Pitie Salpetriere, HepatoGastroenterol Dept, Paris, France.
   [Marthey, Lysianne] Bicetre Hosp, HepatoGastroenterol Dept, Paris, France.
   [Desrame, Jerome] Jean Mermoz Private Hosp, Cancerol Inst, Lyon, France.
   [Lepage, Come] Univ Burgundy & Franche Comte, Univ Hosp Dijon, HepatoGastroenterol & Digest Oncol Dept, FFCD,EPICAD INSERM LNC UMR 1231, Dijon, France.
C3 Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Europeen Georges-Pompidou - APHP; Aix-Marseille
   Universite; Assistance Publique-Hopitaux de Marseille; Institut Agro;
   AgroSup Dijon; Universite de Bourgogne; Assistance Publique Hopitaux
   Paris (APHP); Hopital Universitaire Avicenne - APHP; Assistance Publique
   Hopitaux Paris (APHP); Universite Paris Cite; Hopital Universitaire
   Saint-Louis - APHP; Universite d'Angers; Centre Hospitalier
   Universitaire d'Angers; CHU Tours; Sorbonne Universite; Assistance
   Publique Hopitaux Paris (APHP); Hopital Universitaire Pitie-Salpetriere
   - APHP; Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
   Bicetre - APHP; CHU Dijon Bourgogne; Universite de Bourgogne; Institut
   National de la Sante et de la Recherche Medicale (Inserm); Institut
   Agro; AgroSup Dijon
RP Taieb, J (corresponding author), Hop Europeen Georges Pompidou, Dept Hepatogastroenterol & Gastrointestinal Oncol, 20 Rue Leblanc, F-75015 Paris, France.
EM jtaieb75@gmail.com
RI Dahan, Laetitia/M-3441-2016
OI taieb, julien/0000-0002-9955-4753; LECOMTE, Thierry/0000-0001-5093-0212;
   Le Malicot, Karine/0000-0002-3226-8525
CR Aparicio T, 2018, J CLIN ONCOL, V36, P674, DOI 10.1200/JCO.2017.75.2931
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NR 18
TC 5
Z9 5
U1 0
U2 0
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1533-0028
EI 1938-0674
J9 CLIN COLORECTAL CANC
JI Clin. Colorectal Canc.
PD DEC
PY 2020
VL 19
IS 4
BP 285
EP 290
DI 10.1016/j.clcc.2020.06.003
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OW6AP
UT WOS:000592967200026
PM 32921581
DA 2025-01-04
ER

PT J
AU Buza, N
AF Buza, Natalia
TI Immunohistochemistry in gynecologic carcinomas: Practical update with
   diagnostic and clinical considerations based on the 2020 WHO
   classification of tumors
SO SEMINARS IN DIAGNOSTIC PATHOLOGY
LA English
DT Review
DE Immunohistochemistry; Cervical carcinoma; Endometrial carcinoma; Ovarian
   carcinoma; Mismatch repair proteins; HER2; PD-L1
ID CLEAR-CELL CARCINOMA; VULVAR INTRAEPITHELIAL NEOPLASIA; MISMATCH REPAIR
   DEFICIENCY; OVARIAN ENDOMETRIOID CARCINOMA; NONPOLYPOSIS
   COLORECTAL-CANCER; HUMAN-PAPILLOMAVIRUS INFECTION; UTERINE SEROUS
   CARCINOMAS; IN-SITU-HYBRIDIZATION; LYNCH-SYNDROME; MICROSATELLITE
   INSTABILITY
AB This review provides an update on immunohistochemistry applications-diagnostic, prognostic, and predictive-in the pathology evaluation of gynecologic carcinomas. The 5th edition of the WHO Classification of Female Genital Tumors introduced important changes in the diagnostic classification of lower genital tract, endometrial, and ovarian carcinomas, with major influence on the routine pathology practice. Lower genital tract carcinomas and their precursor lesions are now classified based on their human papillomavirus (HPV)-associated and HPVindependent pathogenesis, reflecting the clinically significant prognostic differences and impacting the therapeutic decision-making. Immunohistochemical markers have an increasing role in the pathology evaluation of endometrial carcinomas: in addition to their traditional use in the differential diagnosis and histologic subtyping, they have also been recently advocated for prognostic classification as surrogates for the TCGA (The Cancer Genome Atlas) molecular groups. New entities - mesonephric-like adenocarcinoma and gastric (gastrointestinal)type mucinous adenocarcinoma of the endometrium - have also been added and often require immunostains for diagnostic confirmation. Ovarian carcinomas frequently show overlapping morphologic patterns and heterogeneous appearance within the same tumor, necessitating immunohistochemical work-up. Beyond diagnostic applications, there is increasing clinical demand for screening of inherited cancer syndromes, prediction of prognosis and guiding targeted therapy. Practical issues and pitfalls related to mismatch repair protein immunohistochemistry, HER2, and PD-L1 testing are also discussed.
C1 [Buza, Natalia] Yale Univ, Dept Pathol, Sch Med, New Haven, CT 06520 USA.
C3 Yale University
RP Buza, N (corresponding author), Yale Univ, Pathol, Sch Med, 310 Cedar St LH 108,POB 208023, New Haven, CT 06520 USA.
EM natalia.buza@yale.edu
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NR 210
TC 13
Z9 13
U1 1
U2 26
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0740-2570
EI 1930-1111
J9 SEMIN DIAGN PATHOL
JI Semin. Diagn. Pathol.
PD JAN
PY 2022
VL 39
IS 1
BP 58
EP 77
DI 10.1053/j.semdp.2021.10.006
EA DEC 2021
PG 20
WC Medical Laboratory Technology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology; Pathology
GA XT2OQ
UT WOS:000733433900001
PM 34750021
DA 2025-01-04
ER

PT J
AU Ala, M
AF Ala, Moein
TI Tryptophan metabolites modulate inflammatory bowel disease and
   colorectal cancer by affecting immune system
SO INTERNATIONAL REVIEWS OF IMMUNOLOGY
LA English
DT Review
DE Colorectal cancer; IBD; indole; kynurenine; serotonin; tryptophan
ID ARYL-HYDROCARBON RECEPTOR; SULFATE-INDUCED COLITIS; INDOLEAMINE
   2,3-DIOXYGENASE EXPRESSION; KYNURENINE PATHWAY METABOLISM; SULFONIC-ACID
   COLITIS; GUT MICROBIOTA; DENDRITIC CELLS; CROHNS-DISEASE;
   ESCHERICHIA-COLI; INTERFERON-GAMMA
AB Tryptophan is an essential amino acid, going through three different metabolic pathways in the intestines. Indole pathway in the gut microbiota, serotonin system in the enterochromaffin cells and kynurenine pathway in the immune cells and intestinal lining are the three arms of tryptophan metabolism in the intestines. Clinical, in vivo and in vitro studies showed that each one of these arms has a significant impact on IBD. This review explains how different metabolites of tryptophan are involved in the pathophysiology of IBD and colorectal cancer, as a major complication of IBD. Indole metabolites alleviate colitis and protect against colorectal cancer while serotonin arm follows a more complicated and receptor-specific pattern. Indole metabolites and kynurenine interact with aryl hydrocarbon receptor (AHR) to induce T regulatory cells differentiation, confine Th17 and Th1 response and produce anti-inflammatory mediators. Kynurenine decreases tumor-infiltrating CD8+ cells and mediates tumor cells immune evasion. Serotonin system also increases colorectal cancer cells proliferation and metastasis while, indole metabolites can profoundly decrease colorectal cancer growth. Targeted therapy for tryptophan metabolites may improve the management of IBD and colorectal cancer, e.g. supplementation of indole metabolites such as indole-3-carbinol (I3C), inhibition of kynurenine monooxygenase (KMO) and selective stimulation or inhibition of specific serotonergic receptors can mitigate colitis. Furthermore, it will be explained how indole metabolites supplementation, inhibition of indoleamine 2,3-dioxygenase 1 (IDO1), KMO and serotonin receptors can protect against colorectal cancer. Additionally, extensive molecular interactions between tryptophan metabolites and intracellular signaling pathways will be thoroughly discussed.
C1 [Ala, Moein] Univ Tehran Med Sci, Sch Med, Tehran 1416753955, Iran.
C3 Tehran University of Medical Sciences
RP Ala, M (corresponding author), Univ Tehran Med Sci, Sch Med, Tehran 1416753955, Iran.
EM moinala75@yahoo.com
RI Ala, Moein/AAD-5514-2021
OI Ala, Moein/0000-0001-5951-4864
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NR 184
TC 68
Z9 73
U1 5
U2 76
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 0883-0185
EI 1563-5244
J9 INT REV IMMUNOL
JI Int. Rev. Immunol.
PD MAY 4
PY 2022
VL 41
IS 3
BP 326
EP 345
DI 10.1080/08830185.2021.1954638
EA JUL 2021
PG 20
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 1N1BY
UT WOS:000675698200001
PM 34289794
DA 2025-01-04
ER

PT J
AU Chetta, M
   Basile, A
   Tarsitano, M
   Rivieccio, M
   Oro, M
   Capitanio, N
   Bukvic, N
   Priolo, M
   Rosati, A
AF Chetta, Massimiliano
   Basile, Anna
   Tarsitano, Marina
   Rivieccio, Maria
   Oro, Maria
   Capitanio, Nazzareno
   Bukvic, Nenad
   Priolo, Manuela
   Rosati, Alessandra
TI The Target Therapy Hyperbole: "KRAS (p.G12C)"-The Simplification of a
   Complex Biological Problem
SO CANCERS
LA English
DT Article
DE KRAS isoforms (KRAS4A; KRAS4B); sotorasib (AMG 510); p.G12C mutation
ID COVALENT INHIBITOR; SOTORASIB; CANCER
AB Simple Summary: KRAS mutations have critical roles in the etiology of cancers such as NSCLC, CRC, and PDAC. However, therapeutic targeting of KRAS has proven difficult due to the lack of typical drug-binding sites. Recent improvements have seen the emergence of inhibitors specially tailored for the p.G12C mutation, with Sotorasib showing promising results in NSCLC. Nonetheless, the CodeBreaK 200 study found no significant difference in overall survival between Docetaxel and Sotorasib. This study compares the structural configurations of KRAS isoforms KRAS4A and KRAS4B and analyzes the effects of mutations on drug binding. The present study reveals unique aggregation propensities in wild-type and mutant isoforms, highlighting the complexities of KRAS as a therapeutic target. Sotorasib's stable structure may allow for more effective binding to KRAS4B, despite the steric constraints imposed by KRAS4A and its mutations. This emphasizes the necessity for additional research into the complicated dynamics of KRAS targeting in cancer therapy. Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS) gene variations are linked to the development of numerous cancers, including non-small cell lung cancer (NSCLC), colorectal cancer (CRC), and pancreatic ductal adenocarcinoma (PDAC). The lack of typical drug-binding sites has long hampered the discovery of therapeutic drugs targeting KRAS. Since "CodeBreaK 100" demonstrated Sotorasib's early safety and efficacy and led to its approval, especially in the treatment of non-small cell lung cancer (NSCLC), the subsequent identification of specific inhibitors for the p.G12C mutation has offered hope. However, the CodeBreaK 200 study found no significant difference in overall survival (OS) between patients treated with Docetaxel and Sotorasib (AMG 510), adding another degree of complexity to this ongoing challenge. The current study compares the three-dimensional structures of the two major KRAS isoforms, KRAS4A and KRAS4B. It also investigates the probable structural changes caused by the three major mutations (p.G12C, p.G12D, and p.G12V) within Sotorasib's pocket domain. The computational analysis demonstrates that the wild-type and mutant isoforms have distinct aggregation propensities, resulting in the creation of alternate oligomeric configurations. This study highlights the increased complexity of the biological issue of using KRAS as a therapeutic target. The present study stresses the need for a better understanding of the structural dynamics of KRAS and its mutations to design more effective therapeutic approaches. It also emphasizes the potential of computational approaches to shed light on the complicated molecular pathways that drive KRAS-mediated oncogenesis. This study adds to the ongoing efforts to address the therapeutic hurdles presented by KRAS in cancer treatment.
C1 [Chetta, Massimiliano; Tarsitano, Marina; Rivieccio, Maria; Oro, Maria; Priolo, Manuela] AORN Cardarelli, UOC Med & Lab Genet, I-80131 Naples, Italy.
   [Basile, Anna; Rosati, Alessandra] Univ Salerno, Dept Med Surg & Dent Schola Med Salernitana, StressBioLab, I-84081 Baronissi, Italy.
   [Capitanio, Nazzareno] Univ Foggia, Dept Clin & Expt Med, I-71121 Foggia, Italy.
   [Bukvic, Nenad] Univ Hosp Consortium Corp Polyclin Bari, Med Genet Sect, I-70124 Bari, Italy.
C3 University of Salerno; University of Foggia
RP Chetta, M (corresponding author), AORN Cardarelli, UOC Med & Lab Genet, I-80131 Naples, Italy.
EM massimiliano.chetta@aocardarelli.it; abasile@unisa.it;
   marina.tarsitano@aocardarelli.it; riviecciomaria@gmail.com;
   mar.oro94@libero.it; nazzareno.capitanio@unifg.it;
   nenad.bukvic@policlinico.ba.it; manuela.priolo@aocardarelli.it;
   arosati@unisa.it
RI Bukvic, Nenad/ABH-7268-2020; CAPITANIO, NAZZARENO/K-5454-2016
OI Bukvic, MD, PhD, Nenad/0000-0002-9235-8987; CAPITANIO,
   NAZZARENO/0000-0001-9285-051X; Rosati, Alessandra/0000-0001-6675-0857
FU Regione Campania, POR CAMPANIA FESR
FX This study was supported in part by Regione Campania, POR CAMPANIA FESR
   2014-2020 "System Innovation for Cancer Early Diagnosis-SICED".
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NR 30
TC 0
Z9 0
U1 2
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUL
PY 2024
VL 16
IS 13
AR 2389
DI 10.3390/cancers16132389
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YR9I5
UT WOS:001270323300001
PM 39001451
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhou, DD
   Liu, XF
   Lu, CW
   Pant, OP
   Liu, XD
AF Zhou, Dan-Dan
   Liu, Xiu-fen
   Lu, Cheng-wei
   Pant, Om Prakash
   Liu, Xiao-dong
TI Long non-coding RNA PVT1: Emerging biomarker in digestive system cancer
SO CELL PROLIFERATION
LA English
DT Review
ID COLORECTAL-CANCER; POOR-PROGNOSIS; GASTRIC-CANCER; INCREASED EXPRESSION;
   TUMOR-SUPPRESSOR; CELLS PROMOTES; SERUM MARKERS; LNCRNA PVT1; C-MYC;
   TRANSLOCATIONS
AB The digestive system cancers are leading cause of cancer-related death worldwide, and have high risks of morbidity and mortality. More and more long non-coding RNAs (lncRNAs) have been studied to be abnormally expressed in cancers and play a key role in the process of digestive system tumour progression. Plasmacytoma variant translocation 1 (PVT1) seems fairly novel. Since 1984, PVT1 was identified to be an activator of MYC in mice. Its role in human tumour initiation and progression has long been a subject of interest. The expression of PVT1 is elevated in digestive system cancers and correlates with poor prognosis. In this review, we illustrate the various functions of PVT1 during the different stages in the complex process of digestive system tumours (including oesophageal cancer, gastric cancer, colorectal cancer, hepatocellular carcinoma and pancreatic cancer). The growing evidence shows the involvement of PVT1 in both proliferation and differentiation process in addition to its involvement in epithelial to mesenchymal transition (EMT). These findings lead us to conclude that PVT1 promotes proliferation, survival, invasion, metastasis and drug resistance in digestive system cancer cells. We will also discuss PVT1's potential in diagnosis and treatment target of digestive system cancer. There was a great probability PVT1 could be a novel biomarker in screening tumours, prognosis biomarkers and future targeted therapy to improve the survival rate in cancer patients.
C1 [Zhou, Dan-Dan; Liu, Xiao-dong] Jilin Univ, Sch Publ Hlth, Minist Hlth, Key Lab Radiobiol, Changchun, Jilin, Peoples R China.
   [Zhou, Dan-Dan] Jilin Univ, Hosp 1, Dept Radiol, Changchun, Jilin, Peoples R China.
   [Liu, Xiu-fen; Lu, Cheng-wei; Pant, Om Prakash] Jilin Univ, Hosp 1, Dept Ophthalmol, Changchun, Jilin, Peoples R China.
C3 Jilin University; Jilin University; Jilin University
RP Liu, XD (corresponding author), Jilin Univ, Sch Publ Hlth, Minist Hlth, Key Lab Radiobiol, Changchun, Jilin, Peoples R China.; Lu, CW (corresponding author), Jilin Univ, Hosp 1, Dept Ophthalmol, Changchun, Jilin, Peoples R China.
EM lcwchina800@sina.com; doriszhoudan0928@sina.com
RI Liu, Xiaodong/R-5861-2019
OI Pant, Om Prakash/0000-0002-2966-4383; Liu, Xiaodong/0000-0002-6879-990X
FU First Hospital of Jilin University Grant [JDYY72016055]
FX This work was supported by grants from The First Hospital of Jilin
   University Grant (grant number JDYY72016055).
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PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0960-7722
EI 1365-2184
J9 CELL PROLIFERAT
JI Cell Prolif.
PD DEC
PY 2017
VL 50
IS 6
AR e12398
DI 10.1111/cpr.12398
PG 6
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA FM0IV
UT WOS:000414647400021
PM 29027279
OA Bronze, Green Published
DA 2025-01-04
ER

PT J
AU Li, MJ
   Yu, TH
   Hu, YF
AF Li, Meijuan
   Yu, Tinghui
   Hu, Yun-Fu
TI The impact of companion diagnostic device measurement performance on
   clinical validation of personalized medicine
SO STATISTICS IN MEDICINE
LA English
DT Article
DE biomarker; companion diagnostic device; analytical accuracy;
   imprecision; positive and negative percentage agreements; positive and
   negative predictive values; clinical validation trial
ID PREDICTIVE BIOMARKER VALIDATION; ALZHEIMERS-DISEASE; APOLIPOPROTEIN-E;
   TRIAL DESIGNS
AB A key component of personalized medicine is companion diagnostics that measure biomarkers, for example,protein expression, gene amplification or specific mutations. Most of the recent attention concerning molecular cancer diagnostics has been focused on the biomarkers of response to therapy, such as V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations in metastatic colorectal cancer, epidermal growth factor receptor mutations in metastatic malignant melanoma. The presence or absence of these markers is directly linked to the response rates of particular targeted therapies with small-molecule kinase inhibitors or antibodies. Therefore, testing for these markers has become a critical step in the target therapy of the aforementioned tumors. The core capability of personalized medicine is the companion diagnostic devices' (CDx) ability to accurately and precisely stratify patients by their likelihood of benefit (or harm) from a particular therapy. There is no reference in the literature discussing the impact of device's measurement performance, for example,analytical accuracy and precision on treatment effects, variances, and sample sizes of clinical trial for the personalized medicine. In this paper, using both analytical and estimation method, we assessed the impact of CDx measurement performance as a function of positive and negative predictive values and imprecision (standard deviation) on treatment effects, variances of clinical outcome, and sample sizes for the clinical trials. Copyright (c) 2015 John Wiley & Sons, Ltd.
C1 [Li, Meijuan; Yu, Tinghui] US FDA, Div Biostat, Off Surveillance & Biometr, Ctr Devices & Radiol Hlth, Silver Spring, MD 20993 USA.
   [Hu, Yun-Fu] US FDA, Div Mol Genet & Pathol, Off Vitro Diagnost & Radiol Hlth, Ctr Devices & Radiol Hlth, Silver Spring, MD 20993 USA.
C3 US Food & Drug Administration (FDA); US Food & Drug Administration (FDA)
RP Li, MJ (corresponding author), US FDA, Div Biostat, Off Surveillance & Biometr, Ctr Devices & Radiol Hlth, 10903 New Hampshire Ave, Silver Spring, MD 20993 USA.
EM meijuan.li@fda.hhs.gov
CR [Anonymous], 2014, US FOOD DRUG ADM IN
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NR 13
TC 11
Z9 12
U1 1
U2 17
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
EI 1097-0258
J9 STAT MED
JI Stat. Med.
PD JUN 30
PY 2015
VL 34
IS 14
BP 2222
EP 2234
DI 10.1002/sim.6476
PG 13
WC Mathematical & Computational Biology; Public, Environmental &
   Occupational Health; Medical Informatics; Medicine, Research &
   Experimental; Statistics & Probability
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Mathematical & Computational Biology; Public, Environmental &
   Occupational Health; Medical Informatics; Research & Experimental
   Medicine; Mathematics
GA CJ7JY
UT WOS:000355672400007
PM 25779099
DA 2025-01-04
ER

PT J
AU Feng, Y
   Gao, SH
   Gao, YJ
   Song, DF
   Wang, XF
   Chen, Z
AF Feng, Ye
   Gao, Shuohui
   Gao, Yongjian
   Song, Defeng
   Wang, Xuefeng
   Chen, Zhi
TI Runx3 expression in rectal cancer cells and its effect on cell invasion
   and proliferation
SO ONCOLOGY LETTERS
LA English
DT Article
DE rectal cancer; Runx3; HRC-9698 cell strain; proliferation; invasion
ID OUTCOMES
AB Effect of Runx3 gene on the cell proliferation and invasion of rectal cancer was investigated to explore potential new targets for targeted treatment of rectal cancer. The Runx3 overexpression group (OE group), blank plasmid control group, negative control and blank group of the rectal cancer HRC-9698 cell strain were set. The overexpressed Runx3 plasmid was transfected in OE group; the empty plasmid was transfected in blank plasmid control group; only liposome Lipofectamine was added to negative control group; only 1640 medium was used in blank group. RT-qPCR was used for detection of the mRNA expression of Runx3 in different groups; CCK-8 kit for detection of cell proliferation in different groups; Transwell chamber test for detection of cell strain invasion in different groups. The mRNA expression of Runx3 gene in OE group was the highest, significantly higher than that in blank plasmid control group, negative control and blank group (P<0.01). The OD values of overexpressed Runx3 at 96 h after transfection in OE group was significantly lower than each control group (P<0.01). At the same time-point, pairwise comparison in each group found that OE group was significantly lower than blank plasmid control, negative control and blank groups (all P<0.01). In the invasion experiment, the number of invasion cells in OE, blank plasmid control, negative control and blank groups were 38.63 +/- 9.33, 107.87 +/- 5.66, 110.93 +/- 4.33 and 112.86 +/- 6.66, respectively. OE group was significantly lower than each control group (P<0.01). Overexpression of Runx3 gene in vitro inhibits the cell proliferation of rectal cancer and blocks the cell invasion and metastasis. This study provides a new idea and a new molecular therapeutic target for molecular targeted therapy of rectal cancer.
C1 [Feng, Ye; Gao, Shuohui; Gao, Yongjian; Song, Defeng; Wang, Xuefeng] Jilin Univ, China Japan Union Hosp, Dept Gastrointestinal Colorectal & Anal Surg, Changchun 130033, Jilin, Peoples R China.
   [Chen, Zhi] Jilin Univ, Bethune Hosp 1, Dept Nephrol, 71 Xinmin Ave, Changchun 130021, Jilin, Peoples R China.
C3 Jilin University; Jilin University
RP Chen, Z (corresponding author), Jilin Univ, Bethune Hosp 1, Dept Nephrol, 71 Xinmin Ave, Changchun 130021, Jilin, Peoples R China.
EM crt2uq@163.com
RI feng, ye/JMP-7925-2023
FU Jilin Province High Technology Industrialization Program [2014Y083];
   Jilin Provincial Science and Technology Development Program
   [20140204028XY]; Jilin Provincial Direct Health Special Program (2016,
   2017); Jilin Natural Science Foundation Program [20160101115JC]; Jilin
   Provincial Youth Science Technology Innovation Leader and Team Program
   [20180519025JH]
FX This study was supported by Jilin Province High Technology
   Industrialization Program (2014Y083), Jilin Provincial Science and
   Technology Development Program (20140204028XY), Jilin Provincial Direct
   Health Special Program (2016, 2017), Jilin Natural Science Foundation
   Program (20160101115JC) and Jilin Provincial Youth Science Technology
   Innovation Leader and Team Program (20180519025JH).
CR Acuna SA, 2017, JAMA SURG, V152, P986, DOI 10.1001/jamasurg.2017.1724
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NR 23
TC 6
Z9 7
U1 0
U2 3
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD SEP
PY 2019
VL 18
IS 3
BP 3290
EP 3294
DI 10.3892/ol.2019.10654
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JA2UX
UT WOS:000487675500136
PM 31452807
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Smagulova, KK
   Kaidarova, DR
   Chingissova, ZK
   Nasrytdinov, TS
   Khozhayev, AA
AF Smagulova, Kaldygul K.
   Kaidarova, Dilyara R.
   Chingissova, Zhanna K.
   Nasrytdinov, Timur S.
   Khozhayev, Arman A.
TI Effects of metastatic CRC predictors on treatment outcomes
SO SURGICAL ONCOLOGY-OXFORD
LA English
DT Article
DE ?olorectal ?ancer; Metastases; Predictors; Genetic factors; Targeted
   therapy; Efficacy
ID COLORECTAL-CANCER
AB Background: Colorectal cancer (CRC) is the third most commonly diagnosed malignant tumor. The problem of mCRC is urgent due to both an increase in the number of metastatic tumors and the implementation of high-tech treatment methods that have significantly improved the results of a 5-year survival.Methods: The research used the method of experiment and observation. Current study included data of 332 patients with CRC who received comprehensive treatment from 2014 to 2018 in oncology centers of the Republic of Kazakhstan. The patients were treated according to the clinical protocols for the treatment of oncological diseases approved in the Republic of Kazakhstan, including surgical treatment, as well as chemotherapy and radiation therapy, depending on the stage and localization of the process. A comprehensive treatment also included surgical treatment, chemotherapy, targeted chemotherapy and, in some cases, radiation therapy for rectal cancer. The diagnosis was confirmed morphologically in all patients; process dissemination was recorded using standard examination methods. Among the patients, women prevailed - 182 (54.8%) women and 150 men (45.2%) were included; the Caucasian race prevailed - 170 (51.2%) patients and 162 (48.8%) patients were of the Asian race. The mean age of the patients at the time of treatment was 56.4 +/- 0.6 years (from 25 to 79 years). Histologically, adenocarcinoma prevailed represented by glandular - in 95.6%, mucous - in 2.9% and trabecular - in 1.5% of cases. A comprehensive treatment was used in 209 (63.0%) patients and other types of treatment were used in 123 (37.0%) patients (PCT, stoma + PCT). Radiation therapy was administered to 13 (3.9%) patients diagnosed with rectal cancer.Results: A comparative analysis of the results of pharmacotherapy in the patients with mCRC showed that of 332 patients, 263 (79.2%) received targeted chemotherapy and 69 (20.8%) received standard polychemotherapy. At the time of the study, 85 (32.3%) patients in the targeted chemotherapy group were still alive, with a median survival of 42.0 +/- 1.7 months, 95% CI (38.6-45.4). In the polychemotherapy group, 7 (10.1%) patients were alive, while the median survival rate was 20.0 +/- 1.7 months, 95% CI (16.6-23.4). Conclusion: Based on the results, it was concluded that targeted chemotherapy schemes increased progressionfree survival, compared to standard polychemotherapy schemes.
C1 [Smagulova, Kaldygul K.] Kazakh Inst Oncol & Radiol, Dept Chemotherapy, Alma Ata, Kazakhstan.
   [Smagulova, Kaldygul K.; Chingissova, Zhanna K.] Kazakh Med Univ Continuing Educ, Dept Oncol Course Hematol, Alma Ata, Kazakhstan.
   [Kaidarova, Dilyara R.] Kazakh Inst Oncol & Radiol, Dept Adm, Alma Ata, Kazakhstan.
   [Chingissova, Zhanna K.] Kazakh Inst Oncol & Radiol, Consultat & Diagnost Ctr, Alma Ata, Kazakhstan.
   [Nasrytdinov, Timur S.] Kazakh Inst Oncol & Radiol, Operating Theatre, Alma Ata, Kazakhstan.
   [Nasrytdinov, Timur S.; Khozhayev, Arman A.] SD Asfendiyarov Kazakh Natl Med Univ, Dept Oncol, Alma Ata, Kazakhstan.
C3 Kazakh Institute of Oncology & Radiology; Kazakh Institute of Oncology &
   Radiology; Kazakh Institute of Oncology & Radiology; Kazakh Institute of
   Oncology & Radiology; Asfendiyarov Kazakh National Medical University
RP Nasrytdinov, TS (corresponding author), Kazakh Inst Oncol & Radiol, Operating Theatre, Alma Ata, Kazakhstan.
EM nasrytdinov5981@kpi.com.de
RI Khozhayev, Arman/AAC-7566-2022; Kaidarova, Dilyara/CAG-0403-2022
CR Australian Institute of Health and Welfare, 2017, NAT DRUG STRAT HOUS, V101
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NR 19
TC 2
Z9 2
U1 0
U2 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0960-7404
EI 1879-3320
J9 SURG ONCOL
JI Surg. Oncol.-Oxf.
PD SEP
PY 2022
VL 44
AR 101835
DI 10.1016/j.suronc.2022.101835
EA AUG 2022
PG 5
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA 4E8XU
UT WOS:000848104000002
PM 36027665
DA 2025-01-04
ER

PT J
AU Richman, SD
   Southward, K
   Chambers, P
   Cross, D
   Barrett, J
   Hemmings, G
   Taylor, M
   Wood, H
   Hutchins, G
   Foster, JM
   Oumie, A
   Spink, KG
   Brown, SR
   Jones, M
   Kerr, D
   Handley, K
   Gray, R
   Seymour, M
   Quirke, P
AF Richman, Susan D.
   Southward, Katie
   Chambers, Philip
   Cross, Debra
   Barrett, Jennifer
   Hemmings, Gemma
   Taylor, Morag
   Wood, Henry
   Hutchins, Gordon
   Foster, Joseph M.
   Oumie, Assa
   Spink, Karen G.
   Brown, Sarah R.
   Jones, Marc
   Kerr, David
   Handley, Kelly
   Gray, Richard
   Seymour, Matthew
   Quirke, Philip
TI HER2 overexpression and amplification as a potential therapeutic target
   in colorectal cancer: analysis of 3256 patients enrolled in the QUASAR,
   FOCUS and PICCOLO colorectal cancer trials
SO JOURNAL OF PATHOLOGY
LA English
DT Article
DE HER2; colorectal cancer; amplification; overexpression; copy number
   variation
ID GENE AMPLIFICATION; BREAST-CANCER; ADJUVANT CHEMOTHERAPY;
   PROGNOSTIC-FACTOR; POOR-PROGNOSIS; GASTRIC-CANCER; SCORING SYSTEM;
   EXPRESSION; PROTEIN; EGFR
AB HER2 overexpression/amplification is linked to trastuzumab response in breast/gastric cancers. One suggested anti-EGFR resistance mechanism in colorectal cancer (CRC) is aberrant MEK-AKT pathway activation through HER2 up-regulation. We assessed HER2-amplification/overexpression in stage II-III and IV CRC patients, assessing relationships to KRAS/BRAF and outcome. Pathological material was obtained from 1914 patients in the QUASAR stage II-III trial and 1342 patients in stage IV trials (FOCUS and PICCOLO). Tissue microarrays were created for HER2 immunohistochemistry. HER2-amplification was assessed using FISH and copy number variation. KRAS/BRAF mutation status was assessed by pyrosequencing. Progression-free survival (PFS) and overall survival (OS) data were obtained for FOCUS/PICCOLO and recurrence and mortality for QUASAR; 29/1342 (2.2%) stage IV and 25/1914 (1.3%) stage II-III tumours showed HER2 protein overexpression. Of the HER2-overexpressing cases, 27/28 (96.4%) stage IV tumours and 20/24 (83.3%) stage II-III tumours demonstrated HER2 amplification by FISH; 41/47 (87.2%) also showed copy number gains. HER2-overexpression was associated with KRAS/BRAF wild-type (WT) status at all stages: in 5.2% WT versus 1.0% mutated tumours (p < 0.0001) in stage IV and 2.1% versus 0.2% in stage II-III tumours (p = 0.01), respectively. HER2 was not associated with OS or PFS. At stage II-III, there was no significant correlation between HER2 overexpression and 5FU/FA response. A higher proportion of HER2-overexpressing cases experienced recurrence, but the difference was not significant. HER2-amplification/overexpression is identifiable by immunohistochemistry, occurring infrequently in stage II-III CRC, rising in stage IV and further in KRAS/BRAFWT tumours. The value of HER2-targeted therapy in patients with HER2-amplified CRC must be tested in a clinical trial. (c) 2015 The Authors. Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.
C1 [Richman, Susan D.; Southward, Katie; Chambers, Philip; Hemmings, Gemma; Taylor, Morag; Wood, Henry; Hutchins, Gordon; Quirke, Philip] Univ Leeds, Sect Pathol & Tumour Biol, Leeds Inst Canc & Pathol, Leeds LS9 7TF, W Yorkshire, England.
   [Cross, Debra] St James Univ Hosp, Histopathol & Mol Pathol, Leeds LS9 7TF, W Yorkshire, England.
   [Barrett, Jennifer] Univ Leeds, Leeds Inst Canc & Pathol, Epidemiol & Biostat Sect, Leeds LS9 7TF, W Yorkshire, England.
   [Foster, Joseph M.; Oumie, Assa; Spink, Karen G.] Affymetrix UK Ltd, High Wycombe, Bucks, England.
   [Brown, Sarah R.; Jones, Marc] Univ Leeds, Clin Trials Res Unit, Leeds LS9 7TF, W Yorkshire, England.
   [Kerr, David] Univ Oxford, Canc Med, Oxford OX1 2JD, England.
   [Handley, Kelly] Univ Birmingham, Birmingham Clin Trials Unit, Birmingham B15 2TT, W Midlands, England.
   [Gray, Richard] Univ Oxford, Clin Trials Serv Unit, Oxford OX1 2JD, England.
   [Gray, Richard] Univ Oxford, Epidemiol Studies Unit, Oxford OX1 2JD, England.
   [Seymour, Matthew] Univ Leeds, Leeds Inst Canc & Pathol, Sect Oncol, Leeds LS9 7TF, W Yorkshire, England.
C3 University of Leeds; Saint James's University Hospital; University of
   Leeds; University of Leeds; University of Oxford; University of
   Birmingham; University of Oxford; University of Oxford; University of
   Leeds
RP Richman, SD (corresponding author), Univ Leeds, St Jamess Univ Hosp, Sect Pathol & Tumour Biol, Leeds Inst Canc & Pathol, Wellcome Trust Brenner Bldg, Leeds LS9 7TF, W Yorkshire, England.
EM s.d.richman@leeds.ac.uk
RI Quirke, Philip/AAI-1362-2019; Gray, Richard/C-9945-2017
OI Richman, Susan/0000-0003-3993-5041; Kerr, David/0000-0001-7811-6722;
   Wood, Henry/0000-0003-3009-5904; Gray, Richard/0000-0003-4440-574X;
   Taylor, Morag/0000-0002-3907-1290; Seymour, Matthew/0000-0002-2441-9629;
   Quirke, Philip/0000-0002-3597-5444; Handley, Kelly/0000-0003-4036-2375;
   Southward, Katie/0000-0001-9104-5957; Chambers,
   Philip/0000-0002-0926-717X; Brown, Sarah/0000-0002-7975-7537
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NR 35
TC 176
Z9 193
U1 1
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3417
EI 1096-9896
J9 J PATHOL
JI J. Pathol.
PD MAR
PY 2016
VL 238
IS 4
BP 562
EP 570
DI 10.1002/path.4679
PG 9
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA DE7TQ
UT WOS:000370840000010
PM 26690310
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Zhao, RH
   Li, R
   An, TQ
   Liu, XF
AF Zhao, Ruihua
   Li, Rui
   An, Tianqi
   Liu, Xuefeng
TI Conditional Cell Reprogramming in Modeling Digestive System Diseases
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE conditional cell reprogramming; digestive system diseases; cell model;
   CR technology; cell culture technology
ID ADENOID CYSTIC CARCINOMA; IN-VITRO; TARGETED THERAPY; COLORECTAL-CANCER;
   ROCK INHIBITOR; STEM-CELLS; LINES; PROLIFERATION; CULTIVATION;
   GENERATION
AB Digestive diseases have become an important source of morbidity and mortality. The considerable financial and health burdens caused by digestive diseases confirm the importance of extensive research to better understand and treat these diseases. The development of reliable preclinical models is essential for understanding the pathogenesis of digestive diseases and developing treatment and prevention methods. However, traditional established cell lines and animal models still have many limitations in the study of the digestive system. Conditional reprogramming (CR) cell culture is a newly developed primary technology that uses irradiated Swiss-3T3-J2 mouse fibroblast cells and the Rho-associated kinase (ROCK) inhibitor Y-27632 to rapidly and efficiently generate many cells from diseased and normal tissues. CR cells (CRCs) can be reprogrammed to maintain a highly proliferative state and recapitulate the histological and genomic features of the original tissue. Moreover, after removing these conditions, the phenotype was completely reversible. Therefore, CR technology may represent an ideal model to study digestive system diseases, to test drug sensitivity, to perform gene profile analysis, and to undertake xenograft research and regenerative medicine. Indeed, together with organoid cultures, CR technology has been recognized as one of the key new technologies by NIH precision oncology and also used for NCI human cancer model initiatives (HCMI) program with ATCC. In this article, we review studies that use CR technology to conduct research on diseases of the digestive system.
C1 [Zhao, Ruihua; Li, Rui; An, Tianqi] Zhengzhou Univ, Affiliated Hosp 1, Dept Oncol, Zhengzhou, Peoples R China.
   [Li, Rui] Huazhong Univ Sci & Technol, Tongji Hosp, Dept Oncol, Wuhan, Peoples R China.
   [Liu, Xuefeng] Georgetown Univ, Med Ctr, Dept Pathol, Ctr Cell Reprogramming, Washington, DC 20007 USA.
   [Liu, Xuefeng] Georgetown Univ, Med Ctr, Lombardi Comprehens Canc Ctr, Dept Oncol, Washington, DC 20007 USA.
   [Liu, Xuefeng] Ohio State Univ, Sch Med, Dept Pathol, Columbus, OH 43210 USA.
   [Liu, Xuefeng] Ohio State Univ, Sch Med, Dept Urol, Columbus, OH 43210 USA.
   [Liu, Xuefeng] Ohio State Univ, James Comprehens Canc Ctr, Columbus, OH 43210 USA.
C3 Zhengzhou University; Huazhong University of Science & Technology;
   Georgetown University; Georgetown University; University System of Ohio;
   Ohio State University; University System of Ohio; Ohio State University;
   James Cancer Hospital & Solove Research Institute; University System of
   Ohio; Ohio State University
RP Liu, XF (corresponding author), Georgetown Univ, Med Ctr, Dept Pathol, Ctr Cell Reprogramming, Washington, DC 20007 USA.; Liu, XF (corresponding author), Georgetown Univ, Med Ctr, Lombardi Comprehens Canc Ctr, Dept Oncol, Washington, DC 20007 USA.; Liu, XF (corresponding author), Ohio State Univ, Sch Med, Dept Pathol, Columbus, OH 43210 USA.; Liu, XF (corresponding author), Ohio State Univ, Sch Med, Dept Urol, Columbus, OH 43210 USA.; Liu, XF (corresponding author), Ohio State Univ, James Comprehens Canc Ctr, Columbus, OH 43210 USA.
EM xuefeng.liu@georgetown.edu
RI Li, Rui/C-2155-2009; Liu, xuefeng/IUP-1483-2023
FU HPV Vaccine Royalty in Center for Cell Reprogramming/Department of
   Pathology, Georgetown University Medical Center; Henan Natural Science
   Foundation [202300410383]
FX This work was supported by internal support from HPV Vaccine Royalty in
   Center for Cell Reprogramming/Department of Pathology, Georgetown
   University Medical Center. The funders had no role in the data analysis,
   the decision to publish, or preparation of the manuscript, and Henan
   Natural Science Foundation (202300410383).
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NR 65
TC 6
Z9 6
U1 0
U2 28
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-634X
J9 FRONT CELL DEV BIOL
JI Front. Cell. Dev. Biol.
PD JUN 3
PY 2021
VL 9
AR 669756
DI 10.3389/fcell.2021.669756
PG 9
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA ST2WR
UT WOS:000662310700001
PM 34150763
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Aoki, Y
   Nakamura, Y
   Denda, T
   Ohta, T
   Esaki, T
   Shiozawa, M
   Yamaguchi, K
   Yamazaki, K
   Sunakawa, Y
   Kato, T
   Okano, N
   Taniguchi, H
   Sato, T
   Oki, E
   Nishina, T
   Komatsu, Y
   Matsuhashi, N
   Goto, M
   Yasui, H
   Ohtsubo, K
   Moriwaki, T
   Takahashi, N
   Horita, Y
   Boku, S
   Wakabayashi, M
   Ikeno, T
   Mitani, R
   Yuasa, M
   Yoshino, T
AF Aoki, Yu
   Nakamura, Yoshiaki
   Denda, Tadamichi
   Ohta, Takashi
   Esaki, Taito
   Shiozawa, Manabu
   Yamaguchi, Kensei
   Yamazaki, Kentaro
   Sunakawa, Yu
   Kato, Takeshi
   Okano, Naohiro
   Taniguchi, Hiroya
   Sato, Taro
   Oki, Eiji
   Nishina, Tomohiro
   Komatsu, Yoshito
   Matsuhashi, Nobuhisa
   Goto, Masahiro
   Yasui, Hisateru
   Ohtsubo, Koushiro
   Moriwaki, Toshikazu
   Takahashi, Naoki
   Horita, Yosuke
   Boku, Shogen
   Wakabayashi, Masashi
   Ikeno, Takashi
   Mitani, Ryuta
   Yuasa, Mihoko
   Yoshino, Takayuki
TI Clinical Validation of Plasma-Based Genotyping for <i>RAS</i> and
   <i>BRAF</i> V600E Mutation in Metastatic Colorectal Cancer: SCRUM-Japan
   GOZILA Substudy
SO JCO PRECISION ONCOLOGY
LA English
DT Article
ID CIRCULATING TUMOR DNA; TECHNOLOGY; KRAS
AB PURPOSE Circulating tumor DNA (ctDNA) genotyping on the basis of next-generation sequencing (NGS) may guide targeted therapy for metastatic colorectal cancer (mCRC). However, the validity of NGS-based ctDNA genotyping for RAS/BRAF V600E mutation assessment and the efficacy of anti-EGFR and BRAF-targeted therapies on the basis of ctDNA results remains unclear. PATIENTS AND METHODS The performance of NGS-based ctDNA genotyping for RAS/BRAF V600E mutation assessment was compared with that of a validated polymerase chain reaction-based tissue testing in patients with mCRC enrolled in the GOZILA study, a nationwide plasma genotyping study. The primary end points were concordance rate, sensitivity, and specificity. The efficacy of anti-EGFR and BRAF-targeted therapies on the basis of ctDNA were also evaluated. RESULTS In 212 eligible patients, the concordance rate, sensitivity, and specificity were 92.9% (95% CI, 88.6 to 96.0), 88.7% (95% CI, 81.1 to 94.0), and 97.2% (95% CI, 92.0 to 99.4) for RAS and 96.2% (95% CI, 92.7 to 98.4), 88.0% (95% CI, 68.8 to 97.5), and 97.3% (95% CI, 93.9 to 99.1) for BRAF V600E, respectively. In patients with a ctDNA fraction of >= 1.0%, sensitivity rose to 97.5% (95% CI, 91.2 to 99.7) and 100% (95% CI, 80.5 to 100.0) for RAS and BRAF V600E mutations, respectively. In addition to a low ctDNA fraction, previous chemotherapy, lung and peritoneal metastases, and interval between dates of tissue and blood collection were associated with discordance. The progression-free survival of anti-EGFR therapy and BRAF-targeted treatment was 12.9 months (95% CI, 8.1 to 18.5) and 3.7 (95% CI, 1.3 to not evaluated) months, respectively, for matched patients with RAS/BRAF V600E results by ctDNA. CONCLUSION ctDNA genotyping effectively detected RAS/BRAF mutations, especially with sufficient ctDNA shedding. Clinical outcomes support ctDNA genotyping for determining the use of anti-EGFR and BRAF-targeted therapies in patients with mCRC.
C1 [Aoki, Yu; Nakamura, Yoshiaki; Yoshino, Takayuki] Natl Canc Ctr Hosp East, Dept Gastroenterol & Gastrointestinal Oncol, Kashiwa, Japan.
   [Aoki, Yu] Keio Univ, Sch Med, Div Gastroenterol & Hepatol Internal Med, Tokyo, Japan.
   [Nakamura, Yoshiaki; Mitani, Ryuta; Yuasa, Mihoko] Natl Canc Ctr Hosp East, Translat Res Support Off, Kashiwa, Japan.
   [Nakamura, Yoshiaki] Natl Canc Ctr Hosp East, Int Res Promot Off, Kashiwa, Japan.
   [Denda, Tadamichi] Chiba Canc Ctr, Div Gastroenterol, Chiba, Japan.
   [Ohta, Takashi] Kansai Rosai Hosp, Dept Clin Oncol, Amagasaki, Japan.
   [Esaki, Taito] Natl Hosp Org, Dept Gastrointestinal & Med Oncol, Kyushu Canc Ctr, Fukuoka, Japan.
   [Shiozawa, Manabu] Kanagawa Canc Ctr, Dept Gastrointestinal Surg, Yokohama, Japan.
   [Yamaguchi, Kensei] JFCR, Canc Inst Hosp, Gastroenterol Chemotherapy Dept, Tokyo, Japan.
   [Yamazaki, Kentaro] Shizuoka Canc Ctr, Div Gastrointestinal Oncol, Nagaizuma, Japan.
   [Sunakawa, Yu] St Marianna Univ, Dept Clin Oncol, Sch Med, Kawasaki, Japan.
   [Kato, Takeshi] Natl Hosp Org, Osaka Natl Hosp, Dept Surg, Osaka, Japan.
   [Okano, Naohiro] Kyorin Univ, Fac Med, Dept Med Oncol, Tokyo, Japan.
   [Taniguchi, Hiroya] Aichi Canc Ctr Hosp, Dept Clin Oncol, Nagoya, Japan.
   [Sato, Taro] Osaka Univ Hosp, Palliat & Support Care Ctr, Suita, Japan.
   [Oki, Eiji] Kyushu Univ, Grad Sch Med Sci, Dept Surg & Sci, Fukuoka, Japan.
   [Nishina, Tomohiro] Natl Hosp Org, Gastrointestinal Med Oncol, Shikoku Canc Ctr, Matsuyama, Japan.
   [Komatsu, Yoshito] Hokkaido Univ Hosp, Dept Canc Ctr, Sapporo, Japan.
   [Matsuhashi, Nobuhisa] Gifu Univ, Grad Sch Med, Dept Gastroenterol Surg & Pediat Surg, Gifu, Japan.
   [Goto, Masahiro] Osaka Med & Pharmaceut Univ, Canc Chemotherapy Ctr, Takatsuki, Japan.
   [Yasui, Hisateru] Kobe City Med Ctr Gen Hosp, Dept Med Oncol, Kobe, Japan.
   [Ohtsubo, Koushiro] Kanazawa Univ, Canc Res Inst, Div Med Oncol, Kanazawa, Japan.
   [Moriwaki, Toshikazu] Univ Tsukuba Hosp, Dept Gastroenterol, Tsukuba, Japan.
   [Takahashi, Naoki] Saitama Canc Ctr, Dept Gastroenterol, Ina, Japan.
   [Horita, Yosuke] Saitama Med Univ, Int Med Ctr, Dept Med Oncol, Hidaka, Japan.
   [Boku, Shogen] Kansai Med Univ Hosp, Canc Treatment Ctr, Hirakata, Japan.
   [Wakabayashi, Masashi] Natl Canc Ctr Hosp East, Ctr Res Adm & Support, Biostat Div, Kashiwa, Japan.
   [Ikeno, Takashi] Natl Canc Ctr Hosp East, Clin Res Support Off, Kashiwa, Japan.
   [Nakamura, Yoshiaki] Natl Canc Ctr Hosp East, Int Res Promot Off, 6-5-1 Kashiwanoha, Kashiwa, Chiba 2778577, Japan.
C3 National Cancer Center - Japan; Keio University; National Cancer Center
   - Japan; National Cancer Center - Japan; Chiba Cancer Center; Kansai
   Rosai Hospital; Kyushu Cancer Center; Kanagawa Prefectural Cancer
   Center; Japanese Foundation for Cancer Research; Shizuoka Cancer Center;
   Saint Marianna University; Osaka National Hospital; Kyorin University;
   Aichi Cancer Center; Osaka University; Kyushu University; Hokkaido
   University; Gifu University; Osaka Medical & Pharmaceutical University;
   Kobe City Medical Center General Hospital; Kanazawa University;
   University of Tsukuba; Saitama Medical University; Kansai Medical
   University; National Cancer Center - Japan; National Cancer Center -
   Japan; National Cancer Center - Japan
RP Nakamura, Y (corresponding author), Natl Canc Ctr Hosp East, Int Res Promot Off, 6-5-1 Kashiwanoha, Kashiwa, Chiba 2778577, Japan.
EM yoshinak@east.ncc.go.jp
RI Boku, Shogen/AAQ-8874-2021; Sunakawa, Yu/AGW-7031-2022; Oki,
   Eiji/AFO-6423-2022
OI Denda, Tadamichi/0000-0003-2570-9692; Nakamura,
   Yoshiaki/0000-0002-5241-6855
FU Office in National Cancer Center Hospital East; Guardant Health Inc.
FX I would like to thank patients who had participated in the GOZILA study
   and their families, GOZILA investigators and site personnel,
   Translational Research Support Office in National Cancer Center Hospital
   East, and Guardant Health Inc.
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TC 5
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U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
EI 2473-4284
J9 JCO PRECIS ONCOL
JI JCO Precis. Oncol.
PY 2023
VL 7
AR e2200688
DI 10.1200/PO.22.00688
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA NA3W8
UT WOS:001197689200048
PM 37343204
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Yamada, T
   Amann, JM
   Tanimoto, A
   Taniguchi, H
   Shukuya, T
   Timmers, C
   Yano, S
   Shilo, K
   Carbone, DP
AF Yamada, Tadaaki
   Amann, Joseph M.
   Tanimoto, Azusa
   Taniguchi, Hirokazu
   Shukuya, Takehito
   Timmers, Cynthia
   Yano, Seiji
   Shilo, Konstantin
   Carbone, David P.
TI Histone Deacetylase Inhibition Enhances the Antitumor Activity of a MEK
   Inhibitor in Lung Cancer Cells Harboring <i>RAS</i> Mutations
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID SELUMETINIB PLUS DOCETAXEL; RANDOMIZED PHASE-II; COLORECTAL-CANCER;
   KINASE; GENE; COMBINATION; BELINOSTAT; EXPRESSION; ADENOCARCINOMA;
   DOXORUBICIN
AB Non-small cell lung cancer (NSCLC) can be identified by precise molecular subsets based on genomic alterations that drive tumorigenesis and include mutations in EGFR, KRAS, and various ALK fusions. However, despite effective treatments for EGFR and ALK, promising therapeutics have not been developed for patients with KRAS mutations. It has been reported that one way the RAS-ERK pathway contributes to tumorigenesis is by affecting stability and localization of FOXO3a protein, an important regulator of cell death and the cell cycle. This is through regulation of apoptotic proteins BIM and FASL and cell-cycle regulators p21(Cip1) and p27(Kip1). We now show that an HDAC inhibitor affects the expression and localization of FOXO proteins and wanted to determine whether the combination of a MEK inhibitor with an HDAC inhibitor would increase the sensitivity of NSCLC with KRAS mutation. Combined treatment with a MEK inhibitor and an HDAC inhibitor showed synergistic effects on cell metabolic activity of RAS-mutated lung cancer cells through activation of FOXOs, with a subsequent increase in BIM and cell-cycle inhibitors. Moreover, in a mouse xenograft model, the combination of belinostat and trametinib significantly decreases tumor formation through FOXOs by increasing BIM and the cell-cycle inhibitors p21(Cip1) and p27(Kip1). These results demonstrate that control of FOXOs localization and expression is critical in RAS-driven lung cancer cells, suggesting that the dual molecular-targeted therapy for MEK and HDACs may be promising as novel therapeutic strategy in NSCLC with specific populations of RAS mutations. (C) 2017 AACR.
C1 [Yamada, Tadaaki; Amann, Joseph M.; Shukuya, Takehito; Timmers, Cynthia; Shilo, Konstantin; Carbone, David P.] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
   [Yamada, Tadaaki; Tanimoto, Azusa; Taniguchi, Hirokazu; Yano, Seiji] Kanazawa Univ, Canc Res Inst, Div Med Oncol, Kanazawa, Ishikawa, Japan.
   [Yamada, Tadaaki] Kyoto Prefectural Univ Med, Grad Sch Med Sci, Dept Pulm Med, Kyoto, Japan.
   [Taniguchi, Hirokazu] Nagasaki Univ, Grad Sch Biomed Sci, Dept Resp Med, Nagasaki, Japan.
C3 James Cancer Hospital & Solove Research Institute; University System of
   Ohio; Ohio State University; Kanazawa University; Kyoto Prefectural
   University of Medicine; Nagasaki University
RP Carbone, DP (corresponding author), Ohio State Univ, Med Ctr, 460 West 12th Ave, Columbus, OH 43210 USA.
EM david.carbone@osumc.edu
RI 谷本, 梓/JCF-0645-2023; Shilo, K/AAV-2360-2020; Yamada, Tadaaki/L-5378-2015
OI Taniguchi, Hirokazu/0000-0003-2414-8344; Tanimoto,
   Azusa/0000-0002-6643-3867
FU DallePezze Thoracic Oncology Fund; NIH [5U10CA180950]; Kobayashi
   Foundation for Cancer Research; Foundation for Promotion of Cancer
   Research in Japan
FX This study was supported by the DallePezze Thoracic Oncology Fund and
   NIH-funding (5U10CA180950; to D.P. Carbone), and a research grant for
   developing innovative cancer chemotherapy from the Kobayashi Foundation
   for Cancer Research and Foundation for Promotion of Cancer Research in
   Japan (to T. Yamada).
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NR 39
TC 32
Z9 33
U1 0
U2 14
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
EI 1538-8514
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD JAN
PY 2018
VL 17
IS 1
BP 17
EP 25
DI 10.1158/1535-7163.MCT-17-0146
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FR6AS
UT WOS:000419148400002
PM 29079711
OA Green Accepted, Green Submitted, hybrid
DA 2025-01-04
ER

PT J
AU Lefler, DS
   Snook, AE
   Bashir, B
AF Lefler, Daniel S.
   Snook, Adam E.
   Bashir, Babar
TI Immune checkpoint inhibitors in luminal gastrointestinal malignancies:
   going beyond MSI-H/dMMR, TMB and PD-L1
SO IMMUNOTHERAPY
LA English
DT Review
DE colorectal cancer; esophageal cancer; gastric cancer; immune checkpoint
   inhibitors; immunotherapy; microsatellite instability; mismatch repair;
   PD-L1; tumor microenvironment; tumor mutational burden
ID TUMOR MUTATIONAL BURDEN; METASTATIC COLORECTAL-CANCER; MICROSATELLITE
   INSTABILITY; OPEN-LABEL; GASTROESOPHAGEAL JUNCTION; 1ST-LINE TREATMENT;
   PLUS CHEMOTHERAPY; T-CELL; ESOPHAGEAL; NIVOLUMAB
AB In luminal gastrointestinal tumors, immune checkpoint inhibitors (ICIs) targeting PD-1, PD-L1 and CTLA-4 have been investigated in multiple settings. The indications for these drugs are primarily dependent on specific biomarkers that imply immunogenicity: overexpression of PD-L1, tumor mutational burden, loss of mismatch repair proteins (dMMR) and/or high microsatellite instability status. Although these markers can be both predictive and prognostic, there is variability in how they are measured and used to guide therapies. Moreover, the use of ICIs can be further refined with a better understanding of the tumor microenvironment and interactions with other available therapies. The purpose of this review is to characterize luminal gastrointestinal tumors' responses to ICIs considering known predictive biomarkers and discuss emerging therapeutic approaches using ICIs.
   Plain language summary Immune checkpoint inhibitors (ICIs) are medications that help the natural immune system fight cancer cells, preventing their growth. In tumors of the gastrointestinal tract, mounting research has shown that ICIs are useful in treatment regimens. However, this depends on certain characteristics of individual cancers, such as how many mutations they have, if they are missing certain enzymes and other considerations. ICIs can also be paired with standard - and nonstandard - treatments like chemotherapy, radiation and other targeted therapy to increase their effectiveness against cancer. This article discusses how ICIs are used in gastrointestinal tract cancers according to the available evidence in the medical literature, and it explores the directions of the research on the forefront of immunotherapy.
   Tweetable abstract Immune checkpoint inhibitors have become ubiquitous in the treatment of many #cancers. This review explores their role in luminal gastrointestinal tumors, from biomarker-driven therapy to novel drug combinations. #ICIs #oncology.
C1 [Lefler, Daniel S.; Bashir, Babar] Thomas Jefferson Univ Hosp, Sidney Kimmel Canc Ctr, Dept Med Oncol, Philadelphia, PA 19107 USA.
   [Snook, Adam E.; Bashir, Babar] Thomas Jefferson Univ, Dept Pharmacol & Expt Therapeut, Philadelphia, PA 19107 USA.
   [Snook, Adam E.] Thomas Jefferson Univ, Dept Microbiol & Immunol, Philadelphia, PA 19107 USA.
C3 Jefferson University; Jefferson University; Jefferson University
RP Bashir, B (corresponding author), Thomas Jefferson Univ Hosp, Sidney Kimmel Canc Ctr, Dept Med Oncol, Philadelphia, PA 19107 USA.; Bashir, B (corresponding author), Thomas Jefferson Univ, Dept Pharmacol & Expt Therapeut, Philadelphia, PA 19107 USA.
EM babar_bashir@jefferson.edu
RI Bashir, Babar/AGU-8166-2022; Snook, Adam/P-2585-2015
OI Lefler, Daniel/0000-0001-8051-8800; Snook, Adam/0000-0001-9216-4560;
   BASHIR, BABAR/0000-0002-6843-1179
FU Defense Congressionally Directed Medical Research Programs
   [W81XWH-19-1-0263]; West Pharmaceutical Services Inc.; Courtney Ann
   Diacont Memorial Foundation; Lorraine and David Swoyer; Amgen Inc.;
   Boehringer Ingelheim; Bicycle Therapeutics; KAHR Medical; Merck; Pionyr
   Immunotherapeutics; Syros Pharmaceuticals and Tarveda Therapeutics
FX DS Lefler has no conflicts to disclose. AE Snook is a consultant for
   Targeted Diagnostics and Therapeutics Inc., which provided research
   funding that, in part, supported this work and has a license to
   commercialize inventions related to this work. AE Snook was supported by
   the Defense Congressionally Directed Medical Research Programs
   (#W81XWH-19-1-0263), West Pharmaceutical Services Inc., the Courtney Ann
   Diacont Memorial Foundation, and Lorraine and David Swoyer. B Bashir
   reports research funding to the institution from Amgen Inc., Boehringer
   Ingelheim, Bicycle Therapeutics, KAHR Medical, Merck, Pionyr
   Immunotherapeutics, Syros Pharmaceuticals and Tarveda Therapeutics, all
   outside the submitted work. The authors have no other relevant
   affiliations or financial involvement with any organization or entity
   with a financial interest in or financial conflict with the subject
   matter or materials discussed in the manuscript apart from those
   disclosed.
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NR 106
TC 12
Z9 12
U1 1
U2 11
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1750-743X
EI 1750-7448
J9 IMMUNOTHERAPY-UK
JI Immunotherapy
PD AUG
PY 2022
VL 14
IS 11
BP 885
EP 902
DI 10.2217/imt-2022-0012
EA JUN 2022
PG 18
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 2V2ZP
UT WOS:000809877200001
PM 35694998
DA 2025-01-04
ER

PT J
AU Coquerelle, S
   Darlington, M
   Michel, M
   Durand, M
   Borget, I
   Baffert, S
   Marino, P
   Perrier, L
   Durand-Zaleski, I
AF Coquerelle, Severine
   Darlington, Meryl
   Michel, Morgane
   Durand, Manon
   Borget, Isabelle
   Baffert, Sandrine
   Marino, Patricia
   Perrier, Lionel
   Durand-Zaleski, Isabelle
CA NGSEco Grp
TI Impact of Next Generation Sequencing on Clinical Practice in Oncology in
   France: Better Genetic Profiles for Patients Improve Access to
   Experimental Treatments
SO VALUE IN HEALTH
LA English
DT Article
DE clinical practice; NGS; oncology; somatic alterations
ID CELL LUNG-CANCER; COST-EFFECTIVENESS; COLORECTAL-CANCER; MUTATIONS;
   THERAPIES; DIAGNOSIS; MEDICINE; GENOMICS; PROGRAM; PANELS
AB Objectives: We evaluated how next generation sequencing (NGS) can modify care pathways in an observational impact study in France.
   Methods: All patients with lung cancer, colorectal cancer, or melanoma who had NGS analyses of somatic genomic alterations done in 1 of 7 biomolecular platforms certified by the French National Cancer Institute (INCa) between 2013 and 2016 were eligible. We compared patients' pathways before and after their NGS results. Endpoints consisted of the turnaround time in obtaining results, the number of patients with at least 1 genomic alteration identified, the number of actionable alterations, the impact of the genomic multidisciplinary tumor board on care pathways, the number of changes in the treatment plan, and the survival outcome up to 1 year after NGS analyses.
   Results: 1213 patients with a request for NGS analysis were included. NGS was performed for 1155 patients, identified at least 1 genomic alteration for 867 (75%), and provided an actionable alteration for 614 (53%). Turnaround time between analyses and results was on average 8 days (Min: 0; Max: 95) for all cancer types. Before NGS analysis, 33 of 614 patients (5%) were prescribed a targeted therapy compared with 54 of 614 patients (8%) after NGS analysis. Proposition of inclusion in clinical trials with experimental treatments increased from 5% (n = 31 of 614) before to 28% (n = 178 of 614) after NGS analysis. Patients who benefited from a genotype matched treatment after NGS analysis tended to have a better survival outcome at 1 year than patients with nonmatched treatment: 258 days (6107) compared with 234 days (6106), (P =.41).
   Conclusions: NGS analyses resulted in a change in patients' care pathways for 20% of patients (n = 232 of 1155).
C1 [Coquerelle, Severine; Darlington, Meryl; Michel, Morgane; Durand, Manon; Durand-Zaleski, Isabelle] AP HP, Unite Rech Clin Econ Sante Ile France, Paris, France.
   [Coquerelle, Severine; Michel, Morgane] Univ Paris Diderot, Sorbonne Paris Cite, Paris, France.
   [Coquerelle, Severine; Durand-Zaleski, Isabelle] Ctr Res Epidemiol & Stat, INSERM, Joint Res Units, Paris, France.
   [Michel, Morgane] INSERM, Epidemiol Clin & Evaluat Econ, Paris, France.
   [Borget, Isabelle] Gustave Roussy Inst, Etud & Rech Econ Sante, Villejuif, France.
   [Baffert, Sandrine] Rothschild Fdn, Hlth Econ Dept, Paris, France.
   [Marino, Patricia] Inst Paoli Calmettes, Sci Econ & Sociales Sante & Traitement Informat M, Marseille, France.
   [Perrier, Lionel] Univ Lyon, Ctr Leon Berard, Lyon St Etienne Joint Res Units, Grp Anal Theorie Econ, Lyon, France.
   [Durand-Zaleski, Isabelle] Hop Henri Mondor, AP HP, Publ Hlth Dept, Creteil, France.
C3 Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Universite Paris Cite; Institut National de la Sante et de la Recherche
   Medicale (Inserm); Institut National de la Sante et de la Recherche
   Medicale (Inserm); UNICANCER; Gustave Roussy; UNICANCER; Institut
   Paoli-Calmette (IPC); Aix-Marseille Universite; UNICANCER; Centre Leon
   Berard; Centre National de la Recherche Scientifique (CNRS); Ecole
   Normale Superieure de Lyon (ENS de LYON); Universite Claude Bernard Lyon
   1; Universite Jean Monnet; Universite Lyon 2; Assistance Publique
   Hopitaux Paris (APHP); Universite Paris-Est-Creteil-Val-de-Marne (UPEC);
   Hopital Universitaire Henri-Mondor - APHP
RP Coquerelle, S (corresponding author), Hop Hotel Dieu, AP HP, URC Eco, 1 Pl Parvis Notre Dame, F-75004 Paris, France.
EM severine.coquerelle@urc-eco.fr
RI Durand-Zaleski, Isabelle/AFP-1493-2022; Darlington, Meryl/JED-9657-2023;
   Perrier, Lionel/AAC-8048-2021; Michel, Morgane/AEH-1310-2022
OI DARLINGTON, Meryl/0000-0001-8029-1925
FU French National Cancer Institute [2013-1-NGS-02]
FX This work was supported by grants 2013-1-NGS-02 from the French National
   Cancer Institute.
CR [Anonymous], 2005, 2005SANH0530076C NOR
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NR 38
TC 11
Z9 11
U1 1
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1098-3015
EI 1524-4733
J9 VALUE HEALTH
JI Value Health
PD JUL
PY 2020
VL 23
IS 7
BP 898
EP 906
DI 10.1016/j.jval.2020.03.005
PG 9
WC Economics; Health Care Sciences & Services; Health Policy & Services
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Business & Economics; Health Care Sciences & Services
GA MU1PE
UT WOS:000555443700011
PM 32762992
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Tsikalakis, S
   Chatziandreou, I
   Michalopoulos, NV
   Theodoropoulos, GE
   Sakellariou, S
   Korkolopoulou, P
   Patsouris, E
   Saetta, AA
AF Tsikalakis, Spyridon
   Chatziandreou, Ilenia
   Michalopoulos, Nikolaos, V
   Theodoropoulos, Georgios E.
   Sakellariou, Stratigoula
   Korkolopoulou, Penelope
   Patsouris, Efstratios
   Saetta, Angelica A.
TI Comprehensive expression analysis of TNF-related apoptosis-inducing
   ligand and its receptors in colorectal cancer: Correlation with MAPK
   alterations and clinicopathological associations
SO PATHOLOGY RESEARCH AND PRACTICE
LA English
DT Article
DE Apoptosis; mRNA expression; Real time RT-PCR; Colorectal cancer
ID TRAIL RECEPTORS; DEATH; METASTASIS; CARCINOMA; DCR2; RESISTANCE;
   INITIATION; MEMBRANE; CELLS; DR4
AB TNF-related, apoptosis-inducing ligand (TRAIL) apoptotic pathway constitutes a promising therapeutic target due to high selectivity and low toxicity of TRAIL targeting agents when administered in combination therapies. 106 colorectal cancers were examined for: relative mRNA expression of TRAIL pathway genes, decoy receptors TRAIL-R3 and TRAIL-R4 promoter methylation and the presence of KRAS, NRAS, BRAF mutations. Elevated mRNA levels were observed in 26%, 15%, 13%, 12% and 10% of the cases for TRAIL-R4, TRAIL-R3, TRAIL-R2, TRAIL-R1 and TRAIL genes respectively. Reduced mRNA levels were detected in 77%, 65%, 64%, 60% and 37% of the cases for TRAIL, TRAIL-R2, TRAIL-R3, TRAIL-R1 and TRAIL-R4 genes respectively. TRAIL-R3 and TRAIL-R4 promoter methylation was detected in 55% and 16% of the analysed samples respectively. TRAIL-R1, TRAIL-R2 elevated relative mRNA levels inversely correlated with tumor stage (p = .036, p = .048). Strong linear correlations of TRAIL receptors' mRNA levels were found: TRAIL-R1/TRAIL-R2 (R = 0.653, p <.001), TRAIL-R2/TRAIL-R3 (R = 0.573, p < .001). Finally, relative expression of TRAIL was correlated with KRAS, BRAF and NRAS mutation status, defining an inverse correlation between increased TRAIL expression and the absence of mutations in Mitogen-activated protein kinase (MAPK) pathway.
   In conclusion, simultaneous analysis of TRAIL pathway membrane components, pointed towards a significant deregulation of mRNA expression in colorectal tumours. Death receptor overexpression was an indicator of a less aggressive phenotype. The multiple expression patterns of TRAIL pathway components in colorectal tumours underscore the importance of patient selection in order to achieve maximum efficiency with TRAIL targeted therapy.
C1 [Tsikalakis, Spyridon; Chatziandreou, Ilenia; Sakellariou, Stratigoula; Korkolopoulou, Penelope; Patsouris, Efstratios; Saetta, Angelica A.] Natl & Kapodistrian Univ Athens, Dept Pathol 1, Sch Med, Milcras Asias 75, Athens, Goudi, Greece.
   [Michalopoulos, Nikolaos, V; Theodoropoulos, Georgios E.] Natl & Kapodistrian Univ Athens, Dept Propaedeut Surg 1, Hippokrateion Hosp, Sch Med, Vas Sofias 114, Athens, Greece.
C3 Athens Medical School; National & Kapodistrian University of Athens;
   National & Kapodistrian University of Athens; Athens Medical School;
   Hippokration General Hospital
RP Saetta, AA (corresponding author), Natl & Kapodistrian Univ Athens, Dept Pathol 1, Sch Med, Milcras Asias 75, Athens, Goudi, Greece.
EM asaetta@med.uoa.gr
OI Saetta, Angelica A./0000-0002-4862-3413; CHATZIANDREOU,
   ILENIA/0000-0002-4940-5581
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NR 50
TC 6
Z9 8
U1 1
U2 8
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0344-0338
EI 1618-0631
J9 PATHOL RES PRACT
JI Pathol. Res. Pract.
PD JUN
PY 2018
VL 214
IS 6
BP 826
EP 834
DI 10.1016/j.prp.2018.04.019
PG 9
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA GM6ZF
UT WOS:000438326800005
PM 29731264
DA 2025-01-04
ER

PT J
AU Jo, P
   König, A
   Schirmer, M
   Kitz, J
   Conradi, LC
   Azizian, A
   Bernhardt, M
   Wolff, HA
   Grade, M
   Ghadimi, M
   Ströbel, P
   Schildhaus, HU
   Gaedcke, J
AF Jo, Peter
   Koenig, Alexander
   Schirmer, Markus
   Kitz, Julia
   Conradi, Lena-Christin
   Azizian, Azadeh
   Bernhardt, Markus
   Wolff, Hendrik A.
   Grade, Marian
   Ghadimi, Michael
   Stroebel, Philipp
   Schildhaus, Hans-Ulrich
   Gaedcke, Jochen
TI Heterogeneity of <i>KRAS</i> Mutation Status in Rectal Cancer
SO PLOS ONE
LA English
DT Article
ID METASTATIC COLORECTAL-CANCER; BRAF; CETUXIMAB; THERAPY; SPECIMENS;
   CHEMORADIOTHERAPY; CHEMOTHERAPY; EVOLUTION; IMPACT; SITES
AB Introduction
   Anti-EGFR targeted therapy is of increasing importance in advanced colorectal cancer and prior KRAS mutation testing is mandatory for therapy. However, at which occasions this should be performed is still under debate. We aimed to assess in patients with locally advanced rectal cancer whether there is intra-specimen KRAS heterogeneity prior to and upon preoperative chemoradiotherapy (CRT), and if there are any changes in KRAS mutation status due to this intervention.
   Materials and Methods
   KRAS mutation status analyses were performed in 199 tumor samples from 47 patients with rectal cancer. To evaluate the heterogeneity between different tumor areas within the same tumor prior to preoperative CRT, 114 biopsies from 34 patients (mean 3 biopsies per patient) were analyzed (pre-therapeutic intratumoral heterogeneity). For the assessment of heterogeneity after CRT residual tumor tissue (85 samples) from 12 patients (mean 4.2 tissue samples per patient) were analyzed (post-therapeutic intratumoral heterogeneity) and assessment of heterogeneity before and after CRT was evaluated in corresponding patient samples (interventional heterogeneity). Primer extension method (SNaPshot (TM)) was used for initial KRAS mutation status testing for Codon 12, 13, 61, and 146. Discordant results by this method were reevaluated by using the FDA-approved KRAS Pyro Kit 24, V1 and the RAS Extension Pyro Kit 24, V1 Kit (therascreen (R) KRAS test).
   Results
   For 20 (43%) out of the 47 patients, a KRAS mutation was detected. With 12 out of 20, the majority of these mutations affected codon 35. We did not obtained evidence that CRT results in changes of the KRAS mutation pattern. In addition, no intratumoral heterogeneity in the KRAS mutational status could be proven. This was true for both the biopsies prior to CRT and the resection specimens thereafter. The discrepancy observed in some samples when using the SNaPshot (TM) assay was due to insufficient sensitivity of this technique upon massive tumor regression by CRT as application of the therascreen (R) KRAS test revealed concordant results.
   Conclusion
   Our results indicate that the KRAS mutation status at the primary tumor site of rectal cancer is homogenous. Its assessment for therapeutic decisions is feasible in pre-therapeutic biopsies as well as in post-therapeutic resected specimens. The amount of viable tumor cells seems to be an important determinant for assay sensitivity and should thus be considered for selection of the analytical method.
C1 [Jo, Peter; Conradi, Lena-Christin; Azizian, Azadeh; Bernhardt, Markus; Grade, Marian; Ghadimi, Michael; Gaedcke, Jochen] Univ Med Ctr Goettingen, Dept Gen Visceral & Pediat Surg, Gottingen, Germany.
   [Koenig, Alexander] Univ Med Ctr Goettingen, Dept Gastroenterol & Gastrointestinal Oncol, Gottingen, Germany.
   [Schirmer, Markus] Univ Med Ctr Goettingen, Dept Clin Pharmacol, Gottingen, Germany.
   [Kitz, Julia; Stroebel, Philipp; Schildhaus, Hans-Ulrich] Univ Med Ctr Goettingen, Dept Pathol, Gottingen, Germany.
   [Wolff, Hendrik A.] Radiotherapy & Radiol Munich, Munich, Germany.
C3 University of Gottingen; UNIVERSITY GOTTINGEN HOSPITAL; University of
   Gottingen; UNIVERSITY GOTTINGEN HOSPITAL; University of Gottingen;
   UNIVERSITY GOTTINGEN HOSPITAL; University of Gottingen; UNIVERSITY
   GOTTINGEN HOSPITAL
RP Gaedcke, J (corresponding author), Univ Med Ctr Goettingen, Dept Gen Visceral & Pediat Surg, Gottingen, Germany.
EM jochen.gaedcke@med.uni-goettingen.de
RI Schildhaus, Hans Ulrich/KIA-2879-2024
OI Schildhaus, Hans Ulrich/0000-0002-9856-7050
FU Deutsche Forschungsgemeinschaft (DFG)
FX The work is part of the Clinical Research Unit (KFO 179) and was
   supported by the Deutsche Forschungsgemeinschaft (DFG).
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NR 29
TC 12
Z9 14
U1 0
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 11
PY 2016
VL 11
IS 4
AR e0153278
DI 10.1371/journal.pone.0153278
PG 13
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA DJ0KH
UT WOS:000373891000040
PM 27064574
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Keyvani-Ghamsari, S
   Khorsandi, K
   Rasul, A
   Zaman, MK
AF Keyvani-Ghamsari, Saeedeh
   Khorsandi, Khatereh
   Rasul, Azhar
   Zaman, Muhammad Khatir
TI Current understanding of epigenetics mechanism as a novel target in
   reducing cancer stem cells resistance
SO CLINICAL EPIGENETICS
LA English
DT Review
DE Cancer stem cell (CSC); Epigenetic modifications; Signaling pathway;
   Drug resistance; Epi-drugs
ID TUMOR-INITIATING CELLS; BREAST-CANCER; COLORECTAL-CANCER; SELF-RENEWAL;
   DEACETYLASE INHIBITOR; DRUG-RESISTANCE; NONCODING RNAS; OVARIAN-CANCER;
   THERAPEUTIC IMPLICATIONS; MESENCHYMAL TRANSITION
AB At present, after extensive studies in the field of cancer, cancer stem cells (CSCs) have been proposed as a major factor in tumor initiation, progression, metastasis, and recurrence. CSCs are a subpopulation of bulk tumors, with stem cell-like properties and tumorigenic capabilities, having the abilities of self-renewal and differentiation, thereby being able to generate heterogeneous lineages of cancer cells and lead to resistance toward anti-tumor treatments. Highly resistant to conventional chemo- and radiotherapy, CSCs have heterogeneity and can migrate to different organs and metastasize. Recent studies have demonstrated that the population of CSCs and the progression of cancer are increased by the deregulation of different epigenetic pathways having effects on gene expression patterns and key pathways connected with cell proliferation and survival. Further, epigenetic modifications (DNA methylation, histone modifications, and RNA methylations) have been revealed to be key drivers in the formation and maintenance of CSCs. Hence, identifying CSCs and targeting epigenetic pathways therein can offer new insights into the treatment of cancer. In the present review, recent studies are addressed in terms of the characteristics of CSCs, the resistance thereof, and the factors influencing the development thereof, with an emphasis on different types of epigenetic changes in genes and main signaling pathways involved therein. Finally, targeted therapy for CSCs by epigenetic drugs is referred to, which is a new approach in overcoming resistance and recurrence of cancer.
C1 [Keyvani-Ghamsari, Saeedeh] Islamic Azad Univ, Karaj Branch, Dept Microbiol, Karaj, Iran.
   [Khorsandi, Khatereh] ACECR, Yara Inst, Dept Photodynam, Med Laser Res Ctr, Tehran, Iran.
   [Rasul, Azhar] Govt Coll Univ Faisalabad, Dept Zool, Faisalabad 38000, Pakistan.
   [Zaman, Muhammad Khatir] Abdul Wali Khan Univ Mardan AWKUM, Dept Biotechnol, Mardan 23200, Pakistan.
C3 Islamic Azad University; Academic Center for Education, Culture &
   Research (ACECR); Government College University Faisalabad
RP Khorsandi, K (corresponding author), ACECR, Yara Inst, Dept Photodynam, Med Laser Res Ctr, Tehran, Iran.
EM khorsandi.kh@ut.ac.ir
RI , A. Rasul/GMW-9774-2022; keyvani, Saeedeh/AAN-4361-2021; Khorsandi,
   Khatereh/AAV-7192-2020
OI khorsandi, khatereh/0000-0001-6882-5031
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NR 294
TC 39
Z9 43
U1 0
U2 19
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1868-7075
EI 1868-7083
J9 CLIN EPIGENETICS
JI Clin. Epigenetics
PD MAY 29
PY 2021
VL 13
IS 1
AR 120
DI 10.1186/s13148-021-01107-4
PG 31
WC Oncology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Genetics & Heredity
GA SK1FQ
UT WOS:000655967200001
PM 34051847
OA Green Published
DA 2025-01-04
ER

PT J
AU Sjöstedt, S
   Schmidt, AY
   Vieira, FG
   Willemoe, GL
   Agander, TK
   Olsen, C
   Nielsen, FC
   von Buchwald, C
AF Sjoestedt, Sannia
   Schmidt, Ane Yde
   Vieira, Filipe Garrett
   Willemoe, Gro Linno
   Agander, Tina Klitmoller
   Olsen, Caroline
   Nielsen, Finn Cilius
   von Buchwald, Christian
TI Major driver mutations are shared between sinonasal intestinal-type
   adenocarcinoma and the morphologically identical colorectal
   adenocarcinoma
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Article
DE Sinonasal; Cancer; DNA sequencing; Genomics; Mutations; Intestinal type
   adenocarcinoma
ID NASAL CAVITY; ETHMOIDAL MUCOSA; BRAF MUTATIONS; EXPRESSION; COLON;
   CANCER; GENES; KRAS; DIFFERENTIATION; METASTASIS
AB Purpose The purpose of our study was to compare genomic changes in sinonasal intestinal-type adenocarcinoma (sITAC) and colorectal adenocarcinoma (CRC), as they are histomorphologically indistinguishable. This can cause diagnostic difficulties as sinonasal tumours initially diagnosed as sITAC may represent metastasis from CRC, a frequent cancer. Previous studies have not uncovered the underlying mechanism behind the histomorphological resemblance. Methods/patients Tissue samples from all consecutive patients with sITAC at our facility (20 patients) were compared to samples from 20 patients with CRC as well as samples from 2 patients with both CRC and sinonasal tumours. DNA sequencing was performed using Illumina TruSight Oncology 500 panel consisting of 523 cancer-associated genes. Frequent mutations were inspected manually using the Integrative Genomics Viewer. Results Several well-known cancer-associated genes were mutated in the CRC group, but also in the sinonasal ITAC group. These genes includedAPCmutated in 65% of the CRC group and 37% of the sinonasal ITAC group, andTP53mutated in 65% of CRC samples and 58% of ITAC samples. These shared mutations may explain the histomorphological similarities. Successful DNA sequencing was performed on the colorectal sample from one of the two patients with both CRC and sinonasal tumour. Comparing mutations in these samples from one patient we have shown that the sinonasal tumour in all probability was a CRC metastasis. Conclusion We have identified several genetic similarities between sITAC and CRC. This discovery brings us closer to understanding mechanisms behind the development of sITAC-and hopefully in the future targeted therapy.
C1 [Sjoestedt, Sannia; von Buchwald, Christian] Copenhagen Univ Hosp, Dept Otorhinolaryngol Head & Neck Surg & Audiol, Blegdamsvej 9, DK-2100 Copenhagen O, Denmark.
   [Schmidt, Ane Yde; Vieira, Filipe Garrett; Nielsen, Finn Cilius] Copenhagen Univ Hosp, Ctr Genom Med, Blegdamsvej 9, DK-2100 Copenhagen O, Denmark.
   [Willemoe, Gro Linno; Agander, Tina Klitmoller] Copenhagen Univ Hosp, Dept Pathol, Blegdamsvej 9, DK-2100 Copenhagen O, Denmark.
   [Olsen, Caroline] Zealand Univ Hosp Roskilde, Dept Pathol, Sygehusvej 10, DK-4000 Roskilde, Denmark.
C3 University of Copenhagen; University of Copenhagen; University of
   Copenhagen
RP Sjöstedt, S (corresponding author), Copenhagen Univ Hosp, Dept Otorhinolaryngol Head & Neck Surg & Audiol, Blegdamsvej 9, DK-2100 Copenhagen O, Denmark.
EM sannia.mia.svenningsen.sjoestedt.01@regionh.dk
RI Nielsen, Finn/AAA-4926-2020; Garrett Vieira, Filipe/B-9464-2015; von
   Buchwald, Christian/D-5336-2016
OI Sjostedt, Sannia/0000-0001-8027-5204; Garrett Vieira,
   Filipe/0000-0002-8464-7770; von Buchwald, Christian/0000-0001-6753-8129
FU King Christian XI Foundation; Harboe Foundation; Copenhagen University
   Hospital
FX Sannia Mia Svenningsen Sjostedt has received grants from King Christian
   XI Foundation and Harboe Foundation (both non-profit foundations) and
   Copenhagen University Hospital.
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NR 62
TC 16
Z9 16
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0171-5216
EI 1432-1335
J9 J CANCER RES CLIN
JI J. Cancer Res. Clin. Oncol.
PD APR
PY 2021
VL 147
IS 4
BP 1019
EP 1027
DI 10.1007/s00432-020-03421-5
EA OCT 2020
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QV8QA
UT WOS:000578372000001
PM 33051725
DA 2025-01-04
ER

PT J
AU Ma, TN
   Xu, FF
   Hou, YY
   Shu, YQ
   Zhao, ZP
   Zhang, YR
   Bai, L
   Feng, L
   Zhong, L
AF Ma, Tingnan
   Xu, Feifei
   Hou, Yingying
   Shu, Yongquan
   Zhao, Zhipeng
   Zhang, Yaru
   Bai, Lan
   Feng, Lu
   Zhong, Lei
TI SETDB1: Progress and prospects in cancer treatment potential and
   inhibitor research
SO BIOORGANIC CHEMISTRY
LA English
DT Review
DE SETDB1; Tumorigenesis and progression; Antagonist; Anti -tumor target;
   Immune evasion
ID HISTONE METHYLTRANSFERASE SETDB1; EPITHELIAL-MESENCHYMAL TRANSITION;
   CELL-PROLIFERATION; COLORECTAL-CANCER; SMAD7 EXPRESSION;
   GENE-EXPRESSION; POOR-PROGNOSIS; BETA-CATENIN; PROMOTES; ACTIVATION
AB SET domain bifurcated methyltransferase 1 (SETDB1) serves as a histone lysine methyltransferase, catalyzing the di- and tri-methylation of histone H3K9. Mounting evidence indicates that the abnormal expression or activity of SETDB1, either through amplification or mutation, plays a crucial role in tumorigenesis and progression. This is particularly evident in the context of tumor immune evasion and resistance to immune checkpoint blockade therapy. Furthermore, there is a robust association between SETDB1 dysregulation and an unfavorable prognosis across various types of tumors. The oncogenic role of SETDB1 primarily arises from its methyltransferase function, which contributes to the establishment of a condensed and transcriptionally inactive heterochromatin state. This results in the inactivation of genes that typically hinder cancer development and silencing of retrotransposons that could potentially trigger an immune response. These findings underscore the substantial potential for SETDB1 as an anti-tumor therapeutic target. Nevertheless, despite significant strides in recent years in tumor biology research, challenges persist in SETDB1-targeted therapy. To better facilitate the development of anti-tumor therapy targeting SETDB1, we have conducted a comprehensive review of SETDB1 in this account. We present the structure and function of SETDB1, its role in various tumors and immune regulation, as well as the advancements made in SETDB1 antagonists. Furthermore, we discuss the challenges encountered and provide perspectives for the development of SETDB1-targeted anti-tumor therapy.
C1 [Ma, Tingnan; Xu, Feifei; Hou, Yingying; Shu, Yongquan; Zhao, Zhipeng; Zhang, Yaru; Bai, Lan; Zhong, Lei] Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Personalized Drug Therapy Key Lab Sichuan Prov, Sch Med,Dept Pharm, Chengdu 610041, Peoples R China.
   [Xu, Feifei] Chengdu Univ Tradit Chinese Med, State Key Lab Southwestern Chinese Med Resources, Key Lab Standardizat Chinese Herbal Med, Minist Educ,Pharm Coll, Chengdu 610075, Peoples R China.
   [Feng, Lu] Univ Elect Sci & Technol China, Sichuan Acad Med Sci & Sichuan Prov Peoples Hosp, Dept Emergency, Chengdu 610041, Peoples R China.
C3 University of Electronic Science & Technology of China; Sichuan
   Provincial People's Hospital; Chengdu University of Traditional Chinese
   Medicine; University of Electronic Science & Technology of China;
   Sichuan Provincial People's Hospital
RP Bai, L; Zhong, L (corresponding author), Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Personalized Drug Therapy Key Lab Sichuan Prov, Sch Med,Dept Pharm, Chengdu 610041, Peoples R China.; Feng, L (corresponding author), Univ Elect Sci & Technol China, Sichuan Acad Med Sci & Sichuan Prov Peoples Hosp, Dept Emergency, Chengdu 610041, Peoples R China.
EM blci@163.com; feenglu1974@sina.com; zhl7235301@163.com
RI Zhang, Yaru/KDP-3280-2024; Zhao, Zhipeng/ISA-3448-2023; Zhong,
   Lei/KSM-6502-2024; Hou, Yingying/KQU-9653-2024
OI Hou, Yingying/0009-0001-0561-5835
FU Research Project of Chengdu Science and Technology Bureau
   [2022-YF05-01611-SN]; Research Funds of Science & Technology Department
   of Sichuan Province [2021YJ0134]; Fundamental Research Funds for the
   Central Universities [ZYGX2019J106]
FX This work was supported by the Research Project of Chengdu Science and
   Technology Bureau [2022-YF05-01611-SN] ; the Research Funds of Science &
   Technology Department of Sichuan Province [2021YJ0134] ; and the
   Fundamental Research Funds for the Central Universities [ZYGX2019J106] .
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NR 139
TC 1
Z9 1
U1 8
U2 12
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0045-2068
EI 1090-2120
J9 BIOORG CHEM
JI Bioorganic Chem.
PD APR
PY 2024
VL 145
AR 107219
DI 10.1016/j.bioorg.2024.107219
EA FEB 2024
PG 19
WC Biochemistry & Molecular Biology; Chemistry, Organic
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA NA2Z1
UT WOS:001197665100001
PM 38377821
DA 2025-01-04
ER

PT J
AU Cignetto, S
   Modica, C
   Chiriaco, C
   Fontani, L
   Milla, P
   Michieli, P
   Comoglio, PM
   Vigna, E
AF Cignetto, Simona
   Modica, Chiara
   Chiriaco, Cristina
   Fontani, Lara
   Milla, Paola
   Michieli, Paolo
   Comoglio, Paolo M.
   Vigna, Elisa
TI Dual Constant Domain-Fab: A novel strategy to improve half-life and
   potency of a Met therapeutic antibody
SO MOLECULAR ONCOLOGY
LA English
DT Article
DE Cancer targeted therapy; Met; Antibody; Fab; Half-life; Protein
   engineering
ID HEPATOCYTE GROWTH-FACTOR; RECEPTOR TYROSINE KINASE; LUNG-CANCER; C-MET;
   ACQUIRED-RESISTANCE; COLORECTAL-CANCER; SOMATIC MUTATIONS;
   SCATTER-FACTOR; AMPLIFICATION; INHIBITORS
AB The kinase receptor encoded by the Met oncogene is a sensible target for cancer therapy. The chimeric monovalent Fab fragment of the DN30 monoclonal antibody (MvIDN30) has an odd mechanism of action, based on cell surface removal of Met via activation of specific plasma membrane proteases. However, the short half-life of the Fab, due to its low molecular weight, is a severe limitation for the deployment in therapy. This issue was addressed by increasing the Fab molecular weight above the glomerular filtration threshold through the duplication of the constant domains, in tandem (DCD-1) or reciprocally swapped (DCD-2). The two newly engineered molecules showed biochemical properties comparable to the original MyDN30 in vitro, acting as full Met antagonists, impairing Met phosphorylation and activation of downstream signaling pathways. As a consequence, Met-mediated biological responses were inhibited, including anchorage-dependent and-independent cell growth. In vivo DCD-1 and DCD-2 showed a pharmacokinetic profile significantly improved over the original MvDN30, doubling the circulating half-life and reducing the clearance. In pre-clinical models of cancer, generated by injection of tumor cells or implant of patient derived samples, systemic administration of the engineered molecules inhibited the growth of Met-addicted tumors. (C) 2016 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
C1 [Cignetto, Simona; Modica, Chiara; Chiriaco, Cristina; Fontani, Lara; Michieli, Paolo; Comoglio, Paolo M.; Vigna, Elisa] Candiolo Canc Inst, FPO IRCCS, Str Prov 142, I-10060 Candiolo, Italy.
   [Cignetto, Simona; Modica, Chiara; Michieli, Paolo; Comoglio, Paolo M.; Vigna, Elisa] Univ Turin, Dept Oncol, Str Prov 142, I-10060 Candiolo, Italy.
   [Milla, Paola] Univ Turin, Dept Sci & Drug Technol, Via P Giuria 9, I-10125 Turin, Italy.
C3 IRCCS Fondazione del Piemonte per l'Oncologia; University of Turin;
   University of Turin
RP Comoglio, PM; Vigna, E (corresponding author), Str Prov 142, I-10060 Candiolo, Italy.
EM pcomoglio@gmail.com; elisa.vigna@ircc.it
RI Comoglio, Paolo/G-6323-2011; Michieli, Paolo/A-2588-2011; Vigna,
   Elisa/JWO-5055-2024; Milla, Paola/H-7596-2012; Cignetto,
   Simona/J-5359-2018
OI Comoglio, Paolo/0000-0002-7056-5328; Vigna, Elisa/0000-0001-9787-5732;
   MICHIELI, Paolo/0000-0002-3093-8871; modica, chiara/0000-0002-7000-5216;
   Fontani, Lara/0000-0003-3593-5781; Cignetto, Simona/0000-0001-5515-7185
FU AIRC [11852, 15572, 9970]
FX This work was supported by AIRC grants (IG Project no 11852, IG Project
   no 15572 and 2010 Special Program Molecular Clinical Oncology 5xMille,
   Project no 9970) to PMC.
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NR 53
TC 10
Z9 12
U1 0
U2 6
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1574-7891
EI 1878-0261
J9 MOL ONCOL
JI Mol. Oncol.
PD JUN
PY 2016
VL 10
IS 6
BP 938
EP 948
DI 10.1016/j.molonc.2016.03.004
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DQ7FJ
UT WOS:000379372000012
PM 27103110
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Yang, M
   Shen, C
   Zhu, SJ
   Zhang, Y
   Jiang, HL
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   Yang, GY
   Liu, JP
AF Yang, Ming
   Shen, Chen
   Zhu, Si-jia
   Zhang, Yao
   Jiang, Hong-lin
   Bao, Yu-dong
   Yang, Guo-yan
   Liu, Jian-ping
TI Chinese patent medicine Aidi injection for cancer care: An overview of
   systematic reviews and meta-analyses
SO JOURNAL OF ETHNOPHARMACOLOGY
LA English
DT Review
DE Aidi injection; Overview; Cancer care; Systematic reviews; Chinese
   patent medicine; AMSTAR2
ID CELL LUNG-CANCER; CHEMOTHERAPY; EFFICACY; CARCINOMA; SAFETY
AB Ethnopharmacological relevance: Aidi injection is one of the China Food and Drug Administration approved Chinese herbal injections and the most competitive product in cancer care in China. It is composed of the extracts from Mylabris Phalerata, Astragalus Membranaceus, Panax Ginseng, and Acanthopanax Senticosus. Aim of the study: This overview aims to map systematic reviews (SRs) of Aidi injection for cancer and provide a summarized evidence for clinical practice and decision making. Materials and methods: Seven databases were searched for SRs and/or meta-analyses of randomized controlled trials on Aidi injection for cancer care until December 2020. Six authors worked in pairs independently identified studies, collected data, and assessed the quality of included studies according to the revised Assessment of Multiple Systematic Reviews (AMSTAR 2) and the Preferred Reporting Items for Systematic Reviews and MetaAnalyses (PRISMA). A narrative synthesis was used for the evidence mapping. Results: Fifty-two SRs on Aidi injection as adjuvant therapy were included, involving lung cancer (20 SRs), liver cancer (10), colorectal cancer (7), gastric cancer (6), lymphoma (2), breast cancer (2), esophageal cancer (1), ovary cancer (1), and a mix of different cancers (4). Except for one SR focusing on Aidi injection used alone, other SRs evaluated Aidi injection in combination with chemotherapy (43), radiotherapy (4), or chemo/radiology/ targeting therapy (4). Aidi injection showed additional beneficial effects on survival (9), objective response rate (44), quality of life (42), and the reduction of side-effects from chemo/radiotherapy (48). Using AMSTAR 2 tool, two reviews were assessed as low and the rest as critically low methodological quality mainly due to the lack of prospective registration. The reporting quality was insufficient assessed with PRISMA in the reporting of search strategy (26, 50.0%), additional analysis (19, 36.5%), and the summary of evidence (2, 3.8%). Conclusion: Aidi injection has been evaluated for its adjuvant beneficial effects on cancer survival, tumor responses, quality of life, and reducing the side effects of chemo/radiotherapy, mainly focusing on lung, liver and colorectal cancer. The methodological and reporting quality are weak and need to be improved in the future.
C1 [Yang, Ming; Shen, Chen; Zhu, Si-jia; Liu, Jian-ping] Beijing Univ Chinese Med, Ctr Evidence Based Chinese Med, 11 Bei San Huan Dong Lu, Beijing 100029, Peoples R China.
   [Jiang, Hong-lin; Bao, Yu-dong] Beijing Univ Chinese Med, Affiliated Hosp 1, Beijing 100029, Peoples R China.
   [Jiang, Hong-lin; Bao, Yu-dong] Beijing Univ Chinese Med, Inst Acupuncture & Moxibust Canc Care, Beijing 100029, Peoples R China.
   [Zhang, Yao] China Acad Chinese Med Sci, Xiyuan Hosp, Beijing 100091, Peoples R China.
   [Zhang, Yao] Beijing Univ Chinese Med, Beijing 100029, Peoples R China.
   [Yang, Guo-yan] Univ Western Sydney, NICM Hlth Res Inst, Penrith, NSW 2751, Australia.
C3 Beijing University of Chinese Medicine; Beijing University of Chinese
   Medicine; Beijing University of Chinese Medicine; Xiyuan Hospital,
   CACMS; China Academy of Chinese Medical Sciences; Beijing University of
   Chinese Medicine; Western Sydney University
RP Liu, JP (corresponding author), Beijing Univ Chinese Med, Ctr Evidence Based Chinese Med, 11 Bei San Huan Dong Lu, Beijing 100029, Peoples R China.
EM yangming@bucm.edu.cn; shenchensophia@bucm.edu.cn; zhusijia2018@163.com;
   zhangyaonkyd@163.com; joylin68@163.com; 18811385356@163.com;
   e.yang@westernsydney.edu.au; liujp@bucm.edu.cn
RI Shen, Chen/GQP-1025-2022; Jianping, Liu/J-5248-2018; Yang,
   Guoyan/AAG-7873-2021; Bao, Yudong/IUP-5101-2023
OI Yang, Guoyan/0000-0002-8012-2379; Shen, Chen/0000-0002-5439-7133; Liu,
   Jianping/0000-0002-0320-061X; Zhu, Si Jia/0000-0001-6508-4979
FU Key Project of the National Natural Science Foundation of China
   [81830115]
FX This work was supported by the Key Project of the National Natural
   Science Foundation of China (No.81830115) "Key techniques and outcome
   research for therapeutic effect of traditional Chinese medicine as
   complex intervention based on holistic system and pattern
   differen-tiation & prescription", China.
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NR 67
TC 29
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U2 96
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0378-8741
EI 1872-7573
J9 J ETHNOPHARMACOL
JI J. Ethnopharmacol.
PD JAN 10
PY 2022
VL 282
AR 114656
DI 10.1016/j.jep.2021.114656
EA SEP 2021
PG 12
WC Plant Sciences; Chemistry, Medicinal; Integrative & Complementary
   Medicine; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Plant Sciences; Pharmacology & Pharmacy; Integrative & Complementary
   Medicine
GA WE0SP
UT WOS:000705340000006
PM 34551361
DA 2025-01-04
ER

PT J
AU DiNardo, CD
   Venugopal, S
   Lachowiez, C
   Takahashi, K
   Loghavi, S
   Montalban-Bravo, G
   Wang, XM
   Carraway, H
   Sekeres, M
   Sukkur, A
   Hammond, D
   Chien, KLY
   Maiti, A
   Masarova, L
   Sasaki, K
   Alvarado, Y
   Kadia, T
   Short, NJ
   Daver, N
   Borthakur, G
   Ravandi, F
   Kantarjian, HM
   Patel, B
   Dezern, A
   Roboz, G
   Garcia-Manero, G
AF DiNardo, Courtney D.
   Venugopal, Sangeetha
   Lachowiez, Curtis
   Takahashi, Koichi
   Loghavi, Sanam
   Montalban-Bravo, Guillermo
   Wang, Xuemei
   Carraway, Hetty
   Sekeres, Mikkael
   Sukkur, Ameenah
   Hammond, Danielle
   Chien, Kelly
   Maiti, Abhishek
   Masarova, Lucia
   Sasaki, Koji
   Alvarado, Yesid
   Kadia, Tapan
   Short, Nicholas J.
   Daver, Naval
   Borthakur, Gautam
   Ravandi, Farhad
   Kantarjian, Hagop M.
   Patel, Bhumika
   Dezern, Amy
   Roboz, Gail
   Garcia-Manero, Guillermo
TI Targeted therapy with the mutant <i>IDH2</i> inhibitor enasidenib for
   high-risk IDH2-mutant myelodysplastic syndrome
SO BLOOD ADVANCES
LA English
DT Article
ID OPEN-LABEL; AZACITIDINE; CLASSIFICATION; DECITABINE; MUTATIONS; CARE
AB The isocitrate dehydrogenase enzyme 2 (IDH2) gene is mutated in similar to 5% of patients with myelodysplastic syndrome (MDS). Enasidenib is an oral, selective, mutant IDH2 inhibitor approved for IDH2-mutated (mIDH2) relapsed/refractory acute myeloid leukemia. We designed a 2-arm multicenter study to evaluate safety and efficacy of (A) the combination of enasidenib with azacitidine for newly diagnosed mIDH2 MDS, and (B) enasidenib monotherapy for mIDH2 MDS after prior hypomethylating agent (HMA) therapy. Fifty patients with mIDH2 MDS enrolled: 27 in arm A and 23 in arm B. Median age of patients was 73 years. The most common adverse events were neutropenia (40%), nausea (36%), constipation (32%), and fatigue (26%). Hyperbilirubinemia from off-target UGT1A1 inhibition occurred in 14% of patients (8%; grades 3 and 4), and IDH-inhibitor-associated differentiation syndrome (IDH-DS) in 8 patients (16%). In the combination arm, the overall response rate (ORR: complete remission [CR] + marrow CR [mCR] + partial remission) was 74%, including 70% composite CR (CRc: CR + mCR). Median time to best response was 1 month (range, 1-4), anda median of 4 cycles was received (1-32). The median overall survival (OS) was 26 months (range, 14 to not reached). In the enasidenib monotherapy cohort after HMA failure, ORR and CRc were both 35% (n = 8), with 22% CR (n = 5). Median time to first response was 27 days, and time to best response was 4.6 months (2.7-7.6 months). A median of 7 cycles was received (range, 1-29), and the median OS was 20 months (range, 11 to not reached). Enasidenib is an effective treatment option for mIDH2 MDS, both in combination with azacitidine for treatment-naive high-risk MDS, and as a single agent after prior HMA therapy. This trial is registered at www.clinicaltrials.gov as #NCT03383575.
C1 [DiNardo, Courtney D.; Venugopal, Sangeetha; Lachowiez, Curtis; Takahashi, Koichi; Montalban-Bravo, Guillermo; Hammond, Danielle; Chien, Kelly; Maiti, Abhishek; Masarova, Lucia; Sasaki, Koji; Alvarado, Yesid; Kadia, Tapan; Short, Nicholas J.; Daver, Naval; Borthakur, Gautam; Ravandi, Farhad; Kantarjian, Hagop M.; Garcia-Manero, Guillermo] Univ Texas MD Anderson Canc Ctr Houston, Dept Leukemia, Houston, TX USA.
   [Loghavi, Sanam] Univ Texas MD Anderson Canc Ctr Houston, Dept Hematopathol, Houston, TX USA.
   [Wang, Xuemei] Univ Texas MD Anderson Canc Ctr Houston, Dept Biostat, Houston, TX USA.
   [Carraway, Hetty; Patel, Bhumika] Cleveland Clin, Taussig Canc Inst, Leukemia Program, Cleveland, OH USA.
   [Sekeres, Mikkael] Univ Miami, Sylvester Canc Ctr, Div Hematol, Miami, FL USA.
   [Sukkur, Ameenah; Roboz, Gail] Weill Cornell Med Coll, New York Presbyterian Hosp, New York, NY USA.
   [Dezern, Amy] Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Div Hematol Malignancies & Bone Marrow Transplanta, Baltimore, MD USA.
   [DiNardo, Courtney D.] UT MD Anderson Canc Ctr, Dept Leukemia, 1515 Holcombe Blvd, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; University of
   Texas System; UTMD Anderson Cancer Center; University of Texas System;
   UTMD Anderson Cancer Center; Cleveland Clinic Foundation; University of
   Miami; Cornell University; Weill Cornell Medicine; NewYork-Presbyterian
   Hospital; Johns Hopkins University; Johns Hopkins Medicine; University
   of Texas System; UTMD Anderson Cancer Center
RP DiNardo, CD (corresponding author), UT MD Anderson Canc Ctr, Dept Leukemia, 1515 Holcombe Blvd, Houston, TX 77030 USA.
EM cdinardo@mdanderson.org
RI Borthakur, Gautam/AAQ-4490-2021; Kantarjian, Hagop/B-4264-2015; DiNardo,
   Courtney/KYO-7203-2024; Ravandi, Farhad/GOH-3538-2022; Daver,
   Naval/AFU-9643-2022; Short, Nicholas/I-3319-2019; Loghavi,
   Sanam/H-8485-2019; Carraway, Hetty/AAR-4977-2020; Sasaki,
   Koji/T-1218-2019
OI Loghavi, Sanam/0000-0001-8980-3202; Carraway, Hetty/0000-0001-5241-3614;
   Sasaki, Koji/0000-0002-9140-0610; Venugopal,
   Sangeetha/0000-0002-8641-6415; DiNardo, Courtney/0000-0001-9003-0390
FU Celgene and Bristol Myers Squibb (BMS); University of Texas MD Anderson
   Cancer Center [CA016672]; V Foundation Lloyd Family Clinical Scholar and
   LLS Scholar in Clinical Research Award; University of Texas MD Anderson
   Cancer Center MDS/AML Moon Shot
FX This study was funded in part by research funding from Celgene and
   Bristol Myers Squibb (BMS) (C.D.D.) and in part by the University of
   Texas MD Anderson Cancer Center Support grant CA016672 and the
   University of Texas MD Anderson Cancer Center MDS/AML Moon Shot. C.D.D.
   is supported by a V Foundation Lloyd Family Clinical Scholar and LLS
   Scholar in Clinical Research Award.
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NR 19
TC 29
Z9 30
U1 1
U2 8
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2473-9529
EI 2473-9537
J9 BLOOD ADV
JI Blood Adv.
PD JUN 13
PY 2023
VL 7
IS 11
BP 2378
EP 2387
DI 10.1182/bloodadvances.2022008378
EA MAY 2023
PG 10
WC Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Hematology
GA O5LH2
UT WOS:001044218100001
PM 35973199
OA gold, Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Telang, N
AF Telang, Nitin
TI Stem cell models for genetically predisposed colon cancer
SO ONCOLOGY LETTERS
LA English
DT Review
DE adenomatous polyposis coli; drug resistance; stem cells
ID FAMILIAL ADENOMATOUS POLYPOSIS; MULTIPLE INTESTINAL NEOPLASIA;
   COLORECTAL-CANCER; CYCLOOXYGENASE-2 INHIBITOR; CHEMOPREVENTIVE EFFICACY;
   CARCINOGENIC RISK; HCT-116 CELLS; PREVENTION; SULINDAC; MUTATION
AB Negative growth regulatory tumor suppressor genes and positive growth regulatory oncogenes serve important roles in initiation/progression of colon cancer. Germline mutation in the adenomatous polyposis coli (APC) tumor suppressor gene represents a primary genetic defect for familial adenomatous polyposis (FAP) syndrome, a predisposing factor for clinical colon cancer. Somatic mutations in the APC gene are common in sporadic colon cancer. Preclinical and clinical efficacy is documented for targeted therapy with non-steroidal anti-inflammatory drugs, selective cyclo-oxygenase-2 inhibitors for prostaglandin biosynthesis and selective inhibitor of ornithine decarboxylase for polyamine biosynthesis. However, these therapeutic options lead to systemic toxicity, acquired tumor resistance and emergence of therapy resistant cancer stem cells. By contrast, non-toxic natural products are unlikely to exhibit drug resistance and may represent testable alternatives for therapy resistant colon cancer. Tumorigenic Apc [-/-] colonic epithelial cell lines derived from preclinical FAP models provide novel cellular models for drug resistant cancer stem cells. Apc [-/-] Sulindac resistant (SUL-R) cells exhibit upregulated expression levels of cancer stem cell markers. Natural products, such as naturally occurring vitamin A derivative all-trans retinoic acid (ATRA) and the anti-cancer agent from Turmeric root curcumin (CUR), represent testable alternatives. Relative to the non-tumorigenic Apc [+/+] C57 COL colonic epithelial cells, the tumorigenic Apc [-/-] 1638N COL and Apc [-/-] 850 (MIN) COL cells exhibit aneuploid cell hyper-proliferation and upregulated expression of Apc target genes beta -catenin, cyclin D1, c-myc and COX-2. The SUL-R phenotypes exhibit enhanced tumor spheroid formation and upregulated expression levels of stem cell markers CD44, CD133 and c-Myc. Treatment of the SUL-R stem cells with ATRA and CUR inhibits tumor spheroid formation and reduces the expression of stem cell markers. Stem cell models developed for FAP syndrome provide a novel experimental approach to identify mechanistic leads for efficacious natural products as testable alternatives for therapy-resistant, genetically predisposed colon cancer.
C1 [Telang, Nitin] Palindrome Liaisons Consultants, Canc Prevent Res Program, 10 Rolling Ridge,Suite B, Montvale, NJ 07645 USA.
RP Telang, N (corresponding author), Palindrome Liaisons Consultants, Canc Prevent Res Program, 10 Rolling Ridge,Suite B, Montvale, NJ 07645 USA.
EM ntelang3@gmail.com
FU US National Cancer Institute [CN 75029-63]; US National Institutes of
   Health [CA 29502-S1]
FX This research has been funded in the past through US National Cancer
   Institute Contract Research Master Agreement (grant no. CN 75029-63), US
   National Institutes of Health (grant no. CA 29502-S1) and philanthropic
   research support to Strang Cancer Prevention Center, New York, USA.
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NR 50
TC 6
Z9 6
U1 1
U2 5
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD NOV
PY 2020
VL 20
IS 5
AR 138
DI 10.3892/ol.2020.11998
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OS4ZJ
UT WOS:000590173300015
PM 32934706
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yang, FL
   Hu, M
   Chang, SY
   Huang, J
   Si, Y
   Wang, JH
   Cheng, S
   Jiang, WG
AF Yang, Fenglian
   Hu, Mu
   Chang, Siyuan
   Huang, Jing
   Si, Yang
   Wang, Jinghui
   Cheng, Shan
   Jiang, Wen G.
TI Alteration in the sensitivity to crizotinib by
   Na<SUP>+</SUP>/H<SUP>+</SUP> exchanger regulatory factor 1 is dependent
   to its subcellular localization in ALK-positive lung cancers
SO BMC CANCER
LA English
DT Article
DE NHERF1; Crizotinib; ALK; Lung cancer; PDZ protein
ID COLORECTAL-CANCER; BREAST-CANCER; NUCLEAR NHERF1; EXPRESSION; EBP50;
   FEATURES; MARKER; GROWTH; GENE
AB Background Na+/H+ exchanger regulatory factor 1 (NHERF1) is an important scaffold protein participates in the modulation of a variety of intracellular signal pathways. NHERF1 was able to enhance the effects of chemo-drugs in breast and cervical cancer cells. Anaplastic lymphoma kinase (ALK) fusion mutations are validated molecules targeted therapy in lung cancers, where crizotinib can be used as the specific inhibitor to suppress tumor progression. However, due to the less frequent occurrence of ALK mutations and the complexity for factors to determine drug responses, the genes that could alter crizotinib sensitivity are unclear. Methods Both ALK-translocated and ALK-negative lung adenocarcinoma specimens in tissue sections were collected for immunohistochemistry. The possible mechanisms of NHERF1 and its role in the cell sensitivity to crizotinib were investigated using an ALK-positive and crizotinib-sensitive lung adenocarcinoma cell line H3122. Either a NHERF1 overexpression vector or agents for NHERF1 knockdown was used for crizotinib sensitivity measures, in association with cell viability and apoptosis assays. Results The expression level of NHERF1 in ALK-translocated NSCLC was significantly higher than that in other lung cancer tissues. NHERF1 expression in ALK positive lung cancer cells was regulated by ALK activities, and was in return able to alter the sensitivity to crizotinib. The function of NHERF1 to influence crizotinib sensitivity was depending on its subcellular distribution in cytosol instead of its nucleus localized form. Conclusion Ectopically overexpressed NHERF1 could be a functional protein for consideration to suppress lung cancers. The determination of NHERF1 levels in ALK positive NSCLC tissues might be useful to predict crizotinib resistance, especially by distinguishing cytosolic or nuclear localized NHERF1 for the overexpressed molecules.
C1 [Yang, Fenglian; Chang, Siyuan; Huang, Jing; Si, Yang; Cheng, Shan; Jiang, Wen G.] Capital Med Univ, Sch Basic Med Sci, Beijing 100069, Peoples R China.
   [Yang, Fenglian; Hu, Mu; Chang, Siyuan; Huang, Jing; Si, Yang; Cheng, Shan; Jiang, Wen G.] Capital Med Univ, Beijing Key Lab Canc & Metastasis Res, Beijing, Peoples R China.
   [Hu, Mu] Beijing Xuanwu Hosp, Dept Thorac Surg, Beijing 100053, Peoples R China.
   [Wang, Jinghui] Beijing Chest Hosp, Dept Med Oncol, Beijing 101149, Peoples R China.
   [Jiang, Wen G.] Cardiff Univ, Sch Med, Cardiff China Med Res Collaborat, Heath Pk, Cardiff CF14 4XN, Wales.
C3 Capital Medical University; Capital Medical University; Capital Medical
   University; Capital Medical University; Cardiff University
RP Cheng, S (corresponding author), Capital Med Univ, Sch Basic Med Sci, Beijing 100069, Peoples R China.; Cheng, S (corresponding author), Capital Med Univ, Beijing Key Lab Canc & Metastasis Res, Beijing, Peoples R China.
EM chengs@ccmu.edu.cn
RI , firhill/HGE-6886-2022; Jiang, Wen/AAF-1876-2020; Chang,
   Siyuan/V-8277-2019; Jiang, Wen G./B-1293-2010
OI Jiang, Wen G./0000-0002-3283-1111
FU Supporting Project for High Caliber Teachers in Beijing Municipal
   Universities during the "13th Five-year Plan" [IDHT20170516]
FX This work was funded by the Supporting Project for High Caliber Teachers
   in Beijing Municipal Universities during the "13th Five-year Plan"
   (IDHT20170516). The funding source has no role in study design, data
   collection, analysis, interpretation, the writing of the manuscript, or
   the decision to submit the current study.
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NR 28
TC 4
Z9 4
U1 0
U2 4
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD MAR 12
PY 2020
VL 20
IS 1
AR 202
DI 10.1186/s12885-020-6687-9
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KW4CD
UT WOS:000521112100007
PM 32164629
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Viji, MP
   Matada, GSP
   Pal, R
   Ghara, A
   Das, PK
   Manjushree, B
   Mounika, S
   Haripriya, E
   Sk, MA
AF Viji, M. P.
   Matada, Gurubasavaraja Swamy Purawarga
   Pal, Rohit
   Ghara, Abhishek
   Das, Pronoy Kanti
   Manjushree, B., V
   Mounika, S.
   Haripriya, E.
   Sk, Md Ashadul
TI Exploring Thiazolidine-2,4-dione derivatives as privileged scaffolds for
   targeted anticancer agents: Biological activity and structure-activity
   relationship (SAR) insights
SO JOURNAL OF MOLECULAR STRUCTURE
LA English
DT Review
DE Targeted therapy; Thiazolidinedione; Anticancer; SAR; Resistance
ID ACTIVATED RECEPTOR-GAMMA; INHIBITS CELL-GROWTH; PPAR-GAMMA; IN-VITRO;
   BREAST-CANCER; INDUCE APOPTOSIS; GASTRIC-CANCER; COLON-CANCER; CYCLE
   ARREST; CARCINOMA
AB Cancer remains one of the most pressing global public health challenges. While chemotherapy has long been a cornerstone of cancer treatment, its inability to distinguish between cancerous and healthy cells often leads to significant toxicity and side effects. Over the past two decades, there has been a remarkable shift from these broad-spectrum cytotoxic drugs to more targeted therapies, which offer superior efficacy and a more favourable profile. Targeted treatments, unlike traditional chemotherapy, selectively attack cancer cells, and minimizing the side effect. However, a major obstacle with targeted therapies is the development of drug resistance, which continues to challenge the medical community's efforts to develop highly selective and low-toxicity anticancer drugs. In the quest for new anticancer agents that are both effective and have a favourable toxicity profile, heterocyclic compounds containing thiazolidinedione (TZD) derivatives have attracted significant attention in both preclinical and clinical research. TZDs can modulate multiple signalling pathways involved in cancer cell proliferation, apoptosis, and metastasis. The structural versatility of TZD compounds enables the development of derivatives with enhanced selectivity and potency against cancer cells. Beyond improving therapeutic efficacy and selectivity, TZD hybrid compounds hold the potential to overcome drug resistance. Over the past decade, several TZD-based hybrids have been developed and evaluated for their anticancer activity, with some showing promising in-vitro efficacy, indicating their potential as future anticancer agents. This study highlights the antitumor efficacy and potential mechanisms of action of these TZD hybrids and summarizes recent advancements in their development as promising anticancer drugs. Additionally, the study will explore the role of structure-activity relationship (SAR) studies in guiding the rational design of TZD hybrids to create more potent and selective candidates.
C1 [Viji, M. P.; Matada, Gurubasavaraja Swamy Purawarga; Pal, Rohit; Ghara, Abhishek; Das, Pronoy Kanti; Manjushree, B., V; Mounika, S.; Haripriya, E.; Sk, Md Ashadul] Acharya & BM Reddy Coll Pharm, Integrated Drug Discovery Ctr, Dept Pharmaceut Chem, Bengaluru 560107, Karnataka, India.
RP Matada, GSP; Pal, R (corresponding author), Acharya & BM Reddy Coll Pharm, Integrated Drug Discovery Ctr, Dept Pharmaceut Chem, Bengaluru 560107, Karnataka, India.
EM gurubasavarajaswamy@gmail.com; rohitpal.rp096@gmail.com
RI swamy, Gurubasavaraja/ABD-7194-2021; Ghara, Abhishek/KGM-4288-2024; PAL,
   ROHIT/GPX-1264-2022
OI Purawarga Matada, Gurubasavaraja Swamy/0000-0002-1978-6029; PAL,
   ROHIT/0000-0002-2763-5757
FU Acharya & B M Reddy College of Pharmacy in Bengaluru; ICMR
   [5/13/12/2020/NCD-III, 5/13/79/2020/NCD-III]
FX This study was sponsored by the Acharya & B M Reddy College of Pharmacy
   in Bengaluru and the ICMR (No. 5/13/12/2020/NCD-III and No
   5/13/79/2020/NCD-III) programs.
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NR 91
TC 1
Z9 1
U1 1
U2 1
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0022-2860
EI 1872-8014
J9 J MOL STRUCT
JI J. Mol. Struct.
PD FEB 15
PY 2025
VL 1322
AR 140529
DI 10.1016/j.molstruc.2024.140529
EA NOV 2024
PN 3
PG 16
WC Chemistry, Physical
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA L8E9I
UT WOS:001353010200001
DA 2025-01-04
ER

PT J
AU Zhang, QF
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   Liu, Furong
   Qin, Lu
   Liao, Zhibin
   Song, Jia
   Liang, Huifang
   Chen, Xiaoping
   Zhang, Zhanguo
   Zhang, Bixiang
TI Characterization of TGFβ-associated molecular features and drug
   responses in gastrointestinal adenocarcinoma
SO BMC GASTROENTEROLOGY
LA English
DT Article
DE Gastrointestinal adenocarcinoma; Transforming growth factor beta;
   Multi-omics signatures; Drug susceptibility; Deep neural network
ID CANCER; METASTASIS; EXPRESSION; LANDSCAPE; CELLS
AB BackgroundGastrointestinal adenocarcinoma (GIAD) has caused a serious disease burden globally. Targeted therapy for the transforming growth factor beta (TGF-beta) signaling pathway is becoming a reality. However, the molecular characterization of TGF-beta associated signatures in GIAD requires further exploration.MethodsMulti-omics data were collected from TCGA and GEO database. A pivotal unsupervised clustering for TGF-beta level was performed by distinguish status of TGF-beta associated genes. We analyzed differential mRNAs, miRNAs, proteins gene mutations and copy number variations in both clusters for comparison. Enrichment of pathways and gene sets were identified in each type of GIAD. Then we performed differential mRNA related drug response by collecting data from GDSC. At last, a summarized deep neural network for TGF-beta status and GIADs was constracted.ResultsThe TGF-beta (high) group had a worse prognosis in overall GIAD patients, and had a worse prognosis trend in gastric cancer and colon cancer specifically. Signatures (including mRNA and proteins) of the TGF-beta (high) group is highly correlated with EMT. According to miRNA analysis, miR-215-3p, miR-378a-5p, and miR-194-3p may block the effect of TGF-beta. Further genomic analysis showed that TGF-beta (low) group had more genomic changes in gastric cancer, such as TP53 mutation, EGFR amplification, and SMAD4 deletion. And drug response dataset revealed tumor-sensitive or tumor-resistant drugs corresponding to TGF-beta associated mRNAs. Finally, the DNN model showed an excellent predictive effect in predicting TGF-beta status in different GIAD datasets.ConclusionsWe provide molecular signatures associated with different levels of TGF-beta to deepen the understanding of the role of TGF-beta in GIAD and provide potential drug possibilities for therapeutic targets in different levels of TGF-beta in GIAD.
C1 [Zhang, Qiaofeng; Liu, Furong; Liao, Zhibin; Song, Jia; Liang, Huifang; Chen, Xiaoping; Zhang, Zhanguo; Zhang, Bixiang] Huazhong Univ Sci & Technol, Tongji Hosp, Hubei Prov Clin Med Res Ctr Hepat Surg, Hepat Surg Ctr,Tongji Med Coll, 1095 Jiefang Ave, Wuhan 430030, Peoples R China.
   [Zhang, Qiaofeng; Liu, Furong; Liao, Zhibin; Song, Jia; Liang, Huifang; Chen, Xiaoping; Zhang, Zhanguo; Zhang, Bixiang] Hubei Prov Clin Med Res Ctr Hepat Surg, Wuhan 430030, Hubei, Peoples R China.
   [Zhang, Qiaofeng; Liu, Furong; Liao, Zhibin; Song, Jia; Liang, Huifang; Chen, Xiaoping; Zhang, Zhanguo; Zhang, Bixiang] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Hubei Key Lab Hepatopancreatobiliary Dis, Wuhan 430030, Hubei, Peoples R China.
   [Qin, Lu] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Anesthesiol, Wuhan 430022, Peoples R China.
C3 Huazhong University of Science & Technology; Huazhong University of
   Science & Technology; Huazhong University of Science & Technology
RP Zhang, ZG; Zhang, BX (corresponding author), Huazhong Univ Sci & Technol, Tongji Hosp, Hubei Prov Clin Med Res Ctr Hepat Surg, Hepat Surg Ctr,Tongji Med Coll, 1095 Jiefang Ave, Wuhan 430030, Peoples R China.; Zhang, ZG; Zhang, BX (corresponding author), Hubei Prov Clin Med Res Ctr Hepat Surg, Wuhan 430030, Hubei, Peoples R China.; Zhang, ZG; Zhang, BX (corresponding author), Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Hubei Key Lab Hepatopancreatobiliary Dis, Wuhan 430030, Hubei, Peoples R China.
EM zhanguo_tjh@hust.edu.cn; bixiangzhang@163.com
RI Zhang, Biao/A-8662-2013; Zhang, Qiaofeng/AGU-6778-2022; Zhang,
   Zhanguo/AAZ-6366-2020
FU State Key Project on Infection Disease of China [2018ZX10723204-003];
   Chinese Ministry of Public Health for Key Clinical Project [[2010]
   493-51]; National Natural Science Foundation of China [81502530,
   81874189]
FX This study was funded by the State Key Project on Infection Disease of
   China (No. 2018ZX10723204-003); the Chinese Ministry of Public Health
   for Key Clinical Project (No. [2010] 493-51); National Natural Science
   Foundation of China (81502530 and 81874189).
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NR 54
TC 7
Z9 7
U1 0
U2 6
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-230X
J9 BMC GASTROENTEROL
JI BMC Gastroenterol.
PD JUL 12
PY 2021
VL 21
IS 1
AR 284
DI 10.1186/s12876-021-01869-4
PG 15
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA TK7PV
UT WOS:000674348300001
PM 34247571
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Vachani, A
   Wong, YN
   Israelite, J
   Mitra, N
   Hin, S
   Yang, L
   Smith-McLallen, A
   Armstrong, K
   Groeneveld, PW
   Epstein, AJ
AF Vachani, Anil
   Wong, Yu-Ning
   Israelite, Jennifer
   Mitra, Nandita
   Hin, Sakhena
   Yang, Lin
   Smith-McLallen, Aaron
   Armstrong, Katrina
   Groeneveld, Peter W.
   Epstein, Andrew J.
TI Validation of Molecular Pathology Codes for the Identification of
   Mutational Testing in Lung and Colon Cancer
SO MEDICAL CARE
LA English
DT Article
DE lung cancer; colon cancer; molecular diagnostic testing; sensitivity;
   specificity
ID GROWTH-FACTOR RECEPTOR; AMERICAN SOCIETY; COLORECTAL-CANCER; THERAPY;
   KRAS
AB Background:Targeted therapy for patients with lung and colon cancer based on tumor molecular profiles is an important cancer treatment strategy, but the impact of gene mutation tests on cancer treatment and outcomes in large populations is not clear. In this study, we assessed the accuracy of an algorithm to identify tumor mutation testing in administrative claims data during a period before test-specific Current Procedural Terminology codes were available.Materials and Methods:We used Pennsylvania Cancer Registry data to select patients with lung or colon cancer diagnosed between 2007 and 2011 who were treated at the University of Pennsylvania Health System, and we obtained their administrative claims. A combination of Current Procedural Terminology laboratory codes (stacking codes) was used to identify potential tumor mutation testing in the claims data. Patients' electronic medical records were then searched to determine whether tumor mutation testing actually had been performed. The sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were calculated.Results:An algorithm using stacking codes had moderate sensitivity (86% for lung cancer and 81% for colon cancer) and high specificity (98% for lung cancer and 96% for colon cancer). Sensitivity and specificity did not vary significantly during 2007-2011. In patients with lung cancer, PPV was 98% and NPV was 92%. In patients with colon cancer, PPV was 96% and NPV was 83%.Conclusions:An algorithm using stacking codes can identify tumor mutation testing in administrative claims data among patients with lung and colon cancer with a high degree of accuracy.
C1 [Vachani, Anil; Israelite, Jennifer] Univ Penn, Dept Med, Perelman Sch Med, Pulm Allergy & Crit Care Div, Philadelphia, PA 19104 USA.
   [Wong, Yu-Ning] Temple Univ Hlth Syst, Fox Chase Canc Ctr, Hematol & Med Oncol, Philadelphia, PA USA.
   [Mitra, Nandita] Univ Penn, Perelman Sch Med, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA.
   [Mitra, Nandita; Groeneveld, Peter W.; Epstein, Andrew J.] Univ Penn, Leonard Davis Inst Hlth Econ, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Hin, Sakhena; Yang, Lin] Univ Penn, Dept Med, Perelman Sch Med, Div Gen Internal Med, Philadelphia, PA 19104 USA.
   [Smith-McLallen, Aaron] Independence Blue Cross, Philadelphia, PA USA.
   [Armstrong, Katrina; Groeneveld, Peter W.; Epstein, Andrew J.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
   [Groeneveld, Peter W.; Epstein, Andrew J.] Philadelphia Vet Affairs Med Ctr, Ctr Hlth Equity Res & Promot, Dept Vet Affairs, Philadelphia, PA USA.
C3 University of Pennsylvania; Fox Chase Cancer Center; Pennsylvania
   Commonwealth System of Higher Education (PCSHE); Temple University;
   University of Pennsylvania; University of Pennsylvania; University of
   Pennsylvania; Harvard University; Massachusetts General Hospital;
   University of Pennsylvania; Pennsylvania Medicine; US Department of
   Veterans Affairs; Veterans Health Administration (VHA); Philadelphia
   Veterans Affairs Medical Center
RP Vachani, A (corresponding author), Univ Penn, Pulm Allergy & Crit Care Div, Abramson Res Ctr 1016E, Perelman Sch Med,Dept Med, 3615 Civ Ctr Blvd, Philadelphia, PA 19104 USA.
EM avachani@mail.med.upenn.edu
OI Groeneveld, Peter/0000-0002-7374-4292; Epstein,
   Andrew/0000-0001-5078-6564; Smith-McLallen, Aaron/0009-0000-5361-0679
FU NIEHS NIH HHS [P30 ES013508] Funding Source: Medline
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   [Anonymous], 2012, FED REG
   Association for Molecular Pathology, ASS MOL PATH AMP PRO
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NR 14
TC 1
Z9 1
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7079
EI 1537-1948
J9 MED CARE
JI Med. Care
PD DEC
PY 2017
VL 55
IS 12
BP E131
EP E136
DI 10.1097/MLR.0000000000000484
PG 6
WC Health Care Sciences & Services; Health Policy & Services; Public,
   Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Health Care Sciences & Services; Public, Environmental & Occupational
   Health
GA FN4FR
UT WOS:000415960200007
PM 29135776
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Cui, Q
   Wang, JQ
   Assaraf, YG
   Ren, L
   Gupta, P
   Wei, LY
   Ashby, CR 
   Yang, DH
   Chen, ZS
AF Cui, Qingbin
   Wang, Jing-Quan
   Assaraf, Yehuda G.
   Ren, Liang
   Gupta, Pranav
   Wei, Liuya
   Ashby, Charles R., Jr.
   Yang, Dong-Hua
   Chen, Zhe-Sheng
TI Modulating ROS to overcome multidrug resistance in cancer
SO DRUG RESISTANCE UPDATES
LA English
DT Review
DE Cancer chemotherapy; Multidrug resistance; Redox balance; ROS
   modulators; Sensitizing agents
ID CELL LUNG-CANCER; MANGANESE SUPEROXIDE-DISMUTASE; MITOCHONDRIAL
   UNCOUPLING PROTEIN-2; MAMMALIAN THIOREDOXIN REDUCTASE; REVERSES
   CISPLATIN RESISTANCE; INDUCED OXIDATIVE STRESS; GROWTH-FACTOR RECEPTOR;
   CHRONIC MYELOGENOUS LEUKEMIA; GLUTATHIONE-PEROXIDASE 7; HUMAN
   COLORECTAL-CANCER
AB The successful treatment of cancer has significantly improved as a result of targeted therapy and immunotherapy. However, during chemotherapy, cancer cells evolve and can acquire "multidrug resistance" (MDR), which significantly limits the efficacy of cancer treatment and impacts patient survival and quality of life. Among the approaches to reverse MDR, modulating reactive oxidative species (ROS) may represent a strategy to kill MDR cancer cells that are mechanistically diverse. ROS in cancer cells play a central role in regulating and inducing apoptosis, thereby modulating cancer cells proliferation, survival and drug resistance. The levels of ROS and the activity of scavenging/anti-oxidant enzymes in drug resistant cancer cells are typically increased compared to non-MDR cancer and normal cells. Consequently, MDR cancer cells may be more susceptible to alterations in ROS levels. Numerous studies suggest that compounds modulating cellular ROS levels can enhance MDR cancer cell death and sensitize MDR cancer cells to certain chemotherapeutic drugs.
   In the current review, we discuss the critical and targetable redox-regulating enzymes, including mitochondrial electron transport chain (ETC) complexes, NADPH oxidases (NOXs), enzymes related to glutathione metabolism, glutamate/cystine antiporter xCT, thioredoxin reductases (TrxRs), nuclear factor erythroid 2-related factor 2 (Nrf2), and their roles in regulating cellular ROS levels, drug resistance as well as their clinical significance. We also discuss and summarize the findings in the past decade regarding the efficacy of ROS modulators for the treatment of MDR cancer alone or as sensitizing compounds. Compounds that are efficacious in modulating ROS generation represent a prominent class of drug candidates that warrants evaluation in clinical trials for patients harboring MDR cancers.
C1 [Cui, Qingbin; Ren, Liang] Guangzhou Med Univ, Sch Publ Hlth, Guangzhou 511436, Guangdong, Peoples R China.
   [Cui, Qingbin; Wang, Jing-Quan; Gupta, Pranav; Ashby, Charles R., Jr.; Yang, Dong-Hua; Chen, Zhe-Sheng] St Johns Univ, Coll Pharm & Hlth Sci, Dept Pharmaceut Sci, Queens, NY 11439 USA.
   [Assaraf, Yehuda G.] Technion Israel Inst Technol, Dept Biol, Fred Wyszkowski Canc Res Lab, IL-32000 Haifa, Israel.
   [Wei, Liuya] Weifang Med Univ, Sch Pharm, Weifang 261053, Peoples R China.
C3 Guangzhou Medical University; Saint John's University; Technion Israel
   Institute of Technology; Shandong Second Medical University
RP Yang, DH; Chen, ZS (corresponding author), St Johns Univ, Dept Pharmaceut Sci, Queens, NY 11439 USA.
EM yangd1@stjohns.edu; chenz@stjohns.edu
RI Gupta, Pranav/L-4913-2019; Cui, Qingbin/U-4132-2019; Assaraf, Yehuda
   G/JPA-0451-2023; Wang, Jingquan/AAQ-5977-2020; yu, xinyue/KCY-8249-2024
OI Chen, Zhe-Sheng/0000-0002-8289-097X; Yang, Dong-Hua/0000-0001-8649-5531;
   Cui, Qingbin/0000-0003-2561-2962; Wang, Jingquan/0000-0003-4331-0482;
   Assaraf, Yehuda G./0000-0001-6692-8221
FU Guangzhou Postdoctoral Foundation of International Training for Dr.
   Qingbin Cui; NIH [1R15GM116043-01]
FX We thank the supporting of Guangzhou Postdoctoral Foundation of
   International Training for Dr. Qingbin Cui and NIH funding (No.
   1R15GM116043-01) to Zhe-Sheng Chen.
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NR 482
TC 472
Z9 501
U1 22
U2 432
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
   LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 1368-7646
EI 1532-2084
J9 DRUG RESIST UPDATE
JI Drug Resist. Update
PD NOV
PY 2018
VL 41
BP 1
EP 25
DI 10.1016/j.drup.2018.11.001
PG 25
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA HF8AV
UT WOS:000454464200001
PM 30471641
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Harlé, A
   Filhine-Tresarrieu, P
   Husson, M
   Boidot, R
   Rouyer, M
   Dubois, C
   Leroux, A
   Merlin, JL
AF Harle, Alexandre
   Filhine-Tresarrieu, Pierre
   Husson, Marie
   Boidot, Romain
   Rouyer, Marie
   Dubois, Cindy
   Leroux, Agnes
   Merlin, Jean-Louis
TI Rare <i>RAS</i> Mutations in Metastatic Colorectal Cancer Detected
   During Routine <i>RAS</i> Genotyping Using Next Generation Sequencing
SO TARGETED ONCOLOGY
LA English
DT Article
ID ACQUIRED-RESISTANCE; STRUCTURAL BASIS; KRAS MUTATIONS; HETEROGENEITY;
   ACTIVATION; THERAPY; GTPASE
AB Overall survival of metastatic colorectal cancer (mCRC) patients has been improved with the addition of targeted therapy such as anti-epithelial growth factor receptor monoclonal antibodies (anti-EGFR mAbs) to standard chemotherapy. Retrospective studies and randomized trials showed that the presence of RAS mutations was linked to the absence of clinical response to anti-EGFR mAbs. Patients harboring KRAS and NRAS mutations on exons 2, 3 or 4 have little or no benefit from anti-EGFR therapies. Polymerase chain reaction (PCR)-based assays are routinely used to assess KRAS and NRAS status, whereas deep sequencing with next generation sequencing (NGS) currently represents an alternative method.
   The objective of our study was to identify KRAS and NRAS non-hotspot mutations using NGS of mCRC tumor samples.
   DNA was extracted from 188 consecutive formalin-fixed paraffin embedded samples of histologically proven colorectal cancer tumor tissue from patients with mCRC. Following amplification, DNA was sequenced by ultra-deep pyrosequencing. Non-hotspot mutations identified by NGS (frequency of mutated allele range [1.8-70.6 %]) were confirmed by Sanger direct-sequencing when possible.
   NGS procedure was applicable in 94 % of the cases and detected mutations in 62 % of the samples. Nine uncommon mutational profiles were found with a frequency of mutated allele > 1 %. Silent mutations were found in 3.6 % of the samples. Mutations at or near functional domains of RAS proteins, other than defined hotspots, were found in 3.6 %. NGS proved to be accurate, sensitive and suitable for routine RAS genotyping.
   Clinical responses to anti-EGFR mAbs are potentially impaired in the presence of these uncommon RAS mutations.
C1 [Harle, Alexandre; Merlin, Jean-Louis] Univ Lorraine, Fac Pharm, F-54001 Nancy, France.
   [Harle, Alexandre; Merlin, Jean-Louis] CRAN, CNRS, UMR 7039, F-54506 Vandoeuvre Les Nancy, France.
   [Harle, Alexandre; Filhine-Tresarrieu, Pierre; Husson, Marie; Rouyer, Marie; Dubois, Cindy; Leroux, Agnes; Merlin, Jean-Louis] Inst Cancerol Lorraine, Serv Biopathol, 6 Ave Bourgogne,CS30519, F-54519 Vandoeuvre Les Nancy, France.
   [Boidot, Romain] Ctr Georges Francois Leclerc, Dept Biol & Pathol Tumors, F-21000 Dijon, France.
   [Boidot, Romain] Ctr Georges Francois Leclerc, Platform Transfer Canc Biol, F-21000 Dijon, France.
   [Boidot, Romain] INSERM, U866, F-21000 Dijon, France.
C3 Universite de Lorraine; Centre National de la Recherche Scientifique
   (CNRS); Universite de Lorraine; UNICANCER; Institut de cancerologie de
   Lorraine (ICL); UNICANCER; Centre Georges-Francois Leclerc; Universite
   de Bourgogne; UNICANCER; Centre Georges-Francois Leclerc; Institut Agro;
   AgroSup Dijon; Institut National de la Sante et de la Recherche Medicale
   (Inserm); Universite de Bourgogne; Institut Agro; AgroSup Dijon
RP Harlé, A (corresponding author), Univ Lorraine, Fac Pharm, F-54001 Nancy, France.; Harlé, A (corresponding author), CRAN, CNRS, UMR 7039, F-54506 Vandoeuvre Les Nancy, France.; Harlé, A (corresponding author), Inst Cancerol Lorraine, Serv Biopathol, 6 Ave Bourgogne,CS30519, F-54519 Vandoeuvre Les Nancy, France.
EM a.harle@nancy.unicancer.fr
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NR 32
TC 17
Z9 17
U1 1
U2 7
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1776-2596
EI 1776-260X
J9 TARGET ONCOL
JI Target. Oncol.
PD JUN
PY 2016
VL 11
IS 3
BP 363
EP 370
DI 10.1007/s11523-015-0404-7
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DO6TV
UT WOS:000377917300010
PM 26661077
DA 2025-01-04
ER

PT J
AU Deng, YH
   Cai, Y
   Lin, JY
   Jiang, L
   Hu, HB
AF Deng, Yanhong
   Cai, Yue
   Lin, Jiayu
   Jiang, Ling
   Hu, Huabin
TI Survival of patients with KRAS wild-type metastatic colorectal cancer is
   identical after sequential treatment with cetuximab and bevacizumab
   regardless of the sequence - A retrospective single-center study
SO GASTROENTEROLOGY REPORT
LA English
DT Article
DE metastatic colorectal cancer; sequential treatment; bevacizumab;
   cetuximab
ID 1ST-LINE TREATMENT; MUTATION STATUS; PHASE-III; FOLFIRI; FLUOROURACIL;
   LEUCOVORIN; IRINOTECAN; TRIAL
AB Objective: To investigate the overall survival of patients with KRAS wild-type metastatic colorectal cancer (mCRC) after sequentially receiving both bevacizumab and cetuximab during the course of treatment.
   Methods: Twenty-six mCRC patients who received both bevacizumab and cetuximab at the Sun Yat-sen University Gastrointestinal Hospital were retrospectively analyzed. Group A (n = 8) comprised patients who received bevacizumab first, and group B (n = 18) comprised those who received cetuximab first. The objective response rate, progression-free survival, and overall survival were compared.
   Results: Baseline characteristics between the two groups were statistically similar. The objective response in groups A and B patients was 62.5% and 66.6%, respectively (P = 0.132). The median progression-free survival for groups A and B patients was 13 and 10 months, respectively (P = 0.798). The median overall survival for the entire cohort was 42 months, 44 months for group A and 39 months for group p B (P = 0.862) patients, respectively. Patients aged <40 years had worse survival than those aged >= 40 years (22 vs 44 months; P = 0.029). Patients with synchronous metastasis had worse survival than those with metachronous metastasis (unreached and 36 months, respectively). In multivariate analyses, synchronous metastasis and age remained statistically significant. The hazard ratio for synchronous metastasis was 4.548, and the HR for patients aged >= 40 years was 0.237.
   Conclusion: A longer median survival time was observed in patients regardless of the targeted therapy sequence, which warrants further investigation.
C1 [Deng, Yanhong; Cai, Yue; Lin, Jiayu; Jiang, Ling; Hu, Huabin] Sun Yat Sen Univ, Affiliated Hosp 6, Dept Med Oncol, 2 Cross Rd Tianhe Dist,Village 26, Guangzhou 510655, Guangdong, Peoples R China.
C3 Sun Yat Sen University
RP Deng, YH (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 6, Dept Med Oncol, 2 Cross Rd Tianhe Dist,Village 26, Guangzhou 510655, Guangdong, Peoples R China.
EM dengyanh@mail.sysu.edu.cn
FU China National Natural Science Foundation [81472249]
FX The study was supported by the China National Natural Science Foundation
   (No. 81472249)
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U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
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J9 GASTROENTEROL REP
JI Gastroenterol. Rep.
PD NOV
PY 2015
VL 3
IS 4
SI SI
BP 339
EP 343
DI 10.1093/gastro/gov051
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CW9FX
UT WOS:000365305300008
PM 26468218
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Nwaokorie, A
   Fey, D
AF Nwaokorie, Annabelle
   Fey, Dirk
TI Personalised Medicine for Colorectal Cancer Using Mechanism-Based
   Machine Learning Models
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE cancer; colorectal cancer; signal transduction networks; pathways;
   event-free survival; biomarkers; WNT pathway; targeted therapy
ID INHIBITION; PLATFORM; GENES; KEGG
AB Gaining insight into the mechanisms of signal transduction networks (STNs) by using critical features from patient-specific mathematical models can improve patient stratification and help to identify potential drug targets. To achieve this, these models should focus on the critical STNs for each cancer, include prognostic genes and proteins, and correctly predict patient-specific differences in STN activity. Focussing on colorectal cancer and the WNT STN, we used mechanism-based machine learning models to identify genes and proteins with significant associations to event-free patient survival and predictive power for explaining patient-specific differences of STN activity. First, we identified the WNT pathway as the most significant pathway associated with event-free survival. Second, we built linear-regression models that incorporated both genes and proteins from established mechanistic models in the literature and novel genes with significant associations to event-free patient survival. Data from The Cancer Genome Atlas and Clinical Proteomic Tumour Analysis Consortium were used, and patient-specific STN activity scores were computed using PROGENy. Three linear regression models were built, based on; (1) the gene-set of a state-of-the-art mechanistic model in the literature, (2) novel genes identified, and (3) novel proteins identified. The novel genes and proteins were genes and proteins of the extant WNT pathway whose expression was significantly associated with event-free survival. The results show that the predictive power of a model that incorporated novel event-free associated genes is better compared to a model focussing on the genes of a current state-of-the-art mechanistic model. Several significant genes that should be integrated into future mechanistic models of the WNT pathway are DVL3, FZD5, RAC1, ROCK2, GSK3B, CTB2, CBT1, and PRKCA. Thus, the study demonstrates that using mechanistic information in combination with machine learning can identify novel features (genes and proteins) that are important for explaining the STN heterogeneity between patients and their association to clinical outcomes.
C1 [Nwaokorie, Annabelle; Fey, Dirk] Univ Coll Dublin, Sch Med, Syst Biol Ireland, Dublin 4, Ireland.
C3 University College Dublin
RP Fey, D (corresponding author), Univ Coll Dublin, Sch Med, Syst Biol Ireland, Dublin 4, Ireland.
EM annabelle.nwaokorie@ucdconnect.ie; dirk.fey@ucd.ie
OI Nwaokorie, Annabelle/0000-0002-9993-2953; Fey, Eric/0009-0005-7847-7479;
   Fey, Dirk/0000-0002-5558-0167
FU UCD Ad Astra Fellowship [64998]; European Union [754923]; H2020 Societal
   Challenges Programme [754923] Funding Source: H2020 Societal Challenges
   Programme
FX This project has received funding from the UCD Ad Astra Fellowship No
   64998 and the European Union's Horizon 2020 research and innovation
   programme under grant agreement No 754923. The material presented and
   views expressed here are the responsibility of the author(s) only. The
   EU Commission takes no responsibility for any use made of the
   information set out.
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NR 60
TC 7
Z9 7
U1 2
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD SEP
PY 2021
VL 22
IS 18
AR 9970
DI 10.3390/ijms22189970
PG 26
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA UV5NK
UT WOS:000699524700001
PM 34576133
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Luo, YY
   Humayun, A
   Murray, TA
   Kemp, BS
   McFarland, A
   Liu, X
   Mills, DK
AF Luo, Yangyang
   Humayun, Ahmed
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   Kemp, Benjamin S.
   McFarland, Antwine
   Liu, Xuan
   Mills, David K.
TI Cellular Analysis and Chemotherapeutic Potential of a Bi-Functionalized
   Halloysite Nanotube
SO PHARMACEUTICS
LA English
DT Article
DE targeted drug delivery; halloysite nanotube; osteosarcoma; methotrexate;
   surface modification
ID DRUG-DELIVERY; CO-DELIVERY; TARGETED THERAPY; CLAY NANOTUBES;
   NANOPARTICLES; METHOTREXATE; CURCUMIN; CARRIER; DOXORUBICIN; SYSTEMS
AB The surface of halloysite nanotubes (HNTs) was bifunctionalized with two ligands-folic acid and a fluorochrome. In tandem, this combination should selectively target cancer cells and provide a means for imaging the nanoparticle. Modified bi-functionalized HNTs (bi-HNTs) were then doped with the anti-cancer drug methotrexate. bi-HNTs were characterized and subjected to in vitro tests to assess cellular growth and changes in cellular behavior in three cell lines-colon cancer, osteosarcoma, and a pre-osteoblast cell line (MC3T3-E1). Cell viability, proliferation, and cell uptake efficiency were assessed. The bi-HNTs showed cytocompatibility at a wide range of concentrations. Compared with regular-sized HNTs, reduced HNTs (similar to 6 microns) were taken up by cells in more significant amounts, but increased cytotoxicity lead to apoptosis. Multi-photon images confirmed the intracellular location of bi-HNTs, and the method of cell entry was mainly through caveolae-mediated endocytosis. The bi-HNTs showed a high drug loading efficiency with methotrexate and a prolonged period of release. Most importantly, bi-HNTs were designed as a drug carrier to target cancer cells specifically, and imaging data shows that non-cancerous cells were unaffected after exposure to MTX-doped bi-HNTs. All data provide support for our nanoparticle design as a mechanism to selectively target cancer cells and significantly reduce the side-effects caused by off-targeting of anti-cancer drugs.
C1 [Luo, Yangyang; Humayun, Ahmed; Murray, Teresa A.; Kemp, Benjamin S.; McFarland, Antwine; Liu, Xuan] Louisiana Tech Univ, Mol Sci & Nanotechnol, Ruston, LA 71272 USA.
   [Mills, David K.] Louisiana Tech Univ, Sch Biol Sci, Ruston, LA 71272 USA.
   [Mills, David K.] Louisiana Tech Univ, Ctr Biomed Engn, Ruston, LA 71272 USA.
C3 University of Louisiana System; Louisiana Technical University;
   University of Louisiana System; Louisiana Technical University;
   University of Louisiana System; Louisiana Technical University
RP Mills, DK (corresponding author), Louisiana Tech Univ, Sch Biol Sci, Ruston, LA 71272 USA.; Mills, DK (corresponding author), Louisiana Tech Univ, Ctr Biomed Engn, Ruston, LA 71272 USA.
EM yangyang317luo@gmail.com; ah.humayun@gmail.com; tmurray@latech.edu;
   bscott.kemp@gmail.com; awm011@latech.edu; Xliu@latech.edu;
   dkmills@latech.edu
RI Luo, Yangyang/LTE-0459-2024; Murray, Teresa/AAG-3531-2019; Mills,
   D/KFT-3273-2024
OI McFarland, Antwine/0000-0003-4572-2376; Luo,
   Yangyang/0000-0003-3441-6621; Humayun, Ahmed/0000-0002-6139-7609
FU Louisiana Biomedical Research Network (through an Institutional
   Development Award (IDeA) from the National Institute of General Medical
   Sciences of the National Institutes of Health [P20 GM103424-17]
FX Funding for this study was provided by a grant (to DKM) from the
   Louisiana Biomedical Research Network (through an Institutional
   Development Award (IDeA) from the National Institute of General Medical
   Sciences of the National Institutes of Health under grant number P20
   GM103424-17.
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NR 40
TC 20
Z9 20
U1 1
U2 12
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1999-4923
J9 PHARMACEUTICS
JI Pharmaceutics
PD OCT
PY 2020
VL 12
IS 10
AR 962
DI 10.3390/pharmaceutics12100962
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA ON8LF
UT WOS:000586944400001
PM 33066206
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Ruess, DA
   Heynen, GJ
   Ciecielski, KJ
   Ai, JY
   Berninger, A
   Kabacaoglu, D
   Görgülü, K
   Dantes, Z
   Wörmann, SM
   Diakopoulos, KN
   Karpathaki, AF
   Kowalska, M
   Kaya-Aksoy, E
   Song, L
   van der Laan, EAZ
   López-Alberca, MP
   Nazaré, M
   Reichert, M
   Saur, D
   Erkan, MM
   Hopt, UT
   Sainz, B
   Birchmeier, W
   Schmid, RM
   Lesina, M
   Algül, H
AF Ruess, Dietrich A.
   Heynen, Guus J.
   Ciecielski, Katrin J.
   Ai, Jiaoyu
   Berninger, Alexandra
   Kabacaoglu, Derya
   Goerguelue, Kivanc
   Dantes, Zahra
   Woermann, Sonja M.
   Diakopoulos, Kalliope N.
   Karpathaki, Angeliki F.
   Kowalska, Marlena
   Kaya-Aksoy, Ezgi
   Song, Liang
   van der Laan, Eveline A. Zeeuw
   Lopez-Alberca, Maria P.
   Nazare, Marc
   Reichert, Maximilian
   Saur, Dieter
   Erkan, Mert M.
   Hopt, Ulrich T.
   Sainz, Bruno, Jr.
   Birchmeier, Walter
   Schmid, Roland M.
   Lesina, Marina
   Alguel, Hana
TI Mutant KRAS-driven cancers depend on <i>PTPN11</i>/SHP2 phosphatase
SO NATURE MEDICINE
LA English
DT Article
ID MOUSE MODEL; PHOSPHOTYROSINE PHOSPHATASE; TYROSINE PHOSPHATASES;
   PANCREATIC-CANCER; COLON-CANCER; LUNG-CANCER; SHP2; INHIBITION;
   PROGRESSION; MEK
AB The ubiquitously expressed non-receptor protein tyrosine phosphatase SHP2, encoded by PTPN11, is involved in signal transduction downstream of multiple growth factor, cytokine and integrin receptors(1). Its requirement for complete RAS-MAPK activation and its role as a negative regulator of JAK-STAT signaling have established SHP2 as an essential player in oncogenic signaling pathways(1-7). Recently, a novel potent allosteric SHP2 inhibitor was presented as a viable therapeutic option for receptor tyrosine kinase-driven cancers, but was shown to be ineffective in KRAS-mutant tumor cell lines in vitro(8). Here, we report a central and indispensable role for SHP2 in oncogenic KRAS-driven tumors. Genetic deletion of Ptpn11 profoundly inhibited tumor development in mutant KRAS-driven murine models of pancreatic ductal adenocarcinoma and non-small-cell lung cancer. We provide evidence for a critical dependence of mutant KRAS on SHP2 during carcinogenesis. Deletion or inhibition of SHP2 in established tumors delayed tumor progression but was not sufficient to achieve tumor regression. However, SHP2 was necessary for resistance mechanisms upon blockade of MEK. Synergy was observed when both SHP2 and MEK were targeted, resulting in sustained tumor growth control in murine and human patient-derived organoids and xenograft models of pancreatic ductal adenocarcinoma and non-small-cell lung cancer. Our data indicate the clinical utility of dual SHP2/MEK inhibition as a targeted therapy approach for KRAS-mutant cancers.
C1 [Ruess, Dietrich A.; Ciecielski, Katrin J.; Ai, Jiaoyu; Berninger, Alexandra; Kabacaoglu, Derya; Goerguelue, Kivanc; Dantes, Zahra; Woermann, Sonja M.; Diakopoulos, Kalliope N.; Karpathaki, Angeliki F.; Kowalska, Marlena; Kaya-Aksoy, Ezgi; Song, Liang; Reichert, Maximilian; Saur, Dieter; Schmid, Roland M.; Lesina, Marina; Alguel, Hana] Tech Univ Munich, Klinikum Rechts Isar, Internal Med 2, Mildred Scheel Chair Tumor Metab, Munich, Germany.
   [Ruess, Dietrich A.; Hopt, Ulrich T.] Univ Freiburg, Med Ctr, Fac Med, Dept Surg, Freiburg, Germany.
   [Heynen, Guus J.; van der Laan, Eveline A. Zeeuw; Birchmeier, Walter] Helmholtz Soc, Max Delbruck Ctr Mol Med MDC, Canc Res Program, Berlin, Germany.
   [Lopez-Alberca, Maria P.; Nazare, Marc] Leibniz Forschungsinst Mol Pharmakol, Med Chem, Berlin, Germany.
   [Erkan, Mert M.] Koc Univ, Sch Med, Istanbul, Turkey.
   [Sainz, Bruno, Jr.] Univ Autonoma Madrid, Dept Biochem, Sch Med, Inst Invest Biomed Alberto Sols, Madrid, Spain.
C3 Technical University of Munich; University of Freiburg; Helmholtz
   Association; Max Delbruck Center for Molecular Medicine; Leibniz
   Association; Leibniz Forschungsinstitut furr Molekulare Pharmakologie
   (FMP); Koc University; Consejo Superior de Investigaciones Cientificas
   (CSIC); CSIC - Instituto de Investigaciones Biomedicas Alberto Sols
   (IIBM); Autonomous University of Madrid
RP Algül, H (corresponding author), Tech Univ Munich, Klinikum Rechts Isar, Internal Med 2, Mildred Scheel Chair Tumor Metab, Munich, Germany.
EM hana.alguel@mri.tum.de
RI Kabacaoglu, Derya/HDL-8563-2022; Lesina, Marina/AAV-3845-2020; Erkan,
   Mert/IQS-9553-2023; Reichert, Maximilian/GOH-1246-2022; Ruess,
   Dietrich/J-6983-2019; Görgülü, Kıvanç/AAV-6525-2020; Saur,
   Dieter/O-8355-2015; Nazare, Marc/X-4996-2018; Sainz Anding,
   Bruno/ABH-5365-2020
OI Ruess, Dietrich A./0000-0003-4371-2246; Lesina,
   Marina/0000-0001-8427-3548; Berninger, Alexandra/0000-0002-6494-2369;
   Saur, Dieter/0000-0001-5874-0210; Kaya Aksoy, Ezgi/0000-0002-9375-9686;
   Gorgulu, Kivanc/0000-0002-1613-1422; Zeeuw van der Laan,
   Eveline/0000-0002-2784-5236; Kabacaoglu, Derya/0000-0002-3601-0265;
   Nazare, Marc/0000-0002-1602-2330; Sainz Anding,
   Bruno/0000-0003-4829-7651; Frank, Katrin Jana/0000-0002-7913-4794;
   Diakopoulos, Kalliope/0000-0002-9236-0489
FU Deutsche Forschungsgemeinschaft [DFG AL1174/5-1, LE3222/1-1]; Deutsche
   Krebshilfe [111646, 111464, 111273]; Wilhelm Sander Stiftung
   [2014.052.1]; Fundacion Asociacion Espanola Contra el Cancer; Academy of
   Finland (AKA) [111464] Funding Source: Academy of Finland (AKA)
FX We thank G.-S. Feng (Department of Pathology, School of Medicine, and
   Molecular Biology, Division of Biological Sciences, University of
   California, San Diego, La Jolla, CA, USA) for sharing the
   Ptpn11<SUP>fl</SUP> allele. We also thank R. F. Braren and D. C.
   Karampinos (both Institute of Radiology, Klinikum rechts der Isar,
   Technische Universitat Munchen) for providing the infrastructure and A.
   Gupta for help with the setup for MRI studies. This work was supported
   by grants from Deutsche Forschungsgemeinschaft (DFG AL1174/5-1 to H.A.
   and LE3222/1-1 to M.L.), Deutsche Krebshilfe (no. 111646 and no. 111464
   to H.A.; Max Eder Program no. 111273 to M.R.), the Wilhelm Sander
   Stiftung (2014.052.1 to H.A.) and the Fundacion Asociacion Espanola
   Contra el Cancer (to B.S.).
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NR 53
TC 279
Z9 318
U1 2
U2 88
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD JUL
PY 2018
VL 24
IS 7
BP 954
EP +
DI 10.1038/s41591-018-0024-8
PG 10
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
   Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
   Medicine
GA GM5NV
UT WOS:000438187700023
PM 29808009
DA 2025-01-04
ER

PT J
AU Jifu, C
   Lu, LX
   Ding, JX
   Lv, MJ
   Xia, J
   Wang, JT
   Wang, PJ
AF Jifu, Cili
   Lu, Linxia
   Ding, Jiaxin
   Lv, Mengjun
   Xia, Jun
   Wang, Jingtao
   Wang, Peijun
TI USP18 Is Associated with PD-L1 Antitumor Immunity and Improved Prognosis
   in Colorectal Cancer
SO BIOMOLECULES
LA English
DT Article
DE USP18; colorectal cancer; tumor immune microenvironment; immune
   checkpoint genes; PD-L1; anticancer immunity
ID T-CELLS; EXPRESSION; ISG15; REGULATOR; SERVER; UBP43
AB Background: Compared with conventional chemotherapy and targeted therapy, immunotherapy has improved the treatment outlook for a variety of solid tumors, including lung cancer, colorectal cancer (CRC), and melanoma. However, it is effective only in certain patients, necessitating the search for alternative strategies to targeted immunotherapy. The deubiquitinating enzyme USP18 is known to play an important role in various aspects of the immune response, but its role in tumor immunity in CRC remains unclear. Methods: In this study, multiple online datasets were used to systematically analyze the expression, prognosis, and immunomodulatory role of USP18 in CRC. The effect of USP18 on CRC was assessed via shRNA-mediated knockdown of USP18 expression in combination with CCK-8 and colony formation assays. Finally, molecular docking analysis of USP18/ISG15 and programmed death-ligand 1 (PD-L1) was performed via HDOCK, and an ELISA was used to verify the potential of USP18 to regulate PD-L1. Results: Our study revealed that USP18 expression was significantly elevated in CRC patients and closely related to clinicopathological characteristics. The experimental data indicated that silencing USP18 significantly promoted the proliferation and population-dependent growth of CRC cells. In addition, high USP18 expression was positively correlated with the CRC survival rate and closely associated with tumor-infiltrating CD8+ T cells and natural killer (NK) cells. Interestingly, USP18 was correlated with the expression of various chemokines and immune checkpoint genes. The results of molecular docking simulations suggest that USP18 may act as a novel regulator of PD-L1 and that its deficiency may potentiate the antitumor immune response to PD-L1 blockade immunotherapy in CRC. Conclusions: In summary, USP18 shows great promise for research and clinical application as a potential target for CRC immunotherapy.
C1 [Jifu, Cili; Lu, Linxia; Ding, Jiaxin; Xia, Jun; Wang, Jingtao; Wang, Peijun] Jiamusi Univ, Coll Basic Med, Jiamusi 154007, Peoples R China.
   [Lv, Mengjun] Jiamusi Univ, Coll Publ Hlth, Jiamusi 154007, Peoples R China.
C3 Jiamusi University; Jiamusi University
RP Wang, JT; Wang, PJ (corresponding author), Jiamusi Univ, Coll Basic Med, Jiamusi 154007, Peoples R China.
EM 208053016@stu.jmsu.edu.cn; lulinxia@stu.jmsu.edu.cn;
   wjingtao@jmsu.edu.cn; wangpj6877@163.com
FU National Natural Science Foundation of China; Basic Medical Research and
   Translational Team [DJXSTD202405];  [81872706]
FX This research was funded by the National Natural Science Foundation of
   China (81872706) and the Basic Medical Research and Translational Team
   (DJXSTD202405) for financial support.
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NR 57
TC 0
Z9 0
U1 2
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2218-273X
J9 BIOMOLECULES
JI Biomolecules
PD SEP
PY 2024
VL 14
IS 9
AR 1191
DI 10.3390/biom14091191
PG 20
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA H4Y3G
UT WOS:001323508300001
PM 39334957
OA gold
DA 2025-01-04
ER

PT J
AU Tobore, TO
AF Tobore, Tobore Onojighofia
TI On the need for the development of a cancer early detection, diagnostic,
   prognosis, and treatment response system
SO FUTURE SCIENCE OA
LA English
DT Article
DE bioelectronics; bioengineering; biomarkers; biosensors; biotechnology;
   cancer early detection; diagnostic biomarkers; ISWEBDS; nanotechnology;
   personalized; precision medicine; predictive biomarkers; prognostic
   biomarkers; targeted therapy; wearables
ID OXIDATIVE STRESS; ELECTROCHEMICAL BIOSENSORS; CYTOGENETIC BIOMARKERS;
   COLORECTAL-CANCER; RISK; FUTURE; COST; SENSOR; CARE
AB Cancer is the second leading cause of noncommunicable disease deaths in the world. In 2018, there were over 18 million new cancer cases and approximately 10 million people died from the disease globally. In 2019, almost two million new cases of cancer will be diagnosed in USA and over 600,000 people are expected to die from the disease. The incidence of cancer is expected to rise because of lifestyle changes and a rapidly aging population. Evidence suggests that early detection is critical to reducing cancer morbidity and mortality. In this paper, the development of an integrated smart wearable and biomarker detection system is proposed to help reduce cancer morbidity and mortality. The potential benefits and limitations of the system are discussed.
   Lay abstract Cancer is one of the leading causes of death in the world. Evidence suggests that its incidence will continue to rise in the future because of lifestyle changes and a rapidly aging population. There is currently no cure for the disease and the best way to reduce its incidence and morbidity is to detect it early. In this paper, an integrated smart wearable and biomarker detection system to help in the early detection, prognosis, diagnosis and treatment of cancer is proposed.
EM tonojig1@jhu.edu
OI Tobore, Tobore Onojighofia/0000-0001-7334-2915
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NR 67
TC 26
Z9 27
U1 1
U2 10
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 2056-5623
J9 FUTUR SCI OA
JI Futur. Sci. OA
PD FEB
PY 2020
VL 6
IS 2
AR FSO439
DI 10.2144/fsoa-2019-0028
PG 8
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA LS9ZZ
UT WOS:000536738600002
PM 32025328
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Geyik, OG
   Efe, H
   Köse, SB
   Uysal, O
   Yüce, Z
AF Geyik, Oyku Gonul
   Efe, Hande
   Kose, Seda Baykal
   Uysal, Ozge
   Yuce, Zeynep
TI Generation of an in vitro Intratumoral Heterogeneity Model by Lentiviral
   Fluorescent Labeling of Colon Cancer Cell Line DLD-1 Subclones
SO JOURNAL OF BASIC AND CLINICAL HEALTH SCIENCES
LA English
DT Article
DE colon cancer; DLD-1; fluorescent labeling; lentiviral transduction;
   cancer therapy resistance
ID TRANSCRIPTOME; ABERRATIONS; ANEUPLOIDY; LANDSCAPE; GENESIS; PATTERN
AB Purpose: Studying genomic changes during tumor progression has helped to understand the biology of many different cancers and has been the basis for targeted therapy strategies. However, resistance and differences in response to therapy in patients are still very important issues. One of the major underlying reasons is intratumoral cellular heterogeneity. Clones harbor mutations and/or epigenetic patterns providing a survival advantage under changing micro-environmental conditions are the main culprits of therapy resistance. Therefore, it is crucial to define and to study the properties and the contributions of these deviant subclones in vitro. In order to achieve that, we have generated a fluorescent intratumoral heterogeneity model of the colon cancer cell line DLD-1.
   Methods: We used 2N subclones (C3 and C34) and 4N subclones (B9 and B12) of DLD-1, isolated by our team previously. Subclones were stably transduced using lentiviral vectors carrying different fluorescent labels and selected by puromycin.
   Results: Labeled subclones were mixed in equal proportions and a co-culture model of intratumoral heterogeneity was generated. Fluorescent signals were then confirmed by fluorescence microscope.
   Conclusion: The in vitro model we have generated may be used in many tumor kinetic studies. By co-culturing different clones, profiles that have a selective advantage under different conditions can be detected. After exposure to different chemotherapeutic agents, radiation and/or combinations, real time changes in population kinetics can be tracked. By comparing these results to the genomic profiling of subclones, it will be possible to relate variations that are responsible for any observed therapeutic resistance in vitro.
C1 [Geyik, Oyku Gonul; Efe, Hande; Kose, Seda Baykal; Uysal, Ozge; Yuce, Zeynep] Dokuz Eylul Univ, Fac Med, Dept Med Biol & Genet, Izmir, Turkey.
   [Geyik, Oyku Gonul] Istinye Univ, Fac Hlth Sci, Dept Nutr & Dietet, Istanbul, Turkey.
C3 Dokuz Eylul University; Istinye University
RP Yüce, Z (corresponding author), Dokuz Eylul Univ, Fac Med, Dept Med Biol & Genet, Izmir, Turkey.
EM zeynyuce@gmail.com
RI Yuce, Zeynep/JDW-8153-2023; Baykal, Seda/ABI-4548-2020; GÖNÜL GEYİK,
   Öykü/AHB-4716-2022
OI Uysal Yoca, Ozge/0000-0002-3906-6918; Gonul Geyik,
   Oyku/0000-0003-3014-1253; Baykal, Seda/0000-0001-8654-5332
FU TUBITAK 1001 Research Grant [116Z300]
FX This study was funded by TUBITAK 1001 Research Grant; 116Z300.
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NR 23
TC 0
Z9 0
U1 0
U2 1
PU DOKUZ EYLUL UNIV INST HEALTH SCIENCES
PI IZMIR
PA DEPT MEDICAL BIOCHEMISTRY, FAC MEDICINE, DOKUZ EYLUL UNIV, IZMIR, TURKEY
SN 2458-8938
EI 2564-7288
J9 J BASIC CLIN HEALTH
JI J. Basic Clin. Health Sci.
PY 2020
VL 4
IS 2
BP 149
EP 153
DI 10.30621/jbachs.2020.921
PG 5
WC Health Care Sciences & Services
WE Emerging Sources Citation Index (ESCI)
SC Health Care Sciences & Services
GA LO4LI
UT WOS:000533600300012
DA 2025-01-04
ER

PT J
AU Zheng, H
   Liu, HS
   Li, HY
   Dou, WD
   Wang, JG
   Zhang, JL
   Liu, T
   Wu, YC
   Liu, YC
   Wang, X
AF Zheng, Hang
   Liu, Heshu
   Li, Huayu
   Dou, Weidong
   Wang, Jingui
   Zhang, Junling
   Liu, Tao
   Wu, Yingchao
   Liu, Yucun
   Wang, Xin
TI Characterization of stem cell landscape and identification of
   stemness-relevant prognostic gene signature to aid immunotherapy in
   colorectal cancer
SO STEM CELL RESEARCH & THERAPY
LA English
DT Article
DE Colorectal cancer; Stemness; Bioinformatics; Tumor microenvironment;
   Immunotherapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; TUMOR-ASSOCIATED MACROPHAGES;
   EXTRACELLULAR-MATRIX; HETEROGENEITY; EXPRESSION; GROWTH; METASTASIS;
   CYTOKINE; INVASION; FEATURES
AB Background It is generally accepted that colorectal cancer (CRC) originates from cancer stem cells (CSCs), which are responsible for CRC progression, metastasis and therapy resistance. The high heterogeneity of CSCs has precluded clinical application of CSC-targeting therapy. Here, we aimed to characterize the stemness landscapes and screen for certain patients more responsive to immunotherapy. Methods Twenty-six stem cell gene sets were acquired from StemChecker database. Consensus clustering algorithm was applied for stemness subtypes identification on 1,467 CRC samples from TCGA and GEO databases. The differences in prognosis, tumor microenvironment (TME) components, therapy responses were evaluated among subtypes. Then, the stemness-risk model was constructed by weighted gene correlation network analysis (WGCNA), Cox regression and random survival forest analyses, and the most important marker was experimentally verified. Results Based on single-sample gene set enrichment analysis (ssGSEA) enrichments scores, CRC patients were classified into three subtypes (C1, C2 and C3). C3 subtype exhibited the worst prognosis, highest macrophages M0 and M2 infiltrations, immune and stromal scores, and minimum sensitivity to immunotherapies, but was more sensitive to drugs like Bosutinib, Docetaxel, Elesclomol, Gefitinib, Lenalidomide, Methotrexate and Sunitinib. The turquoise module was identified by WGCNA that it was most positively correlated with C3 but most negatively with C2, and five hub genes in turquoise module were identified for stemness model construction. CRC patients with higher stemness scores exhibited worse prognosis, more immunosuppressive components in TME and lower immunotherapeutic responses. Additionally, the model's immunotherapeutic prediction efficacy was further confirmed from two immunotherapy cohorts (anti-PD-L1 in IMvigor210 cohort and anti-PD-1 in GSE78220 cohort). Mechanistically, Gene Set Enrichment Analysis (GSEA) results revealed high stemness score group was enriched in interferon gamma response, interferon alpha response, P53 pathway, coagulation, apoptosis, KRAS signaling upregulation, complement, epithelial-mesenchymal transition (EMT) and IL6-mediated JAK-STAT signaling gene sets. Conclusions Our study characterized three stemness-related subtypes with distinct prognosis and TME patterns in CRC patients, and a 5-gene stemness-risk model was constructed by comprehensive bioinformatic analyses. We suggest our stemness model has prospective clinical implications for prognosis evaluation and might facilitate physicians selecting prospective responders for preferential use of current immune checkpoint inhibitors.
C1 [Zheng, Hang; Li, Huayu; Dou, Weidong; Wang, Jingui; Zhang, Junling; Liu, Tao; Wu, Yingchao; Liu, Yucun; Wang, Xin] Peking Univ, Peking Univ First Hosp, Dept Gen Surg, Beijing, Peoples R China.
   [Liu, Heshu] Capital Med Univ, Beijing Chaoyang Hosp, Dept Oncol, Beijing, Peoples R China.
C3 Peking University; Capital Medical University
RP Wang, X (corresponding author), Peking Univ, Peking Univ First Hosp, Dept Gen Surg, Beijing, Peoples R China.
EM wangxin_guo@126.com
RI Dou, Weidong/A-1528-2012; Liu, Tao/AAK-8973-2021; Liu,
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NR 89
TC 59
Z9 61
U1 2
U2 19
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1757-6512
J9 STEM CELL RES THER
JI Stem Cell Res. Ther.
PD JUN 9
PY 2022
VL 13
IS 1
AR 244
DI 10.1186/s13287-022-02913-0
PG 20
WC Cell & Tissue Engineering; Cell Biology; Medicine, Research &
   Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA 1Z8CU
UT WOS:000809046200001
PM 35681225
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Voutsadakis, IA
AF Voutsadakis, Ioannis A.
TI PIK3CA Mutated Colorectal Cancers Without KRAS, NRAS and BRAF Mutations
   Possess Common and Potentially Targetable Mutations in Epigenetic
   Modifiers and DNA Damage Response Genes
SO CANCER GENOMICS & PROTEOMICS
LA English
DT Article
DE PI3K; genomic studies; targeted therapy; quadruple wild type; extended
   RAS panel
ID UBIQUITIN-PROTEASOME SYSTEM; PI3K PATHWAY; CETUXIMAB; EFFICACY;
   RESISTANCE; INHIBITORS; COLON
AB Background/Aim: Despite therapeutic advancements, metastatic colorectal cancer is usually fatal, necessitating novel approaches based on the molecular pathogenesis to improve outcomes. Some colorectal cancers have no mutations in the extended RAS panel (KRAS, NRAS, BRAF) genes and represent a special subset, which deserves particular therapeutic considerations. Materials and Methods: The genomic landscape of colorectal cancers from publicly available genomic series was interrogated, using the cBioportal platform. Colorectal cancer cohorts with cancers devoid of KRAS/NRAS or BRAF mutations were evaluated for the presence of mutations in the catalytic sub-unit alpha of kinase PI3K, encoded by the gene PIK3CA. Results: PIK3CA mutations in the absence of KRAS/NRAS/BRAF mutations were observed in 3.7% to 7.6% of colorectal cancers in the different series examined. Patients with all four genes in wildtype configuration (quadruple wild type) represented 32.2% to 39.9% of cases in the different series examined. Compared with quadruple wild type cancers, triple (KRAS/NRAS/BRAF) wild type/PIK3CA mutated cancers had a higher prevalence of high TMB cases and additional mutations in colorectal cancer associated genes except for mutations in TP53. Mutations in genes encoding for epigenetic modifiers and the DNA damage response (DDR) were also more frequent in triple wild type/PIK3CA mutated cancers. The prognosis of the two groups was comparable. Conclusion: Colorectal cancers with PIK3CA mutations in the absence of KRAS/NRAS/BRAF mutations have frequently mutations in epigenetic modifiers and DDR response genes, which may provide opportunities for targeting. These mutations are present in a smaller subset of quadruple wild type cancers.
C1 [Voutsadakis, Ioannis A.] Sault Area Hosp, Algoma Dist Canc Program, Sault Ste Marie, ON, Canada.
   [Voutsadakis, Ioannis A.] Northern Ontario Sch Med, Div Clin Sci, Sect Internal Med, Sudbury, ON, Canada.
   [Voutsadakis, Ioannis A.] Sault Area Hosp, Div Med Oncol, 750 Great Northern Rd, Sault Ste Marie, ON P6B 0A8, Canada.
C3 NOSM University
RP Voutsadakis, IA (corresponding author), Sault Area Hosp, Div Med Oncol, 750 Great Northern Rd, Sault Ste Marie, ON P6B 0A8, Canada.
EM ivoutsadakis@nosm.ca
RI Voutsadakis, Ioannis/AAU-7224-2020
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NR 51
TC 0
Z9 0
U1 0
U2 0
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
   ATHENS 19014, GREECE
SN 1109-6535
EI 1790-6245
J9 CANCER GENOM PROTEOM
JI Cancer Genomics Proteomics
PD SEP-OCT
PY 2024
VL 21
IS 5
BP 533
EP 548
DI 10.21873/cgp.20470
PG 16
WC Oncology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Genetics & Heredity
GA F2G1C
UT WOS:001308044000010
PM 39191495
OA gold
DA 2025-01-04
ER

PT J
AU Vauléon, E
   Behal, H
   Lebellec, L
   Desbarbieux, R
   Baldacci, S
   Simon, N
   Pannier, D
   Vieillard, MH
   Turpin, A
AF Vauleon, Enora
   Behal, Helene
   Lebellec, Loic
   Desbarbieux, Renaud
   Baldacci, Simon
   Simon, Nicolas
   Pannier, Diane
   Vieillard, Marie-Helene
   Turpin, Anthony
TI Does bevacizumab increase joint pain in patients with cancer? Results of
   the prospective observational BEVARTHRALGIA study
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE Arthralgia; Targeted therapy; Colorectal cancer; Ovarian cancer; Lung
   cancer
ID OVARIAN-CARCINOMA; PALMAR-FASCIITIS; PACLITAXEL
AB Purpose The occurrence of arthralgia and myalgia during treatment with bevacizumab (Bev) has been described but not spontaneously reported. We aimed to evaluate the frequency of arthralgia in patients treated with Bev and identify the risk factors. Methods In this observational prospective study, a self-administered questionnaire was distributed to patients at the initiation of Bev and at 3 and 6 months of treatment. Bev (5-15 mg/kg) was administered every 2 or 3 weeks, with or without chemotherapy. Results A total of 71 patients (42 with colorectal cancer, 22 with ovarian cancer, and 7 with lung cancer) were enrolled from January to November 2018. All patients completed the questionnaire at initiation, while only 56 (78.9%) and 36 (50.7%) patients completed the questionnaire at 3 and 6 months, respectively. The frequency of joint pain was 29.6% before Bev treatment and increased to 41.8% and 50% at 3 and 6 months, respectively, without reaching significance. The evolution of pain was significant according to the Common Terminology Criteria for Adverse Events grades (P = 0.032). No significant increase in the impact of pain on instrumental or elementary activities was observed over time. The frequency of arthralgia significantly increased at 3 months in patients with ovarian cancer versus those with colorectal cancer (odds ratio: 19.50; 95% confidence interval 4.53-83.98; P < 0.001). Conclusions Bev-including regimens tend to be associated with a significant increase in the frequency of arthralgia in women treated for ovarian cancer. Physicians should be aware of this side effect.
C1 [Vauleon, Enora] Univ Lille, Dept Med Oncol, CHU Lille, Lille, France.
   [Behal, Helene] Univ Lille, ULR 2694, METR Evaluat Technol Sante & Prat Med, CHU Lille, Lille, France.
   [Lebellec, Loic; Pannier, Diane; Vieillard, Marie-Helene] Oscar Lambret Ctr, Dept Med Oncol, Lille, France.
   [Desbarbieux, Renaud] Hop Duchenne, Boulogne Sur Mer, France.
   [Baldacci, Simon] Univ Lille, CNRS, INSERM,Thorac Oncol Dept,CHRU Lille, Inst Pasteur Lille,UMR9020,UMR S 1277,Canther,Can, Lille, France.
   [Simon, Nicolas] Univ Lille, ULR 7365 GRITA Grp Rech Formes Injectables & Tech, CHU Lille, F-59000 Lille, France.
   [Vieillard, Marie-Helene] Univ Lille, CNRS, INSERM,Univ Dept Rheumatol,CHU Lille, Inst Pasteur Lille,UMR9020,UMR S 1277,Canther,Can, Lille, France.
   [Turpin, Anthony] Univ Lille, CNRS, INSERM,Med Oncol Dept,CHU Lille, Inst Pasteur Lille,UMR9020,UMR S 1277,Canther,Can, Lille, France.
C3 Universite de Lille; CHU Lille; Universite de Lille; CHU Lille;
   UNICANCER; Centre Oscar Lambret; Universite de Lille; CHU Lille; Pasteur
   Network; Institut Pasteur Lille; Institut National de la Sante et de la
   Recherche Medicale (Inserm); Centre National de la Recherche
   Scientifique (CNRS); Universite de Lille; CHU Lille; Centre National de
   la Recherche Scientifique (CNRS); Universite de Lille; CHU Lille;
   Pasteur Network; Institut Pasteur Lille; Institut National de la Sante
   et de la Recherche Medicale (Inserm); Pasteur Network; Universite de
   Lille; Institut Pasteur Lille; Institut National de la Sante et de la
   Recherche Medicale (Inserm); CHU Lille; Centre National de la Recherche
   Scientifique (CNRS)
RP Turpin, A (corresponding author), Univ Lille, CNRS, INSERM,Med Oncol Dept,CHU Lille, Inst Pasteur Lille,UMR9020,UMR S 1277,Canther,Can, Lille, France.
EM Anthony.turpin@chru-lille.fr
RI SIMON, Nicolas/IAO-0588-2023; Turpin, Anthony/F-2481-2018; SIMON,
   Nicolas/G-4328-2016
OI Baldacci, Simon/0000-0003-3610-1316; Turpin,
   Anthony/0000-0002-2282-0101; Lebellec, Loic/0000-0002-6079-0185; SIMON,
   Nicolas/0000-0001-5257-440X
CR Bannwarth B., 2010, REV RHUMATISME MONOG, V77, P173
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NR 28
TC 2
Z9 2
U1 1
U2 2
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0344-5704
EI 1432-0843
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD APR
PY 2021
VL 87
IS 4
BP 533
EP 541
DI 10.1007/s00280-020-04226-6
EA JAN 2021
PG 9
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA QU6NG
UT WOS:000607318900001
PM 33438069
DA 2025-01-04
ER

PT J
AU Das, PK
   Asha, SY
   Abe, I
   Islam, F
   Lam, AK
AF Das, Plabon Kumar
   Asha, Saharia Yeasmin
   Abe, Ichiro
   Islam, Farhadul
   Lam, Alfred K.
TI Roles of Non-Coding RNAs on Anaplastic Thyroid Carcinomas
SO CANCERS
LA English
DT Review
DE Anaplastic thyroid carcinoma; non-coding RNAs; miRNAs; lncRNAs; siRNAs;
   targeted therapy
ID DOUBLE-STRAND BREAKS; MESENCHYMAL TRANSITION; TUMOR-SUPPRESSOR;
   DOWN-REGULATION; LNCRNA NEAT1; CANCER-CELLS; INCREASED EXPRESSION;
   COLORECTAL-CANCER; MALAT1 PROMOTES; POOR-PROGNOSIS
AB Simple Summary
   Anaplastic thyroid carcinoma (ATC) is a biological aggressive human carcinoma and causes most of the thyroid cancer related deaths. Non-protein producing RNAs, such as long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), play crucial roles in formation and therapy resistance of ATC by regulating the production of key proteins. These RNAs alter the proteome of cells, which in turn controls cancer cells' growth, division, invasion, migration, metastasis, and recurrence of ATC. Thus, the exogenous manipulation of these RNAs could interfere cells growth and development of ATC. Considering this, we discuss the roles of various miRNAs and lncRNAs in the pathogenesis of ATC and their potential therapeutic applications.
   Anaplastic thyroid cancer (ATC) remains as one of the most aggressive human carcinomas with poor survival rates in patients with the cancer despite therapeutic interventions. Novel targeted and personalized therapies could solve the puzzle of poor survival rates of patients with ATC. In this review, we discuss the role of non-coding RNAs in the regulation of gene expression in ATC as well as how the changes in their expression could potentially reshape the characteristics of ATCs. A broad range of miRNA, such as miR-205, miR-19a, miR-17-3p and miR-17-5p, miR-618, miR-20a, miR-155, etc., have abnormal expressions in ATC tissues and cells when compared to those of non-neoplastic thyroid tissues and cells. Moreover, lncRNAs, such as H19, Human leukocyte antigen (HLA) complex P5 (HCP5), Urothelial carcinoma-associated 1 (UCA1), Nuclear paraspeckle assembly transcript 1 (NEAT1), etc., participate in transcription and post-transcriptional regulation of gene expression in ATC cells. Dysregulations of these non-coding RNAs were associated with development and progression of ATC by modulating the functions of oncogenes during tumour progression. Thus, restoration of the abnormal expression of these miRNAs and lncRNAs may serve as promising ways to treat the patients with ATC. In addition, siRNA mediated inhibition of several oncogenes may act as a potential option against ATC. Thus, non-coding RNAs can be useful as prognostic biomarkers and potential therapeutic targets for the better management of patients with ATC.
C1 [Das, Plabon Kumar; Asha, Saharia Yeasmin; Islam, Farhadul] Rajshahi Univ, Dept Biochem & Mol Biol, Rajshahi 6205, Bangladesh.
   [Abe, Ichiro; Lam, Alfred K.] Griffith Univ, Sch Med, Gold Coast, Qld 4222, Australia.
   [Abe, Ichiro] Fukuoka Univ, Dept Endocrinol & Diabet Mellitus, Chikushi Hosp, Fukuoka 8188502, Japan.
   [Islam, Farhadul] Griffith Univ, Inst Glyc, Gold Coast Campus, Gold Coast, Qld 4222, Australia.
C3 University of Rajshahi; Griffith University; Griffith University - Gold
   Coast Campus; Fukuoka University; Griffith University; Griffith
   University - Gold Coast Campus
RP Islam, F (corresponding author), Rajshahi Univ, Dept Biochem & Mol Biol, Rajshahi 6205, Bangladesh.; Lam, AK (corresponding author), Griffith Univ, Sch Med, Gold Coast, Qld 4222, Australia.; Islam, F (corresponding author), Griffith Univ, Inst Glyc, Gold Coast Campus, Gold Coast, Qld 4222, Australia.
EM plabonsb5208@gmail.com; saharia.yeasmin@gmail.com;
   i.abe@griffith.edu.au; farhad_bio83@ru.ac.bd; a.lam@griffith.edu.au
RI Abe, Ichiro/JLL-1354-2023; Islam, Farhadul/R-5643-2017; Lam,
   Alfred/C-1652-2008
OI Islam, Farhadul/0000-0001-5262-4702; Abe, Ichiro/0000-0002-7545-9751;
   Lam, Alfred/0000-0003-2771-564X; DAS, PLABON KUMAR/0000-0003-3339-1346
FU School of Medicine, Griffith University, Gold coast campus, Queensland,
   Australia
FX This research received no external funding and the APC was funded by
   School of Medicine, Griffith University, Gold coast campus, Queensland,
   Australia.
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NR 137
TC 15
Z9 15
U1 0
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD NOV
PY 2020
VL 12
IS 11
AR 3159
DI 10.3390/cancers12113159
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OW3ZD
UT WOS:000592828200001
PM 33126409
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kennedy, AS
   Brown, DB
   Fakih, M
   Jeyarajah, R
   Jones, S
   Liu, DV
   Pinato, DJ
   Sangro, B
   Sharma, NK
   Sze, DY
   Van Cutsem, E
   Wasan, HS
AF Kennedy, Andrew S.
   Brown, Daniel B.
   Fakih, Marwan
   Jeyarajah, Rohan
   Jones, Suzanne
   Liu, David
   Pinato, David J.
   Sangro, Bruno
   Sharma, Navesh K.
   Sze, Daniel Y.
   Van Cutsem, Eric
   Wasan, Harpreet S.
TI Multidisciplinary Delphi Consensus on Safety of Combining Transarterial
   Radioembolization with Yttrium-90 Microspheres with Systemic Anticancer
   Agents for the Treatment of Liver Malignancy
SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY
LA English
DT Article
ID INTERNAL RADIATION-THERAPY; METASTATIC NEUROENDOCRINE TUMORS; RECEPTOR
   RADIONUCLIDE THERAPY; PHASE-II TRIAL; COLORECTAL-CANCER; RESIN
   MICROSPHERES; SIR-SPHERES; RADIOTHERAPY; CHEMOTHERAPY; SORAFENIB
AB Purpose: To provide guidance, via multidisciplinary consensus statements, on the safety interactions between systemic anticancer agents (such as radiosensitizing chemotherapy, immunotherapy, targeted therapy, and peptide receptor radionuclide therapy) and transarterial radioembolization (TARE) with yttrium-90 (90Y)-labeled 90 Y)-labeled microspheres in the treatment of primary and metastatic liver malignancies. Materials and Methods: A literature search identified 59 references that informed 26 statements on the safety of 90 Y TARE combined with systemic therapies. Modified Delphi method was used to develop consensus on statements through online anonymous surveys of the 12 panel members representing the fields of interventional radiology, medical oncology, surgical oncology, hepatology, and pharmacy, focusing on hepatocellular carcinoma (HCC), metastatic colorectal cancer (mCRC), neuroendocrine tumors, metastatic breast cancer, and intrahepatic cholangiocarcinoma. Results: High-level evidence was limited. Level 1 data in patients with mCRC suggest that some radiosensitizing chemotherapies (eg, oxaliplatin) require temporary dose reduction when used concomitantly with 90 Y TARE, and some targeted therapies (eg, vascular endothelial growth factor inhibitors and antiangiogenic tyrosine kinase inhibitors) should be avoided for at least 4 weeks before 90 Y TARE. In patients with HCC, the feasibility of 90 Y TARE and immunotherapy has been demonstrated with Level 4 evidence. Data are more limited for other primary and secondary liver malignancies, and consensus statements were driven by expert opinion (Level 5). Conclusions: Given the absence of evidence-based guidelines on the safety of 90 Y TARE in combination with systemic anticancer therapy, these consensus statements provide expert guidance on the potential risks when considering specific combinations.
C1 [Kennedy, Andrew S.] Sarah Cannon Res Inst, Radiat Oncol, Nashville, TN 37203 USA.
   [Brown, Daniel B.] Vanderbilt Univ, Med Ctr, Intervent Radiol, Nashville, TN USA.
   [Fakih, Marwan] City Hope Comprehens Canc Ctr Duarte, Med Oncol & Therapeut Res, Duarte, CA USA.
   [Jeyarajah, Rohan] TCU Burnett Sch Med, Ft Worth, TX USA.
   [Jones, Suzanne] Sarah Cannon Res Inst, Drug Dev, Nashville, TN USA.
   [Liu, David] Univ British Columbia, Fac Med, Sch Biomed Engn, Vancouver, BC, Canada.
   [Pinato, David J.] Imperial Coll London, Hammersmith Hosp, Dept Surg & Canc, London, England.
   [Pinato, David J.] Univ Piemonte Orientale, Dept Translat Med, Div Oncol, Novara, Italy.
   [Sangro, Bruno] Clin Univ Navarra, Liver Unit, Pamplona Madrid, Spain.
   [Sangro, Bruno] CIBEREHD, Pamplona Madrid, Spain.
   [Sharma, Navesh K.; Sze, Daniel Y.] WellSpan Canc Ctr, Dept Radiat Oncol, New York, NY USA.
C3 Sarah Cannon Research Institute; Vanderbilt University; Sarah Cannon
   Research Institute; University of British Columbia; Imperial College
   London; University of Eastern Piedmont Amedeo Avogadro; University of
   Navarra; CIBER - Centro de Investigacion Biomedica en Red; CIBEREHD
RP Kennedy, AS (corresponding author), Sarah Cannon Res Inst, Radiat Oncol, Nashville, TN 37203 USA.
EM andrew.kennedy@sarahcannon.com
RI Pinato, David/ABB-3719-2020; Sangro, Bruno/AFW-4106-2022
OI Kennedy, Andrew/0000-0001-9761-2262; Sangro, Bruno/0000-0002-4177-6417;
   Liu, Dave/0000-0002-5891-3609
FU Sirtex Medical
FX The authors thank Martin Gilmour, PhD, of Empowering Strategic
   Performance for providing editorial assistance andconducting the Delphi
   consensus methodology under thedirection of the panel. This editorial
   assistance was fundedby Sirtex Medical, which did not influence the
   content ofthe recommendations. Sirtex Medical funded project management
   (including logistical arrangements for WorkingGroup Meetings and
   delivering the Delphi surveys) andeditorial support (literature search
   and analysis, statementdrafting, and manuscript development). The
   authors did notreceive compensation for their participation in the
   initiative.
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NR 90
TC 1
Z9 1
U1 4
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1051-0443
EI 1535-7732
J9 J VASC INTERV RADIOL
JI J. Vasc. Interv. Radiol.
PD SEP
PY 2024
VL 35
IS 9
DI 10.1016/j.jvir.2024.06.006
EA AUG 2024
PG 16
WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular
   Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System &
   Cardiology
GA E6T6H
UT WOS:001304313500001
PM 38885899
OA hybrid
DA 2025-01-04
ER

PT J
AU Ahn, M
   Lee, TB
   Kim, KS
   Lee, SH
   Na, K
AF Ahn, Minji
   Lee, Taebum
   Kim, Kyoung Sub
   Lee, Sanghee
   Na, Kun
TI Synergistic Approach of Antibody-Photosensitizer Conjugate Independent
   of KRAS-Mutation and Its Downstream Blockade Pathway in Colorectal
   Cancer
SO ADVANCED HEALTHCARE MATERIALS
LA English
DT Article
DE antibody drug conjugates; cetuximab conjugates; KRAS mutation; linker
   chemistry; photoimmunotherapy
ID EGFR-TARGETED THERAPIES; DRUG; RESISTANCE; CETUXIMAB; LINKERS
AB Here, a novel approach is presented to improve the efficacy of antibody-drug conjugates (ADC) by integrating antibody-mediated immunotherapy and photodynamic therapy (PDT) in a combination therapy system utilizing an antibody-photosensitizer conjugate (APC) platform based on a poloxamer polymer linker. To specifically target Kirsten rat sarcoma 2 viral oncogene homolog (KRAS)-mutated cancer cells, an antibody antiepidermal growth factor receptor (EGFR), cetuximab, with a poloxamer linker coupled with the photosensitizer chlorin e6 through click chemistry (cetuximab-maleimide-poly(ethylene oxide)-poly(propylene oxide)-poly(ethylene oxide)-chlorine e6 conjugate, CMPXC) is synthesized. CMPXC is cytotoxic upon laser treatment, achieving a 90% cell death by suppressing KRAS downstream signaling pathways associated with ERK and AKT proteins, confirmed using RNA sequencing analysis. In KRAS-mutated colorectal cancer mouse models, CMPXC significantly enhances antitumor efficacy compared with cetuximab treatment alone, resulting in an 86% reduction in tumor growth. Furthermore, CMPXC treatment leads to a 2.24- and 1.75-fold increase in dendritic and priming cytotoxic T cells, respectively, highlighting the immune-activating potential of this approach. The findings suggest that the APC platform addresses the challenges associated with ADC development and EGFR-targeted therapy, including the synergistic advantages of antibody-mediated immunotherapy and PDT.
   To improve the efficacy of antibody-drug conjugates, a novel platform by combining antibody-mediated immunotherpay and photodynamic therapy is constructed. Upon spatiotemporal light exposure, the antibody-photosensitizer conjugate exhibits a remarkable anticancer effect, independent Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) mutation, by suppressing KRAS downstream signaling pathways and providing innate and adaptive immune system induction through a synergistic approach.image
C1 [Ahn, Minji; Lee, Taebum; Na, Kun] Catholic Univ Korea, Dept Biomed Chem Engn, 43 Jibong Ro, Bucheon Si 14662, Gyeonggi Do, South Korea.
   [Ahn, Minji; Lee, Taebum; Kim, Kyoung Sub; Na, Kun] Catholic Univ Korea, Dept Biotechnol, 43 Jibong Ro, Bucheon Si 14662, Gyeonggi Do, South Korea.
   [Lee, Sanghee] Northwestern Univ, Feinberg Sch Med, Dept Radiol, Chicago, IL 60611 USA.
C3 Catholic University of Korea; Catholic University of Korea; Northwestern
   University; Feinberg School of Medicine
RP Na, K (corresponding author), Catholic Univ Korea, Dept Biomed Chem Engn, 43 Jibong Ro, Bucheon Si 14662, Gyeonggi Do, South Korea.; Na, K (corresponding author), Catholic Univ Korea, Dept Biotechnol, 43 Jibong Ro, Bucheon Si 14662, Gyeonggi Do, South Korea.
EM kna6997@catholic.ac.kr
RI Lee, Tae/F-9916-2010
FU Korean Fund for Regenerative Medicine (KFRM) - Korea government (the
   Ministry of Science and ICT) [KFRM 21A0501L1]; National Research
   Foundation of Korea - Ministry of Science and ICT (MSIT)
FX This research was supported by the Korean Fund for Regenerative Medicine
   (KFRM) grant funded by the Korea government (the Ministry of Science and
   ICT, the Ministry of Health and Welfare) (code: KFRM 21A0501L1). This
   work was supported by the Basic Science Research Program
   (NRF-2022R1A2B5B03001432) of the National Research Foundation of Korea
   funded by the Ministry of Science and ICT (MSIT).
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NR 49
TC 5
Z9 5
U1 10
U2 21
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2192-2640
EI 2192-2659
J9 ADV HEALTHC MATER
JI Adv. Healthc. Mater.
PD DEC
PY 2023
VL 12
IS 31
DI 10.1002/adhm.202302374
EA SEP 2023
PG 12
WC Engineering, Biomedical; Nanoscience & Nanotechnology; Materials
   Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Science & Technology - Other Topics; Materials Science
GA CQ6G2
UT WOS:001070768900001
PM 37722358
OA Bronze
DA 2025-01-04
ER

PT J
AU Yang, L
   Chen, XM
   Lee, CSY
   Shi, JJ
   Lawrence, EB
   Zhang, LJ
   Li, YM
   Gao, N
   Jung, SY
   Creighton, CJ
   Li, JJ
   Cui, Y
   Arimura, S
   Lei, YP
   Li, W
   Shen, LL
AF Yang, Li
   Chen, Xiaomin
   Lee, Christy
   Shi, Jiejun
   Lawrence, Emily B.
   Zhang, Lanjing
   Li, Yumei
   Gao, Nan
   Jung, Sung Yun
   Creighton, Chad J.
   Li, Jingyi Jessica
   Cui, Ya
   Arimura, Sumimasa
   Lei, Yunping
   Li, Wei
   Shen, Lanlan
TI Functional characterization of age-dependent <i>p16</i> epimutation
   reveals biological drivers and therapeutic targets for colorectal cancer
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Article
DE Colon cancer; p16 epimutation; Tumor microenvironment; Epigenetic and
   immunotherapy
ID SUPPRESSES TUMOR-GROWTH; CPG ISLAND METHYLATION; DNA METHYLATION;
   EPIGENETIC THERAPY; EPIGENOME; CELLS; TUMORIGENESIS; INACTIVATION;
   PROGRESSION; INHIBITION
AB BackgroundMethylation of the p16 promoter resulting in epigenetic gene silencing-known as p16 epimutation-is frequently found in human colorectal cancer and is also common in normal-appearing colonic mucosa of aging individuals. Thus, to improve clinical care of colorectal cancer (CRC) patients, we explored the role of age-related p16 epimutation in intestinal tumorigenesis.MethodsWe established a mouse model that replicates two common genetic and epigenetic events observed in human CRCs: Apc mutation and p16 epimutation. We conducted long-term survival and histological analysis of tumor development and progression. Colonic epithelial cells and tumors were collected from mice and analyzed by RNA sequencing (RNA-seq), quantitative PCR, and flow cytometry. We performed single-cell RNA sequencing (scRNA-seq) to characterize tumor-infiltrating immune cells throughout tumor progression. We tested whether anti-PD-L1 immunotherapy affects overall survival of tumor-bearing mice and whether inhibition of both epigenetic regulation and immune checkpoint is more efficacious.ResultsMice carrying combined Apc mutation and p16 epimutation had significantly shortened survival and increased tumor growth compared to those with Apc mutation only. Intriguingly, colon tumors with p16 epimutation exhibited an activated interferon pathway, increased expression of programmed death-ligand 1 (Pdl1), and enhanced infiltration of immune cells. scRNA-seq further revealed the presence of Foxp3(+) Tregs and gamma delta T17 cells, which contribute to an immunosuppressive tumor microenvironment (TME). Furthermore, we showed that a combined therapy using an inhibitor of DNA methylation and a PD-L1 immune checkpoint inhibitor is more effective for improving survival in tumor-bearing mice than blockade of either pathway alone.ConclusionsOur study demonstrated that age-dependent p16 epimutation creates a permissive microenvironment for malignant transformation of polyps to colon cancer. Our findings provide a mechanistic rationale for future targeted therapy in patients with p16 epimutation.
C1 [Yang, Li; Chen, Xiaomin; Lawrence, Emily B.; Shen, Lanlan] USDA, Baylor Coll Med, Dept Pediat, Childrens Nutr Res Ctr, Houston, TX 77065 USA.
   [Lee, Christy; Li, Jingyi Jessica] Univ Calif Los Angeles, Dept Stat, Los Angeles, CA USA.
   [Shi, Jiejun; Cui, Ya; Li, Wei] Univ Calif Irvine, Sch Med, Dept Biol Chem, Div Computat Biomed, Irvine, CA USA.
   [Shi, Jiejun] Tongji Univ, Shanghai Tongji Hosp, Sch Life Sci & Technol, Dept Gen Surg, Shanghai, Peoples R China.
   [Zhang, Lanjing] Med Ctr Princeton, Dept Pathol, Plainsboro, NJ USA.
   [Zhang, Lanjing] Rutgers State Univ, Earnest Mario Sch Pharm, Dept Chem Biol, Piscataway, NJ USA.
   [Li, Yumei; Creighton, Chad J.] Baylor Coll Med, Human Genome Sequencing Ctr, Houston, TX USA.
   [Gao, Nan] Rutgers State Univ, Dept Biol Sci, Newark, NJ USA.
   [Jung, Sung Yun] Baylor Coll Med, Dept Biochem, Houston, TX USA.
   [Creighton, Chad J.; Arimura, Sumimasa] Baylor Coll Med, Dept Med, Houston, TX USA.
   [Creighton, Chad J.] Baylor Coll Med, Dan Duncan Comprehens Canc Ctr, Houston, TX USA.
   [Arimura, Sumimasa] Baylor Coll Med, Sect Gastroenterol & Hepatol, Houston, TX USA.
   [Lei, Yunping] Baylor Coll Med, Ctr Precis Environm Hlth, Dept Mol & Cellular Biol, Houston, TX USA.
C3 Baylor College of Medicine; United States Department of Agriculture
   (USDA); University of California System; University of California Los
   Angeles; University of California System; University of California
   Irvine; Tongji University; Rutgers University System; Rutgers University
   New Brunswick; Baylor College of Medicine; Rutgers University System;
   Rutgers University Newark; Rutgers University New Brunswick; Baylor
   College of Medicine; Baylor College of Medicine; Baylor College of
   Medicine; Baylor College of Medicine; Baylor College of Medicine
RP Shen, LL (corresponding author), USDA, Baylor Coll Med, Dept Pediat, Childrens Nutr Res Ctr, Houston, TX 77065 USA.
EM Lanlan.Shen@bcm.edu
RI Lei, Yunping/LMM-9159-2024; Zhang, Lanjing/AGY-7838-2022; lifeng,
   yang/AAD-6519-2021; Shi, Jiejun/P-3329-2019; Li, Jingyi
   Jessica/I-2779-2019; Li, Wei/AFW-2599-2022; Chen, Xiaomin/AAJ-3021-2020;
   ARIMURA, SUMIMASA/IQT-4772-2023; Zhang, Lanjing/D-1544-2009
OI Shen, Lanlan/0000-0002-1532-5807; Shi, Jiejun/0000-0001-9777-1183;
   Zhang, Lanjing/0000-0001-5436-887X
FU US Department of Agriculture [CRIS 3092-51000-060]; National Institutes
   of Health [R21CA229727, R01HD100914, R01CA233472]
FX This research was supported by grants from US Department of Agriculture
   (CRIS 3092-51000-060 to L.S.) and National Institutes of Health
   (R21CA229727, R01HD100914, and R01CA233472 to L.S.).
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NR 70
TC 7
Z9 7
U1 2
U2 9
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1756-9966
J9 J EXP CLIN CANC RES
JI J. Exp. Clin. Cancer Res.
PD MAY 4
PY 2023
VL 42
IS 1
AR 113
DI 10.1186/s13046-023-02689-y
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA F3UN4
UT WOS:000981630200001
PM 37143122
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Song, F
   Hou, C
   Huang, YZ
   Liang, JF
   Cai, HS
   Tian, GL
   Jiang, YQ
   Wang, ZY
   Hou, JS
AF Song, Fan
   Hou, Chen
   Huang, Yingzhao
   Liang, Jianfeng
   Cai, Hongshi
   Tian, Guoli
   Jiang, Yaoqi
   Wang, Ziyi
   Hou, Jinsong
TI Lactylome analyses suggest systematic lysine-lactylated substrates in
   oral squamous cell carcinoma under normoxia and hypoxia
SO CELLULAR SIGNALLING
LA English
DT Article
DE Oral squamous cell carcinoma; Post-translational modifications; Lysine
   lactylation; Alternative splicing; Ribosome pathway; Glycolysis
ID EPITHELIAL-MESENCHYMAL TRANSITION; METABOLIC ADAPTATION; CANCER;
   MECHANISM; PROTEIN; PHOSPHORYLATION; GLYCOSYLATION; RECRUITMENT;
   SUMOYLATION
AB Cancer cells tend to live in hypoxic environment characterized by enhanced glycolysis and accumulation of lactate. Intracellular lactate is shown to drive a novel type of post-translational modification (PTM), lysine lactylation (Kla). Kla has been confirmed to affect the malignant progression of tumors such as hepatocellular carcinoma (HCC) and colon cancer, whereas the global lactylomic profiling of oral squamous cell carcinoma (OSCC) is unclear. Here, the integrative lactylome and proteome analyses by using liquid chromatography- tandem mass spectrometry (LC-MS/MS) identified 1011 Kla sites within 532 proteins and 1197 Kla sites within 608 proteins in SCC25 cells under normoxic and hypoxic environments, respectively. Among these lactylated proteins, histones accounted for only a small fraction, suggesting the presence of Kla modification of OSCC in a large number of non-histone proteins. Notably, Kla preferred to enrich in spliceosome, ribosome and glycolysis/gluconeogenesis pathway in both normoxic and hypoxic cultures. Compared with normoxia, 589 differential proteins with 898 differentially lactylated sites were detected under hypoxia, which were mainly associated with the glycolysis/gluconeogenesis pathway by KEGG analysis. Importantly, we verified the presence of lactylation modification in the spliceosomal proteins hnRNPA1, SF3A1, hnRNPU and SLU7, as well as in glycolytic enzyme PFKP. In addition, the differential alternative splicing analysis described the divergence of premRNA splicing patterns in the presence or absence of sodium lactate and at different oxygen concentrations. Finally, a negative correlation between tissue Kla levels and the prognosis of OSCC patients was revealed by immunohistochemistry. Our study is the first report to elucidate the lactylome and its biological function in OSCC, which deepens our understanding of the mechanisms underlying OSCC progression and provides a novel strategy for targeted therapy for OSCC.
C1 [Song, Fan; Hou, Chen; Huang, Yingzhao; Liang, Jianfeng; Cai, Hongshi; Tian, Guoli; Jiang, Yaoqi; Wang, Ziyi; Hou, Jinsong] Sun Yat Sen Univ, Hosp Stomatol, Guanghua Sch Stomatol, Dept Oral & Maxillofacial Surg, Guangzhou 510055, Guangdong, Peoples R China.
   [Song, Fan; Hou, Chen; Huang, Yingzhao; Liang, Jianfeng; Cai, Hongshi; Tian, Guoli; Jiang, Yaoqi; Wang, Ziyi; Hou, Jinsong] Sun Yat Sen Univ, Guangdong Prov Key Lab Stomatol, Guangzhou 510055, Guangdong, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University
RP Hou, JS (corresponding author), Sun Yat Sen Univ, Hosp Stomatol, Guanghua Sch Stomatol, Dept Oral & Maxillofacial Surg, Guangzhou 510055, Guangdong, Peoples R China.; Hou, JS (corresponding author), Sun Yat Sen Univ, Guangdong Prov Key Lab Stomatol, Guangzhou 510055, Guangdong, Peoples R China.
EM houjs@mail.sysu.edu.cn
RI HOU, CHEN/IQT-3648-2023
FU National Natural Science Foundation of China [81874128, 82072994]; Sun
   Yat-sen University Clinical Research 5010 Program [2015018]
FX We thank J. Silvio Gutkind for providing NOK cell lines. This research
   was funded by the National Natural Science Foundation of China (grant
   no. 81874128, 82072994) , Sun Yat-sen University Clinical Research 5010
   Program (grant no. 2015018) .
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NR 66
TC 2
Z9 3
U1 6
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0898-6568
EI 1873-3913
J9 CELL SIGNAL
JI Cell. Signal.
PD AUG
PY 2024
VL 120
AR 111228
DI 10.1016/j.cellsig.2024.111228
EA MAY 2024
PG 16
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA H8D1D
UT WOS:001325681000001
PM 38750680
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Tesfaye, AA
   Wang, HK
   Hartley, ML
   He, AR
   Weiner, L
   Gabelia, N
   Kapanadze, L
   Shezad, M
   Brody, JR
   Marshall, JL
   Pishvaian, MJ
AF Tesfaye, Anteneh A.
   Wang, Hongkun
   Hartley, Marion L.
   He, Aiwu Ruth
   Weiner, Louis
   Gabelia, Nina
   Kapanadze, Lana
   Shezad, Muhammad
   Brody, Jonathan R.
   Marshall, John L.
   Pishvaian, Michael J.
TI A Pilot Trial of Molecularly Tailored Therapy for Patients with
   Metastatic Pancreatic Ductal Adenocarcinoma
SO JOURNAL OF PANCREATIC CANCER
LA English
DT Article
DE chemotherapy; metastatic pancreatic cancer; molecular testing
ID PHASE-II TRIAL; THYMIDYLATE SYNTHASE EXPRESSION; 1ST-LINE TREATMENT;
   OXALIPLATIN COMBINATION; 2ND-LINE TREATMENT; NAB-PACLITAXEL;
   ONCOLOGY-GROUP; FOLINIC ACID; COLON-CANCER; GEMCITABINE
AB Purpose: Despite the wide adoption of tumormolecular profiling, there is a dearth of evidence linking molecular biomarkers for treatment selection to prediction of treatment outcomes in patients with metastatic pancreatic cancer. We initiated a pilot study to test the feasibility of designing a larger phase II trial of molecularly tailored treatment for metastatic pancreatic cancer.
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C1 [Tesfaye, Anteneh A.] Wayne State Univ, Karmanos Canc Inst, Detroit, MI USA.
   [Wang, Hongkun; Hartley, Marion L.; He, Aiwu Ruth; Weiner, Louis; Gabelia, Nina; Kapanadze, Lana; Shezad, Muhammad; Marshall, John L.; Pishvaian, Michael J.] Georgetown Univ, Lombardi Comprehens Canc Ctr, Podium B,3800 Reservoir Rd NW, Washington, DC 20007 USA.
   [Brody, Jonathan R.] Thomas Jefferson Univ, Dept Surg, Sidney Kimmel Canc Ctr, Philadelphia, PA 19107 USA.
C3 Wayne State University; Barbara Ann Karmanos Cancer Institute;
   Georgetown University; Jefferson University
RP Pishvaian, MJ (corresponding author), Georgetown Univ, Lombardi Comprehens Canc Ctr, Podium B,3800 Reservoir Rd NW, Washington, DC 20007 USA.
EM pishvaim@georgetown.edu
RI Tesfaye, Anteneh/IYJ-9752-2023
FU 2015 Pancreatic Cancer Action Network American Association for Cancer
   Research Acceleration Network Grant [15-90-25-BROD]; Ruesch Center for
   the Cure of Gastrointestinal Cancers at Lombardi Comprehensive Cancer
   Center
FX M.J.P. and J.R.B. are supported by a 2015 Pancreatic Cancer Action
   Network American Association for Cancer Research Acceleration Network
   Grant (15-90-25-BROD). The trial was funded by The Ruesch Center for the
   Cure of Gastrointestinal Cancers at Lombardi Comprehensive Cancer
   Center.
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NR 48
TC 3
Z9 4
U1 0
U2 1
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
EI 2475-3246
J9 J PANCREATIC CANCER
JI J. Pancreatic Cancer
PD MAY 2
PY 2019
VL 5
IS 1
BP 12
EP 21
DI 10.1089/pancan.2019.0003
PG 10
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA JF1JS
UT WOS:000491144000001
PM 31065624
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Hu, HF
   Xu, WW
   Wang, Y
   Zheng, CC
   Zhang, WX
   Li, B
   He, QY
AF Hu, Hui-Fang
   Xu, Wen Wen
   Wang, Yang
   Zheng, Can-Can
   Zhang, Wei-Xia
   Li, Bin
   He, Qing-Yu
TI Comparative Proteomics Analysis Identifies Cdc42-Cdc42BPA Signaling as
   Prognostic Biomarker and Therapeutic Target for Colon Cancer Invasion
SO JOURNAL OF PROTEOME RESEARCH
LA English
DT Article
DE SILAC proteomics; Cdc42; Cdc42BPA; colon cancer invasion; prognostic
   biomarker; targeted therapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; CELL LUNG-CANCER; ESOPHAGEAL CANCER;
   BREAST-CANCER; COLORECTAL-CANCER; TUMOR-METASTASIS; POOR-PROGNOSIS; RHO
   GTPASES; CDC42; INHIBITION
AB Metastasis is one of the major causes of treatment failure in the patients with colon cancer. The aim of our study is to find key proteins and pathways that drive invasion and metastasis in colon cancer. Eight rounds of selection of cancer cells invading through matrigel-coated chamber were performed to obtain highly invasive colon cancer sublines HCT116-I8 and RKO-I8. Stable Isotope Labeling by Amino Acids in Cell Culture technology was used to identify the differently expressed proteins, and the proteomics data were analyzed by ingenuity pathway analysis. PAK1-PBD immunoprecipitation combined with Western blot were carried out to determine Cdc42 activity, and qRT-PCR and Western blot were used to determine gene expression. The functional role of Cdc42BPA and Cdc42 pathway in colon cancer invasion was studied by loss-of-function experiments including pharmacological blockade, siRNA knockdown, chamber invasion, and WST-1 assays. Human colon cancer tissue microarray was analyzed by immunohistochemistry for overexpression of Cdc42BPA and its correlation with clinicopathological parameters and patient survival outcomes. HCT116-I8 and RKO-I8 cells showed significantly stronger invasive potential as well as decreased E-cadherin and increased vimentin expressions compared with parental cells. The differently expressed proteins in I8 cells compared with parental cells were identified. Bioinformatics analysis of proteomics data suggested that Cdc42BPA protein and Cdc42 signaling pathway are important for colon cancer invasion, which was confirmed by experimental data showing upregulation of Cdc42BPA and higher expression of active GTP-bound form of Cdc42 in HCT116-18 and RKO-I8 cells. Functionally, pharmacological and genetic blockade of Cdc42BPA and Cdc42 signaling markedly suppressed colon cancer cell invasion and reversed epithelial mesenchymal transition process. Furthermore, compared with adjacent normal tissues, Cdc42BPA expression was significantly higher in colon cancer tissues and further upregulated in metastatic tumors in lymph nodes. More importantly, Cdc42BPA expression was correlated with metastasis and poor survival of the patients with colon cancer. This study provides the first evidence that Cdc42BPA and Cdc42 signaling are important for colon cancer invasion, and Cdc42BPA has potential implications for colon cancer prognosis and treatment.
C1 [Hu, Hui-Fang; Wang, Yang; Zheng, Can-Can; Zhang, Wei-Xia; Li, Bin; He, Qing-Yu] Jinan Univ, Coll Life Sci & Technol, Inst Life & Hlth Engn, Key Lab Funct Prot Res,Guangdong Higher Educ Inst, Guangzhou 510632, Guangdong, Peoples R China.
   [Xu, Wen Wen] Jinan Univ, Guangdong Prov Key Lab Bioengn Med, Natl Engn Res Ctr Genet Med, Inst Biomed, Guangzhou 510632, Guangdong, Peoples R China.
C3 Jinan University; Jinan University
RP Li, B; He, QY (corresponding author), Jinan Univ, Coll Life Sci & Technol, Inst Life & Hlth Engn, Key Lab Funct Prot Res,Guangdong Higher Educ Inst, Guangzhou 510632, Guangdong, Peoples R China.
EM libin2015@jnu.edu.cn; qyhe@jnu.edu.cn
RI Wang, Yang/JCD-7420-2023; cancan, zheng/JRX-5084-2023; Xu,
   Wenwen/KXR-5605-2024; He, Qing-Yu/H-7078-2014
OI Li, Bin/0000-0002-8979-610X; He, Qing-Yu/0000-0003-0503-9492; Hu,
   Hui-Fang/0009-0001-0223-5044; Wang, Yang/0000-0001-6440-0204
FU National Key Research and Development Program of China [2017YFA0505100];
   National Natural Science Foundation of China [31570828, 81672953];
   Guangdong Natural Science Research Grant [2016A030313838]; Fundamental
   Research Funds for the Central Universities [21617434]
FX This work was supported by the National Key Research and Development
   Program of China (no. 2017YFA0505100), the National Natural Science
   Foundation of China (31570828, 81672953), Guangdong Natural Science
   Research Grant (2016A030313838), and the Fundamental Research Funds for
   the Central Universities (21617434). We thank Mr. Xing-Feng Yin and Mr.
   Zheng-Hua Sun for their technical assistance on mass spectrometry.
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NR 49
TC 15
Z9 16
U1 0
U2 30
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1535-3893
EI 1535-3907
J9 J PROTEOME RES
JI J. Proteome Res.
PD JAN
PY 2018
VL 17
IS 1
BP 265
EP 275
DI 10.1021/acs.jproteome.7b00550
PG 11
WC Biochemical Research Methods
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA FS4HN
UT WOS:000419749800025
PM 29072916
DA 2025-01-04
ER

PT J
AU He, LW
   Li, HG
   Pan, CY
   Hua, YT
   Peng, JY
   Zhou, ZC
   Zhao, Y
   Lin, MB
AF He, Luwei
   Li, Huaguang
   Pan, Chenyu
   Hua, Yutong
   Peng, Jiayin
   Zhou, Zhaocai
   Zhao, Yun
   Lin, Moubin
TI Squalene epoxidase promotes colorectal cancer cell proliferation through
   accumulating calcitriol and activating CYP24A1-mediated MAPK signaling
SO CANCER COMMUNICATIONS
LA English
DT Article
DE calcitriol; cell proliferation; cholesterol biosynthesis; colorectal
   cancer; MAPK signaling; squalene epoxidase; terbinafine
ID CONSENSUS MOLECULAR SUBTYPES; CHOLESTEROL ESTER HYDROLASE; VITAMIN-D;
   DIETARY-CHOLESTEROL; IN-VITRO; METABOLISM; CYP24A1; PATHWAY; PROTEIN;
   OVEREXPRESSION
AB Background Colorectal cancer (CRC) is one of the most malignant tumors with high incidence, yet its molecular mechanism is not fully understood, hindering the development of targeted therapy. Metabolic abnormalities are a hallmark of cancer. Targeting dysregulated metabolic features has become an important direction for modern anticancer therapy. In this study, we aimed to identify a new metabolic enzyme that promotes proliferation of CRC and to examine the related molecular mechanisms. Methods We performed RNA sequencing and tissue microarray analyses of human CRC samples to identify new genes involved in CRC. Squalene epoxidase (SQLE) was identified to be highly upregulated in CRC patients. The regulatory function of SQLE in CRC progression and the therapeutic effect of SQLE inhibitors were determined by measuring CRC cell viability, colony and organoid formation, intracellular cholesterol concentration and xenograft tumor growth. The molecular mechanism of SQLE function was explored by combining transcriptome and untargeted metabolomics analysis. Western blotting and real-time PCR were used to assess MAPK signaling activation by SQLE. Results SQLE-related control of cholesterol biosynthesis was highly upregulated in CRC patients and associated with poor prognosis. SQLE promoted CRC growth in vitro and in vivo. Inhibition of SQLE reduced the levels of calcitriol (active form of vitamin D3) and CYP24A1, followed by an increase in intracellular Ca2+ concentration. Subsequently, MAPK signaling was suppressed, resulting in the inhibition of CRC cell growth. Consistently, terbinafine, an SQLE inhibitor, suppressed CRC cell proliferation and organoid and xenograft tumor growth. Conclusions Our findings demonstrate that SQLE promotes CRC through the accumulation of calcitriol and stimulation of CYP24A1-mediated MAPK signaling, highlighting SQLE as a potential therapeutic target for CRC treatment.
C1 [He, Luwei; Li, Huaguang; Pan, Chenyu; Hua, Yutong; Lin, Moubin] Tongji Univ, Yangpu Hosp, Ctr Clin Res & Translat Med, Sch Med, Shanghai 200090, Peoples R China.
   [He, Luwei; Li, Huaguang; Pan, Chenyu; Hua, Yutong; Lin, Moubin] Tongji Univ, Inst Gastrointestinal Surg & Translat Med, Sch Med, Shanghai 200090, Peoples R China.
   [Lin, Moubin] Tongji Univ, Yangpu Hosp, Dept Gen Surg, Sch Med, Shanghai 200090, Peoples R China.
   [Peng, Jiayin; Zhao, Yun] Chinese Acad Sci, Shanghai Inst Biochem & Cell Biol, CAS Ctr Excellence Mol Cell Sci, State Key Lab Cell Biol,Univ Chinese Acad Sci, Shanghai 200031, Peoples R China.
   [Zhou, Zhaocai] Fudan Univ, Zhongshan Hosp, Sch Life Sci, State Key Lab Genet Engn, Shanghai 200438, Peoples R China.
   [Zhao, Yun] ShanghaiTech Univ, Sch Life Sci & Technol, Shanghai 201210, Peoples R China.
C3 Tongji University; Tongji University; Tongji University; Chinese Academy
   of Sciences; Center for Excellence in Molecular Cell Science, CAS;
   University of Chinese Academy of Sciences, CAS; Fudan University;
   ShanghaiTech University
RP He, LW; Lin, MB (corresponding author), Tongji Univ, Yangpu Hosp, Ctr Clin Res & Translat Med, Sch Med, Shanghai 200090, Peoples R China.; Zhao, Y (corresponding author), Chinese Acad Sci, Shanghai Inst Biochem & Cell Biol, CAS Ctr Excellence Mol Cell Sci, State Key Lab Cell Biol,Univ Chinese Acad Sci, Shanghai 200031, Peoples R China.
EM medichembio1992@163.com; yunzhao@sibcb.ac.cn; lmbin@hotmail.com
RI peng, jiayin/HOH-1860-2023
OI He, Luwei/0000-0001-6564-848X
FU National Natural Science Foundation of China [31630047, 81874201,
   81725014]; Natural Science Foundation of Shanghai [20ZR1452300];
   ShanghaiMunicipal Health Bureau [201840359]; NationalKeyResearch and
   Development Programof China [2020YFA0509000, 2017YFA0503600]
FX National Natural Science Foundation of China, Grant/Award Numbers:
   31630047, 81874201, 81725014; Natural Science Foundation of Shanghai,
   Grant/AwardNumber: 20ZR1452300; ShanghaiMunicipal Health Bureau,
   Grant/Award Number: 201840359; TheNationalKeyResearch and Development
   Programof China, Grant/Award Numbers: 2020YFA0509000, 2017YFA0503600
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NR 63
TC 35
Z9 37
U1 7
U2 30
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2523-3548
J9 CANCER COMMUN
JI Cancer Commun.
PD AUG
PY 2021
VL 41
IS 8
BP 726
EP 746
DI 10.1002/cac2.12187
EA JUL 2021
PG 21
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UA5CY
UT WOS:000673909900001
PM 34268906
OA Green Published
DA 2025-01-04
ER

PT J
AU Davodabadi, F
   Far, BF
   Sargazi, S
   Sajjadi, SF
   Fathi-karkan, S
   Mirinejad, S
   Ghotekar, S
   Sargazi, S
   Rahman, MM
AF Davodabadi, Fatemeh
   Farasati Far, Bahareh
   Sargazi, Saman
   Fatemeh Sajjadi, Seyedeh
   Fathi-karkan, Sonia
   Mirinejad, Shekoufeh
   Ghotekar, Suresh
   Sargazi, Sara
   Rahman, Mohammed M.
TI Nanomaterials-Based Targeting of Long Non-Coding RNAs in Cancer: A
   Cutting-Edge Review of Current Trends
SO CHEMMEDCHEM
LA English
DT Review
DE Cancer; Drug Delivery; Nanotherapeutics; Nanotechnology; Long non-coding
   RNA; Diagnosis
ID COLORECTAL-CANCER; BREAST-CANCER; PROSTATE-CANCER; POLYMERIC
   NANOPARTICLES; BIOMEDICAL APPLICATIONS; PROGNOSTIC VALUE;
   OVARIAN-CANCER; UP-REGULATION; GENE-THERAPY; CELL-GROWTH
AB This review article spotlights the burgeoning potential of using nanotherapeutic strategies to target long non-coding RNAs (lncRNAs) in cancer cells. This updated discourse underlines the prominent role of lncRNAs in instigating cancer, facilitating its progression, and metastasis, validating lncRNAs ' potential for being effective diagnostic biomarkers and therapeutic targets. The manuscript offers an in-depth examination of different strategies presently employed to modulate lncRNA expression and function for therapeutic purposes. Among these strategies, Antisense Oligonucleotides (ASOs), RNA interference (RNAi) technologies, and the innovative clustered regularly interspaced short palindromic repeats (CRISPR)-based gene editing tools garner noteworthy mention. A significant section of the review is dedicated to nanocarriers and their crucial role in drug delivery. These nanocarriers ' efficiency in targeting lncRNAs in varied types of cancers is elaborated upon, validating the importance of targeted therapy. The manuscript culminates by reaffirming the promising prospects of targeting lncRNAs to enhance the accuracy of cancer diagnosis and improve treatment efficacy. Consequently, new paths are opened to more research and innovation in employing nanotherapeutic approaches against lncRNAs in cancer cells. Thus, this comprehensive manuscript serves as a valuable resource that underscores the vital role of lncRNAs and the various nano-strategies for targeting them in cancer treatment. Future research should also focus on unraveling the complex regulatory networks involving lncRNAs and identifying fundamental functional interactions to refine therapeutic strategies targeting lncRNAs in cancer.
   Researchers have targeted lncRNAs via iRNAs, ASOs and CRISPR-based gene editing, considering the role they play in the development and metastasis of cancer. Different nanocarriers have been used to deliver these anti-lncRNA agents, such as polymeric, liposomal, exosomes, and microbubbles. Through this strategy, metastasis and cancer development are reduced via increased efficiency. Nanotherapeutic strategies targeting lncRNAs offer a promising and emerging approach to cancer therapeutics. image
C1 [Davodabadi, Fatemeh] Payame Noor Univ, Fac Basic Sci, Dept Biol, Tehran, Iran.
   [Farasati Far, Bahareh] Iran Univ Sci & Technol, Dept Chem, Tehran, Iran.
   [Sargazi, Saman; Mirinejad, Shekoufeh; Sargazi, Sara] Zahedan Univ Med Sci, Res Inst Cellular & Mol Sci Infect Dis, Cellular & Mol Res Ctr, Zahedan, Iran.
   [Sargazi, Saman] Zahedan Univ Med Sci, Sch Med, Dept Clin Biochem, Zahedan, Iran.
   [Fatemeh Sajjadi, Seyedeh] Inst Res Fundamental Sci IPM, Sch Biol Sci, Tehran, Iran.
   [Fathi-karkan, Sonia] North Khorasan Univ Med Sci, Nat Prod & Med Plants Res Ctr, Bojnurd 9453155166, Iran.
   [Fathi-karkan, Sonia] North Khorasan Univ Med Sci, Sch Med, Dept Adv Sci & Technol Med, Bojnurd 9414974877, Iran.
   [Ghotekar, Suresh] Chettinad Acad Res & Educ, Chettinad Hosp & Res Inst, Ctr Herbal Pharmacol & Environm Sustainabil, Kelambakkam 603103, Tamil Nadu, India.
   [Rahman, Mohammed M.] King Abdulaziz Univ, Fac Sci, Ctr Excellence Adv Mat Res CEAMR, Jeddah 21589, Saudi Arabia.
   [Rahman, Mohammed M.] King Abdulaziz Univ, Fac Sci, Dept Chem, Jeddah, Saudi Arabia.
C3 Payame Noor University; Iran University Science & Technology; Zahedan
   University of Medical Sciences; Zahedan University of Medical Sciences;
   North Khorasan University of Medical Sciences; North Khorasan University
   of Medical Sciences; King Abdulaziz University; King Abdulaziz
   University
RP Sargazi, S (corresponding author), Zahedan Univ Med Sci, Res Inst Cellular & Mol Sci Infect Dis, Cellular & Mol Res Ctr, Zahedan, Iran.; Sargazi, S (corresponding author), Zahedan Univ Med Sci, Sch Med, Dept Clin Biochem, Zahedan, Iran.; Fathi-karkan, S (corresponding author), North Khorasan Univ Med Sci, Nat Prod & Med Plants Res Ctr, Bojnurd 9453155166, Iran.; Fathi-karkan, S (corresponding author), North Khorasan Univ Med Sci, Sch Med, Dept Adv Sci & Technol Med, Bojnurd 9414974877, Iran.; Rahman, MM (corresponding author), King Abdulaziz Univ, Fac Sci, Ctr Excellence Adv Mat Res CEAMR, Jeddah 21589, Saudi Arabia.; Rahman, MM (corresponding author), King Abdulaziz Univ, Fac Sci, Dept Chem, Jeddah, Saudi Arabia.
EM sgz.biomed@gmail.com; Soniafathi92@gmail.com; mmrahman@kau.edu.sa
RI Davodabadi, Fatemeh/LWI-2494-2024; Rahman, Mohammed/H-5823-2012; fathi
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OI Rahman, Mohammed M./0000-0003-2229-5121
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NR 200
TC 5
Z9 5
U1 6
U2 11
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA POSTFACH 101161, 69451 WEINHEIM, GERMANY
SN 1860-7179
EI 1860-7187
J9 CHEMMEDCHEM
JI ChemMedChem
PD APR 16
PY 2024
VL 19
IS 8
DI 10.1002/cmdc.202300528
EA FEB 2024
PG 30
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA OF2Q1
UT WOS:001168992600001
PM 38267373
DA 2025-01-04
ER

PT J
AU Edraki, N
   Jamei, MH
   Haghighijoo, Z
   Kayani, Z
   Raufi, E
   Eskandari, M
   Firouzi, M
   Sadeghpour, H
   Miri, R
   Khoshneviszadeh, M
   Firuzi, O
AF Edraki, Najmeh
   Jamei, Mohammad Hasan
   Haghighijoo, Zahra
   Kayani, Zahra
   Raufi, Elaheh
   Eskandari, Masoomeh
   Firouzi, Maryam
   Sadeghpour, Hossein
   Miri, Ramin
   Khoshneviszadeh, Mehdi
   Firuzi, Omidreza
TI Phenanthrotriazine Derivatives Containing Arylidine Hydrazone Moieties
   as Novel Potential c-Met Inhibitors with Anticancer Effect
SO IRANIAN JOURNAL OF PHARMACEUTICAL RESEARCH
LA English
DT Article
DE Targeted therapy; Receptor tyrosine kinase inhibitor; Breast cancer;
   Schiff base; Cell cycle block; Antiproliferative
ID SIGNALING PATHWAYS; APOPTOSIS; AGENTS; DISCOVERY; DESIGN;
   1,2,4-TRIAZINES; IDENTIFICATION; PHENANTHRENE; ACTIVATION; DENBINOBIN
AB Cancer is the second cause of death in the world and the discovery of novel anticancer agents is of vital importance to provide better therapeutic options for cancer patients. In this study, a new series of 12 arylidene hydrazone phenanthrotriazine derivatives were designed, synthesized, and tested in-vitro for antiproliferative activity against three cancer cell lines including colorectal cancer (HT-29), breast cancer (MCF-7) and leukemia (MOLT-4) cells and also against Vero normal cells. The effect of derivatives on cell cycle and apoptosis induction were studied by flow cytometric propidium iodide/RNase assay and Hoechst 33258 staining, respectively, while docking analysis was used to investigate the interactions of synthesized derivatives with the c-Met receptor kinase domain. Some compounds showed considerable antiproliferative activity against tested cancer cells. The most potent derivative was 9k bearing pyrrole moiety with IC50 values of 14.3, 4.7 and 1.7 mu M against HT-29, MCF-7 and MOLT-4 cells, respectively, while it showed negligible activity against Vero normal cells (IC50: 95.4 mu M). Derivatives bearing 2-nitrophenyl (9g), 4-cyanophenyl (9j), pyrrole (9k), and thiophene (9l) moieties induced G0/G1 cell cycle arrest and also apoptosis at higher doses in MCF-7 cells. Docking study showed that the phenanthrotriazine backbone form H-bond interactions with Asn1209, while phenyl moieties of the pendants generate different hydrophobic interactions with the Asp1164 and Asp1231 residues of c-Met. In conclusion, phenanthrene 1,2,4-triazines, especially the ones with less influence on normal cells, may constitute promising compounds for the discovery of antiproliferative agents with potential c-Met inhibitory capacity.
C1 [Edraki, Najmeh; Jamei, Mohammad Hasan; Haghighijoo, Zahra; Kayani, Zahra; Raufi, Elaheh; Eskandari, Masoomeh; Firouzi, Maryam; Miri, Ramin; Khoshneviszadeh, Mehdi; Firuzi, Omidreza] Shiraz Univ Med Sci, Med & Nat Prod Chem Res Ctr, Shiraz, Iran.
   [Sadeghpour, Hossein; Khoshneviszadeh, Mehdi] Shiraz Univ Med Sci, Sch Pharm, Dept Med Chem, Shiraz, Iran.
C3 Shiraz University of Medical Science; Shiraz University of Medical
   Science
RP Khoshneviszadeh, M; Firuzi, O (corresponding author), Shiraz Univ Med Sci, Med & Nat Prod Chem Res Ctr, Shiraz, Iran.; Khoshneviszadeh, M (corresponding author), Shiraz Univ Med Sci, Sch Pharm, Dept Med Chem, Shiraz, Iran.
EM khoshnevism@sums.ac.ir; firuzio@sums.ac.ir
RI Firuzi, Omidreza/A-1025-2012; khoshneviszadeh, mehdi/S-1541-2018;
   sadeghpour, hossein/H-5752-2011; Miri, Ramin/F-5813-2011; Firouzi,
   Maryam/JZE-1403-2024
FU Shiraz University of Medical Sciences [95-01-1212113]
FX The authors are thankful for the support of Shiraz University of Medical
   Sciences, Vice Chancellor for Research (Grant No. 95-01-1212113). This
   study was part of the Pharm. D. thesis of Mohammad Hassan Jamei.
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NR 45
TC 4
Z9 4
U1 0
U2 5
PU BRIEFLANDS
PI Shertogenbosch
PA 25 Derde Morgen, Shertogenbosch, NETHERLANDS
SN 1735-0328
EI 1726-6890
J9 IRAN J PHARM RES
JI Iran. J. Pharm. Res.
PY 2021
VL 20
IS 3
BP 516
EP 531
DI 10.22037/ijpr.2021.114371.14835
PG 16
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA XS8OQ
UT WOS:000733161300039
PM 34904005
DA 2025-01-04
ER

PT J
AU Deans, ZC
   Butler, R
   Cheetham, M
   Dequeker, EMC
   Fairley, JA
   Fenizia, F
   Hall, JA
   Keppens, C
   Normanno, N
   Schuuring, E
   Patton, SJ
AF Deans, Zandra C.
   Butler, Rachel
   Cheetham, Melanie
   Dequeker, Elisabeth M. C.
   Fairley, Jennifer A.
   Fenizia, Francesca
   Hall, Jacqueline A.
   Keppens, Cleo
   Normanno, Nicola
   Schuuring, Ed
   Patton, Simon J.
TI IQN path ASBL report from the first European cfDNA consensus meeting:
   expert opinion on the minimal requirements for clinical ctDNA testing
SO VIRCHOWS ARCHIV
LA English
DT Article
DE ctDNA; cfDNA; Liquid biopsy testing
ID CELL-FREE-DNA; METASTATIC COLORECTAL-CANCER; TYROSINE KINASE INHIBITORS;
   LUNG-CANCER; MOLECULAR PATHOLOGY; PLASMA; BLOOD; QUANTIFICATION;
   HETEROGENEITY; LABORATORIES
AB Liquid biopsy testing is a new laboratory-based method that detects tumour mutations in circulating free DNA (cfDNA) derived from minimally invasive blood sampling techniques. Recognising the significance for clinical testing, in 2017, IQN Path provided external quality assessment for liquid biopsy testing. Representatives of those participating laboratories were invited to attend a workshop to discuss the findings and how to achieve quality implementation of cfDNA testing in the clinical setting, the discussion and outcomes of this consensus meeting are described below. Predictive molecular profiling using tumour tissue in order to select cancer patients eligible for targeted therapy is now routine in diagnostic pathology. If insufficient tumour tissue material is available, in some circumstances, recent European Medicines Agency (EMA) guidance recommends mutation testing with plasma cfDNA. Clinical applications of cfDNA include treatment selection based on clinically relevant mutations derived from pre-treatment samples and the detection of resistant mutations upon progression of the disease. In order to identify tumour-related mutations in amongst other nucleic acid material found in plasma samples, highly sensitive laboratory methods are needed. In the workshop, we discussed the variable approaches taken with regard to cfDNA extraction methods, the tests, and considered the impact of false-negative test results. We explored the lack of standardisation of complex testing procedures ranging from plasma collection, transport, processing and storage, cfDNA extraction, and mutation analysis, to interpretation and reporting of results. We will also address the current status of clinical validation and clinical utility, and its use in current diagnosis. This workshop revealed a need for guidelines on with standardised procedures for clinical cfDNA testing and reporting, and a requirement for cfDNA-based external quality assessment programs.
C1 [Deans, Zandra C.; Fairley, Jennifer A.] Royal Infirm Edinburgh NHS Trust, Dept Lab Med, UK NEQAS Mol Genet, Edinburgh EH16 4SA, Midlothian, Scotland.
   [Butler, Rachel] Univ Hosp Wales, Inst Med Genet, All Wales Genet Lab, Heath Pk, Cardiff CF14 4XW, S Glam, Wales.
   [Cheetham, Melanie; Patton, Simon J.] St Marys Hosp, Manchester Ctr Genom Med, European Mol Genet Qual Network, Manchester M13 9WL, Lancs, England.
   [Dequeker, Elisabeth M. C.; Keppens, Cleo] Katholieke Univ Leuven, Biomed Qual Assurance Res Unit, Dept Publ Hlth & Primary Care, Leuven, Belgium.
   [Dequeker, Elisabeth M. C.] Univ Hosp Leuven, Leuven, Belgium.
   [Fenizia, Francesca; Normanno, Nicola] Fdn G Pascale IRCCS, Cell Biol & Biotherapy Unit, Ist Nazl Tumori, Naples, Italy.
   [Hall, Jacqueline A.] Int Qual Network Pathol IQN Path ASBL, 3A Sentier Esperance, L-1474 Luxembourg, Luxembourg.
   [Schuuring, Ed] Univ Groningen, Univ Med Ctr Groningen, Dept Pathol, Groningen, Netherlands.
C3 University of Edinburgh; Royal Infirmary of Edinburgh; Cardiff
   University; University of Manchester; KU Leuven; KU Leuven; University
   Hospital Leuven; Fondazione IRCCS Istituto Nazionale Tumori Milan; IRCCS
   Fondazione Pascale; University of Groningen
RP Deans, ZC (corresponding author), Royal Infirm Edinburgh NHS Trust, Dept Lab Med, UK NEQAS Mol Genet, Edinburgh EH16 4SA, Midlothian, Scotland.
EM sandi.deans@ed.ac.uk
RI Normanno, Nicola/AAT-1107-2021; Fenizia, Francesca/AAC-1394-2019
OI Keppens, Cleo/0000-0002-4498-8386; Deans, Zandra/0000-0001-9361-6012
FU IQN Path
FX The workshop was funded by IQN Path.
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NR 38
TC 29
Z9 30
U1 0
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0945-6317
EI 1432-2307
J9 VIRCHOWS ARCH
JI Virchows Arch.
PD JUN
PY 2019
VL 474
IS 6
BP 681
EP 689
DI 10.1007/s00428-019-02571-3
PG 9
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA IE1AE
UT WOS:000472117200004
PM 31028539
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Chung, JH
   Sanford, E
   Johnson, A
   Klempner, SJ
   Schrock, AB
   Palma, NA
   Erlich, RL
   Frampton, GM
   Chalmers, ZR
   Vergilio, J
   Rubinson, DA
   Sun, JX
   Chmielecki, J
   Yelensky, R
   Suh, JH
   Lipson, D
   George, TJ
   Elvin, JA
   Stephens, PJ
   Miller, VA
   Ross, JS
   Ali, SM
AF Chung, J. H.
   Sanford, E.
   Johnson, A.
   Klempner, S. J.
   Schrock, A. B.
   Palma, N. A.
   Erlich, R. L.
   Frampton, G. M.
   Chalmers, Z. R.
   Vergilio, J.
   Rubinson, D. A.
   Sun, J. X.
   Chmielecki, J.
   Yelensky, R.
   Suh, J. H.
   Lipson, D.
   George, T. J., Jr.
   Elvin, J. A.
   Stephens, P. J.
   Miller, V. A.
   Ross, J. S.
   Ali, S. M.
TI Comprehensive genomic profiling of anal squamous cell carcinoma reveals
   distinct genomically defined classes
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE anal squamous cell carcinoma; comprehensive genomic profiling; HPV;
   PI3KCA; targeted therapy
ID COLORECTAL-CANCER; GENE; HEAD; EGFR; CHEMOTHERAPY; MUTATIONS; SURVIVAL;
   TUMORS
AB Treatment of advanced anal squamous cell carcinoma (ASCC) with cisplatin-based chemotherapy, which is recommended by the National Comprehensive Cancer Network, provides limited benefit. An improved genomic understanding could guide therapeutic approaches. In this comprehensive genomic analysis of human papilloma-virus-positive and negative ASCC, we identify clinically relevant genomic alterations.Squamous cell cancers of the anal canal (ASCC) are increasing in frequency and lack effective therapies for advanced disease. Although an association with human papillomavirus (HPV) has been established, little is known about the molecular characterization of ASCC. A comprehensive genomic analysis of ASCC was undertaken to identify novel genomic alterations (GAs) that will inform therapeutic choices for patients with advanced disease.
   Hybrid-capture-based next-generation sequencing of exons from 236 cancer-related genes and intronic regions from 19 genes commonly rearranged in cancer was performed on 70 patients with ASCC. HPV status was assessed by aligning tumor sequencing reads to HPV viral genomes. GAs were identified using an established algorithm and correlated with HPV status.
   Sixty-one samples (87%) were HPV-positive. A mean of 3.5 GAs per sample was identified. Recurrent alterations in phosphoinositol-3-kinase pathway (PI3K/AKT/mTOR) genes including amplifications and homozygous deletions were present in 63% of cases. Clinically relevant GAs in genes involved in DNA repair, chromatin remodeling, or receptor tyrosine kinase signaling were observed in 30% of cases. Loss-of-function mutations in TP53 and CDKN2A were significantly enhanced in HPV-negative cases (P < 0.0001).
   This is the first comprehensive genomic analysis of ASCC, and the results suggest new therapeutic approaches. Differing genomic profiles between HPV-associated and HPV-negative ASCC warrants further investigation and may require novel therapeutic and preventive strategies.
C1 [Chung, J. H.; Sanford, E.; Johnson, A.; Schrock, A. B.; Palma, N. A.; Erlich, R. L.; Frampton, G. M.; Chalmers, Z. R.; Vergilio, J.; Sun, J. X.; Chmielecki, J.; Yelensky, R.; Suh, J. H.; Lipson, D.; Elvin, J. A.; Stephens, P. J.; Miller, V. A.; Ross, J. S.; Ali, S. M.] Fdn Med, Cambridge, MA USA.
   [Klempner, S. J.] Univ Calif Irvine, Div Hematol Oncol, Irvine, CA USA.
   [Rubinson, D. A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
   [George, T. J., Jr.] Univ Florida, Div Hematol Oncol, Gainesville, FL USA.
   [Ross, J. S.] Albany Med Coll, Dept Pathol & Lab Med, Albany, NY 12208 USA.
C3 Foundation Medicine; University of California System; University of
   California Irvine; Harvard University; Dana-Farber Cancer Institute;
   State University System of Florida; University of Florida; Albany
   Medical College
RP Chung, JH (corresponding author), Fdn Med Inc, 150 Second St,1st Floor, Cambridge, MA 02141 USA.
EM jchung@foundationmedicine.com
RI Rubinson, Douglas/G-3502-2019; Klempner, Samuel/U-2235-2019; George,
   Thomas/L-9119-2019; Ali, Siraj/AAE-2958-2019
OI George, Thomas/0000-0002-6249-9180; Rubinson,
   Douglas/0000-0002-5337-5231; Chung, Jon/0000-0003-0526-3670; Sanford,
   Eric/0000-0002-9232-9334; Klempner, Samuel/0000-0002-4062-0808;
   Frampton, Garrett/0000-0002-2361-2750
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NR 31
TC 75
Z9 76
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
EI 1569-8041
J9 ANN ONCOL
JI Ann. Oncol.
PD JUL
PY 2016
VL 27
IS 7
BP 1336
EP 1341
DI 10.1093/annonc/mdw152
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DR2UZ
UT WOS:000379760700022
PM 27052656
OA Bronze
DA 2025-01-04
ER

PT J
AU Macdonald, JB
   Macdonald, B
   Golitz, LE
   LoRusso, P
   Sekulic, A
AF Macdonald, James B.
   Macdonald, Brooke
   Golitz, Loren E.
   LoRusso, Patricia
   Sekulic, Aleksandar
TI Cutaneous adverse effects of targeted therapies Part I: Inhibitors of
   the cellular membrane
SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY
LA English
DT Article
DE adverse sequelae; alopecia; antiangiogenic agents; anticancer; BCR-ABL;
   bevacizumab; cancer treatment; canertinib; cetuximab; chemotherapy;
   cutaneous adverse effects; dasatinib; dermatologic toxicities; disturbed
   wound healing; drug eruption; drug rash; drug reaction; dry skin; dual
   kinase inhibitors; epidermal growth factor receptor inhibitors; erbB
   receptor; erlotinib; gefitinib; genital rash; HER2; hyperkeratotic
   hand-foot skin reaction; imatinib; KIT; lapatinib; macular eruption;
   monoclonal antibodies; morbilliform; mucocutaneous hemorrhage;
   mucositis; multikinase inhibitors; nilotinib; panitumumab;
   papulopustular eruption; paronychia; pazopanib; platelet-derived growth
   factor receptor; photosensitivity; pigment changes; ranibizumab; side
   effects; small molecule; sorafenib; stomatitis; sunitinib; supportive
   oncodermatology; targeted therapy; toxic erythema; tyrosine kinase
   inhibitors; vandetanib; vascular endothelial growth factor; xerosis
ID EPIDERMAL-GROWTH-FACTOR; CHRONIC MYELOID-LEUKEMIA; FACTOR RECEPTOR
   INHIBITORS; METASTATIC COLORECTAL-CANCER; FOOT SKIN REACTION;
   PLACEBO-CONTROLLED TRIAL; ADVANCED HEPATOCELLULAR-CARCINOMA; EYELASH
   TRICHOMEGALY SECONDARY; IMATINIB-INDUCED ERYTHRODERMA; CHRONIC
   MYELOGENOUS LEUKEMIA
AB There has been a rapid emergence of numerous targeted agents in the oncology community in the last decade. This exciting paradigm shift in drug development lends promise for the future of individualized medicine. Given the pace of development and clinical deployment of targeted agents with novel mechanisms of action, dermatology providers may not be familiar with the full spectrum of associated skin-related toxicities. Cutaneous adverse effects are among the most frequently observed toxicities with many targeted agents, and their intensity can be dose-limiting or lead to therapy discontinuation. In light of the often life-saving nature of emerging oncotherapeutics, it is critical that dermatologists both understand the mechanisms and recognize clinical signs and symptoms of such toxicities in order to provide effective clinical management. Part I of this continuing medical education article will review in detail the potential skin-related adverse sequelae, the frequency of occurrence, and the implications associated with on- and off-target cutaneous toxicities of inhibitors acting at the cell membrane level, chiefly inhibitors of epidermal growth factor receptor, KIT, and BCR-ABL, angiogenesis, and multikinase inhibitors.
C1 [Macdonald, James B.] Cent Utah Clin, Dept Dermatol, Provo, UT 84604 USA.
   [Macdonald, James B.] Cent Utah Clin, Dept Pathol, Provo, UT 84604 USA.
   [Macdonald, Brooke] Macdonald Graph Design Inc, Provo, UT USA.
   [Golitz, Loren E.] Univ Colorado Denver, Dept Dermatol, Aurora, CO USA.
   [Golitz, Loren E.] Univ Colorado Denver, Dept Pathol, Aurora, CO USA.
   [LoRusso, Patricia] Wayne State Univ, Dept Oncol, Detroit, MI USA.
   [Sekulic, Aleksandar] Mayo Clin Scottsdale, Dept Dermatol, Scottsdale, AZ USA.
C3 Children's Hospital Colorado; University of Colorado System; University
   of Colorado Anschutz Medical Campus; University of Colorado System;
   University of Colorado Anschutz Medical Campus; Children's Hospital
   Colorado; Wayne State University; Mayo Clinic; Mayo Clinic Phoenix
RP Macdonald, JB (corresponding author), Cent Utah Clin, Dept Dermatol, 1055 N 500 W,Ste 111, Provo, UT 84604 USA.
EM macdonjb@gmail.com
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NR 177
TC 161
Z9 179
U1 1
U2 45
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0190-9622
J9 J AM ACAD DERMATOL
JI J. Am. Acad. Dermatol.
PD FEB
PY 2015
VL 72
IS 2
BP 203
EP 218
DI 10.1016/j.jaad.2014.07.032
PG 16
WC Dermatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dermatology
GA AY9YH
UT WOS:000347903200009
PM 25592338
DA 2025-01-04
ER

PT J
AU Mahgoub, E
   Taneera, J
   Sulaiman, N
   Saber-Ayad, M
AF Mahgoub, Eglal
   Taneera, Jalal
   Sulaiman, Nabil
   Saber-Ayad, Maha
TI The role of autophagy in colorectal cancer: Impact on pathogenesis and
   implications in therapy
SO FRONTIERS IN MEDICINE
LA English
DT Review
DE colorectal cancer; autophagy; tumor microenvironment; endothelial cells;
   hypoxia; oxidative stress; targeted therapy; MSI-H
ID CHAPERONE-MEDIATED AUTOPHAGY; HYPOXIA-INDUCED AUTOPHAGY; ADVANCED SOLID
   TUMORS; PHASE-I TRIAL; CELL-SURVIVAL; MOLECULAR-MECHANISMS;
   PYRUVATE-KINASE; BECLIN 1; INHIBITION; EXPRESSION
AB Colorectal cancer (CRC) is considered as a global major cause of cancer death. Surgical resection is the main line of treatment; however, chemo-, radiotherapy and other adjuvant agents are crucial to achieve good outcomes. The tumor microenvironment (TME) is a well-recognized key player in CRC progression, yet the processes linking the cancer cells to its TME are not fully delineated. Autophagy is one of such processes, with a controversial role in the pathogenesis of CRC, with its intricate links to many pathological factors and processes. Autophagy may apparently play conflicting roles in carcinogenesis, but the precise mechanisms determining the overall direction of the process seem to depend on the context. Additionally, it has been established that autophagy has a remarkable effect on the endothelial cells in the TME, the key substrate for angiogenesis that supports tumor metastasis. Favorable response to immunotherapy occurs only in a specific subpopulation of CRC patients, namely the microsatellite instability-high (MSI-H). In view of such limitations of immunotherapy in CRC, modulation of autophagy represents a potential adjuvant strategy to enhance the effect of those relatively safe agents on wider CRC molecular subtypes. In this review, we discussed the molecular control of autophagy in CRC and how autophagy affects different processes and mechanisms that shape the TME. We explored how autophagy contributes to CRC initiation and progression, and how it interacts with tumor immunity, hypoxia, and oxidative stress. The crosstalk between autophagy and the TME in CRC was extensively dissected. Finally, we reported the clinical efforts and challenges in combining autophagy modulators with various cancer-targeted agents to improve CRC patients' survival and restrain cancer growth.
C1 [Mahgoub, Eglal; Taneera, Jalal; Sulaiman, Nabil; Saber-Ayad, Maha] Univ Sharjah, Coll Med, Sharjah, U Arab Emirates.
   [Mahgoub, Eglal; Taneera, Jalal; Sulaiman, Nabil; Saber-Ayad, Maha] Univ Sharjah, Sharjah Inst Med Res, Sharjah, U Arab Emirates.
   [Sulaiman, Nabil] Baker Heart & Diabet Inst, Melbourne, Vic, Australia.
   [Saber-Ayad, Maha] Cairo Univ, Fac Med, Giza, Egypt.
C3 University of Sharjah; University of Sharjah; Baker Heart and Diabetes
   Institute; Egyptian Knowledge Bank (EKB); Cairo University
RP Saber-Ayad, M (corresponding author), Univ Sharjah, Coll Med, Sharjah, U Arab Emirates.; Saber-Ayad, M (corresponding author), Univ Sharjah, Sharjah Inst Med Res, Sharjah, U Arab Emirates.; Saber-Ayad, M (corresponding author), Cairo Univ, Fac Med, Giza, Egypt.
EM msaber@sharjah.ac.ae
RI Saber-Ayad, Maha/AAQ-2386-2021; Sulaiman, Nabil/AGL-5557-2022
OI Saber-Ayad, Maha/0000-0002-9287-7621
FU University of Sharjah, United Arab Emirates [22010902104];
   MBRU-AlMahmeed Research Award, (ALM) [1914];  [0309];  [0304]
FX This work was supported by research grant Nos. (CoV19 #0309 and #0304),
   Competitive grant (#22010902104), University of Sharjah, United Arab
   Emirates, and the MBRU-AlMahmeed Research Award, (ALM #1914).
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NR 154
TC 13
Z9 14
U1 1
U2 8
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-858X
J9 FRONT MED-LAUSANNE
JI Front. Med.
PD SEP 7
PY 2022
VL 9
AR 959348
DI 10.3389/fmed.2022.959348
PG 15
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 4Q4UT
UT WOS:000856079800001
PM 36160153
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Lin, L
   Wu, Q
   Lu, FF
   Lei, JM
   Zhou, YH
   Liu, YF
   Zhu, N
   Yu, Y
   Ning, ZF
   She, TH
   Hu, MC
AF Lin, Li
   Wu, Qing
   Lu, Feifei
   Lei, Jiaming
   Zhou, Yanhong
   Liu, Yifei
   Zhu, Ni
   Yu, You
   Ning, Zhifeng
   She, Tonghui
   Hu, Meichun
TI Nrf2 signaling pathway: current status and potential therapeutic
   targetable role in human cancers
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE Nrf2; Nrf2 signaling pathway; oxidative stress; cancer; therapeutic
   target
ID CELL-CYCLE PROGRESSION; OXIDATIVE STRESS; COLORECTAL-CANCER;
   LUNG-CANCER; DOWN-REGULATION; CLINICOPATHOLOGICAL FEATURES; CISPLATIN
   RESISTANCE; DRUG-RESISTANCE; GASTRIC-CANCER; EXPRESSION
AB Cancer is a borderless global health challenge that continues to threaten human health. Studies have found that oxidative stress (OS) is often associated with the etiology of many diseases, especially the aging process and cancer. Involved in the OS reaction as a key transcription factor, Nrf2 is a pivotal regulator of cellular redox state and detoxification. Nrf2 can prevent oxidative damage by regulating gene expression with antioxidant response elements (ARE) to promote the antioxidant response process. OS is generated with an imbalance in the redox state and promotes the accumulation of mutations and genome instability, thus associated with the establishment and development of different cancers. Nrf2 activation regulates a plethora of processes inducing cellular proliferation, differentiation and death, and is strongly associated with OS-mediated cancer. What's more, Nrf2 activation is also involved in anti-inflammatory effects and metabolic disorders, neurodegenerative diseases, and multidrug resistance. Nrf2 is highly expressed in multiple human body parts of digestive system, respiratory system, reproductive system and nervous system. In oncology research, Nrf2 has emerged as a promising therapeutic target. Therefore, certain natural compounds and drugs can exert anti-cancer effects through the Nrf2 signaling pathway, and blocking the Nrf2 signaling pathway can reduce some types of tumor recurrence rates and increase sensitivity to chemotherapy. However, Nrf2's dual role and controversial impact in cancer are inevitable consideration factors when treating Nrf2 as a therapeutic target. In this review, we summarized the current state of biological characteristics of Nrf2 and its dual role and development mechanism in different tumor cells, discussed Keap1/Nrf2/ARE signaling pathway and its downstream genes, elaborated the expression of related signaling pathways such as AMPK/mTOR and NF-kappa B. Besides, the main mechanism of Nrf2 as a cancer therapeutic target and the therapeutic strategies using Nrf2 inhibitors or activators, as well as the possible positive and negative effects of Nrf2 activation were also reviewed. It can be concluded that Nrf2 is related to OS and serves as an important factor in cancer formation and development, thus provides a basis for targeted therapy in human cancers.
C1 [Lin, Li; Wu, Qing; Lu, Feifei; Lei, Jiaming; Zhu, Ni; Yu, You; Ning, Zhifeng; She, Tonghui; Hu, Meichun] Hubei Univ Sci & Technol, Xianning Med Coll, Sch Basic Med Sci, Key Lab Environm Related Dis & One Hlth, Xianning, Peoples R China.
   [Zhou, Yanhong] Hubei Univ Sci & Technol, Xianning Med Coll, Dept Med Sch Facial Features, Xianning, Peoples R China.
   [Liu, Yifei] Hubei Univ Sci & Technol, Xianning Med Coll, Sch Biomed Engn, Xianning, Peoples R China.
C3 Hubei University of Science & Technology; Hubei University of Science &
   Technology; Hubei University of Science & Technology
RP She, TH; Hu, MC (corresponding author), Hubei Univ Sci & Technol, Xianning Med Coll, Sch Basic Med Sci, Key Lab Environm Related Dis & One Hlth, Xianning, Peoples R China.
EM xnsth@hbust.edu.cn; humeichun.530@163.com
RI 溜, 达猫/HNP-4158-2023; Yu, You/HZH-8705-2023; Hu, Meichun/JAX-1849-2023
OI Hu, Meichun/0009-0007-9752-8977
FU This study was supported by grants from the National Natural Science
   Foundation of China (31900853), the Natural Science Foundation of Hubei
   Province (2022CFB394, 2016CFB491), the Scientific Projects of Health
   Commission of Hubei Province (WJ2019Q022, WJ20 [31900853]; National
   Natural Science Foundation of China [2022CFB394, 2016CFB491]; Natural
   Science Foundation of Hubei Province [WJ2019Q022, WJ2021M089];
   Scientific Projects of Health Commission of Hubei Province [2020WG09];
   Medical School of Facial Features of Hubei University of Science and
   Technology [2022YKY08]; Medical Scientific Research Projects of Hubei
   University of Science and Technology
FX The authors thank the School of Basic Medicinal Sciences, Xianning
   Medical College, Hubei University of Science and Technology.r This study
   was supported by grants from the National Natural Science Foundation of
   China (31900853), the Natural Science Foundation of Hubei Province
   (2022CFB394, 2016CFB491), the Scientific Projects of Health Commission
   of Hubei Province (WJ2019Q022, WJ2021M089), the Medical School of Facial
   Features of Hubei University of Science and Technology (2020WG09), and
   the Medical Scientific Research Projects of Hubei University of Science
   and Technology (2022YKY08).
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NR 217
TC 26
Z9 27
U1 3
U2 13
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD SEP 22
PY 2023
VL 13
AR 1184079
DI 10.3389/fonc.2023.1184079
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA T2ER3
UT WOS:001076170200001
PM 37810967
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Pan, HM
   Lang, WY
   Yao, LJ
   Wang, Y
   Li, XL
AF Pan, Hong-Ming
   Lang, Wei-Ya
   Yao, Li-Jie
   Wang, Yan
   Li, Xiao-Ling
TI shRNA-interfering LSD1 inhibits proliferation and invasion of gastric
   cancer cells <i>via</i> VEGF-C/PI3K/AKT signaling pathway
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Gastric cancer; Lysine specific histone demethylase 1; Cell
   proliferation; Cell invasion; VEGF-C/PI3K/AKT signaling pathway
ID ENHANCED ENDOSCOPIC ULTRASOUND; FINE-NEEDLE-ASPIRATION;
   COLORECTAL-CANCER; EXPRESSION; TRANYLCYPROMINE; DERIVATIVES; METASTASIS;
   DESIGN; GROWTH
AB BACKGROUND
   Histone Lysine Specific Demethylase 1 (LSD1) is the first histone demethylase to be discovered, which regulates various biological functions by making lysine of histone H3K4, H3K9 and non-histone substrates demethylated. Abnormal regulation of LSD1 is closely related to the occurrence and development of gastric cancer. The change of LSD1 expression level plays an important role in the proliferation and metastasis of gastric cancer cells. The study of its function and mechanism may provide a theoretical basis for early diagnosis and targeted therapy of gastric cancer.
   AIM
   To investigate the effect of downregulation of lysine-specific demethylase 1 (LSD1) expression on proliferation and invasion of gastric cancer cells and the possible regulatory mechanisms of the VEGF-C/PI3K/AKT signaling pathway.
   METHODS
   The LSD1-specific short hairpin RNA (shRNA) interference plasmid was transiently transfected, and expression of LSD1 was downregulated. The cell proliferation ability of LSD1 was observed by CCK-8 assay after downregulating expression of LSD1. Transwell invasion assay was used to observe the change of cell invasion ability after downregulating expression of LSD1. Expression of phosphorylated phosphoinositide 3-kinase (p-PI3K), PI3K, p-AKT, AKT, vascular endothelial growth factor receptor (VEGFR)-3, matrix metalloproteinase (MMP)-2 and MMP-9 in each group was detected by Western blotting.
   RESULTS
   The cell proliferation ability of transiently transfected LSD1-shRNA interference plasmid group was significantly lower than that of the control group (P < 0.05). Transwell invasion assay showed that the number of cells across the membrane of the LSD1-shRNA transfection group (238.451 +/- 5.216) was significantly lower than that of the control group (49.268 +/- 6.984) (P < 0.01). Western blotting showed that expression level of VEGF-C, p-PI3K, PI3K, p-AKT, AKT, VEGFR-3, MMP-2 and MMP-9 in the LSD1-shRNA group was significantly lower than that in the control group (P < 0.05).
   CONCLUSION
   Downregulation of LSD1 expression inhibits metastatic potential of gastric cancer cells, and VEGF-C-mediated activation of PI3K/AKT signaling pathway, which may be an important mechanism for inhibiting lymph node metastasis in gastric cancer cells.
C1 [Pan, Hong-Ming] Qiqihar Med Univ, Dept Biochem, Qiqihar 161000, Heilongjiang, Peoples R China.
   [Lang, Wei-Ya] Qiqihar Med Univ, Dept Histol & Embryol, Qiqihar 161000, Heilongjiang, Peoples R China.
   [Yao, Li-Jie; Wang, Yan; Li, Xiao-Ling] Qiqihar Med Univ, Dept Anat, 333 Bukui North St, Qiqihar 161000, Heilongjiang, Peoples R China.
C3 Qiqihar Medical University; Qiqihar Medical University; Qiqihar Medical
   University
RP Li, XL (corresponding author), Qiqihar Med Univ, Dept Anat, 333 Bukui North St, Qiqihar 161000, Heilongjiang, Peoples R China.
EM lixiaoling0420@126.com
RI Li, Xiaoling/JGD-1624-2023
OI Li, Xiaoling/0000-0002-8806-2788
FU Doctoral Special Research Fund of Qiqihar Medical College [QY2016B-06]
FX Supported by Doctoral Special Research Fund of Qiqihar Medical College,
   No. QY2016B-06.
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NR 37
TC 20
Z9 22
U1 3
U2 21
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD AUG 15
PY 2019
VL 11
IS 8
BP 622
EP 633
DI 10.4251/wjgo.v11.i8.622
PG 12
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA IS5LL
UT WOS:000482194000005
PM 31435463
OA Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Jauw, YWS
   Menke-van der Houven van Oordt, CW
   Hoekstra, OS
   Hendrikse, NH
   Vugts, DJ
   Zijlstra, JM
   Huisman, MC
   van Dongen, GAMS
AF Jauw, Yvonne W. S.
   Menke-van der Houven van Oordt, C. Willemien
   Hoekstra, Otto S.
   Hendrikse, N. Harry
   Vugts, Danielle J.
   Zijlstra, Josee M.
   Huisman, Marc C.
   van Dongen, Guus A. M. S.
TI Immuno-Positron Emission Tomography with Zirconium-89-Labeled Monoclonal
   Antibodies in Oncology: What Can We Learn from Initial Clinical Trials?
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE molecular imaging; positron emission tomography; (89)zirconium;
   monoclonal antibodies; imaging biomarker; clinical oncology
ID METASTATIC COLORECTAL-CANCER; PHASE-I; ZR-89-BEVACIZUMAB PET;
   BIFUNCTIONAL CHELATE; 1ST-LINE TREATMENT; CELL CARCINOMA;
   BIODISTRIBUTION; LYMPHOMA; HEAD; RECEPTOR
AB Selection of the right drug for the right patient is a promising approach to increase clinical benefit of targeted therapy with monoclonal antibodies (mAbs). Assessment of in vivo biodistribution and tumor targeting of mAbs to predict toxicity and efficacy is expected to guide individualized treatment and drug development. Molecular imaging with positron emission tomography (PET) using zirconium-89 (Zr-89)-labeled monoclonal antibodies also known as Zr-89-immuno-PET, visualizes and quantifies uptake of radiolabeled mAbs. This technique provides a potential imaging biomarker to assess target expression, as well as tumor targeting of mAbs. In this review we summarize results from initial clinical trials with Zr-89-immuno-PET in oncology and discuss technical aspects of trial design. In clinical trials with Zr-89-immuno-PET two requirements should be met for each Zr-89-labeled mAb to realize its full potential. One requirement is that the biodistribution of the Zr-89-labeled mAb (imaging dose) reflects the biodistribution of the drug during treatment (therapeutic dose). Another requirement is that tumor uptake of Zr-89-mAb on PET is primarily driven by specific, antigen-mediated, tumor targeting. Initial trials have contributed toward the development of Zr-89-immuno-PET as an imaging biomarker by showing correlation between uptake of Zr-89-labeled mAbs on PET and target expression levels in biopsies. These results indicate that Zr-89-immuno-PET reflects specific, antigen-mediated binding. Zr-89-immuno-PET was shown to predict toxicity of RIT, but thus far results indicating that toxicity of mAbs or mAb-drug conjugate treatment can be predicted are lacking. So far, one study has shown that molecular imaging combined with early response assessment is able to predict response to treatment with the antibody-drug conjugate trastuzumab-emtansine, in patients with human epithelial growth factor-2 (HER2)-positive breast cancer. Future studies would benefit from a standardized criterion to define positive tumor uptake, possibly supported by quantitative analysis, and validated by linking imaging data with corresponding clinical outcome. Taken together,
C1 [Jauw, Yvonne W. S.; Zijlstra, Josee M.] Vrije Univ Amsterdam, Med Ctr, Dept Hematol, Amsterdam, Netherlands.
   [Menke-van der Houven van Oordt, C. Willemien] Vrije Univ Amsterdam, Med Ctr, Dept Med Oncol, Amsterdam, Netherlands.
   [Hoekstra, Otto S.; Hendrikse, N. Harry; Vugts, Danielle J.; Huisman, Marc C.; van Dongen, Guus A. M. S.] Vrije Univ Amsterdam, Med Ctr, Dept Radiol & Nucl Med, Amsterdam, Netherlands.
   [Hendrikse, N. Harry] Vrije Univ Amsterdam, Med Ctr, Dept Clin Pharmacol & Pharm, Amsterdam, Netherlands.
C3 Vrije Universiteit Amsterdam; Vrije Universiteit Amsterdam; Vrije
   Universiteit Amsterdam; Vrije Universiteit Amsterdam
RP Jauw, YWS (corresponding author), Vrije Univ Amsterdam, Med Ctr, Dept Hematol, Amsterdam, Netherlands.
EM yws.jauw@vumc.nl
RI van+der+Houven+van+Oordt, C./AAE-8064-2020
OI Vugts, Danielle/0000-0001-7068-8152; Hoekstra, Otto
   S/0000-0003-0767-2734; Menke-van der Houven van Oordt, C.
   Willemien/0000-0002-5404-5883
FU Dutch Cancer Society [VU 2013-5839]
FX Financial support was provided by the Dutch Cancer Society, grant number
   VU 2013-5839 to YJ.
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NR 48
TC 153
Z9 159
U1 0
U2 59
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD MAY 24
PY 2016
VL 7
AR 131
DI 10.3389/fphar.2016.00131
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DM8UV
UT WOS:000376640900001
PM 27252651
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Guo, P
   Zu, SJ
   Han, SL
   Yu, WD
   Xue, GQ
   Lu, XA
   Lin, H
   Zhao, XR
   Lu, HB
   Hua, CY
   Wan, XY
   Ru, LY
   Guo, ZY
   Ge, HX
   Lv, K
   Zhang, GH
   Deng, WG
   Luo, C
   Guo, W
AF Guo, Ping
   Zu, Shijia
   Han, Shilong
   Yu, Wendan
   Xue, Guoqing
   Lu, Xiaona
   Lin, Hua
   Zhao, Xinrui
   Lu, Haibo
   Hua, Chunyu
   Wan, Xinyu
   Ru, Liyuan
   Guo, Ziyue
   Ge, Hanxiao
   Lv, Kuan
   Zhang, Guohui
   Deng, Wuguo
   Luo, Cheng
   Guo, Wei
TI BPTF inhibition antagonizes colorectal cancer progression by
   transcriptionally inactivating Cdc25A
SO REDOX BIOLOGY
LA English
DT Article
DE Colorectal cancer; BPTF; Cdc25A; c-Myc; Cell cycle
ID CELL-CYCLE PHOSPHATASE; PHD-FINGER; HEPATOCELLULAR-CARCINOMA;
   EXPRESSION; COMPLEXES; THERAPY; COLON; PROLIFERATION; GROWTH
AB As the largest subunit of the nuclear remodeling factor complex, Bromodomain PHD Finger Transcription Factor (BPTF) has been reported to be involved in tumorigenesis and development in several cancers. However, to date, its functions and related molecular mechanisms in colorectal cancer (CRC) are still poorly defined and deserve to be revealed. In this study, we uncovered that, under the expression regulation of c-Myc, BPTF promoted CRC progression by targeting Cdc25A. BPTF was found to be highly expressed in CRC and promoted the proliferation and metastasis of CRC cells through BPTF specific siRNAs, shRNAs or inhibitors. Based on RNA-seq, combined with DNA-pulldown, ChIP and luciferase reporter assay, we proved that, by binding to-178/+107 region within Cdc25A promoter, BPTF transcriptionally activated Cdc25A, thus accelerating the cell cycle process of CRC cells. Meanwhile, BPTF itself was found to be transcriptionally regulated by c-Myc. Moreover, BPTF knockdown or inactivation was verified to sensitize CRC cells to chemotherapeutics, 5-Fluorouracil (5FU) and Oxaliplatin (Oxa), c-Myc inhibitor and cell cycle inhibitor not just at the cellular level in vitro, but in subcutaneous xeno-grafts or AOM/DSS-induced in situ models of CRC in mice, while Cdc25A overexpression partially reversed BPTF silencing-caused tumor growth inhibition. Clinically, BPTF, c-Myc and Cdc25A were highly expressed in CRC tissues simultaneously, the expression of any two of the three was positively correlated, and their expressions were highly relevant to tumor differentiation, TNM staging and poor prognosis of CRC patients. Thus, our study indicated that the targeted inhibition of BPTF alone, or together with chemotherapy and/or cell cycle-targeted therapy, might act as a promising new strategy for CRC treatment, while c-Myc/BPTF/Cdc25A signaling axis is expected to be developed as an associated set of candidate biomarkers for CRC diagnosis and prognosis prediction.
C1 [Guo, Ping; Han, Shilong; Yu, Wendan; Xue, Guoqing; Lu, Xiaona; Zhao, Xinrui; Hua, Chunyu; Wan, Xinyu; Ru, Liyuan; Guo, Ziyue; Ge, Hanxiao; Lv, Kuan; Zhang, Guohui; Guo, Wei] Dalian Med Univ, Inst Canc Stem Cells, Dalian 116044, Peoples R China.
   [Deng, Wuguo] Sun Yat sen Univ Canc Ctr, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Canc Ctr, Guangzhou 510060, Peoples R China.
   [Zu, Shijia; Lin, Hua; Lu, Haibo; Luo, Cheng] Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Shanghai 201203, Peoples R China.
   [Zu, Shijia; Luo, Cheng] China Univ Chinese Acad Sci, Beijing 100049, Peoples R China.
   [Lu, Haibo; Luo, Cheng] Fudan Univ, Sch Pharm, 826 Zhangheng Rd, Shanghai 201203, Peoples R China.
   [Guo, Wei] Dalian Med Univ, Dalian, Peoples R China.
   [Deng, Wuguo] Sun Yat Sen Univ, Canc Ctr, Guangzhou, Peoples R China.
   [Luo, Cheng] Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai, Peoples R China.
C3 Dalian Medical University; State Key Lab Oncology South China; Sun Yat
   Sen University; Chinese Academy of Sciences; Shanghai Institute of
   Materia Medica, CAS; Chinese Academy of Sciences; University of Chinese
   Academy of Sciences, CAS; Fudan University; Dalian Medical University;
   Sun Yat Sen University; Chinese Academy of Sciences; Shanghai Institute
   of Materia Medica, CAS
RP Guo, W (corresponding author), Dalian Med Univ, Dalian, Peoples R China.; Deng, WG (corresponding author), Sun Yat Sen Univ, Canc Ctr, Guangzhou, Peoples R China.; Luo, C (corresponding author), Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai, Peoples R China.
EM dengwg@sysucc.org.cn; cluo@simm.ac.cn; wei1015@dmu.edu.cn
RI Lin, Hua/U-1529-2019; Zhao, Xinrui/AAK-7972-2020; xue,
   guoqing/AAC-7903-2021
FU National Natural Science Foundation of China [82072711, 81772975,
   81821005, 91853205]; Scientific Research Fund project of Education
   Department of Liaoning Province-Service local project [LZ2020005];
   Liaoning Bai-Qian-Wan Talents Program, and LiaoNing Revitalization
   Talents Prograrn [XLYC2007172]; National Key R&D Program of China
   [2021ZD0203900]
FX We are particularly grateful to the support of the funds from the
   National Natural Science Foundation of China [grant number: 82072711,
   81772975 to W.G., 81821005, 91853205 to C.L.], the Scientific Research
   Fund project of Education Department of Liaoning Province-Service local
   project [grant number: LZ2020005], the Liaoning Bai-Qian-Wan Talents
   Program, and LiaoNing Revitalization Talents Prograrn [grant number:
   XLYC2007172] and the National Key R&D Program of China [2021ZD0203900 to
   C.L.].
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TC 9
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U2 27
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2213-2317
J9 REDOX BIOL
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AR 102418
DI 10.1016/j.redox.2022.102418
EA AUG 2022
PG 16
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 5W1ET
UT WOS:000877664700003
PM 35932692
OA Green Published
DA 2025-01-04
ER

PT J
AU Gao, B
   Shao, Q
   Choudhry, H
   Marcus, V
   Dong, K
   Ragoussis, J
   Gao, ZH
AF Gao, Bo
   Shao, Qin
   Choudhry, Hani
   Marcus, Victoria
   Dong, Kung
   Ragoussis, Jiannis
   Gao, Zu-Hua
TI Weighted gene co-expression network analysis of colorectal cancer liver
   metastasis genome sequencing data and screening of anti-metastasis drugs
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE weighted gene co-expression network analysis; colorectal cancer liver
   metastasis; gene module; anti-metastasis drugs
ID BREAST-CANCER; TUMOR-GROWTH; PROLIFERATION; RECEPTOR; PREVENTION;
   SEROTONIN; RESECTION; SURVIVAL; INVASION; ACID
AB Approximately 9% of cancer-related deaths are caused by colorectal cancer (CRC). CRC patients are prone to liver metastasis, which is the most important cause for the high CRC mortality rate. Understanding the molecular mechanism of CRC liver metastasis could help us to find novel targets for the effective treatment of this deadly disease. Using weighted gene co-expression network analysis on the sequencing data of CRC with and with metastasis, we identified 5 colorectal cancer liver metastasis related modules which were labeled as brown, blue, grey, yellow and turquoise. In the brown module, which represents the metastatic tumor in the liver, gene ontology (GO) analysis revealed functions including the G-protein coupled receptor protein signaling pathway, epithelial cell differentiation and cell surface receptor linked signal transduction. In the blue module, which represents the primary CRC that has metastasized, GO analysis showed that the genes were mainly enriched in GO terms including G-protein coupled receptor protein signaling pathway, cell surface receptor linked signal transduction, and negative regulation of cell differentiation. In the yellow and turquoise modules, which represent the primary non-metastatic CRC, 13 downregulated CRC liver metastasis-related candidate miRNAs were identified (e.g. hsa-miR-204, hsa-miR-455, etc.). Furthermore, analyzing the DrugBank database and mining the literature identified 25 and 12 candidate drugs that could potentially block the metastatic processes of the primary tumor and inhibit the progression of metastatic tumors in the liver, respectively. Data generated from this study not only furthers our understanding of the genetic alterations that drive the metastatic process, but also guides the development of molecular-targeted therapy of colorectal cancer liver metastasis.
C1 [Gao, Bo] Harbin Med Univ, Dept Gen Surg, Affiliated Hosp 1, Harbin 150001, Heilongjiang, Peoples R China.
   [Shao, Qin; Marcus, Victoria; Gao, Zu-Hua] McGill Univ, Dept Pathol, Res Inst, Ctr Hlth, 1001 Blvd Decarie, Montreal, PQ H4A 3J1, Canada.
   [Choudhry, Hani; Ragoussis, Jiannis] McGill Univ, Montreal, PQ H3B 1S6, Canada.
   [Choudhry, Hani; Ragoussis, Jiannis] Genome Quebec Innovat Ctr, Montreal, PQ H3B 1S6, Canada.
   [Dong, Kung] Capital Med Univ, Dept Pathol, Beijing Youan Hosp, Beijing 100069, Peoples R China.
C3 Harbin Medical University; McGill University; McGill University; Capital
   Medical University
RP Gao, ZH (corresponding author), McGill Univ, Dept Pathol, Res Inst, Ctr Hlth, 1001 Blvd Decarie, Montreal, PQ H4A 3J1, Canada.
EM zu-hua.gao@mcgill.ca
RI Ragoussis, Ioannis/AAD-9790-2022; gao, bo/HHC-7855-2022
OI Ragoussis, Ioannis/0000-0002-8515-0934; Choudhry,
   Hani/0000-0003-0401-6619
FU Harbin Medical University Postgraduate Innovative Research Projects
   [YJSCX2015-19HYD]
FX This study was supported by Harbin Medical University Postgraduate
   Innovative Research Projects (grant no. YJSCX2015-19HYD).
CR Adachi Y, 2001, TUMOR BIOL, V22, P247, DOI 10.1159/000050623
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NR 35
TC 21
Z9 21
U1 0
U2 8
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1019-6439
EI 1791-2423
J9 INT J ONCOL
JI Int. J. Oncol.
PD SEP
PY 2016
VL 49
IS 3
BP 1108
EP 1118
DI 10.3892/ijo.2016.3591
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DU8EY
UT WOS:000382447300026
PM 27571956
OA Bronze
DA 2025-01-04
ER

PT J
AU Li, ZY
   Liu, Y
   Yi, HJ
   Cai, T
   Wei, YW
AF Li, Zhiyong
   Liu, Yang
   Yi, Huijie
   Cai, Ting
   Wei, Yunwei
TI Identification of N6-methylandenosine related lncRNA signatures for
   predicting the prognosis and therapy response in colorectal cancer
   patients
SO FRONTIERS IN GENETICS
LA English
DT Article
DE colorectal cancer1; N6-methylandenosine2; long non-coding RNA3;
   prognostic4; genetic alteration5; immune cell infiltration6; single-cell
   sequencing7; 5-fluorouracil8
ID LONG NONCODING RNA; B-CELLS; TARGETED THERAPY; SURVIVAL; HETEROGENEITY;
   MECHANISM; BLOCKADE
AB Despite recent advances in surgical and multimodal therapies, the overall survival (OS) of advanced colorectal cancer (CRC) patients remains low. Thus, discerning sensitive prognostic biomarkers to give the optimistic treatment for CRC patients is extremely critical. N6-methyladenosine (m6A) and long noncoding RNAs (lncRNAs) play an important role in CRC progression. Nonetheless, few studies have focused on the impact of m6A-related lncRNAs on the prognosis, tumor microenvironment (TME) and treatment of CRC. In this study, 1707 m6A-related lncRNAs were identified through Pearson correlation analysis and Weighted co-expression network analysis (WGCNA) using The Cancer Genome Atlas (TCGA) cohort. Then, 28 m6A-related prognostic lncRNAs were screened by univariate Cox regression analysis, followed by identifying two clusters by consensus clustering analysis. A prognostic model consisted of 8 lncRNA signatures was constructed by the least absolute shrinkage and selection operator (LASSO). Kaplan-Meier curve analysis and a nomogram were performed to investigate the prognostic ability of this model. The risk score of prognostic model act as an independent risk factor for OS rate. Functional enrichment analysis indicated that lncRNA signatures related tumor immunity. The low-risk group characterized by increased microsatellite instability-high (MSI-H), mutation burden, and immunity activation, indicated favorable odds of OS. Moreover, the lncRNA signatures were significantly associated with the cancer stem cell (CSC) index and drug sensitivity. In addition, 3 common immune genes shared by the lncRNA signatures were screened out. We found that these immune genes were widely distributed in 2 cell types of TME. Finally, a ceRNA network was constructed to identify ZEB1-AS1 regulatory axis in CRC. We found that ZEB1-AS1 was significantly overexpressed in tumor tissues, and was related to the metastasis of EMT and the chemoresistance of 5-Fu in CRC. Therefore, our study demonstrated the important role of m6A-related lncRNAs in TME remodeling. Moreover, these results illustrated the levels of ZEB1-AS1 might be valuable for predicting the progression and prognosis of CRC, and further provided a new target for the diagnosis and treatment of CRC patients.
C1 [Li, Zhiyong; Wei, Yunwei] Harbin Med Univ, Affiliated Hosp 1, Dept Oncol & Endoscop Surg, Harbin, Peoples R China.
   [Li, Zhiyong; Liu, Yang; Wei, Yunwei] Univ Chinese Acad Sci, HwaMei Hosp, Pancreat & Gastrointestinal Surg Div, Ningbo, Peoples R China.
   [Li, Zhiyong] Heilongjiang Acad Med Sci, Translat Med Res & Cooperat Ctr Northern China, Harbin, Peoples R China.
   [Yi, Huijie] Peking Univ, Sch Nursing, Beijing, Peoples R China.
   [Yi, Huijie] Peking Univ Peoples Hosp, Resp & Crit Care Med, Beijing, Peoples R China.
   [Cai, Ting] Univ Chinese Acad Sci, HwaMei Hosp, Dept Expt Med Sci, Ningbo, Peoples R China.
   [Cai, Ting] Key Lab Diag & Treatment Digest Syst Tumors, Ningbo, Zhejiang, Peoples R China.
C3 Harbin Medical University; Chinese Academy of Sciences; University of
   Chinese Academy of Sciences, CAS; Peking University; Chinese Academy of
   Sciences; University of Chinese Academy of Sciences, CAS
RP Wei, YW (corresponding author), Harbin Med Univ, Affiliated Hosp 1, Dept Oncol & Endoscop Surg, Harbin, Peoples R China.; Wei, YW (corresponding author), Univ Chinese Acad Sci, HwaMei Hosp, Pancreat & Gastrointestinal Surg Div, Ningbo, Peoples R China.; Cai, T (corresponding author), Univ Chinese Acad Sci, HwaMei Hosp, Dept Expt Med Sci, Ningbo, Peoples R China.; Cai, T (corresponding author), Key Lab Diag & Treatment Digest Syst Tumors, Ningbo, Zhejiang, Peoples R China.
EM caiting@ucas.ac.cn; hydwyw11@hotmail.com
RI li, zy/HZM-1892-2023
FU Ningbo Digestive System Tumor Clinical Medical Research Center; National
   Nature Science Foundation of China (NSFC) [2019A21003];  [81970466]
FX This research was funded by the Ningbo Digestive System Tumor Clinical
   Medical Research Center (Grant No. 2019A21003) and National Nature
   Science Foundation of China (NSFC) (Grant No. 81970466).
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NR 64
TC 5
Z9 5
U1 0
U2 3
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1664-8021
J9 FRONT GENET
JI Front. Genet.
PD SEP 30
PY 2022
VL 13
AR 947747
DI 10.3389/fgene.2022.947747
PG 25
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA 5K9JM
UT WOS:000870034500001
PM 36246627
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Alnuaimi, AR
   Nair, VA
   Malhab, LJB
   Abu-Gharbieh, E
   Ranade, AV
   Pintus, G
   Hamad, M
   Busch, H
   Kirfel, J
   Hamoudi, R
   Abdel-Rahman, WM
AF Alnuaimi, Alya R.
   Nair, Vidhya A.
   Malhab, Lara J. Bou
   Abu-Gharbieh, Eman
   Ranade, Anu Vinod
   Pintus, Gianfranco
   Hamad, Mohamad
   Busch, Hauke
   Kirfel, Jutta
   Hamoudi, Rifat
   Abdel-Rahman, Wael M.
TI Emerging role of caldesmon in cancer: A potential biomarker for
   colorectal cancer and other cancers
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Bladder cancer; CALD1; Caldesmon; Chemoresistance; Colorectal cancer;
   Gastric cancer; Glioma; Epithelial to mesenchymal transition; Invasion;
   Metastasis
ID SMOOTH-MUSCLE; COLON-CANCER; DIFFERENTIAL EXPRESSION; MOLECULAR
   SUBTYPES; DRUG-RESISTANCE; CELL INVASION; UP-REGULATION; ACTIN; PROTEIN;
   TUMOR
AB Colorectal cancer (CRC) is a devastating disease, mainly because of metastasis. As a result, there is a need to better understand the molecular basis of invasion and metastasis and to identify new biomarkers and therapeutic targets to aid in managing these tumors. The actin cytoskeleton and actin-binding proteins are known to play an important role in the process of cancer metastasis because they control and execute essential steps in cell motility and contractility as well as cell division. Caldesmon (CaD) is an actin-binding protein encoded by the CALD1 gene as multiple transcripts that mainly encode two protein isoforms: High-molecular-weight CaD, expressed in smooth muscle, and low-molecular weight CaD (l-CaD), expressed in nonsmooth muscle cells. According to our comprehensive review of the literature, CaD, particularly l-CaD, plays a key role in the development, metastasis, and resistance to chemoradiotherapy in colorectal, breast, and urinary bladder cancers and gliomas, among other malignancies. CaD is involved in many aspects of the carcinogenic hallmarks, including epithelial mesenchymal transition via transforming growth factor-beta signaling, angiogenesis, resistance to hormonal therapy, and immune evasion. Recent data show that CaD is expressed in tumor cells as well as in stromal cells, such as cancer-associated fibroblasts, where it modulates the tumor microenvironment to favor the tumor. Interestingly, CaD undergoes selective tumor-specific splicing, and the resulting isoforms are generally not expressed in normal tissues, making these transcripts ideal targets for drug design. In this review, we will analyze these features of CaD with a focus on CRC and show how the currently available data qualify CaD as a potential candidate for targeted therapy in addition to its role in the diagnosis and prognosis of cancer.
C1 [Alnuaimi, Alya R.; Nair, Vidhya A.; Malhab, Lara J. Bou; Abu-Gharbieh, Eman; Ranade, Anu Vinod; Pintus, Gianfranco; Hamad, Mohamad; Hamoudi, Rifat; Abdel-Rahman, Wael M.] Univ Sharjah, Sharjah Inst Med Res, Sharjah 27272, U Arab Emirates.
   [Alnuaimi, Alya R.] Univ Sharjah, Coll Med, Sharjah 27272, U Arab Emirates.
   [Abu-Gharbieh, Eman; Hamoudi, Rifat] Univ Sharjah, Dept Clin Sci, Sharjah 27272, U Arab Emirates.
   [Ranade, Anu Vinod] Univ Sharjah, Dept Basic Med Sci, Sharjah 27272, U Arab Emirates.
   [Pintus, Gianfranco; Hamad, Mohamad; Abdel-Rahman, Wael M.] Univ Sharjah, Dept Med Lab Sci, Sharjah 27272, U Arab Emirates.
   [Pintus, Gianfranco] Univ Sassari, Dept Biomed Sci, I-07100 Sassari, Italy.
   [Busch, Hauke] Univ Canc Ctr Schleswig Holstein, Univ Luebeck, Luebeck Inst Expt Dermatol, D-23560 Lubeck, Germany.
   [Kirfel, Jutta] Univ Hosp Schleswig Holstein, Inst Pathol, D-23560 Lubeck, Germany.
   [Hamoudi, Rifat] UCL, Div Surg & Intervent Sci, London WC1E 6BT, England.
   [Abdel-Rahman, Wael M.] Univ Sharjah, Dept Med Lab Sci, Sharjah 27272, U Arab Emirates.
C3 University of Sharjah; University of Sharjah; University of Sharjah;
   University of Sharjah; University of Sharjah; University of Sassari;
   University of Lubeck; University of Kiel; Schleswig Holstein University
   Hospital; University of London; University College London; University of
   Sharjah
RP Abdel-Rahman, WM (corresponding author), Univ Sharjah, Dept Med Lab Sci, Sharjah 27272, U Arab Emirates.
EM whassan@sharjah.ac.ae
RI Pintus, Gianfranco/C-2975-2009; Abdelrahman, Wael/V-8032-2018; Busch,
   Hauke/R-6452-2016; Abu-Gharbieh, Eman/F-3635-2010; Ranade,
   Anu/AAU-4965-2020
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NR 117
TC 6
Z9 7
U1 1
U2 9
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD SEP 15
PY 2022
VL 14
IS 9
BP 1637
EP 1653
DI 10.4251/wjgo.v14.i9.1637
PG 17
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA 4Z7MW
UT WOS:000862388900003
PM 36187394
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zalba, S
   Contreras, AM
   Haeri, A
   ten Hagen, TLM
   Navarro, I
   Koning, G
   Garrido, MJ
AF Zalba, Sara
   Contreras, Ana M.
   Haeri, Azadeh
   ten Hagen, Timo L. M.
   Navarro, Inigo
   Koning, Gerben
   Garrido, Maria J.
TI Cetuximab-oxaliplatin-liposomes for epidermal growth factor receptor
   targeted chemotherapy of colorectal cancer
SO JOURNAL OF CONTROLLED RELEASE
LA English
DT Article
DE EGFR; Targeted liposomes; Oxaliplatin; Cetuximab; Fab'; Colorectal
   cancer
ID DRUG-DELIVERY SYSTEMS; IN-VITRO; STEALTH LIPOSOMES; CELLS;
   IMMUNOLIPOSOMES; NANOPARTICLES; PHARMACOKINETICS
AB Oxaliplatin (L-OH), a platinum derivative with good tolerability is currently combined with Cetuximab (CTX), a monoclonal antibody (mAb), for the treatment of certain (wild-type KRAS) metastatic colorectal cancer (CRC) expressing epidermal growth factor receptor (EGFR).
   Improvement of L-OH pharmacokinetics (PK) can be provided by its encapsulation into liposomes, allowing a more selective accumulation and delivery to the tumor. Here, we aim to associate both agents in a novel liposomal targeted therapy by linking CTX to the drug-loaded liposomes. These EGFR-targeted liposomes potentially combine the therapeutic activity and selectivity of CTX with tumor-cell delivery of L-OH in a single therapeutic approach.
   L-OH liposomes carrying whole CTX or CTX-Fab' fragments on their surface were designed and characterized. Their functionality was tested in vitro using four human CRC cell lines, expressing different levels of EGFR to investigate the role of CTX-EGFR interactions in the cellular binding and uptake of the nanocarriers and encapsulated drug. Next, those formulations were evaluated in vivo in a colorectal cancer xenograftmodelwith regard to tumor drug accumulation, toxicity and therapeutic activity.
   In EGFR-overexpressing cell lines, intracellular drug delivery by targeted liposomes increased with receptor density reaching up to 3-fold higher levels than with non-targeted liposomes. Receptor specific uptake was demonstrated by competition with free CTX, which reduced internalization to levels similar to non-targeted liposomes. In a CRC xenograftmodel, drug deliverywas strongly enhanced upon treatmentwith targeted formulations. Liposomes conjugated with monovalent CTX-Fab' fragments showed superior drug accumulation in tumor tissue (2916.0 +/- 507.84 ng/g) compared to CTX liposomes (1546.02 +/- 362.41 ng/g) or non-targeted liposomes (891.06 +/- 155.1 ng/g). Concomitantly, CTX-Fab' targeted L-OH liposomes outperformed CTX-liposomes, which on its turn was still more efficacious than non-targeted liposomes and free drug treatment in CRC bearing mice.
   These results showthat site-directed conjugation ofmonovalent CTX-Fab' provides targeted L-OHliposomes that display an increased tumor drug delivery and efficacy over a formulation with CTX and non-targeted liposomes. (C) 2015 Elsevier B.V. All rights reserved.
C1 [Zalba, Sara; Contreras, Ana M.; Garrido, Maria J.] Univ Navarra, Dept Pharm & Pharmaceut Technol, Pamplona 31008, Spain.
   [Zalba, Sara; Haeri, Azadeh; ten Hagen, Timo L. M.; Koning, Gerben] Erasmus MC, Dept Surg, Lab Expt Surg Oncol, Inst Canc, NL-3015 GE Rotterdam, Netherlands.
   [Navarro, Inigo] Univ Navarra, Dept Chem & Edaphol, Pamplona 31008, Spain.
C3 University of Navarra; Erasmus University Rotterdam; Erasmus MC;
   University of Navarra
RP Koning, G (corresponding author), Erasmus MC, Dept Surg, Lab Expt Surg Oncol, Inst Canc, NL-3015 GE Rotterdam, Netherlands.
EM g.koning@erasmusmc.nl; mgarrido@unav.es
RI Sara, Zalba/AAE-8470-2019; Koning, Gerben/K-2326-2012; Garrido, Maria
   J/J-1802-2017; Navarro-Blasco, Inigo/D-8148-2012
OI Contreras-Sandoval, Ana/0000-0002-4324-9610; Garrido, Maria
   J/0000-0003-3559-4710; Zalba, Sara/0000-0001-5203-2985; Navarro-Blasco,
   Inigo/0000-0003-1863-0580
FU Spanish Government (Instituto de Salud Carlos III) [PS09/02512-FISS];
   Government of Navarra [IIQ14334.RI1]; University of Navarra
FX Funding for this project came from the Spanish Government (Instituto de
   Salud Carlos III, ref: PS09/02512-FISS), Government of Navarra (ref:
   IIQ14334.RI1) and from the University of Navarra. Sara Zalba was
   supported by a grant from the Government of Navarra. The authors want to
   thank the Imaging Unit from CIMA (Pamplona, Spain) for their support to
   this work.
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NR 46
TC 94
Z9 101
U1 3
U2 98
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-3659
EI 1873-4995
J9 J CONTROL RELEASE
JI J. Control. Release
PD JUL 28
PY 2015
VL 210
BP 26
EP 38
DI 10.1016/j.jconrel.2015.05.271
PG 13
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA CK5CC
UT WOS:000356238700004
PM 25998052
DA 2025-01-04
ER

PT J
AU Szemitko, M
   Falkowski, A
   Modrzejewska, M
   Golubinska-Szemitko, E
AF Szemitko, Marcin
   Falkowski, Aleksander
   Modrzejewska, Monika
   Golubinska-Szemitko, Elzbieta
TI Efficacy and Safety of Liver Chemoembolization Procedures, Combined with
   FOLFIRI Chemotherapy, in First-Line Treatment of Metastatic Colorectal
   Cancer in Patients with Oncogene Mutations
SO CANCERS
LA English
DT Article
DE DEB-TACE; FOLFIRI; FOLFOX; irinotecan; microspheres
ID PLUS CETUXIMAB; MICROSPHERES; BEVACIZUMAB; TACE
AB Simple Summary Colorectal cancer (CRC) is the the second leading cause of cancer-related mortality. The aim of the study was to evaluate the efficacy and safety of transarterial chemoembolization (DEB-TACE) procedures for the treatment of metastatic liver lesions from CRC, using irinotecan-loaded microspheres as first-line treatment together with FOLFIRI chemotherapy. The response and disease control rates were 55% and 80%, respectively. The toxicity profiles among our patients were generally acceptable and no serious events were recorded. The combination of FOLFIRI with chemoembolization may provide a valuable treatment option for patients with oncogene mutations who do not qualify for monoclonal antibody therapy.Abstract Purpose. The usual first- and second-line treatments for inoperable liver metastases from colorectal cancer (CRC) involve systemic chemotherapy, often with molecular targeted therapy. Chemoembolization, using microspheres loaded with irinotecan, has also been available as a treatment option for many years, used mainly in later lines of treatment when, due to increasing resistance, other chemotherapy regimens may have been exhausted. However, when there are contraindications to molecular therapies, the use of chemoembolization as first or second lines of treatment, in combination with FOLFIRI chemotherapy, may provide greater efficacy due to reduced irinotecan resistance. Objective. The aim of the study was to evaluate the efficacy and safety of transarterial chemoembolization (DEB-TACE) procedures for the treatment of metastatic liver lesions from CRC, using irinotecan-loaded microspheres as first-line treatment together with FOLFIRI chemotherapy. Patients and methods. The analysis included 20 patients (12 females; 8 males) with unresectable liver metastases in the course of CRC with KRAS, NRAS and BRAF mutations, who underwent 73 chemoembolization procedures with microspheres loaded with 100 mg of irinotecan, in combination with interspersed FOLFIRI chemotherapy. Response to treatment was assessed through computed tomography according to the Modified Response Evaluation Criteria in Solid Tumors (mRECIST). Progression-free survival (PFS) and overall survival (OS) were calculated using the Kaplan-Meier method. Assessment of adverse events utilized the Cancer Therapy Evaluation Program's Common Terminology Criteria for Adverse Events (CTCAE; version 5.0). Results. Partial remission (PR) was observed in 11 (55%) patients while 5 (25%) patients showed stable disease (SD). Progression (PD) was observed in 4 (20%) patients. Median PFS was 9.1 months (95% CI: 7.2-10.1 months) and median OS was 20.7 months (95% CI: 18.2-23.3 months). The most common adverse events (AEs) resulting in treatment delay were hematological disorders, notably neutropenia (CTCAE grades 1-3). No deaths or AEs above grade 3 occurred during TACE. Continued FOLFIRI chemotherapy after TACE treatments resulted in grade 4 neutropenia in two patients, grade 3 in four patients and grade 2 thrombocytopenia in two patients. Conclusion. Combining FOLFIRI chemotherapy with chemoembolization procedures for liver metastatic lesions from colorectal cancer may provide a valuable treatment option for patients not qualified for monoclonal antibody therapy.
C1 [Szemitko, Marcin; Falkowski, Aleksander] Pomeranian Med Univ, Dept Intervent Radiol, Al Pow Wielkopolskich 72, PL-70111 Szczecin, Poland.
   [Modrzejewska, Monika] Pomeranian Med Univ, Dept Ophthalmol 2, Al Pow Wielkopolskich 72, PL-70111 Szczecin, Poland.
   [Golubinska-Szemitko, Elzbieta] Pomeranian Med Univ, Dept Gen & Dent Diagnost Imaging, Al Pow Wielkopolskich 72, PL-70111 Szczecin, Poland.
C3 Pomeranian Medical University; Pomeranian Medical University; Pomeranian
   Medical University
RP Szemitko, M (corresponding author), Pomeranian Med Univ, Dept Intervent Radiol, Al Pow Wielkopolskich 72, PL-70111 Szczecin, Poland.
EM szemitko@gmail.com; zrz@pum.edu.pl; monika_modrzej@op.pl;
   e.golubinska@gmail.com
RI Szemitko, Marcin/IWM-2075-2023; Falkowski, Aleksander/I-2324-2014
OI Szemitko, Marcin/0000-0002-7271-7495
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NR 28
TC 0
Z9 0
U1 0
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JAN
PY 2024
VL 16
IS 1
AR 71
DI 10.3390/cancers16010071
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EM1K2
UT WOS:001139249900001
PM 38201500
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhang, Y
   Li, Y
   Zuo, Z
   Li, T
   An, Y
   Zhang, WJ
AF Zhang, Yu
   Li, Yan
   Zuo, Zan
   Li, Ting
   An, Ying
   Zhang, Wenjing
TI An epithelial-mesenchymal transition-related mRNA signature associated
   with the prognosis, immune infiltration and therapeutic response of
   colon adenocarcinoma
SO PATHOLOGY & ONCOLOGY RESEARCH
LA English
DT Article
DE epithelial-mesenchymal transition; bioinformatics; prognostic signature;
   tumor immune microenvironment; colon adenocarcinoma
ID COLORECTAL-CANCER; TUMOR MICROENVIRONMENT; EXPRESSION; PROMOTES;
   IDENTIFICATION; METASTASIS; EMT; PROGRESSION; SURVIVAL; GENES
AB Background: Epithelial-mesenchymal transition (EMT) is closely associated with cancer cell metastasis. Colon adenocarcinoma (COAD) is one of the most common malignancies in the world, and its metastasis leading to poor prognosis remains a challenge for clinicians. The purpose of this study was to explore the prognostic value of EMT-related genes (EMTRGs) by bioinformatics analysis and to develop a new EMTRGs prognostic signature for COAD.Methods: The TCGA-COAD dataset was downloaded from the TCGA portal as the training cohort, and the GSE17538 and GSE29621 datasets were obtained from the GEO database as the validation cohort. The best EMTRGs prognostic signature was constructed by differential expression analysis, Cox, and LASSO regression analysis. Gene set enrichment analysis (GSEA) is used to reveal pathways that are enriched in high-risk and low-risk groups. Differences in tumor immune cell levels were analyzed using microenvironmental cell population counter and single sample gene set enrichment analysis. Subclass mapping analysis and Genomics of Drug Sensitivity in Cancer were applied for prediction of immunotherapy response and chemotherapy response, respectively.Results: A total of 77 differentially expressed EMTRGs were identified in the TCGA-COAD cohort, and they were significantly associated with functions and pathways related to cancer cell metastasis, proliferation, and apoptosis. We constructed EMTRGs prognostic signature with COMP, MYL9, PCOLCE2, SCG2, and TIMP1 as new COAD prognostic biomarkers. The high-risk group had a poorer prognosis with enhanced immune cell infiltration. The GSEA demonstrated that the high-risk group was involved in "ECM Receptor Interaction," "WNT Signaling Pathway" and "Colorectal Cancer." Furthermore, patients with high risk scores may respond to anti-CTLA4 therapy and may be more resistant to targeted therapy agents BI 2536 and ABT-888.Conclusion: Together, we developed a new EMTRGs prognostic signature that can be an independent prognostic factor for COAD. This study has guiding implications for individualized counseling and treatment of COAD patients.
C1 [Zhang, Yu; Li, Yan; Zuo, Zan; Li, Ting; An, Ying] Kunming Univ Sci & Technol, Peoples Hosp Yunnan Prov 1, Dept Gastroenterol, Affiliated Hosp, Kunming, Peoples R China.
   [Zhang, Yu; Li, Yan; Zuo, Zan; Li, Ting; An, Ying] Yunnan Digest Endoscopy Clin Med Ctr, Kunming, Peoples R China.
   [Zhang, Wenjing] Kunming Univ Sci & Technol, Fac Med, Kunming, Peoples R China.
   [Zhang, Wenjing] Kunming Univ Sci & Technol, Peoples Hosp Yunnan Prov 1, Dept Med Oncol, Affiliated Hosp, Kunming, Peoples R China.
C3 Kunming University of Science & Technology; Kunming University of
   Science & Technology; Kunming University of Science & Technology
RP Zhang, WJ (corresponding author), Kunming Univ Sci & Technol, Fac Med, Kunming, Peoples R China.; Zhang, WJ (corresponding author), Kunming Univ Sci & Technol, Peoples Hosp Yunnan Prov 1, Dept Med Oncol, Affiliated Hosp, Kunming, Peoples R China.
EM wenjing_zhang1@163.com
FU National Natural Science Foundation of China [81860522, 81860509]; Young
   Academic Talents Cultivation Foundation of Yunnan Province
   [202205AC160070]; Yunnan Medical Training Program [YNWR-QNBJ-2019-147]
FX Funding This study was supported by grant from the National Natural
   Science Foundation of China (81860522, 81860509), Young Academic Talents
   Cultivation Foundation of Yunnan Province (202205AC160070), Yunnan
   Medical Training Program (YNWR-QNBJ-2019-147).
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NR 85
TC 4
Z9 4
U1 0
U2 3
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1219-4956
EI 1532-2807
J9 PATHOL ONCOL RES
JI Pathol. Oncol. Res.
PD FEB 24
PY 2023
VL 29
AR 1611016
DI 10.3389/pore.2023.1611016
PG 14
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA E0OJ0
UT WOS:000972629100001
PM 36910014
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Peng, K
   Liu, RQ
   Yu, YY
   Liang, L
   Yu, S
   Xu, XJ
   Liu, TS
AF Peng, Ke
   Liu, Ruiqi
   Yu, Yiyi
   Liang, Li
   Yu, Shan
   Xu, Xiaojing
   Liu, Tianshu
TI Identification and validation of cetuximab resistance associated long
   noncoding RNA biomarkers in metastatic colorectal cancer
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Metastatic colorectal cancer; EGFR inhibitor; Cetuximab; lncRNA;
   Progression-free survival
ID PHASE-III TRIAL; PANITUMUMAB; PLUS; CHEMOTHERAPY; OXALIPLATIN;
   EXPRESSION; THERAPIES; SIGNATURE; KRAS
AB Background: Cetuximab is one of the most widely used epidermal growth factor receptor (EGFR) inhibitors to treat patients with metastatic colorectal cancer (mCRC) harboring wild-type of RAS/RAF status. However, primary and acquired resistance to cetuximab is often found during target therapy.
   Methods: To gain insights into the functions of long non-coding RNA (lncRNA) in cetuximab resistance, we used a lncRNA-mining approach to distinguish lncRNA specific probes in Affymetrix HG-U133A 2.0 arrays. Then we performed lncRNA expression profiling in a cetuximab treated mCRC cohort from Gene Expression Ominus (GEO). The potential lncRNAs were further validated in acquired cetuximab resistant cell lines and clinical samples of our hospital. The functions and associated pathways of the prognostic lncRNA were predicted by GO and KEGG analyses.
   Results: 249 lncRNA-specific probe sets (corresponding to 212 lncRNAs) were represented in Affymetrix HG-U133A 2.0 arrays. We found that 9 lncRNAs were differentially expressed between disease control group (DCG) and non-responders, and 5 of these 9 lncRNAs were significantly related with the progression-free survival (PFS) of the patients. Among those 5 lncRNAs, POU5F1P4 was also down-regulated in acquired cetuximab resistant cells, as well as in cetuximab resistant patients. Downregulation of POU5F1P4 decreased the sensitivity of colorectal cancer cells to cetuximab.
   Conclusion: Our findings indicate the potential roles of lncRNAs in cetuximab resistance, and may provide the useful information for discovery of new biomarkers and therapeutic targets.
C1 [Peng, Ke; Liu, Ruiqi; Yu, Yiyi; Liang, Li; Yu, Shan; Xu, Xiaojing; Liu, Tianshu] Fudan Univ, Zhongshan Hosp, Dept Oncol, Shanghai 200032, Peoples R China.
   [Liu, Tianshu] Fudan Univ, Ctr Evidence Based Med, Shanghai, Peoples R China.
C3 Fudan University; Fudan University
RP Liu, TS (corresponding author), Fudan Univ, Zhongshan Hosp, 180 Fenglin Rd, Shanghai 200032, Peoples R China.
EM liu.tianshu@zs-hospital.sh.cn
RI xu, xiaojing/C-2759-2014; yu, yiyi/HMP-5697-2023; Liu,
   Ruiqi/JTU-2973-2023; Liu, Tianshu/H-6879-2019
OI liu, tianshu/0000-0002-2318-2869
FU National Natural Science Foundation of China [81772511, 81602038,
   81502003]
FX This study was funded by: 1. National Natural Science Foundation of
   China (No. 81772511); 2. National Natural Science Foundation of China
   (No. 81602038); 3. National Natural Science Foundation of China (No.
   81502003).
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NR 32
TC 23
Z9 28
U1 0
U2 14
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD JAN
PY 2018
VL 97
BP 1138
EP 1146
DI 10.1016/j.biopha.2017.11.031
PG 9
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA FR4NC
UT WOS:000419041300137
PM 29136952
DA 2025-01-04
ER

PT J
AU Li, BX
   Wang, Y
   Wang, Y
   Li, SM
   Liu, KR
AF Li, Baoxuan
   Wang, Yang
   Wang, Yue
   Li, Siman
   Liu, Kuiran
TI Deep Infiltrating Endometriosis Malignant Invasion of Cervical Wall and
   Rectal Wall With Lynch Syndrome: A Rare Case Report and Review of
   Literature
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE endometriosis; deep infiltrating endometriosis; malignant
   transformation; Lynch syndrome; malignant tumor
ID CLEAR-CELL CARCINOMA; OVARIAN-CANCER; MUTATIONS; ADENOCARCINOMA;
   EXPRESSION; PIK3CA
AB BackgroundMalignant transformation of deep infiltrating endometriosis (DIE) invading the cervix and rectum is quite rare, especially in patients combined with Lynch syndrome (LS). We report a rare case of a 49-year-old perimenopausal woman with endometrioid carcinoma arising from the pouch of Douglas, invading the cervix and rectum 1 year after a unilateral salpingo-oophorectomy treatment for ovarian endometriosis. The genetic testing of the patient showed germline mutations in MSH2, which combined with the special family history of colorectal cancer of the patient, was also thought to be associated with LS. We have analyzed the reported cases of DIE malignant transformation over the last 10 years, and reviewed the relevant literature, in order to strengthen the clinical management of patients with endometriosis, particularly patients with DIE, and reveal a possible correlation between malignant transformation of endometriosis and LS. Case PresentationA 49-year-old perimenopausal woman presented with hypogastralgia, diarrhea, and intermittent fever for more than 1 month. A Transvaginal ultrasound (TVS) showed a cervix isthmus mass, and a magnetic resonance imaging (MRI) showed a mass in pouch of Douglas with high suspicion of malignancy, possibly invading the anterior wall of the rectum. Prior to surgery, the patient performed the ultrasound guided pelvic mass biopsy through the vagina, and the pathology of the mass showed endometrioid carcinoma. The patient received a gynecological-surgical laparotomy and enterostomy, and a histopathology revealed endometrioid carcinoma infiltrating the cervical wall and rectal wall. In the family genetic history of the patient, her mother and two sisters suffered from colorectal cancer, so lesion tissue and blood were taken for genetic testing, which showed a germline mutation in MSH2, with LS being considered. After the surgical treatment, the patient received six courses of paclitaxel-carboplatin chemotherapy. During the course of treatment, bone marrow suppression occurred, but was healed after symptomatic treatment. To date, the patient is generally in good health, and imaging examination showed no evidence of recurrence. ConclusionThe risk of malignant transformation of endometriosis is increased in perimenopause and postmenopause, as DIE is a rare malignant transformation of endometriosis. DIE can invade other adjacent organs and cause poor prognosis, thus, comprehensive gynecological-surgical treatment should be necessary. In addition, if histopathology showed endometrioid carcinoma, the possibility of LS should be considered, and if necessary, immunohistochemical staining and gene detection should be improved to provide follow-up targeted therapy and immunotherapy.
C1 [Li, Baoxuan; Wang, Yang; Wang, Yue; Li, Siman; Liu, Kuiran] China Med Univ, Shengjing Hosp, Dept Obstet & Gynecol, Shenyang, Peoples R China.
C3 China Medical University
RP Liu, KR (corresponding author), China Med Univ, Shengjing Hosp, Dept Obstet & Gynecol, Shenyang, Peoples R China.
EM liukr0412@163.com
FU "Scientific research funding project of the Liaoning Provincial
   Department of Science and Technology [2020JH2/10300050]
FX This research received the support from a "Scientific research funding
   project of the Liaoning Provincial Department of Science and Technology
   (No.2020JH2/10300050)".
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NR 36
TC 12
Z9 12
U1 0
U2 6
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD MAR 23
PY 2022
VL 12
AR 832228
DI 10.3389/fonc.2022.832228
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 0J7LO
UT WOS:000780283500001
PM 35402227
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Ito, T
   Takashima, A
   Yamazaki, K
   Yukami, H
   Uetake, H
   Tsuda, M
   Suto, T
   Moriwaki, T
   Sugimoto, N
   Ojima, H
   Takii, Y
   Yasui, H
   Esaki, T
   Tsuji, A
   Goto, M
   Saruta, M
   Otsu, S
   Shinozaki, K
   Fujiwara, T
   Tamura, T
   Baba, E
   Shiozawa, M
   Denda, T
   Ueno, H
   Nagashima, K
   Shimada, Y
AF Ito, Takahiko
   Takashima, Atsuo
   Yamazaki, Kentaro
   Yukami, Hiroki
   Uetake, Hiroyuki
   Tsuda, Masahiro
   Suto, Takeshi
   Moriwaki, Toshikazu
   Sugimoto, Naotoshi
   Ojima, Hitoshi
   Takii, Yasumasa
   Yasui, Hisateru
   Esaki, Taito
   Tsuji, Akihito
   Goto, Masahiro
   Saruta, Masayuki
   Otsu, Satoshi
   Shinozaki, Katsunori
   Fujiwara, Toshiyoshi
   Tamura, Takao
   Baba, Eishi
   Shiozawa, Manabu
   Denda, Tadamichi
   Ueno, Hideki
   Nagashima, Kengo
   Shimada, Yasuhiro
TI Primary tumor location as a predictor of survival in patients with
   <i>RAS</i> wild-type colorectal cancer who receive molecularly targeted
   drugs as first-line therapy: a multicenter real-world observational
   study by the Japanese Society for Cancer of the Colon and Rectum
SO INTERNATIONAL JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
DE Metastatic colorectal cancer; Tumor sidedness; Bevacizumab; Cetuximab;
   Panitumumab
ID FOLFIRI PLUS BEVACIZUMAB; MFOLFOX6 PLUS; OPEN-LABEL; ANTI-EGFR;
   PHASE-III; CHEMOTHERAPY; CETUXIMAB; METAANALYSIS; PANITUMUMAB;
   OXALIPLATIN
AB Background Primary tumor location is considered a predictor of overall survival (OS) in RAS wild-type (WT) metastatic colorectal cancer (mCRC) treated with bevacizumab (BEV) or an anti-epidermal growth factor antibody (cetuximab or panitumumab [CET/PAN]) as first-line molecularly targeted therapy. BEV is recommended for right-sided mCRC and CET/PAN for left-sided mCRC based on post-hoc analyses of clinical trial data, but real-world evidence is lacking. Methods We retrospectively collected data of patients who started BEV or CET/PAN plus 5-fluorouracil-based doublet chemotherapy between January 2013 and December 2016 as first-line treatment for RAS WT mCRC at any of 24 Japanese institutions. OS was compared between the BEV and CET/PAN groups according to primary tumor location by Cox multivariate regression analysis in the full cohort and in a propensity score-matched cohort. Results In total, 935 patients were enrolled. Median OS was 24.6 months with BEV and 20.9 months with CET/PAN in right-sided mCRC (n = 213; adjusted hazard ratio [HR] 0.73, 95% confidence interval [CI] 0.50-1.06) and 35.7 months and 30.0 months, respectively, in left-sided mCRC (n = 722; adjusted HR 0.92, 95% CI 0.74-1.13). In the propensity score-matched cohort, OS was significantly better in the BEV group than in the CET/PAN group in right-sided mCRC (HR 0.52, 95% CI 0.28-0.96) but was not significantly different in left-sided mCRC (HR 0.78, 95% CI 0.53-1.07). Conclusion Real-world data showed that OS was better with BEV than with CET/PAN in right-sided mCRC. However, there was no significant difference in OS in left-sided mCRC.
C1 [Ito, Takahiko; Takashima, Atsuo] Natl Canc Ctr, Chuo Ku, 5-1-1 Tsukiji, Tokyo 1040045, Japan.
   [Ito, Takahiko] Kyoto Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Sakyo Ku, 54 Shogoin Kawahara Cho, Kyoto 6068507, Japan.
   [Yamazaki, Kentaro] Shizuoka Canc Ctr, Dept Gastrointestinal Oncol, 1007 Shimonagakubo, Shizuoka 4118777, Japan.
   [Yukami, Hiroki] Natl Canc Ctr East, Dept Gastroenterol & Gastrointestinal Oncol, 6-5-1 Kashiwanoha, Kashiwa, Chiba 2778577, Japan.
   [Yukami, Hiroki; Goto, Masahiro] Osaka Med & Pharmaceut Univ Hosp, 2-7 Daigaku Machi, Takatsuki, Osaka 5698686, Japan.
   [Uetake, Hiroyuki] Natl Hosp Org Disaster Med Ctr, 3256 Midori Cho, Tachikawa, Tokyo 1900014, Japan.
   [Tsuda, Masahiro] Hyogo Canc Ctr, 13-70 Kitaouji Cho, Akashi, Hyogo 6738558, Japan.
   [Suto, Takeshi] Yamagata Prefectural Cent Hosp, Dept Gastroenterol Surg, 1800 Aoyagi, Yamagata 9902292, Japan.
   [Moriwaki, Toshikazu] Univ Tsukuba, Fac Med, Dept Gastroenterol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan.
   [Sugimoto, Naotoshi] Osaka Int Canc Inst, Chuo Ku, 3-1-69 Otemae, Osaka 5418567, Japan.
   [Ojima, Hitoshi] Gunma Prefectural Canc Ctr, Dept Gastrointestinal Surg, 617-1 Takabayashi, Ota, Gunma 3738550, Japan.
   [Takii, Yasumasa] Niigata Canc Ctr Hosp, Dept Gastroenterol Surg, Chuo Ku, 2-15-3 Kawagichi Cho, Niigata 9518566, Japan.
   [Yasui, Hisateru] Kobe City Med Ctr, Dept Med Oncol, Gen Hosp, Chuo Ku, 2-1-1 Minatojima Minamimachi, Kobe, Hyogo 6500047, Japan.
   [Esaki, Taito] Natl Hosp Org Kyushu Canc Ctr, Dept Gastrointestinal & Med Oncol, Minami Ku, 3-1-1 Notame, Fukuoka 8111395, Japan.
   [Tsuji, Akihito] Kagawa Univ, Fac Med, 1750-1 Ikenobe, Kita, Kagawa 7610793, Japan.
   [Saruta, Masayuki] Jikei Univ, Dept Internal Med, Div Gastroenterol & Hepatol, Sch Med,Minato Ku, 3-25-8 Nishi Shinbashi, Tokyo 1058461, Japan.
   [Otsu, Satoshi] Oita Univ, Dept Med Oncol & Hematol, Fac Med, 1-1 Idaigaoka, Yufu, Oita 8795593, Japan.
   [Shinozaki, Katsunori] Hiroshima Prefectural Hosp, Div Clin Oncol, Minami Ku, 1-5-54 Ujinakanda, Hiroshima 7348530, Japan.
   [Fujiwara, Toshiyoshi] Okayama Univ, Dept Gastroenterol Surg, Grad Sch Med Dent & Pharmaceut Sci, Kita Ku, 2-5-1 Shikata Cho, Okayama 7008558, Japan.
   [Tamura, Takao] Kindai Univ, Dept Med Oncol, Fac Med, 377-2 Ohno Higashi, Osaka 5890014, Japan.
   [Baba, Eishi] Kyushu Univ, Grad Sch Med Sci, Dept Oncol & Social Med, Higashi Ku, 3-1-1 Maidashi, Fukuoka 8128582, Japan.
   [Shiozawa, Manabu] Kanagawa Canc Ctr, Gastrointestinal Surg, Asahi Ku, 2-3-2 Nakao, Yokohama, Kanagawa 2418512, Japan.
   [Denda, Tadamichi] Chiba Canc Ctr, Chuo Ku, 666-2 Nitona Cho, Chiba 2608717, Japan.
   [Ueno, Hideki] Natl Def Med Coll, Dept Surg, 3-2 Namiki, Tokorozawa, Saitama 3598513, Japan.
   [Nagashima, Kengo] Keio Univ Hosp, Shinjuku Ku, 35 Shinanomachi, Tokyo 1608582, Japan.
   [Shimada, Yasuhiro] Kochi Hlth Sci Ctr, 2125-1 Ike, Kochi 7818555, Japan.
C3 National Cancer Center - Japan; Kyoto University; Shizuoka Cancer
   Center; National Cancer Center - Japan; Hyogo Cancer Center; Yamagata
   Prefectural Central Hospital; University of Tsukuba; Kobe City Medical
   Center General Hospital; Kyushu Cancer Center; Kagawa University; Jikei
   University; Oita University; Okayama University; Kindai University
   (Kinki University); Kyushu University; Kanagawa Prefectural Cancer
   Center; Chiba Cancer Center; National Defense Medical College - Japan;
   Keio University
RP Takashima, A (corresponding author), Natl Canc Ctr, Chuo Ku, 5-1-1 Tsukiji, Tokyo 1040045, Japan.
EM atakashi@ncc.go.jp
RI Nagashima, Kengo/I-4258-2019; Saruta, Masayuki/ABL-4991-2022; Uetake,
   Hiroyuki/AAC-2669-2020; Ueno, Hideki/L-1237-2016
FU Grants-in-Aid for Scientific Research [22K07272] Funding Source: KAKEN
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NR 28
TC 1
Z9 1
U1 0
U2 0
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
   JAPAN
SN 1341-9625
EI 1437-7772
J9 INT J CLIN ONCOL
JI Int. J. Clin. Oncol.
PD SEP
PY 2022
VL 27
IS 9
BP 1450
EP 1458
DI 10.1007/s10147-022-02208-7
EA JUL 2022
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3W6BF
UT WOS:000828454300001
PM 35861943
DA 2025-01-04
ER

PT J
AU Voutsadakis, IA
AF Voutsadakis, Ioannis A.
TI Sensitivities and Dependencies of <i>BRAF</i> Mutant Colorectal Cancer
   Cell Lines with or without <i>PIK3CA</i> Mutations for Discovery of
   Vulnerabilities with Therapeutic Potential
SO MEDICINA-LITHUANIA
LA English
DT Article
DE colon cancer; cell line models; dependencies; targeted therapy; signal
   transduction
ID GENOMIC LANDSCAPE; EXPRESSION; SPECIFICITY; ENCORAFENIB; ACTIVATION;
   CETUXIMAB; PATHWAY; ARK5
AB Background: Colorectal cancer represents a common malignancy and remains incurable in the metastatic stage. Identification of molecular alterations that are present in colorectal cancer has led to the introduction of targeted therapies that improve outcomes. BRAF and PIK3CA mutations are observed in a subset of colorectal cancers. Colorectal cancers bearing BRAF mutations may be treated with specific BRAF inhibitors. These drugs benefit patients with BRAF mutant colorectal cancers but responses are rather brief, and progression is the rule. In contrast, no PI3K inhibitors have proven successful yet in the disease. Thus, new treatments to supplement the currently available drugs would be welcome to further improve survival. Methods: Profiled colorectal cancer cell lines from the Cancer Cell Line Encyclopedia (CCLE) were examined for BRAF and PIK3CA mutations and were interrogated for molecular characteristics and concomitant alterations that mirror clinical sample alterations. The Genomics of Drug Sensitivity in Cancer (GDSC) project was used for determination of drug sensitivities of BRAF mutated colorectal cell lines with or without concomitant PIK3CA mutations. The Cancer Dependency Map project served as the basis for identification of molecular dependencies and vulnerabilities in these cell lines. Results: CCLE includes 84 colorectal cancer cell lines, which recapitulate the molecular landscape of colorectal cancer. Of these, 23 and 24 cell lines possess BRAF and PIK3CA mutations, respectively. Seven BRAF mutant cell lines have V600E mutations and 14 PIK3CA mutant cell lines have hotspot helical or kinase domain mutations. V600E BRAF mutant cell lines with or without hotspot PIK3CA mutations are heterogeneous in their MSI status and mimic colorectal cancer tissues in other prevalent abnormalities including APC and TP53 mutations. Essential genes for survival include CTNNB1, WRN, and pyrimidine metabolism enzyme CAD. Besides BRAF mutations, BRAF inhibitor sensitivity in colorectal cancer cell lines is conferred by SACS mutations and PRKN locus loss. Conclusions: Colorectal cancer cell lines bearing the frequent BRAF and PIK3CA mutations present many alterations of the parental cancer tissue. Described vulnerabilities represent leads for therapeutic exploration in colorectal cancers with the corresponding alterations.
C1 [Voutsadakis, Ioannis A.] Sault Area Hosp, Algoma Dist Canc Program, 750 Great Northern Rd, Sault Ste Marie, ON P6B 0A8, Canada.
   [Voutsadakis, Ioannis A.] Northern Ontario Sch Med, Div Clin Sci, Sect Internal Med, Sudbury, ON P3E 2C6, Canada.
C3 NOSM University
RP Voutsadakis, IA (corresponding author), Sault Area Hosp, Algoma Dist Canc Program, 750 Great Northern Rd, Sault Ste Marie, ON P6B 0A8, Canada.; Voutsadakis, IA (corresponding author), Northern Ontario Sch Med, Div Clin Sci, Sect Internal Med, Sudbury, ON P3E 2C6, Canada.
EM ivoutsadakis@yahoo.com
RI Voutsadakis, Ioannis/AAU-7224-2020
OI Voutsadakis, Ioannis/0000-0002-9301-5951
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NR 63
TC 3
Z9 3
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1010-660X
EI 1648-9144
J9 MEDICINA-LITHUANIA
JI Med. Lith.
PD OCT
PY 2022
VL 58
IS 10
AR 1498
DI 10.3390/medicina58101498
PG 15
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 5P3MU
UT WOS:000873059500001
PM 36295658
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Liang, L
   Guo, XM
   Ye, W
   Liu, YX
AF Liang, Liu
   Guo, Xuemin
   Ye, Wei
   Liu, Yuxiang
TI KRAS Gene Mutation Associated with Grade of Tumor Budding and Peripheral
   Immunoinflammatory Indices in Patients with Colorectal Cancer
SO INTERNATIONAL JOURNAL OF GENERAL MEDICINE
LA English
DT Article
DE colorectal cancer; KRAS; systemic immune inflammation index; tumor
   budding
ID INFLAMMATION RESPONSE INDEX; METASTASIS; MICROENVIRONMENT; SURVIVAL;
   FEATURES
AB Background: The efficacy of targeted therapy for colorectal cancer (CRC) is affected by hub genes of epidermal growth factor receptor (EGFR) signaling pathways, such as KRAS. Immune cell infiltration may lead to gene mutation, but the relationship between KRAS status and peripheral immune-inflammatory indices has not been clarified in CRC. Methods: Clinical records of CRC patients were collected. The relationship between KRAS status and clinicopathological charactersystemic immune inflammation index (SII) (plateletxneutrophil/lymphocyte), and system inflammation response index (SIRI) (monocytexneutrophil/lymphocyte)) were analyzed. Results: 1033 CRC patients were collected, there were 514 (49.8%) patients with KRAS wild-type and 519 (50.2%) with KRAS mutation. Patients with KRAS mutation had higher proportions of female, III-IV stage, and lymph node metastasis and lower proportion of low grade of tumor budding (the presence of single tumor cells or small clusters of up to 5 cells in mesenchyma at the front of tumor invasion) than those with KRAS wild-type. The PIV, SII, and SIRI levels in KRAS mutation patients were significantly higher than those in KRAS wild-type patients. The proportion of aged >= 65 years old, dMMR, distant metastasis, and KRAS mutation were high in patients with high PIV, SII, and SIRI levels. Logistic regression analysis showed that non-low grade of tumor budding (odds ratio (OR): 1.970, 95% confidence interval (CI): 1.287-3.016, p=0.002), and high SII level (>= 807.81 vs <807.81, OR: 1.915, 95% CI: 1.120-3.272, p=0.018) were independently associated with KRAS mutation. Conclusion: Non-low grade of tumor budding, and high SII level were independently associated with KRAS mutation in CRC. It provides additional references for diagnosis and treatment options for patients with CRC.
C1 [Liang, Liu; Guo, Xuemin; Ye, Wei] Meizhou Peoples Hosp, Dept Lab Med, Meizhou, Peoples R China.
   [Liu, Yuxiang] Meizhou Peoples Hosp, Dept Med Oncol, Meizhou, Peoples R China.
RP Liang, L (corresponding author), Meizhou Peoples Hosp, Dept Lab Med, Meizhou, Peoples R China.
EM 19926117315@163.com
FU Project of Medical and Health Scientific Research of Meizhou City
   [2024-B-63]
FX <B>Funding</B> This work was supported by the Project of Medical and
   Health Scientific Research of Meizhou City (Grant No.: 2024-B-63) .
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NR 67
TC 0
Z9 0
U1 0
U2 0
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
EI 1178-7074
J9 INT J GEN MED
JI Int. J. Gen. Med.
PY 2024
VL 17
BP 4769
EP 4780
DI 10.2147/IJGM.S487525
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA J6E1G
UT WOS:001337967400001
PM 39440104
OA gold
DA 2025-01-04
ER

PT J
AU Reis, H
   van der Vos, KE
   Niedworok, C
   Herold, T
   Módos, O
   Szendroi, A
   Hager, T
   Ingenwerth, M
   Vis, DJ
   Behrendt, MA
   Jong, J
   van der Heijden, MS
   Peyronnet, B
   Mathieu, R
   Wiesweg, M
   Ablat, J
   Okon, K
   Tolkach, Y
   Keresztes, D
   Nagy, N
   Bremmer, F
   Gaisa, NT
   Chlosta, P
   Kriegsmann, J
   Kovalszky, I
   Timar, J
   Kristiansen, G
   Radzun, HJ
   Knüchel, R
   Schuler, M
   Black, PC
   Rübben, H
   Hadaschik, BA
   Schmid, KW
   van Rhijn, BWG
   Nyirády, P
   Szarvas, T
AF Reis, Henning
   van der Vos, Kristan E.
   Niedworok, Christian
   Herold, Thomas
   Modos, Orsolya
   Szendroi, Attila
   Hager, Thomas
   Ingenwerth, Marc
   Vis, Daniel J.
   Behrendt, Mark A.
   de Jong, Jeroen
   van der Heijden, Michiel S.
   Peyronnet, Benoit
   Mathieu, Romain
   Wiesweg, Marcel
   Ablat, Jason
   Okon, Krzysztof
   Tolkach, Yuri
   Keresztes, David
   Nagy, Nikolett
   Bremmer, Felix
   Gaisa, Nadine T.
   Chlosta, Piotr
   Kriegsmann, Joerg
   Kovalszky, Ilona
   Timar, Jozsef
   Kristiansen, Glen
   Radzun, Heinz-Joachim
   Knuechel, Ruth
   Schuler, Martin
   Black, Peter C.
   Ruebben, Herbert
   Hadaschik, Boris A.
   Schmid, Kurt Werner
   van Rhijn, Bas W. G.
   Nyirady, Peter
   Szarvas, Tibor
TI Pathogenic and targetable genetic alterations in 70 urachal
   adenocarcinomas
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE urachal cancer; molecular genetics; targeted therapy; colorectal cancer;
   urothelial carcinoma
ID COMPREHENSIVE MOLECULAR CHARACTERIZATION; MICROSATELLITE INSTABILITY;
   GENOMIC ALTERATIONS; PROMOTER MUTATIONS; COLORECTAL-CANCER; CARCINOMA;
   RARE; KRAS; BRAF; EXPRESSION
AB Urachal cancer (UrC) is a rare but aggressive malignancy often diagnosed in advanced stages requiring systemic treatment. Although cytotoxic chemotherapy is of limited effectiveness, prospective clinical studies can hardly be conducted. Targeted therapeutic treatment approaches and potentially immunotherapy based on a biological rationale may provide an alternative strategy. We therefore subjected 70 urachal adenocarcinomas to targeted next-generation sequencing, conducted in situ and immunohistochemical analyses (including PD-L1 and DNA mismatch repair proteins [MMR]) and evaluated the microsatellite instability (MSI) status. The analytical findings were correlated with clinicopathological and outcome data and Kaplan-Meier and univariable/multivariable Cox regression analyses were performed. The patients had a mean age of 50 years, 66% were male and a 5-year overall survival (OS) of 58% and recurrence-free survival (RFS) of 45% was detected. Sequence variations were observed in TP53 (66%), KRAS (21%), BRAF (4%), PIK3CA (4%), FGFR1 (1%), MET (1%), NRAS (1%), and PDGFRA (1%). Gene amplifications were found in EGFR (5%), ERBB2 (2%), and MET (2%). We detected no evidence of MMR-deficiency (MMR-d)/MSI-high (MSI-h), whereas 10 of 63 cases (16%) expressed PD-L1. Therefore, anti-PD-1/PD-L1 immunotherapy approaches might be tested in UrC. Importantly, we found aberrations in intracellular signal transduction pathways (RAS/RAF/PI3K) in 31% of UrCs with potential implications for anti-EGFR therapy. Less frequent potentially actionable genetic alterations were additionally detected in ERBB2 (HER2), MET, FGFR1, and PDGFRA. The molecular profile strengthens the notion that UrC is a distinct entity on the genomic level with closer resemblance to colorectal than to bladder cancer.
C1 [Reis, Henning; Herold, Thomas; Hager, Thomas; Ingenwerth, Marc; Schmid, Kurt Werner] Univ Duisburg Essen, Univ Hosp Essen, West German Canc Ctr, Inst Pathol, Hufelandstr 55, D-45147 Essen, Germany.
   [van der Vos, Kristan E.; Vis, Daniel J.; van der Heijden, Michiel S.] Antoni van Leeuwenhoek Hosp, Netherlands Canc Inst, Div Mol Carcinogenesis, Amsterdam, Netherlands.
   [Niedworok, Christian; Ruebben, Herbert; Hadaschik, Boris A.; Szarvas, Tibor] Univ Duisburg Essen, Univ Hosp Essen, West German Canc Ctr, Dept Urol, Essen, Germany.
   [Reis, Henning; Herold, Thomas; Schuler, Martin; Hadaschik, Boris A.; Schmid, Kurt Werner] Partner Site Univ Hosp Essen, German Canc Consortium DKTK, Essen, Germany.
   [Modos, Orsolya; Szendroi, Attila; Keresztes, David; Nagy, Nikolett; Nyirady, Peter; Szarvas, Tibor] Semmelweis Univ, Dept Urol, Budapest, Hungary.
   [Behrendt, Mark A.; van Rhijn, Bas W. G.] Antoni van Leeuwenhoek Hosp, Netherlands Canc Inst, Dept Surg Oncol Urol, Amsterdam, Netherlands.
   [Behrendt, Mark A.] Univ Hosp Basel, Div Urol, Dept Surg, Basel, Switzerland.
   [de Jong, Jeroen] Antoni van Leeuwenhoek Hosp, Netherlands Canc Inst, Dept Pathol, Amsterdam, Netherlands.
   [van der Heijden, Michiel S.] Antoni van Leeuwenhoek Hosp, Netherlands Canc Inst, Dept Med Oncol, Amsterdam, Netherlands.
   [Peyronnet, Benoit; Mathieu, Romain] Univ Rennes, Dept Urol, Rennes, France.
   [Wiesweg, Marcel; Schuler, Martin] Univ Duisburg Essen, Univ Hosp Essen, West German Canc Ctr, Dept Med Oncol, Essen, Germany.
   [Ablat, Jason; Black, Peter C.] Univ British Columbia, Vancouver Prostate Ctr, Vancouver, BC, Canada.
   [Okon, Krzysztof; Chlosta, Piotr] Jagiellonian Univ, Dept Pathomorphol, Krakow, Poland.
   [Tolkach, Yuri; Kristiansen, Glen] Univ Bonn, Inst Pathol, Bonn, Germany.
   [Bremmer, Felix; Radzun, Heinz-Joachim] Univ Gottingen, Inst Pathol, Gottingen, Germany.
   [Gaisa, Nadine T.; Knuechel, Ruth] Rhein Westfal TH Aachen, Inst Pathol, Aachen, Germany.
   [Kriegsmann, Joerg] Ctr Histol Cytol & Mol Diagnost Trier, Trier, Germany.
   [Kovalszky, Ilona] Semmelweis Univ, Inst Pathol & Expt Canc Res 1, Budapest, Hungary.
   [Timar, Jozsef] Semmelweis Univ, Dept Pathol 2, Budapest, Hungary.
C3 University of Duisburg Essen; Netherlands Cancer Institute; University
   of Duisburg Essen; Helmholtz Association; German Cancer Research Center
   (DKFZ); Semmelweis University; Netherlands Cancer Institute; University
   of Basel; Netherlands Cancer Institute; Netherlands Cancer Institute;
   Universite de Rennes; University of Duisburg Essen; University of
   British Columbia; Jagiellonian University; University of Bonn;
   University of Gottingen; RWTH Aachen University; Semmelweis University;
   Semmelweis University
RP Reis, H (corresponding author), Univ Duisburg Essen, Univ Hosp Essen, West German Canc Ctr, Inst Pathol, Hufelandstr 55, D-45147 Essen, Germany.
EM Henning.Reis@uk-essen.de
RI Schuler, Markus/AAI-6535-2020; Hadaschik, Boris/HNP-2417-2023;
   Peyronnet, benoit/AGV-9053-2022; van Rhijn, Bas/JWP-8591-2024; Black,
   Peter/AAE-8424-2020; VIEILLARD, Philippe/B-8544-2008; Reis,
   Henning/AAX-9545-2020; Kovalszky, Ilona/ABH-2832-2020; Okon,
   Krzysztof/D-1345-2011; Szarvas, Tibor/L-4422-2017
OI Hadaschik, Boris/0000-0002-1052-2692; Okon,
   Krzysztof/0000-0002-1921-5007; Wiesweg, Marcel/0000-0002-9698-9559;
   Szarvas, Tibor/0000-0002-6321-0799; Reis, Henning/0000-0003-1373-5295;
   Schuler, Martin/0000-0002-2166-3394
FU Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences;
   National Research, Development and Innovation Office
   [NVKP_16-1-2016-004]
FX Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences;
   Grant sponsor: National Research, Development and Innovation Office;
   Grant number: NVKP_16-1-2016-004
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NR 40
TC 46
Z9 46
U1 0
U2 13
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD OCT 1
PY 2018
VL 143
IS 7
BP 1764
EP 1773
DI 10.1002/ijc.31547
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GS2PB
UT WOS:000443392100022
PM 29672836
OA Green Submitted, Bronze
DA 2025-01-04
ER

PT J
AU Yuan, HH
   Zhang, XC
   Wei, XL
   Zhang, WJ
   Du, XX
   Huang, P
   Chen, H
   Bai, L
   Zhang, HF
   Han, Y
AF Yuan, Heng-Heng
   Zhang, Xin-Chen
   Wei, Xiao-Li
   Zhang, Wen-Jie
   Du, Xiao-Xue
   Huang, Peng
   Chen, Hao
   Bai, Lu
   Zhang, Hong-Feng
   Han, Yu
TI LncRNA UCA1 mediates Cetuximab resistance in Colorectal Cancer via the
   MiR-495 and HGF/c-MET Pathways
SO JOURNAL OF CANCER
LA English
DT Article
DE UCA1; cetuximab; metastatic colorectal cancer; miR-495; hepatocyte
   growth factor; c-MET signalling pathway
ID ANTI-EGFR THERAPY; EXPRESSION; CELLS; METASTASIS; MECHANISMS; GROWTH;
   IDENTIFICATION; ASSOCIATION; SENSITIVITY; ACTIVATION
AB Background: Cetuximab is one of the most widely used monoclonal antibodies to treat patients with RAS/BRAF wild-type metastatic colorectal cancer (mCRC). Unfortunately, cetuximab resistance often occurs during targeted therapy. However, the underlying epigenetic mechanisms remain unclear. Our previous study demonstrated that the exosomal transfer of urothelial carcinoma-associated 1 (UCA1) confers cetuximab resistance to CRC cells. The goal of this study was to elucidate the detailed role of UCA1 in cetuximab resistance in CRC and the underlying molecular mechanism. Methods: In vitro and in vivo functional studies were performed to assess the role of UCA1 in cetuximab resistance in CRC cell lines and xenograft models. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to examine UCA1 localization and expression. Bioinformatics analysis was performed to predict the potential mechanism of UCA1, which was further validated by the dual-luciferase reporter assay and the RNA immunoprecipitation (RIP) assay. Cells treated with indicators were subjected to Cell Counting Kit-8 (CCK-8) and western blotting to investigate the role of hepatocyte growth factor (HGF)/c-mesenchymal-epithelial transition (c-MET) signalling in UCA1-mediated cetuximab resistance. Results: We showed that UCA1 decreased CRC cell sensitivity to cetuximab by suppressing apoptosis. Mechanistic studies revealed that UCA1 promoted cetuximab resistance by competitively binding miR-495 to facilitate HGF and c-MET expression in CRC cells. Moreover, HGF was shown to attenuate the cetuximab-induced inhibition of cell proliferation by activating the HGF/c-MET pathway in CRC cells. Conclusion: We provide the first evidence of a UCA1-miR-495-HGF/c-MET regulatory network involved in cetuximab resistance in CRC. Therefore, UCA1 has potential as a predictor and therapeutic target for cetuximab resistance.
C1 [Yuan, Heng-Heng; Wei, Xiao-Li; Zhang, Wen-Jie; Du, Xiao-Xue; Huang, Peng; Chen, Hao; Bai, Lu; Han, Yu] Harbin Med Univ, Dept Gastrointestinal Oncol, Canc Hosp, 150 Haping Rd, Harbin 150081, Heilongjiang, Peoples R China.
   [Zhang, Xin-Chen] Harbin Med Univ, Dept Gen Surg, Affiliated Hosp 2, Harbin, Heilongjiang, Peoples R China.
   [Zhang, Hong-Feng] Harbin Med Univ, Dept Gastr Surg, Canc Hosp, 150 Haping Rd, Harbin 150081, Heilongjiang, Peoples R China.
C3 Harbin Medical University; Harbin Medical University; Harbin Medical
   University
RP Han, Y (corresponding author), Harbin Med Univ, Dept Gastrointestinal Oncol, Canc Hosp, 150 Haping Rd, Harbin 150081, Heilongjiang, Peoples R China.; Zhang, HF (corresponding author), Harbin Med Univ, Dept Gastr Surg, Canc Hosp, 150 Haping Rd, Harbin 150081, Heilongjiang, Peoples R China.
EM zhanghf@hrbmu.edu.cn; hanyu@hrbmu.edu.cn
RI huang, peng/KBC-5715-2024; Zhang, Wenjie/O-5336-2014
OI Zhang, Hongfeng/0009-0001-3186-3357
FU Key Project of Haiyan Research Fund of Harbin Medical University Cancer
   Hospital [JJZD2018-06]; Harbin Science and Technology Bureau Project
   [2017RAQXJ198]
FX This study was supported by the Key Project of Haiyan Research Fund of
   Harbin Medical University Cancer Hospital (No. JJZD2018-06) and the
   Harbin Science and Technology Bureau Project (No. 2017RAQXJ198).
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NR 65
TC 18
Z9 20
U1 1
U2 6
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1837-9664
J9 J CANCER
JI J. Cancer
PY 2022
VL 13
IS 1
BP 253
EP 267
DI 10.7150/jca.65687
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YI2XX
UT WOS:000743717900002
PM 34976187
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Shek, D
   Akhuba, L
   Carlino, MS
   Nagrial, A
   Moujaber, T
   Read, SA
   Gao, B
   Ahlenstiel, G
AF Shek, Dmitrii
   Akhuba, Liia
   Carlino, Matteo S.
   Nagrial, Adnan
   Moujaber, Tania
   Read, Scott A.
   Gao, Bo
   Ahlenstiel, Golo
TI Immune-Checkpoint Inhibitors for Metastatic Colorectal Cancer: A
   Systematic Review of Clinical Outcomes
SO CANCERS
LA English
DT Review
DE colorectal cancer; pembrolizumab; atezolizumab; nivolumab; ipilimumab;
   targeted therapy; immune-checkpoint inhibitors
ID NIVOLUMAB; SURVIVAL; VEGF
AB Simple Summary In 2018, colorectal cancer (CRC) was declared the fourth most deadly cancer worldwide. Unfortunately, a quarter of all patients are diagnosed at late stages, when curative surgery is not possible, rendering systemic therapy and/or best supportive care as the only options. To our knowledge, this is the first systematic review assessing response and survival rates in patients with mCRC treated with immune-checkpoint inhibitors (ICIs). Our study established that ICIs show potentially superior response rates in mCRC patients, though only in those with high microsatellite instability (MSI). Nivolumab + regorafenib was reported to provide encouraging response in low-MSI (MSI-L) patients; however, additional studies using cohort randomization are required. Further studies are required, particularly regarding the mechanism of resistance to ICIs in MSI-L patients. Background. Colorectal cancer (CRC) is the fourth most deadly cancer worldwide. Unfortunately, a quarter of the patients are diagnosed at late stages, when surgical options are limited. Targeted therapies, particularly immune-checkpoint inhibitors (ICIs), are the latest addition and have been studied herein regarding their efficacy outcomes. Methods. Clinical studies were identified through the PubMed, Scopus and Cochrane databases. Any trial that evaluated ICIs in patients with metastatic CRC (mCRC) and reported the objective response rate was deemed eligible. Data analysis was performed by employing the random-effects model in STATA v.17. Results. A total of 461 articles were identified; 13 clinical trials were included, encompassing a total cohort of 1209 patients. Our study determined that a single PD-1/PD-L1 checkpoint blockade provides durable clinical response in mCRC patients with high microsatellite instability (MSI-H). The combinatorial therapy of CTLA-4 + PD-1 inhibitors also showed high response rates in pre-treated MSI-H patients. The single-arm REGONIVO trial reported durable clinical response in patients with microsatellite stable (MSS) status. Conclusions. Our study surmises that PD-1/PD-L1 inhibitors as well as combination therapy with CTLA-4 and PD-1 inhibitors show encouraging response rates in mCRC patients, albeit exclusively in patients with cancer that are of MSI-H status. A single study suggests that nivolumab + regorafenib can reach a durable response rate in MSS patients; however, further studies in larger randomized settings are required.
C1 [Shek, Dmitrii; Read, Scott A.; Ahlenstiel, Golo] Univ Western Sydney, Blacktown Clin Sch, Sydney, NSW 2148, Australia.
   [Shek, Dmitrii; Carlino, Matteo S.; Nagrial, Adnan; Moujaber, Tania; Read, Scott A.; Gao, Bo; Ahlenstiel, Golo] Blacktown Hosp, Sydney, NSW 2148, Australia.
   [Shek, Dmitrii; Akhuba, Liia] RUDN Univ, Accreditat Ctr, Moscow 117198, Russia.
   [Carlino, Matteo S.; Nagrial, Adnan; Moujaber, Tania; Gao, Bo] Westmead Hosp, Crown Princess Mary Canc Ctr, Sydney, NSW 2145, Australia.
   [Carlino, Matteo S.; Nagrial, Adnan; Ahlenstiel, Golo] Univ Sydney, Westmead Clin Sch, Sydney, NSW 2145, Australia.
   [Carlino, Matteo S.] Melanoma Inst, Sydney, NSW 2065, Australia.
   [Read, Scott A.; Ahlenstiel, Golo] Storr Liver Ctr, Westmead Inst Med Res, Sydney, NSW 2145, Australia.
C3 Western Sydney University; NSW Health; Blacktown & Mount Druitt
   Hospital; Peoples Friendship University of Russia; University of Sydney;
   NSW Health; Westmead Hospital; University of Sydney; Melanoma Institute
   Australia; University of Sydney; Westmead Institute for Medical Research
RP Ahlenstiel, G (corresponding author), Univ Western Sydney, Blacktown Clin Sch, Sydney, NSW 2148, Australia.; Ahlenstiel, G (corresponding author), Blacktown Hosp, Sydney, NSW 2148, Australia.; Ahlenstiel, G (corresponding author), Univ Sydney, Westmead Clin Sch, Sydney, NSW 2145, Australia.; Ahlenstiel, G (corresponding author), Storr Liver Ctr, Westmead Inst Med Res, Sydney, NSW 2145, Australia.
EM Dmitri.Shek@health.nsw.gov.au; Akhuba_lg@rudn.university;
   Matteo.Carlino@health.nsw.gov.au; Adnan.Nagrial@health.nsw.gov.au;
   Tania.Moujaber@health.nsw.gov.au; S.Read@westernsydney.edu.au;
   Bo.Gao@health.nsw.gov.au; Golo.Ahlenstiel@health.nsw.gov.au
RI Read, Scott/K-6462-2019; Akhuba, Liia/AAE-7954-2021; Carlino,
   Matteo/GRS-7198-2022; Shek, Dmitrii/A-5061-2017; gao, bo/HHC-7855-2022;
   Ahlenstiel, Golo/U-1990-2017
OI Carlino, Matteo S/0000-0002-7861-4104; Nagrial,
   Adnan/0000-0003-0275-2479; Akhuba, Liia/0000-0002-4505-1616; Moujaber,
   Tania/0000-0002-0688-3364; Read, Scott/0000-0001-6775-2061; Gao,
   Bo/0000-0002-7881-6603; Ahlenstiel, Golo/0000-0003-0026-1457; Shek,
   Dmitrii/0000-0001-9013-0842
FU Ainsworth Bequest; Robert W. Storr Bequest; Western Sydney Local Health
   District Research and Education Network Grant
FX This project was supported by the Ainsworth Bequest to the School of
   Medicine of Western Sydney University, the Robert W. Storr Bequest to
   the Sydney Medical Foundation of the University of Sydney and the
   Western Sydney Local Health District Research and Education Network
   Grant 2021.
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NR 44
TC 15
Z9 17
U1 0
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD SEP
PY 2021
VL 13
IS 17
AR 4345
DI 10.3390/cancers13174345
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UN6JJ
UT WOS:000694120100001
PM 34503155
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Nagasaka, M
   Li, YW
   Sukari, A
   Ou, SHI
   Al-Hallak, MN
   Azmi, AS
AF Nagasaka, Misako
   Li, Yiwei
   Sukari, Ammar
   Ou, Sai-Hong Ignatius
   Al-Hallak, Mohammed Najeeb
   Azmi, Asfar S.
TI KRAS G12C Game of Thrones, which direct KRAS inhibitor will claim the
   iron throne?
SO CANCER TREATMENT REVIEWS
LA English
DT Review
DE Kirsten rat sarcoma viral oncogene homolog; Non-small cell lung cancer;
   Targeted therapy; AMG 510; MRTX 849; ARS 3248
ID SMALL-MOLECULE INHIBITORS; ONCOGENIC K-RAS; MALIGNANT-TRANSFORMATION;
   CANCER; MUTATIONS; MECHANISM; PATHWAYS; GTP; RAF/MEK/ERK; ACTIVATION
AB Mutations in Kirsten rat sarcoma viral oncogene homolog (KRAS) are among the most common aberrations in cancer, including non-small cell lung cancer (NSCLC). The lack of an ideal small molecule binding pocket in the KRAS protein and its high affinity towards the abundance of cellular guanosine triphosphate (GTP) renders the design of specific small molecule drugs challenging. Despite efforts, KRAS remains a challenging therapeutic target.
   Among the different known mutations; the KRAS(G12c) (glycine 12 to cysteine) mutation has been considered potentially druggable. Several novel covalent direct inhibitors targeting KRAS(G12c) with similar covalent binding mechanisms are now in clinical trials. Both AMG 510 from Amgen and MRTX849 from Mirati Therapeutics covalently binds to KRAS(G12c) at the cysteine at residue 12, keeping KRAS(G12c) in its inactive GDP-bound state and inhibiting KRAS-dependent signaling. Both inhibitors are being studied as a single agent or as combination with other targets. In addition, two novel KRAS G12C inhibitors JNJ-74699157 and LY3499446 will have entered phase 1 studies by the end of 2019.
   Given the rapid clinical development of 4 direct covalent KRAS G12C inhibitors within a short period of time, understanding the similarities and differences among these will be important to determine the best treatment option based on tumor specific response (NSCLC versus colorectal carcinoma), potential resistance mechanisms (i.e. anticipated acquired mutation at the cysteine 12 residue) and central nervous system (CNS) activity. Additionally, further investigation evaluating the efficacy and safety of combination therapies with agents such as immune checkpoint inhibitors will be important next steps.
C1 [Nagasaka, Misako; Li, Yiwei; Sukari, Ammar; Al-Hallak, Mohammed Najeeb; Azmi, Asfar S.] Wayne State Univ, Karmanos Canc Inst, Detroit, MI 48202 USA.
   [Nagasaka, Misako] St Marianna Univ, Grad Sch Med, Kawasaki, Kanagawa, Japan.
   [Li, Yiwei; Azmi, Asfar S.] Wayne State Univ, Sch Med, Detroit, MI 48202 USA.
   [Ou, Sai-Hong Ignatius] Univ Calif Irvine, Sch Med, Dept Med, Chao Family Comprehens Canc Ctr,Div Hematol Oncol, Orange, CA 92668 USA.
C3 Barbara Ann Karmanos Cancer Institute; Wayne State University; Saint
   Marianna University; Wayne State University; University of California
   System; University of California Irvine
RP Azmi, AS (corresponding author), Wayne State Univ, Karmanos Canc Inst, Detroit, MI 48202 USA.; Azmi, AS (corresponding author), Wayne State Univ, Sch Med, Detroit, MI 48202 USA.
EM nagasakm@karmanos.org; liyi@karmanos.org; sukaria@karmanos.org;
   siou@hs.uci.edu; hallakm@karmanos.org; azmia@karmanos.org
RI Ou, Sai-Hong/AAA-3389-2020
OI Al Hallak, Mohammed/0000-0002-4598-8177; AZMI, ASFAR/0000-0003-1178-9505
FU NCI [R37 CA21542702]; SKY Foundation
FX Work in the lab of Asfar S. Azmi is supported by NCI R37 CA21542702 and
   SKY Foundation.
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NR 75
TC 141
Z9 160
U1 0
U2 116
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0305-7372
EI 1532-1967
J9 CANCER TREAT REV
JI Cancer Treat. Rev.
PD MAR
PY 2020
VL 84
AR 101974
DI 10.1016/j.ctrv.2020.101974
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KR0YY
UT WOS:000517347600009
PM 32014824
OA Green Accepted, Green Submitted
DA 2025-01-04
ER

PT J
AU Tang, PA
   Hay, AE
   O'Callaghan, CJ
   Mittmann, N
   Chambers, CR
   Pater, JL
   Leighl, NB
AF Tang, P. A.
   Hay, A. E.
   O'Callaghan, C. J.
   Mittmann, N.
   Chambers, C. R.
   Pater, J. L.
   Leighl, N. B.
TI Estimation of drug cost avoidance and pathology cost avoidance through
   participation in NCIC Clinical Trials Group phase III clinical trials in
   Canada
SO CURRENT ONCOLOGY
LA English
DT Article
DE Cost avoidance; phase III trials
ID STAGE BREAST-CANCER; CELL LUNG-CANCER; ADJUVANT CHEMOTHERAPY;
   COLORECTAL-CARCINOMA; POSTMENOPAUSAL WOMEN; ECONOMIC-BENEFITS;
   RANDOMIZED-TRIAL; 1ST-LINE THERAPY; FLUOROURACIL; OXALIPLATIN
AB Background Cost avoidance occurs when, because of provision of a drug therapy [drug cost avoidance (DCA)] or a pathology test [pathology cost avoidance (PCA)] during trial participation, health care payers need not pay for standard treatments or testing. The aim of our study was to estimate the total DCA and PCA for Canadian patients enrolled in relevant phase III trials conducted by the NCIC Clinical Trials Group.
   Methods Phase III trials that had completed accrual and resulted in DCA or PCA were identified. The PCA was calculated based on the number of patients screened and the test cost. The DCA was estimated based on patients randomized, the protocol dosing regimen, drug cost, median dose intensity, and median duration of therapy. Costs are presented in Canadian dollars. No adjustment was made for inflation.
   Results From 1999 to 2011, 4 trials (1479 patients) resulted in PCA and 17 trials (3195 patients) resulted in DCA. The total PCA was estimated at $4,194,849, which included testing for KRAS ($141,058), microsatellite instability ($18,600), and 21-gene recurrence score ($4,035,191). The total DCA was estimated at $27,952,512, of which targeted therapy constituted 43% (five trials). The combined PCA and DCA was $32,147,361.
   Conclusions Over the study period, trials conducted by the NCIC Clinical Trials Group resulted in total cost avoidance (PCA and DCA) of approximately $7,518 per patient. Although not all trials lead to cost avoidance, such savings should be taken account when the financial impact of conducting clinical research is being considered.
C1 [Tang, P. A.; Chambers, C. R.] Univ Calgary, Tom Baker Canc Ctr, Calgary, AB, Canada.
   [Hay, A. E.; O'Callaghan, C. J.; Mittmann, N.; Pater, J. L.] NCIC Clin Trials Grp, Kingston, ON, Canada.
   [Mittmann, N.] Sunnybrook Hlth Sci Ctr, Hlth Outcomes & Pharmacoecon HOPE Res Ctr, Toronto, ON M4N 3M5, Canada.
   [Leighl, N. B.] Princess Margaret Canc Ctr, Toronto, ON, Canada.
C3 University of Calgary; Tom Baker Cancer Clinic; Queens University -
   Canada; Canadian Cancer Trials Group; University of Toronto; Sunnybrook
   Research Institute; Sunnybrook Health Science Center; University of
   Toronto; University Health Network Toronto; Princess Margaret Cancer
   Centre
RP Tang, PA (corresponding author), Tom Baker Canc Clin, 1331 29 St NW, Calgary, AB T2N 4N2, Canada.
EM Patricia.tang@albertahealthservices.ca
OI Hay, Annette/0000-0003-4581-3390
FU Canadian Cancer Society Research Institute [021039]
FX This study was supported by the Canadian Cancer Society Research
   Institute (grant no. 021039).
CR Alberts SR, 2012, JAMA-J AM MED ASSOC, V307, P1383, DOI 10.1001/jama.2012.385
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NR 26
TC 16
Z9 16
U1 0
U2 4
PU MULTIMED INC
PI TORONTO
PA 66 MARTIN ST, TORONTO, ON L9T 2R2, CANADA
SN 1198-0052
J9 CURR ONCOL
JI Curr. Oncol.
PD FEB
PY 2016
VL 23
SU 1
BP S7
EP S13
DI 10.3747/co.23.2861
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DG1KX
UT WOS:000371828000003
PM 26985151
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Fu, Y
   Ye, YD
   Liu, XR
   Zhu, GF
   Xu, YW
   Sun, JB
   Wu, HM
   Feng, FY
   Wen, ZH
   Jiang, SS
   Li, YY
   Zhang, QL
AF Fu, Yun
   Ye, Yuedian
   Liu, Xiaorong
   Zhu, Guifang
   Xu, Yangwei
   Sun, Jingbo
   Wu, Hongmei
   Feng, Feiyan
   Wen, Zhihui
   Jiang, Shanshan
   Li, Yanyan
   Zhang, Qingling
TI Analyzing microsatellite instability and gene mutation in circulating
   cell-free DNA to monitor colorectal cancer progression
SO TRANSLATIONAL CANCER RESEARCH
LA English
DT Article
DE Colorectal cancer (CRC); microsatellite instability (MSI); gene
   mutation; next-generation sequencing (NGS); circulating cell-free DNA
   (cfDNA)
ID MISMATCH REPAIR DEFICIENCY; FREE TUMOR DNA; CLINICAL ONCOLOGY; AMERICAN
   SOCIETY; COLON-CANCER; VALIDATION; CARCINOMA
AB Background: Colorectal cancer (CRC) is the second leading cause of cancer-related deaths worldwide. Detection of microsatellite instability (MSI) status and gene mutations may be useful for molecular targeted therapy. The liquid biopsy is a newly developed, non-invasive method for tumor diagnosis and monitoring. In this study, we evaluated the possible clinical value of liquid biopsy by analyzing MSI and gene mutation.
   Methods: Next-generation sequencing (NGS) was used to analyze MSI and gene mutation in circulating cell-free DNA (cfDNA) and tissue DNA extracted from 6 CRC patients' plasma and matched primary tumor tissue (MPTT) samples, respectively.
   Results: A total of 6 patients (4 male, 2 female) were included for analysis, whose stage ranges from stage I through stage III. NGS-based panel of 5 quasi-monomorphic microsatellite markers (MSI-NGS) BAT-25, BAT-26, NR21, NR24 as well as NR27, and 4 mismatch repair (MMR) genes (MSH2, MSH6, PMS2, MLH1) expressions assessed by immunohistochemistry (MMR-IHC) and NGS (MMR-NGS) were used to determine MSI status synergistically. Comprehensive analysis of NGS and IHC results showed that the overall incidences of MSI in plasma and MPTT samples from these patients were 1/6 and 2/6, respectively. 4 patients were defined as microsatellite stable (MSS) in both plasma and MPTT. In the above 6 patients, MSI-NGS detection in cfDNA accurately identified 1/2 of tissue high-level microsatellite instability (MSI-H) and 4/4 of tissue MSS for an overall accuracy of 5/6. Gene mutational profiles in these CRC patients' plasma and MPTT samples were analyzed by NGS. Tumor-specific gene mutations were detected in 2/6 of plasma and 4/4 of MPTT samples. The two mutation-positive plasma samples were from CRC patients at stage IIb and stage IIIc.
   Conclusions: Analyzing MSI and gene mutation might be a non-invasive supplementary way to reveal the molecular characteristics of CRC.
C1 [Fu, Yun; Ye, Yuedian; Liu, Xiaorong; Zhu, Guifang; Xu, Yangwei; Sun, Jingbo; Wu, Hongmei; Feng, Feiyan; Wen, Zhihui; Jiang, Shanshan; Li, Yanyan; Zhang, Qingling] Southern Med Univ, Sch Basic Med Sci, Dept Pathol, Guangzhou, Peoples R China.
   [Fu, Yun; Liu, Xiaorong; Xu, Yangwei; Sun, Jingbo; Wu, Hongmei; Feng, Feiyan; Wen, Zhihui; Jiang, Shanshan; Li, Yanyan; Zhang, Qingling] Guangdong Acad Med Sci, Guangdong Prov Peoples Hosp, Dept Pathol, Guangzhou, Peoples R China.
   [Ye, Yuedian] Southern Med Univ, Clin Med Sch 1, Nanfang Hosp, Guangzhou, Peoples R China.
   [Zhu, Guifang] Southern Med Univ, Zhujiang Hosp, Dept Pathol, Guangzhou, Peoples R China.
C3 Southern Medical University - China; Southern Medical University -
   China; Guangdong Academy of Medical Sciences & Guangdong General
   Hospital; Southern Medical University - China; Southern Medical
   University - China
RP Zhang, QL (corresponding author), Guangdong Prov Peoples Hosp, Dept Pathol, 106 Zhongshan Second Rd, Guangzhou 510000, Peoples R China.
EM zqllc8@126.com
RI Li, YanY/ABC-3649-2020; Jiang, Shanshan/O-8265-2019; ZHANG,
   XIAOGUANG/AEX-5387-2022
FU National Natural Science Foundation of China [81772918, 81972277];
   Guangdong Provincial Natural Science Foundation of China
   [2017A030313896]; Guangzhou Science & Technology Project [201804010319]
FX The present study was supported by the National Natural Science
   Foundation of China (grant no. 81772918 and no. 81972277), the Guangdong
   Provincial Natural Science Foundation of China (grant no.
   2017A030313896) and Guangzhou Science & Technology Project (grant no.
   201804010319).
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NR 38
TC 5
Z9 6
U1 0
U2 9
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2218-676X
EI 2219-6803
J9 TRANSL CANCER RES
JI Transl. Cancer Res.
PD JUN
PY 2021
VL 10
IS 6
BP 2812
EP 2821
DI 10.21037/tcr-20-2762
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UN4ZS
UT WOS:000694025800016
PM 35116591
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Styczen, H
   Nagelmeier, I
   Beissbarth, T
   Nietert, M
   Homayounfar, K
   Sprenger, T
   Boczek, U
   Stanek, K
   Kitz, J
   Wolff, HA
   Ghadimi, BM
   Middel, P
   Liersch, T
   Rüschoff, J
   Conradi, LC
AF Styczen, Hanna
   Nagelmeier, Iris
   Beissbarth, Tim
   Nietert, Manuel
   Homayounfar, Kia
   Sprenger, Thilo
   Boczek, Ute
   Stanek, Kathrin
   Kitz, Julia
   Wolff, Hendrik A.
   Ghadimi, B. Michael
   Middel, Peter
   Liersch, Torsten
   Rueschoff, Josef
   Conradi, Lena-Christin
TI HER-2 and HER-3 expression in liver metastases of patients with
   colorectal cancer
SO ONCOTARGET
LA English
DT Article
DE colorectal cancer; HER-2; HER-3; targeted therapy; liver metastases
ID RANDOMIZED CONTROLLED-TRIAL; HER2-POSITIVE BREAST-CANCER;
   POPULATION-BASED ANALYSIS; ADVANCED RECTAL-CANCER; ADVANCED SOLID
   TUMORS; ADJUVANT CHEMOTHERAPY; CORRESPONDING METASTASES; NEOADJUVANT
   CHEMOTHERAPY; COMBINATION CHEMOTHERAPY; PROGNOSTIC-SIGNIFICANCE
AB Objective: In this study, we evaluate the frequency of HER-2 and HER-3 expression in liver metastases from patients with colorectal cancer (CRLM). We analyzed the potential of HER-2 and HER-3 as therapeutic targets and evaluated their prognostic value.
   Patients and Methods: Overall 208 patients with CRLM were enrolled. HER-2 and HER-3 expression were determined in metastatic tissue of diagnostic punch biopsies (n = 29) or resection specimens (n = 179). The results of immunohistochemistry (IHC) scoring and In-situ-hybridization (ISH)-amplification were correlated with clinical parameters and for the 179 resected patients with cancer-specific (CSS) and overall survival (OS). The mean follow-up time was 56.7 months.
   Results: Positivity of HER-2 status (IHC score 2+/ISH+ and IHC 3+) was found in 8.2% of CRLM. High expression of HER-3 (IHC score 2+ and IHC 3+) was detected in 75.0% of liver metastases. CSS after liver surgery was determined and was independent from the HER-2 status (p = 0.963); however HER-3 was prognostic with a favorable course for patients showing an overexpression of HER-3 (p = 0.037).
   Conclusions: HER-2 overexpression occurs in only 8% of patients with CRLM but with 75% of cases HER-3 is frequently overexpressed in CRLM. Therefore, HER-2 and particularly HER-3 could serve as novel targets to be addressed within multimodal treatment approaches.
C1 [Styczen, Hanna; Homayounfar, Kia; Sprenger, Thilo; Boczek, Ute; Stanek, Kathrin; Ghadimi, B. Michael; Liersch, Torsten; Conradi, Lena-Christin] Univ Med Ctr, Dept Gen Visceral & Pediat Surg, Gottingen, Germany.
   [Nagelmeier, Iris; Middel, Peter; Rueschoff, Josef] Pathol Nordhessen, Targos Mol Pathol, Kassel, Germany.
   [Beissbarth, Tim; Nietert, Manuel] Univ Med Ctr, Dept Med Stat, Gottingen, Germany.
   [Kitz, Julia] Univ Med Ctr, Dept Pathol, Gottingen, Germany.
   [Wolff, Hendrik A.] Univ Med Ctr, Dept Radiotherapy & Radiooncol, Gottingen, Germany.
C3 University of Gottingen; UNIVERSITY GOTTINGEN HOSPITAL; Targos Molecular
   Pathology GmbH; University of Gottingen; UNIVERSITY GOTTINGEN HOSPITAL;
   University of Gottingen; UNIVERSITY GOTTINGEN HOSPITAL; University of
   Gottingen; UNIVERSITY GOTTINGEN HOSPITAL
RP Conradi, LC (corresponding author), Univ Med Ctr, Dept Gen Visceral & Pediat Surg, Gottingen, Germany.
EM lena.conradi@med.uni-goettingen.de
RI Beissbarth, Tim/B-3129-2013
OI Nietert, Manuel/0000-0001-5443-7943
FU Deutsche Forschungsgemeinschaft [KFO 179-2]; BMBF consortium MetastaSys
   [0316173A]
FX This work was supported by the Deutsche Forschungsgemeinschaft (KFO
   179-2) and the BMBF consortium MetastaSys (0316173A). Roche Diagnostics
   provided detection kits for the immunohistochemical staining.
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NR 55
TC 20
Z9 21
U1 0
U2 7
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD JUN 20
PY 2015
VL 6
IS 17
BP 15065
EP 15076
DI 10.18632/oncotarget.3527
PG 12
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA CO2TY
UT WOS:000359010700033
PM 25915155
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Syamprasad, NP
   Rajdev, B
   Jain, S
   Panda, SR
   Puppala, ER
   Chaudhari, P
   Vaidya, JR
   Kumar, GJ
   Naidu, VGM
AF Syamprasad, N. P.
   Rajdev, Bishal
   Jain, Siddhi
   Panda, Samir Ranjan
   Puppala, Eswara Rao
   Chaudhari, Pradip
   Vaidya, Jayathirtha Rao
   Kumar, Gangasani Jagadeesh
   Naidu, V. G. M.
TI Pivotal role of AKR1B1 in pathogenesis of colitis associated colorectal
   carcinogenesis
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Article
DE Inflammation; Colorectal carcinoma; Extrinsic apoptosis; NARI-29
ID CANCER CELLS; KAPPA-B; TRAIL; INFLAMMATION; APOPTOSIS; INHIBITION;
   DEFICIENCY; MECHANISM; THERAPY; MICE
AB Identifying the target linking inflammation and oxidative stress to aggravate the disease progression will help to prevent colitis associated carcinogenesis. Since AKR1B1 overexpression is observed in inflammatory diseases and various cancers, we have investigated the role of AKR1B1 in colitis-associated colon carcinogenesis with the aid of epalrestat and its potent analogue NARI-29 (investigational molecule) as pharmacological probes. A TNF-alpha inducible NF-kappa B reporter cell line (GloResponseTM NF-kappa B-RE-luc2P HEK293) and dextran sodium sulfate (DSS) and 1,2 dimethyl hydrazine (DMH))-induced mouse model was used to investigate our hypothesis in vitro and in vivo. Clinically, an increased expression of AKR1B1 was observed in patients with ulcerative colitis. Our in vitro and in vivo findings suggest that the AKR1B1 modulated inflammation and ROS generation for the progression of colitis to colon cancer. AKR1B1 overexpression was observed in DSS + DMH-treated mice colons. Moreover, we could observe histopathological changes like immune cell infiltration, aberrant crypt foci, and tumour formation in DC groups. Mechanistically, we have witnessed modulation of the IKK/I kappa B/NF-kappa B and Akt/FOXO-3a/DR axis, increased inflammatory cytokines, increased expression of proliferative markers, Ki-67 and PCNA, and accu-mulation of beta-catenin in the colon epithelium. However, pharmacological inhibition of AKR1B1 using NARI-29 or EPS has reversed the clinical, histopathological, and molecular alterations induced by DSS + DMH, confirming the obvious role of AKR1B1 in the promotion of colitis-associated carcinogenesis. In conclusion, our findings suggest that AKR1B1 targeted therapy could be a promising strategy for preventing CA-CRC and NARI-29 could be developed as a potent AKR1B1 inhibitor.
C1 [Syamprasad, N. P.; Rajdev, Bishal; Jain, Siddhi; Panda, Samir Ranjan; Puppala, Eswara Rao; Kumar, Gangasani Jagadeesh; Naidu, V. G. M.] Natl Inst Pharmaceut Educ & Res Guwahati, Dept Pharmacol & Toxicol, Changsari 781101, Assam, India.
   [Chaudhari, Pradip] Tata Mem Ctr ACTREC, Adv Ctr Treatment Res & Educ Canc, Plot 1&2,Sect 22, Navi Mumbai 410210, Maharashtra, India.
   [Vaidya, Jayathirtha Rao] CSIR Indian Inst Chem Technol, Fluoro Agro Chem Dept & AcSIR Ghaziabad, Uppal Rd Tarnaka, Hyderabad 500007, India.
C3 National Institute of Pharmaceutical Education & Research, S.A.S. Nagar
   (Mohali); Tata Memorial Centre (TMC); Advance Centre for Treatment,
   Research & Education in Cancer (ACTREC); Council of Scientific &
   Industrial Research (CSIR) - India; CSIR - Indian Institute of Chemical
   Technology (IICT)
RP Kumar, GJ; Naidu, VGM (corresponding author), Natl Inst Pharmaceut Educ & Res Guwahati, Dept Pharmacol & Toxicol, Changsari 781101, Assam, India.
EM jagadeesh@niperguwahati.in; vgmnaidu@niperguwahati.ac.in
RI Puppala, Eswara/ITV-7270-2023; Jain, Siddhi/LHA-7215-2024; Panda, Samir
   Ranjan/GPG-1457-2022
OI Panda, MS, PhD., Samir Ranjan/0000-0001-5327-7917; Gangasani, Jagadeesh
   Kumar/0000-0002-6386-4434; Puppala, Eswara Rao/0000-0002-1677-8904; NP,
   Dr Syamprasad/0000-0003-4232-0291
FU National Institute of Pharmaceutical Education and Research Guwahati;
   Department of Pharmaceuticals, Ministry of chemicals and fertilizers,
   Govt. of India
FX The authors would like to acknowledge Dr. USN Murty, Director, National
   Institute of Pharmaceutical Education and Research Guwahati, for his
   support throughout the research. The authors are also thankful to the
   Department of Pharmaceuticals, Ministry of chemicals and fertilizers,
   Govt. of India for providing funds to carry out the current research
   work.
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NR 36
TC 8
Z9 8
U1 1
U2 8
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD JUN
PY 2023
VL 119
AR 110145
DI 10.1016/j.intimp.2023.110145
EA APR 2023
PG 12
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA F6FY6
UT WOS:000983294100001
PM 37044030
DA 2025-01-04
ER

PT J
AU Wang, Y
   Wang, WL
   Dong, HM
   Wang, G
   Chen, WH
   Chen, J
   Chen, WW
AF Wang, Yan
   Wang, Wenling
   Dong, Hongming
   Wang, Gang
   Chen, Wanghua
   Chen, Juan
   Chen, Weiwei
TI Risk factors for fluoropyrimidine-induced cardiotoxicity in colorectal
   cancer: A retrospective cohort study and establishment of a prediction
   nomogram for 5-FU induced cardiotoxicity
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE fluoropyrimidine-related cardiotoxicity; risk factor; colorectal cancer;
   nomogram; prediction model
ID 5-FLUOROURACIL; CAPECITABINE; SCHEDULES; INJURY
AB BackgroundFluoropyrimidine is an important component of systemic chemotherapy for colorectal cancer (CRC). Fluoropyrimidine-induced cardiotoxicity (FIC) may result in delay and discontinuation of chemotherapy and, in severe cases, can even be life-threatening. To date, risk factors for FIC have not been well identified. This cohort study aimed to identify the predictors of FIC in CRC patients and develop a risk prediction nomogram model. MethodsBetween January 1, 2018 and December 31, 2020, colorectal cancer patients who received 5-fluoropyrimidine(5-Fu)/capecitabine-based chemotherapy in Affiliated Cancer Hospital of Guizhou Medical University were included. FIC was defined as an adverse cardiovascular event related to fluoropyrimidine that occurred during or within four weeks of completing chemotherapy. Risk factors were determined by LASSO algorithm and multivariate logistic regression analysis. Nomogram for predicting 5-Fu-induced cardiotoxicity was established and internally validated. The concordance index (C-index) and calibration curve were used to evaluate the nomogram's discrimination and accuracy. ResultsA total of 916 patients were included for analysis, and 200 [21.8%,95% confidence interval (CI):19.12%-24.47%] experienced FIC. LASSO algorithm and multivariate logistic regression analysis determined that chemotherapy <= 3 cycles (OR=4.694, 95%CI=3.184-6.92), age >= 60 (OR=1.678, 95%CI=1.143-2.464), BMI>22.97 (OR=1.77, 95%CI=1.202-2.606), and simultaneous use of bevacizumab (OR=2.922, 95%CI=1.835-4.653) were significant risk factors, and were included in the prediction model for 5-Fu induced cardiotoxicity. The C-index (95%CI) was 0.751 (0.706-0.795) by internal validation. For patients treated with capecitabine-based regimen, the incidence of FIC increased with the absolute value of neutrophils (OR=5.177, 95%CI=1.684-15.549) and eosinophils (OR=3.377,95% CI=1.237-9.22). ConclusionsOur study identified risk factors for FIC and established a prediction nomogram model based on chemotherapy cycle, age, BMI and use of target therapy for 5-FU induced Cardiotoxicity. The discriminative prediction model can be used for patient counselling and risk-stratification before undergoing chemotherapy in colorectal cancer.
C1 [Wang, Yan; Wang, Wenling; Dong, Hongming; Wang, Gang; Chen, Wanghua; Chen, Juan; Chen, Weiwei] Guizhou Med Univ, Affiliated Hosp, Dept Oncol, Guiyang, Peoples R China.
   [Wang, Yan; Chen, Weiwei] Guizhou Med Univ, Dept Clin Med, Guiyang, Peoples R China.
   [Wang, Yan; Wang, Wenling; Dong, Hongming; Wang, Gang; Chen, Wanghua; Chen, Juan; Chen, Weiwei] Guizhou Med Univ, Affiliated Canc Hosp, Dept Abdominal Oncol, Guiyang, Peoples R China.
C3 Guizhou Medical University; Guizhou Medical University; Guizhou Medical
   University
RP Chen, WW (corresponding author), Guizhou Med Univ, Affiliated Hosp, Dept Oncol, Guiyang, Peoples R China.; Chen, WW (corresponding author), Guizhou Med Univ, Dept Clin Med, Guiyang, Peoples R China.; Chen, WW (corresponding author), Guizhou Med Univ, Affiliated Canc Hosp, Dept Abdominal Oncol, Guiyang, Peoples R China.
EM weiweichen@gmc.edu.cn
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NR 36
TC 7
Z9 7
U1 4
U2 5
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD MAR 1
PY 2023
VL 13
AR 1017237
DI 10.3389/fonc.2023.1017237
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 9W2FZ
UT WOS:000948896700001
PM 36937428
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Lindner, T
   Loktev, A
   Altmann, A
   Giesel, F
   Kratochwil, C
   Debus, J
   Jaeger, D
   Mier, W
   Haberkorn, U
AF Lindner, Thomas
   Loktev, Anastasia
   Altmann, Annette
   Giesel, Frederik
   Kratochwil, Clemens
   Debus, Juergen
   Jaeger, Dirk
   Mier, Walter
   Haberkorn, Uwe
TI Development of Quinoline-Based Theranostic Ligands for the Targeting of
   Fibroblast Activation Protein
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE oncology; PET; radiopharmaceuticals; FAP; small molecules; theranostic
ID CARCINOMA-ASSOCIATED FIBROBLASTS; TUMOR-ASSOCIATED FIBROBLASTS; STROMAL
   FIBROBLASTS; MONOCLONAL-ANTIBODY; SERINE-PROTEASE; COLON-CANCER;
   PHASE-I; CELLS; ALPHA; IMMUNITY
AB Fibroblast activation protein (FAP) is overexpressed in cancer-associated fibroblasts and is involved in a variety of tumor-promoting activities such as matrix remodeling, angiogenesis, chemotherapy resistance, and immunosuppression. Because FAP shows low expression in most normal organs, it presents an interesting target for imaging and endoradiotherapy. In this investigation, FAP inhibitors (FAPIs) were modified and optimized for use as theranostic tracers. Methods: FAPIs based on a quinoline structure were synthesized and characterized with respect to binding, internalization, and efflux in cells expressing human and murine FAP as well as CD26. Preclinical pharmacokinetics were determined in tumor-bearing animals with biodistribution experiments and small-animal PET. Finally, a proof-of-concept approach toward imaging and therapy was chosen for 2 patients with metastasized breast cancer. Results: Of 15 synthesized FAPIs, FAPI-04 was identified as the most promising tracer for clinical application. Compared with the previously published ligand, FAPI-02, FAPI-04 showed excellent stability in human serum, higher affinity for FAP as opposed to CD26, and slower excretion in vitro. In vivo, a higher SUV was reached in tumor-bearing animals, leading to larger areas under the curve as calculated from biodistribution experiments. Finally, PET/CT scans with Ga-68-FAPI-04 in 2 patients with metastasized breast cancer revealed high tracer uptake in metastases and a reduction in pain symptoms after therapy with a considerably low dose of Y-90-FAPI-04. Conclusion: FAPI-04 represents a promising tracer for both diagnostic imaging and, possibly, targeted therapy of malignant tumors with a high content of activated fibroblasts, such as breast cancer.
C1 [Lindner, Thomas; Loktev, Anastasia; Altmann, Annette; Giesel, Frederik; Kratochwil, Clemens; Mier, Walter; Haberkorn, Uwe] Univ Hosp Heidelberg, Dept Nucl Med, Neuenheimer Feld 400, D-69120 Heidelberg, Germany.
   [Loktev, Anastasia; Altmann, Annette; Haberkorn, Uwe] German Canc Res Ctr, Clin Cooperat Unit Nucl Med, Heidelberg, Germany.
   [Loktev, Anastasia] Heidelberg Univ, Fac Biosci, Heidelberg, Germany.
   [Debus, Juergen] Univ Hosp Heidelberg, Dept Radiat Oncol, Heidelberg, Germany.
   [Debus, Juergen] German Canc Res Ctr, Clin Cooperat Unit Radiat Oncol, Heidelberg, Germany.
   [Jaeger, Dirk] Natl Ctr Tumor Dis NCT, Dept Med Oncol, Heidelberg, Germany.
C3 Ruprecht Karls University Heidelberg; Helmholtz Association; German
   Cancer Research Center (DKFZ); Ruprecht Karls University Heidelberg;
   Ruprecht Karls University Heidelberg; Helmholtz Association; German
   Cancer Research Center (DKFZ); Helmholtz Association; German Cancer
   Research Center (DKFZ); Ruprecht Karls University Heidelberg
RP Haberkorn, U (corresponding author), Univ Hosp Heidelberg, Dept Nucl Med, Neuenheimer Feld 400, D-69120 Heidelberg, Germany.
EM uwe.haberkorn@med.uni-heidelberg.de
FU Federal Ministry of Education and Research [13N 13341]
FX We gratefully acknowledge Stefan Bauer (National Center for Tumor
   Diseases, Heidelberg) for supplying the FAP and CD26-transfected cell
   lines. We thank Christian Kleist, Susanne Kramer, Stephanie Biedenstein,
   Kirsten Kunze, Irina Kupin, Vanessa Kohl, Marlene Tesch, Iris Morr,
   Sabine Weiss, Christiane Brenner, Karin Leotta, and Ursula Schierbaum
   for excellent technical assistance. This work was funded in part by
   grant 13N 13341 from the Federal Ministry of Education and Research.
CR Brennen WN, 2012, JNCI-J NATL CANCER I, V104, P1320, DOI 10.1093/jnci/djs336
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NR 30
TC 579
Z9 605
U1 11
U2 164
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD SEP 1
PY 2018
VL 59
IS 9
BP 1415
EP 1422
DI 10.2967/jnumed.118.210443
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA GS6DG
UT WOS:000443772500025
PM 29626119
OA Bronze
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Islam, F
   Gopalan, V
   Smith, RA
   Lam, AKY
AF Islam, Farhadul
   Gopalan, Vinod
   Smith, Robert A.
   Lam, Alfred K. -Y.
TI Translational potential of cancer stem cells: A review of the detection
   of cancer stem cells and their roles in cancer recurrence and cancer
   treatment
SO EXPERIMENTAL CELL RESEARCH
LA English
DT Review
DE Cancer stem cell; Treatment; Metastases; Resistant to therapy; Targeted
   therapy
ID CIRCULATING TUMOR-CELLS; EPITHELIAL-MESENCHYMAL TRANSITION; SIDE
   POPULATION CELLS; RNA-POSITIVE CELLS; COLON-CANCER; INITIATING CELLS;
   BONE-MARROW; MOLECULAR-DETECTION; TUMORIGENIC CELLS; ADHESION MOLECULE
AB Cancer stem cells (CSCs) are a subpopulation of cancer cells with many clinical implications in most cancer types. One important clinical implication of CSCs is their role in cancer metastases, as reflected by their ability to initiate and drive micro and macro-metastases. The other important contributing factor for CSCs in cancer management is their function in causing treatment resistance and recurrence in cancer via their activation of different signalling pathways such as Notch, Wnt/beta-catenin, TGF-beta, Hedgehog, PI3K/Akt/mTOR and JAK/STAT pathways. Thus, many different therapeutic approaches are being tested for prevention and treatment of cancer recurrence. These may include treatment strategies targeting altered genetic signalling pathways by blocking specific cell surface molecules, altering the cancer microenvironments that nurture cancer stem cells, inducing differentiation of CSCs, immunotherapy based on CSCs associated antigens, exploiting metabolites to kill CSCs, and designing small interfering RNA/DNA molecules that especially target CSCs. Because of the huge potential of these approaches to improve cancer management it is important to identify and isolate cancer stem cells for precise study and application of prior the research on their role in cancer. Commonly used methodologies for detection and isolation of CSCs include functional, image-based, molecular, cytological sorting and filtration approaches, the use of different surface markers and xenotransplantation. Overall, given their significance in cancer biology, refining the isolation and targeting of CSCs will play an important role in future management of cancer. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Islam, Farhadul; Gopalan, Vinod; Smith, Robert A.; Lam, Alfred K. -Y.] Griffith Univ, Sch Med, Canc Mol Pathol, Gold Coast, Qld, Australia.
   [Islam, Farhadul; Gopalan, Vinod; Smith, Robert A.; Lam, Alfred K. -Y.] Griffith Univ, Menzies Hlth Inst Queensland, Gold Coast, Qld, Australia.
   [Smith, Robert A.] Queensland Univ Technol, Fac Hlth, Inst Hlth & Biomed Innovat, Genom Res Ctr, Brisbane, Qld 4001, Australia.
   [Lam, Alfred K. -Y.] Gold Coast Univ Hosp, Dept Pathol, Gold Coast, Qld, Australia.
C3 Griffith University; Griffith University - Gold Coast Campus; Griffith
   University; Griffith University - Gold Coast Campus; Menzies Health
   Institute Queensland; Queensland University of Technology (QUT); Gold
   Coast University Hospital
RP Lam, AKY (corresponding author), Griffith Med Sch, Gold Coast Campus, Gold Coast, Qld 4222, Australia.
EM a.lam@griffith.edu.au
RI Islam, Farhadul/R-5643-2017; Gopalan, Vinod/C-4269-2016; Lam,
   Alfred/C-1652-2008
OI Islam, Farhadul/0000-0001-5262-4702; Gopalan, Vinod/0000-0003-0366-9482;
   Lam, Alfred/0000-0003-2771-564X
FU Griffith University; National Natural Science Foundation of China
   [81200796]
FX The authors would like to thank Griffith University (Visiting Fellowship
   and Higher Degree Research scholarship) and National Natural Science
   Foundation of China (Grant no. 81200796) for funding support for this
   manuscript.
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NR 207
TC 96
Z9 107
U1 0
U2 62
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4827
EI 1090-2422
J9 EXP CELL RES
JI Exp. Cell Res.
PD JUL 1
PY 2015
VL 335
IS 1
BP 135
EP 147
DI 10.1016/j.yexcr.2015.04.018
PG 13
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA CK9MG
UT WOS:000356563600014
PM 25967525
DA 2025-01-04
ER

PT J
AU Liu, TT
   You, HL
   Weng, SW
   Wei, YC
   Eng, HL
   Huang, WT
AF Liu, Ting-Ting
   You, Huey-Ling
   Weng, Shao-Wen
   Wei, Yu-Ching
   Eng, Hock-Liew
   Huang, Wan-Ting
TI Recurrent Amplification at 13q34 Targets at <i>CUL4A</i>, <i>IRS2</i>,
   and <i>TFDP1</i> As an Independent Adverse Prognosticator in
   Intrahepatic Cholangiocarcinoma
SO PLOS ONE
LA English
DT Article
ID HUMAN BREAST-CANCER; POLYMORPHISM ARRAY ANALYSIS; GENE AMPLIFICATION;
   COLORECTAL-CANCER; HEPATOCELLULAR CARCINOMAS; LUNG-CANCER;
   OVEREXPRESSION; METASTASIS; EXPRESSION; PATTERNS
AB Amplification of genes at 13q34 has been reported to be associated with tumor proliferation and progression in diverse types of cancers. However, its role in intrahepatic cholangiocarcinoma (iCCA) has yet to be explored. We examined two iCCA cell lines and 86 cases of intrahepatic cholangiocarcinoma to analyze copy number of three target genes, including cullin 4A (CUL4A), insulin receptor substrate 2 (IRS2), and transcription factor Dp-1 (TFDP1) at 13q34 by quantitative real-time polymerase chain reaction. The cell lines and all tumor samples were used to test the relationship between copy number (CN) alterations and protein expression by western blotting and immunohistochemical assays, respectively. IRS2 was introduced, and each target gene was silenced in cell lines. The mobility potential of cells was compared in the basal condition and after manipulation using cell migration and invasion assays. CN alterations correlated with protein expression levels. The SNU1079 cell line containing deletions of the target genes demonstrated decreased protein expression levels and significantly lower numbers of migratory and invasive cells, as opposed to the RBE cell line, which does not contain CN alterations. Overexpression of IRS2 by introducing IRS2 in SUN1079 cells increased the mobility potential. In contrast, silencing each target gene showed a trend or statistical significance toward inhibition of migratory and invasive capacities in RBE cells. In tumor samples, the amplification of each of these genes was associated with poor disease-free survival. Twelve cases (13.9%) demonstrated copy numbers > 4 for all three genes tested (CUL4A, IRS2, and TFDP1), and showed a significant difference in disease-free survival by both univariate and multivariate survival analyses (hazard ratio, 2.69; 95% confidence interval, 1.23 to 5.88; P = 0.013). Our data demonstrate that amplification of genes at 13q34 plays an oncogenic role in iCCA featuring adverse disease-free survival, which may provide new directions for targeted therapy.
C1 [Liu, Ting-Ting; Eng, Hock-Liew; Huang, Wan-Ting] Kaohsiung Chang Gung Mem Hosp, Dept Pathol, Kaohsiung, Taiwan.
   [Liu, Ting-Ting; You, Huey-Ling; Weng, Shao-Wen; Eng, Hock-Liew; Huang, Wan-Ting] Chang Gung Univ, Coll Med, Kaohsiung, Taiwan.
   [Liu, Ting-Ting; You, Huey-Ling; Huang, Wan-Ting] Kaohsiung Chang Gung Mem Hosp, Dept Lab Med, Kaohsiung, Taiwan.
   [Weng, Shao-Wen] Kaohsiung Chang Gung Mem Hosp, Dept Internal Med, Kaohsiung, Taiwan.
   [You, Huey-Ling] Fooyin Univ, Dept Med Lab Sci & Biotechnol, Kaohsiung, Taiwan.
   [Wei, Yu-Ching] Kaohsiung Med Univ Hosp, Kaohsiung Municipal Ta Tung Hosp, Dept Pathol, Kaohsiung, Taiwan.
C3 Chang Gung Memorial Hospital; Chang Gung University; Chang Gung Memorial
   Hospital; Chang Gung Memorial Hospital; Fooyin University; Kaohsiung
   Medical University; Kaohsiung Municipal Ta-Tung Hospital; Kaohsiung
   Medical University Hospital
RP Huang, WT (corresponding author), Kaohsiung Chang Gung Mem Hosp, Dept Pathol, Kaohsiung, Taiwan.
EM huangwanting5@gmail.com
RI Huang, Wan-Ting/E-3497-2010; Hung, Chun-Hsiung/D-5521-2009; Weng, Shape
   wen/GYU-9746-2022
FU Chang Gung Memorial Hospital [CMRPG8A1162, CMRPG8D1321]; National
   Science Council, Taiwan [NSC 104-2320-B-182A-004]
FX This study was supported in part by grants from Chang Gung Memorial
   Hospital (CMRPG8A1162, CMRPG8D1321) and National Science Council, Taiwan
   (NSC 104-2320-B-182A-004). The funders had no role in study design, data
   collection and analysis, decision to publish, or preparation of the
   manuscript.
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NR 32
TC 5
Z9 6
U1 0
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD DEC 18
PY 2015
VL 10
IS 12
AR e0145388
DI 10.1371/journal.pone.0145388
PG 14
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA CY9KM
UT WOS:000366725800072
PM 26684807
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Coliat, P
   Ramolu, L
   Jégu, J
   Gaiddon, C
   Jung, AC
   Pencreach, E
AF Coliat, Pierre
   Ramolu, Ludivine
   Jegu, Jeremie
   Gaiddon, Christian
   Jung, Alain C.
   Pencreach, Erwan
TI Constitutive or Induced HIF-2 Addiction is Involved in Resistance to
   Anti-EGFR Treatment and Radiation Therapy in HNSCC
SO CANCERS
LA English
DT Article
DE head and neck squamous cell carcinoma; anti-EGFR targeted therapy;
   resistance; oncogenic addiction; HIF-2 alpha
ID SQUAMOUS-CELL CARCINOMA; EPIDERMAL-GROWTH-FACTOR; NECK-CANCER; FACTOR
   RECEPTOR; UP-REGULATION; CARBON ION; HUMAN HEAD; HYPOXIA; RADIOTHERAPY;
   EXPRESSION
AB Background: management of head and neck squamous cell carcinomas (HNSCC) include anti-Epidermal Growth Factor Receptor (EGFR) antibodies and radiotherapy, but resistance emerges in most patients. RAS mutations lead to primary resistance to EGFR blockade in metastatic colorectal cancer but are infrequent in HNSCC, suggesting that other mechanisms are implicated. Since hypoxia and Hypoxia Inducible Factor-1 (HIF-1) have been associated with treatment failure and tumor progression, we hypothesized that EGFR/mammalian Target of Rapamycin (mTOR)/HIF-1 axis inhibition could radiosensitize HNSCC. Methods: We treated the radiosensitive Cal27 used as control, and radioresistant SQ20B and UD-SCC1 cells, in vivo and in vitro, with rapamycin and cetuximab before irradiation and evaluated tumor progression and clonogenic survival. Results: Rapamycin and cetuximab inhibited the mTOR/HIF-1 alpha axis, and sensitized the SQ20B cell line to EGFR-inhibition. However, concomitant delivery of radiation to SQ20B xenografts increased tumor relapse frequency, despite effective HIF-1 inhibition. Treatment failure was associated with the induction of HIF-2 alpha expression by cetuximab and radiotherapy. Strikingly, SQ20B and UD-SCC1 cells clonogenic survival dropped <30% after HIF-2 alpha silencing, suggesting a HIF-2-dependent mechanism of oncogenic addiction. Conclusions: altogether, our data suggest that resistance to EGFR inhibition combined with radiotherapy in HNSCC may depend on tumor HIF-2 expression and underline the urgent need to develop novel HIF-2 targeted treatments.
C1 [Coliat, Pierre; Ramolu, Ludivine; Jung, Alain C.] Ctr Lutte Canc Paul Strauss, F-67200 Strasbourg, France.
   [Coliat, Pierre] Ctr Lutte Canc Paul Strauss, Serv Pharm, F-67200 Strasbourg, France.
   [Coliat, Pierre; Ramolu, Ludivine; Jegu, Jeremie; Gaiddon, Christian; Jung, Alain C.; Pencreach, Erwan] Univ Strasbourg, INSERM, UMR S1113, F-67200 Strasbourg, France.
   [Jegu, Jeremie] Univ Strasbourg, Lab Epidemiol & Sante Publ, F-67200 Strasbourg, France.
   [Jegu, Jeremie] Hop Univ Strasbourg, Serv Sante Publ, F-67200 Strasbourg, France.
   [Pencreach, Erwan] Hop Univ Strasbourg, Lab Biochim & Biol Mol, F-67200 Strasbourg, France.
C3 UNICANCER; Centre Paul Strauss; UNICANCER; Centre Paul Strauss; Institut
   National de la Sante et de la Recherche Medicale (Inserm); Universite de
   Lorraine; Universites de Strasbourg Etablissements Associes; Universite
   de Strasbourg; Universites de Strasbourg Etablissements Associes;
   Universite de Strasbourg; Universites de Strasbourg Etablissements
   Associes; Universite de Strasbourg; CHU Strasbourg; Universites de
   Strasbourg Etablissements Associes; Universite de Strasbourg; CHU
   Strasbourg
RP Jung, AC (corresponding author), Ctr Lutte Canc Paul Strauss, F-67200 Strasbourg, France.; Jung, AC; Pencreach, E (corresponding author), Univ Strasbourg, INSERM, UMR S1113, F-67200 Strasbourg, France.; Pencreach, E (corresponding author), Hop Univ Strasbourg, Lab Biochim & Biol Mol, F-67200 Strasbourg, France.
EM pcoliat@strasbourg.unicancer.fr; lramolu@unistra.fr;
   jeremie.jegu@unistra.fr; gaiddon@unistra.fr;
   ajung@strasbourg.unicancer.fr; erwan.pencreach@chru-strasbourg.fr
RI Gaiddon, Christian/F-7321-2012; Jung, Alain/X-5384-2019; coliat,
   pierre/HMW-1218-2023
OI COLIAT, Pierre/0000-0003-3727-7508; Jegu, Jeremie/0000-0001-7671-5465;
   Jung, Alain/0000-0002-4049-4151
FU French Academie de Pharmacie/SFPO; Conference de Coordination
   Interregionale du Grand Est de la Ligue Contre le Cancer; Merck/Serono
   (Bourse oncologie)
FX This work was financially supported by the French Academie de
   Pharmacie/SFPO, the Conference de Coordination Interregionale du Grand
   Est de la Ligue Contre le Cancer, and Merck/Serono (Bourse oncologie).
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NR 46
TC 16
Z9 18
U1 0
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD OCT
PY 2019
VL 11
IS 10
AR 1607
DI 10.3390/cancers11101607
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JQ3CF
UT WOS:000498826000204
PM 31640284
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Chen, ZJ
   Wei, W
   Jiang, GM
   Liu, H
   Wei, WD
   Yang, XL
   Wu, YM
   Liu, HL
   Wong, CKC
   Du, J
   Wang, HS
AF Chen, Zhuo-Jia
   Wei, Wei
   Jiang, Guan-Min
   Liu, Hao
   Wei, Wei-Dong
   Yang, Xiangling
   Wu, Ying-Min
   Liu, Huanliang
   Wong, Chris K. C.
   Du, Jun
   Wang, Hong-Sheng
TI Activation of GPER suppresses epithelial mesenchymal transition of
   triple negative breast cancer cells via NF-κB signals
SO MOLECULAR ONCOLOGY
LA English
DT Article
DE GPER; G-1; EMT; TNBC; NF-kappa B
ID COUPLED RECEPTOR 30; GPR30 INHIBITS PROLIFERATION; ESTROGEN-RELATED
   RECEPTOR; OVARIAN-CANCER; UP-REGULATION; COLORECTAL-CANCER;
   DOWN-REGULATION; E-CADHERIN; MIGRATION; GROWTH
AB The targeted therapy for triple-negative breast cancer (TNBC) is a great challenge due to our poor understanding on its molecular etiology. In the present study, our clinical data showed that the expression of G-protein coupled estrogen receptor (GPER) is negatively associated with lymph node metastasis, high-grade tumor and fibronectin (FN) expression while positively associated with the favorable outcome in 135 TNBC patients. In our experimental studies, both the in vitro migration and invasion of TNBC cells were inhibited by GPER specific agonist G-1, through the suppression of the epithelial mesenchymal transition (EMT). The G-1 treatment also reduced the phosphorylation, nuclear localization, and transcriptional activities of NF-kappa B. While over expression of NF-kappa B attenuated the action of G-1 in suppressing EMT. Our data further illustrated that the phosphorylation of GSK-3 beta by PI3K/Akt and ERK1/2 mediated, at least partially, the inhibitory effect of G-1 on NF-kappa B activities. It was further confirmed in a study of MDA-MB-231 tumor xenografts in nude mice. The data showed that G-1 inhibited the in vivo growth and invasive potential of TNBC via suppression of EMT. Our present study demonstrated that an activation of GPER pathway elicits tumor suppressive actions on TNBC, and supports the use of G-1 therapeutics for TNBC metastasis. (C) 2016 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
C1 [Chen, Zhuo-Jia; Wei, Wei-Dong] Sun Yat Sen Univ, Ctr Canc, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Guangzhou 510060, Guangdong, Peoples R China.
   [Wei, Wei; Wu, Ying-Min; Du, Jun; Wang, Hong-Sheng] Sun Yat Sen Univ, Sch Pharmaceut Sci, Dept Microbial & Biochem Pharm, Guangzhou 510006, Guangdong, Peoples R China.
   [Jiang, Guan-Min] Cent S Univ, Hunan Canc Hosp, Changsha 410013, Hunan, Peoples R China.
   [Jiang, Guan-Min] Cent S Univ, Affiliated Canc Hosp, Xiangya Sch Med, Changsha 410013, Hunan, Peoples R China.
   [Liu, Hao] Guangzhou Med Univ, Canc Res Inst, Guangzhou 510095, Guangdong, Peoples R China.
   [Liu, Hao] Guangzhou Med Univ, Canc Hosp, Guangzhou 510095, Guangdong, Peoples R China.
   [Yang, Xiangling; Liu, Huanliang] Sun Yat Sen Univ, Guangdong Inst Gastroenterol, Dept Clin Lab, Guangdong Prov Key Lab Colorectal & Pelv Floor Di, Guangzhou 510655, Guangdong, Peoples R China.
   [Yang, Xiangling; Liu, Huanliang] Sun Yat Sen Univ, Affiliated Hosp 6, Guangzhou 510655, Guangdong, Peoples R China.
   [Yang, Xiangling; Liu, Huanliang] Sun Yat Sen Univ, Inst Human Virol, Guangzhou 510080, Guangdong, Peoples R China.
   [Yang, Xiangling; Liu, Huanliang] Sun Yat Sen Univ, Key Lab Trop Dis Control, Minist Educ, Guangzhou 510080, Guangdong, Peoples R China.
   [Wong, Chris K. C.] Hong Kong Baptist Univ, Dept Biol, Kowloon Tong, Hong Kong, Peoples R China.
C3 Sun Yat Sen University; State Key Lab Oncology South China; Sun Yat Sen
   University; Central South University; Central South University;
   Guangzhou Medical University; Guangzhou Medical University; Sun Yat Sen
   University; Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen
   University; Hong Kong Baptist University
RP Wang, HS (corresponding author), Sun Yat Sen Univ, Sch Pharmaceut Sci, Dept Microbial & Biochem Pharm, Guangzhou 510006, Guangdong, Peoples R China.
EM whongsh@mail.sysu.edu.cn
RI Wang, Hongsheng/N-1940-2019; Wu, Yingmin/LPR-1553-2024; Wong,
   Kristy/C-8748-2015; Li, Huang/IZE-8023-2023
OI Liu, Huanliang/0000-0002-1006-6666; Wong, Chris/0000-0001-5449-5836
FU National Natural Science Foundation of China [81472470, 81302317];
   Guangdong Natural Science Funds for Distinguished Young Scholar
   [2014A030306025]; Pearl River S&T Nova Program of Guangzhou
   [201506010039]; Fundamental Research Funds for the Central Universities
   (Sun Yatsen University) [12ykpy09]; Science and Technology Planning
   Project of Guangdong Province, China [2012B031500005]; Opening Project
   Program of State Key Laboratory of Oncology in South China [HN2014-09]
FX This research was supported by the National Natural Science Foundation
   of China (Grant No. 81472470 and No. 81302317), the Guangdong Natural
   Science Funds for Distinguished Young Scholar (No. 2014A030306025), the
   Pearl River S&T Nova Program of Guangzhou (No. 201506010039), the
   Fundamental Research Funds for the Central Universities (Sun Yatsen
   University) (No. 12ykpy09), the Science and Technology Planning Project
   of Guangdong Province, China (No. 2012B031500005), and the Opening
   Project Program of State Key Laboratory of Oncology in South China (No.
   HN2014-09).
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NR 57
TC 60
Z9 63
U1 0
U2 32
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1574-7891
EI 1878-0261
J9 MOL ONCOL
JI Mol. Oncol.
PD JUN
PY 2016
VL 10
IS 6
BP 775
EP 788
DI 10.1016/j.molonc.2016.01.002
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DQ7FJ
UT WOS:000379372000001
PM 26842883
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Oh, KY
   Cho, SD
   Yoon, HJ
   Lee, JI
   Hong, SD
AF Oh, Kyu-Young
   Cho, Sung-Dae
   Yoon, Hye-Jung
   Lee, Jae-Il
   Hong, Seong-Doo
TI Discrepancy between immunohistochemistry and sequencing for BRAF V600E
   in odontogenic tumours: Comparative analysis of two VE1 antibodies
SO JOURNAL OF ORAL PATHOLOGY & MEDICINE
LA English
DT Article
DE BRAF V600E; immunohistochemistry; odontogenic tumour; sequencing; VE1
ID COLORECTAL-CARCINOMA; MUTATION; BRAFV600E; MELANOMA
AB Background Although immunohistochemistry (IHC) along with molecular tests has been investigated in ameloblastoma for BRAF V600E detection, VE1 IHC has not been studied in odontogenic carcinomas (OCs) and benign mixed epithelial and mesenchymal odontogenic tumours (BMOTs). Here, we performed BRAF V600E mutation analysis, examined the expression pattern of VE1 IHC, and comparatively evaluated the performance of two VE1 antibodies in ameloblastomas, OCs and BMOTs. Methods BRAF V600E detection was performed using Sanger sequencing in a total of 47 odontogenic tumours: 28 ameloblastomas, 6 OCs and 13 BMOTs. VE1 IHC was conducted using two different antibodies (IHC-A and IHC-V), and their performance was analysed by calculating the sensitivity and specificity compared with sequencing. Results BRAF V600E mutations were identified in 24/28 (85.7%) ameloblastomas, 2/5 (40.0%) ameloblastic carcinomas (ACs), 3/7 (42.9%) ameloblastic fibromas and 1/2 (50.0%) ameloblastic fibro-odontomas. In the presence of the mutation, VE1 showed diffuse cytoplasmic staining in ameloblastomas and ACs, whereas all BMOTs were negative for VE1. IHC-A and IHC-V yielded a sensitivity of 76.7% and 60.0%, respectively, although both antibodies showed 100% specificity. Conclusion OCs and BMOTs have BRAF V600E mutations in common at lower frequencies than ameloblastoma. Diffuse VE1 cytoplasmic staining in AC suggests the utility of MAPK-targeted therapy as selectively applied in ameloblastoma, and consistent VE1 false-negative expression in BMOTs requires further investigation. Considering the high specificity but low sensitivity of VE1 IHC, molecular tests should be performed to determine the presence of BRAF V600E mutations in odontogenic tumours.
C1 [Oh, Kyu-Young; Cho, Sung-Dae; Yoon, Hye-Jung; Lee, Jae-Il; Hong, Seong-Doo] Seoul Natl Univ, Sch Dent, Dept Oral Pathol, 101 Daehak Ro, Seoul, South Korea.
   [Oh, Kyu-Young; Cho, Sung-Dae; Yoon, Hye-Jung; Lee, Jae-Il; Hong, Seong-Doo] Seoul Natl Univ, Dent Res Inst, 101 Daehak Ro, Seoul, South Korea.
C3 Seoul National University (SNU); Seoul National University (SNU)
RP Hong, SD (corresponding author), Seoul Natl Univ, Sch Dent, Dept Oral Pathol, 101 Daehak Ro, Seoul, South Korea.; Hong, SD (corresponding author), Seoul Natl Univ, Dent Res Inst, 101 Daehak Ro, Seoul, South Korea.
EM hongsd@snu.ac.kr
OI Cho, Sung-Dae/0000-0001-8670-9579; Oh, Kyu-Young/0000-0001-5328-0905
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NR 27
TC 17
Z9 17
U1 0
U2 8
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0904-2512
EI 1600-0714
J9 J ORAL PATHOL MED
JI J. Oral Pathol. Med.
PD JAN
PY 2021
VL 50
IS 1
BP 85
EP 91
DI 10.1111/jop.13108
EA OCT 2020
PG 7
WC Dentistry, Oral Surgery & Medicine; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dentistry, Oral Surgery & Medicine; Pathology
GA PZ1YL
UT WOS:000576238400001
PM 32939809
DA 2025-01-04
ER

PT J
AU Jiang, ZH
   Shen, XF
   Wei, YH
   Chen, YJ
   Chai, HB
   Xia, LY
   Leng, WD
AF Jiang, Zhong-Hui
   Shen, Xianfeng
   Wei, Yanhong
   Chen, Yongji
   Chai, Hongbo
   Xia, Lingyun
   Leng, Weidong
TI A Pan-Cancer Analysis Reveals the Prognostic and Immunotherapeutic Value
   of Stanniocalcin-2 (STC2)
SO FRONTIERS IN GENETICS
LA English
DT Review
DE stanniocalcin-2; head and neck squamous cell carcinoma; prognostic
   biomarkers; target therapy; pan-cancer
ID PROMOTES CELL-PROLIFERATION; MICROSATELLITE INSTABILITY;
   COLORECTAL-CANCER; GENE SIGNATURE; EXPRESSION; RESISTANCE; INVASION;
   TARGET
AB Background: Stanniocalcin-2 (STC2) is a secreted glycoprotein which plays an important role in regulating the homeostasis of calcium, glucose homeostasis, and phosphorus metastasis. Accumulating evidence suggests that STC2 is implicated in cancer mechanisms. However, the effects of STC2 on cancer development and progression across pan-cancer are not yet completely known.Methods: Data were downloaded from The Cancer Genome Atlas database to obtain differentially expressed genes significantly associated with prognosis (key genes). A gene was selected for subsequent correlation studies by integrating the significance of prognosis and the time-dependent ROC curve. Gene expression of different tumor types was analyzed based on the UCSC XENA website. Furthermore, our study investigated the correlation of STC2 expression between prognosis, immune cell infiltration, immune checkpoint genes (ICGs), mismatch repair genes (MMRs), tumor mutation burden (TMB), microsatellite instability (MSI), and drug sensitivity in various malignant tumors. Gene set enrichment analysis (GSEA) was conducted for correlated genes of STC2 to explore potential mechanisms.Results: A total of 3,429 differentially expressed genes and 397 prognosis-related genes were identified from the TCGA database. Twenty-six key genes were found by crossing the former and the latter, and the highest risk gene, STC2, was selected for subsequent correlation studies. STC2 had good diagnostic performance for HNSCC, and was closely related to the survival status and clinicopathological stage of HNSCC patients. In pan-cancer analysis, STC2 was upregulated in 20 cancers and downregulated in seven cancers. STC2 overexpression was overall negatively correlated with overall survival, disease-free survival, disease-specific survival, and progress-free survival. STC2 was profoundly correlated with the tumor immune microenvironment, including immune cell infiltration, ICGs, MMRs, TMB, and MSI. Moreover, STC2 was significantly negatively correlated with the sensitivity or resistance of multiple drugs.Conclusion: STC2 was a potential prognostic biomarker for pan-cancer and a new immunotherapy target.
C1 [Jiang, Zhong-Hui; Shen, Xianfeng; Wei, Yanhong; Chen, Yongji; Chai, Hongbo; Xia, Lingyun; Leng, Weidong] Hubei Univ Med, Taihe Hosp, Dept Stomatol, Shiyan, Peoples R China.
C3 Hubei University of Medicine
RP Xia, LY; Leng, WD (corresponding author), Hubei Univ Med, Taihe Hosp, Dept Stomatol, Shiyan, Peoples R China.
EM xialingyun200810@163.com; lwd35@163.com
RI shen, xianfeng/ABA-8025-2020; Chen, Liú/KWU-4813-2024
OI Jiang, Zhong-Hui/0000-0001-9463-4845
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NR 49
TC 13
Z9 14
U1 1
U2 9
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1664-8021
J9 FRONT GENET
JI Front. Genet.
PD JUL 22
PY 2022
VL 13
AR 927046
DI 10.3389/fgene.2022.927046
PG 16
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA 3O8UG
UT WOS:000837109300001
PM 35937984
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Pan, HJ
   Chang, HT
   Huang, WC
   Lin, HC
AF Pan, H-J
   Chang, H-T
   Huang, W-C
   Lin, H-C
TI End of life care for the most common women cancers in Taiwan
SO PUBLIC HEALTH
LA English
DT Article
DE Aggressive treatment; End-of-life care; Hospice; Terminal cancer
ID EARLY PALLIATIVE CARE; HOSPICE UTILIZATION; AGGRESSIVENESS; QUALITY;
   ASSOCIATION; INDICATORS; REFERRALS; SERVICES
AB Objectives: Women with terminal cancer are assumed to choose hospice care over aggressive treatment at the end of life. With new chemotherapy and target therapy options, it becomes more difficult to decide between hospice care and aggressive management. It is also crucial to consider the cost increases leading to severe financial burdens on healthcare systems. To better understand treatment options at the individual level, this study set out to describe trends in end-of-life care for the four leading cancers in women in Taiwan.
   Study design: This was a population-based retrospective cohort study.
   Methods: The data source was obtained between January 1, 2000, and December 31, 2013, from Taiwan's National Health Insurance Research Database. We identified 98,575 women with a diagnosis of breast (18,596), colorectal (23,734), liver and biliary (28,795) or lung (27,450) cancer who had died during the study period. Hospital data for services provided in the last 6 months of life, including hospice services and aggressive managements (chemotherapy, frequent hospitalisation, emergency room [ER] visits, intensive care unit [ICU] admission and endotracheal intubation), were collected.
   Results: Hospice utilisation increased over the study period, with 25.85%, 25.34%, 21.23% and 26.55% of female patients with breast, colorectal, liver and biliary, and lung cancer receiving hospice care, respectively. However, the number of women undergoing aggressive treatments in the last 6 months of life remained high, with the breast cancer group having the highest chemotherapy rate, the colorectal cancer group having frequent hospitalisation and the liver and biliary cancer group having frequent ER visits and ICU admissions.
   Conclusions: Increasing hospice utilisation among women with the four most common cancers in Taiwan indicates that hospice services have gradually become well accepted over the past 13 years; however, the real focus is on the ineffective treatment preceding hospice care, and late referral was also a notable problem. (c) 2020 The Royal Society for Public Health. Published by Elsevier Ltd. All rights reserved.
C1 [Pan, H-J] Kaohsiung Vet Gen Hosp, Dept Family Med, 386 Dazhong 1st Rd, Kaohsiung 81362, Taiwan.
   [Pan, H-J] Fooyin Univ, Kaohsiung, Taiwan.
   [Chang, H-T] Kaohsiung United Municipal Hosp, 976,Zhonghua 1st Rd, Kaohsiung 804, Taiwan.
   [Huang, W-C] Kaohsiung Vet Gen Hosp, Crit Care Ctr, Kaohsiung, Taiwan.
   [Huang, W-C] Kaohsiung Vet Gen Hosp, Cardiovasc Med Ctr, Kaohsiung, Taiwan.
   [Lin, H-C] Kaohsiung Vet Gen Hosp, Res Ctr Med Informat, Kaohsiung, Taiwan.
   [Pan, H-J] 151 Jinxue Rd, Kaohsiung 83102, Taiwan.
C3 Kaohsiung Veterans General Hospital; Fooyin University; Kaohsiung
   Veterans General Hospital; Kaohsiung Veterans General Hospital;
   Kaohsiung Veterans General Hospital
RP Pan, HJ (corresponding author), Kaohsiung Vet Gen Hosp, Dept Family Med, 386 Dazhong 1st Rd, Kaohsiung 81362, Taiwan.
EM philia81301@gmail.com
FU Research Center of Medical Informatics, Kaohsiung Veterans General
   Hospital [VGHKS103-G02, VGHKS104-133]
FX The authors are grateful for the use of the National Health Insurance
   Research Database provided by the Statistic Centre of the Department of
   Health andWelfare. The authors thank the Research Center of Medical
   Informatics, Kaohsiung Veterans General Hospital, No. VGHKS103-G02,
   VGHKS104-133, for managing data. This manuscript was edited by Wallace
   Academic Editing.
CR Amano K, 2015, J PALLIAT MED, V18, P270, DOI 10.1089/jpm.2014.0132
   [Anonymous], 2005, TAIWAN J HOSPICE PAL
   [Anonymous], 2017, HOSPICE PALLIATIVE C
   [Anonymous], 2012, CAUSES DEATH TAIWAN
   [Anonymous], 2018, 2018 TAIWAN HLTH WEL
   Baek YJ, 2011, J PAIN SYMPTOM MANAG, V41, P692, DOI 10.1016/j.jpainsymman.2010.06.019
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NR 37
TC 1
Z9 1
U1 1
U2 5
PU W B SAUNDERS CO LTD
PI LONDON
PA 32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND
SN 0033-3506
EI 1476-5616
J9 PUBLIC HEALTH
JI Public Health
PD SEP
PY 2020
VL 186
BP 119
EP 124
DI 10.1016/j.puhe.2020.05.022
PG 6
WC Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Public, Environmental & Occupational Health
GA NZ1US
UT WOS:000576880300025
PM 32818724
DA 2025-01-04
ER

PT J
AU Chen, H
   Zhang, JH
   Hao, Q
   Wu, XL
   Guo, JX
   Huang, CX
   Zhang, J
   Xing, GS
   An, ZL
   Ling, Y
   Zhao, JG
   Bao, YN
AF Chen, Hong
   Zhang, Ji-Hong
   Hao, Qin
   Wu, Xin-Lin
   Guo, Jia-Xing
   Huang, Cong-Xiu
   Zhang, Jun
   Xing, Guo-Sheng
   An, Zhi-Lin
   Ling, Yu
   Zhao, Jian-Guo
   Bao, Ying-Na
TI Analysis of tumor microenvironment alterations in partially responsive
   rectal cancer patients treated with neoadjuvant chemoradiotherapy
SO INTERNATIONAL JOURNAL OF COLORECTAL DISEASE
LA English
DT Article
DE Neoadjuvant chemoradiotherapy; Tumor microenvironment; Locally advanced
   rectal cancer; Partial response; Immunostimulation; Immunosuppression
ID COLORECTAL-CANCER; T-CELLS; INFILTRATION; RADIOTHERAPY; IMPROVES
AB PurposeAchieving a pathologic complete response (pCR) after neoadjuvant chemoradiotherapy (NCRT) remains a challenge for most patients with rectal cancer. Exploring the potential of combining NCRT with immunotherapy or targeted therapy for those achieving a partial response (PR) offers a promising avenue to enhance treatment efficacy. This study investigated the impact of NCRT on the tumor microenvironment in locally advanced rectal cancer (LARC) patients who exhibited a PR.MethodsThis was a retrospective, observational study. Five patients demonstrating a PR after neoadjuvant treatment for LARC were enrolled in the study. Biopsy samples before treatment and resected specimens after treatment were stained with a panel of 26 antibodies targeting various immune and tumor-related markers, each labeled with distinct metal tags. The labeled samples were then analyzed using the Hyperion imaging system.ResultsHeterogeneity within the tumor microenvironment was observed both before and after NCRT. Notably, tumor-associated macrophages, CD4 + T cells, CD8 + T cells, CD56 + natural killer cells, tumor-associated neutrophils, cytokeratin, and E-cadherin exhibited slight increase in abundance within the tumor microenvironment following treatment (change ratios = 0.78, 0.2, 0.27, 0.32, 0.17, 0.46, 0.32, respectively). Conversely, the number of CD14 + monocytes, CD19 + B cells, CD45 + CD4 + T cells, collagen I, alpha-smooth muscle actin, vimentin, and beta-catenin proteins displayed significant decreases post-treatment (change ratios = 1.73, 1.92, 1.52, 1.25, 1.52, 1.12, 2.66, respectively). Meanwhile, Foxp3 + regulatory cells demonstrated no significant change (change ratio = 0.001).ConclusionsNCRT has diverse effects on various components of the tumor microenvironment in LARC patients who achieve a PR after treatment. Leveraging combination therapies may optimize treatment outcomes in this patient population.
C1 [Chen, Hong] Inner Mongolia Med Univ, Affiliated Hosp, Hohhot 010050, Peoples R China.
   [Zhang, Ji-Hong; Guo, Jia-Xing; Huang, Cong-Xiu; Zhang, Jun; An, Zhi-Lin; Ling, Yu; Zhao, Jian-Guo; Bao, Ying-Na] Inner Mongolia Med Univ, Affiliated Hosp, Dept Radiotherapy, Hohhot 010050, Peoples R China.
   [Hao, Qin; Wu, Xin-Lin; Xing, Guo-Sheng] Inner Mongolia Med Univ, Dept Gastrointestinal Surg, Affiliated Hosp, Hohhot 010050, Peoples R China.
C3 Inner Mongolia Medical University; Inner Mongolia Medical University;
   Inner Mongolia Medical University
RP Bao, YN (corresponding author), Inner Mongolia Med Univ, Affiliated Hosp, Dept Radiotherapy, Hohhot 010050, Peoples R China.
EM baoyingnaq@126.com
RI zhang, yiheng/HQZ-1831-2023; zhanyong, guo/K-3220-2019
FU Inner Mongolia Science and Technology Plan Project [2019GG150]
FX This research was partly funded by the Inner Mongolia Science and
   Technology Plan Project (2019GG150).
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NR 46
TC 0
Z9 0
U1 2
U2 2
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0179-1958
EI 1432-1262
J9 INT J COLORECTAL DIS
JI Int. J. Colorectal Dis.
PD JUN 26
PY 2024
VL 39
IS 1
AR 99
DI 10.1007/s00384-024-04672-1
PG 12
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA WM9V4
UT WOS:001255417500002
PM 38926205
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Shi, F
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   Li, WJ
   Shi, YQ
   Wang, YF
   Wu, SW
AF Shi, Fan
   Wu, Jiatao
   Jia, Qianhao
   Li, Kairui
   Li, Wenjuan
   Shi, Yuqi
   Wang, Yufei
   Wu, Shiwu
TI Relationship between the expression of ARHGAP25 and RhoA in non-small
   cell lung cancer and vasculogenic mimicry
SO BMC PULMONARY MEDICINE
LA English
DT Article
DE ARHGAP25; RhoA; Rho GTPase; Vasculogenic mimicry; NSCLC; Prognosis
ID FASUDIL SUPPRESSES; COLORECTAL-CANCER; MELANOMA-CELLS; IN-VITRO;
   GTPASES; METASTASIS; INHIBITION
AB Background Vasculogenic mimicry (VM) is a recently identified pattern of blood supply to tumor tissue. It has long been considered a functional element in the metastasis and prognosis of malignant tumors. Both Rho GTPase-activating protein 25 (ARHGAP25) and Ras homolog family member A (RhoA) are effective predictors of tumor metastasis. In this study, we examined the expression levels of ARHGAP25 and RhoA and the structure of VM in non-small cell lung cancer (NSCLC). At the same time, we used cytology-related experiments to explore the effect of ARHGAP25 on the migration ability of tumor cells. Furthermore, we analyzed the interaction between the three factors and their association with clinicopathological characteristics and the five-year survival time in patients using statistical tools. Methods A total of 130 well-preserved NSCLC and associated paracancerous tumor-free tissues were obtained. Cell colony formation, wound healing, and cytoskeleton staining assays were used to analyze the effect of ARHGAP25 on the proliferation and migration ability of NSCLC cells. Immunohistochemical staining was used to determine the positivity rates of ARHGAP25, RhoA, and VM. Statistical software was used to examine the relationships between the three factors and clinical case characteristics, overall survival, and disease-free survival. Results Cell colony formation, wound healing, and cytoskeleton staining assays confirmed that ARHGAP25 expression affects the proliferation and migratory abilities of NSCLC cells. ARHGAP25 positivity rates in NSCLC and paracancerous tumor-free tissues were 48.5% and 63.1%, respectively, whereas RhoA positivity rates were 62.3% and 18.5%, respectively. ARHGAP25 had a negative relationship with RhoA and VM, whereas RhoA and VM had a positive relationship (P < 0.05). ARHGAP25, RhoA, and VM affected the prognosis of patients with NSCLC (P < 0.05) according to Kaplan-Meier of survival time and Cox regression analyses. Furthermore, lowering ARHGAP25 expression increased NSCLC cell proliferation and migration. Conclusions ARHGAP25 and RhoA expression is associated with VM and may be of potential value in predicting tumor metastasis, prognosis, and targeted therapy.
C1 [Shi, Fan; Wu, Jiatao; Jia, Qianhao; Li, Kairui; Li, Wenjuan; Shi, Yuqi; Wang, Yufei; Wu, Shiwu] Bengbu Med Coll, Dept Pathol, Affiliated Hosp 1, Changhuai Rd 287, Bengbu 233000, Anhui, Peoples R China.
   [Shi, Fan; Wu, Jiatao; Jia, Qianhao; Li, Kairui; Li, Wenjuan; Shi, Yuqi; Wang, Yufei; Wu, Shiwu] Bengbu Med Coll, Dept Pathol, 2600 Donghai Ave, Bengbu, Anhui, Peoples R China.
C3 Bengbu Medical University; Bengbu Medical University
RP Wu, SW (corresponding author), Bengbu Med Coll, Dept Pathol, Affiliated Hosp 1, Changhuai Rd 287, Bengbu 233000, Anhui, Peoples R China.; Wu, SW (corresponding author), Bengbu Med Coll, Dept Pathol, 2600 Donghai Ave, Bengbu, Anhui, Peoples R China.
EM 13705523357@163.com
RI Wu, Jiatao/K-3007-2018; Li, Kairui/AFU-4963-2022; Shi, Fan/J-2045-2015
FU Key Project of the Anhui Provincial Education Department [KJ2021A0725];
   Postgraduate Innovation Program of Bengbu Medical College [Byycx21091]
FX The Key Project of the Anhui Provincial Education Department (no.
   KJ2021A0725), and the Postgraduate Innovation Program of Bengbu Medical
   College (No. Byycx21091) provided funding for this study.
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NR 48
TC 7
Z9 8
U1 2
U2 8
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2466
J9 BMC PULM MED
JI BMC Pulm. Med.
PD OCT 7
PY 2022
VL 22
IS 1
AR 377
DI 10.1186/s12890-022-02179-5
PG 14
WC Respiratory System
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Respiratory System
GA 5D6NG
UT WOS:000865055200001
PM 36207695
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Warrier, A
   Das Manjulabhai, P
   Rajesh, A
   Shanmughan, U
   Vijayakumar, V
   Raveendran, J
   Gangadharan, D
AF Warrier, Arun
   Das Manjulabhai, Pooja
   Rajesh, Aiswarya
   Shanmughan, Unnimaya
   Vijayakumar, Varsha
   Raveendran, Jeethu
   Gangadharan, Dhanya
TI Screen-printed electrode for electrochemical detection of sunitinib
   malate for therapeutic drug monitoring
SO JOURNAL OF ELECTROCHEMICAL SCIENCE AND ENGINEERING
LA English
DT Article
DE Anticancer drug; electrooxidation; differential pulse voltammetry; real
   samples; electrochemical sensor
ID ANTICANCER MOLECULES IRINOTECAN; ACTIVE METABOLITE; HUMAN PLASMA;
   QUANTIFICATION; NANOPARTICLES; SENSOR; TUMORS
AB Sunitinib is a targeted therapy for colorectal cancer, which needs a precise dosage due to potential severe side effects from overdose. Therapeutic drug monitoring is crucial for maintaining optimal drug levels in body fluids. Traditional anticancer drug dose evaluation methods such as high-pressure liquid chromatography, liquid chromatography with mass spectrophotometry, and immunoassays are cumbersome. This study explores the utilization of electrochemical sensors on indigenously developed screen-printed electrodes for sunitinib malate monitoring. Differential pulse voltammetry, cyclic voltammetry and chrono-amperometric studies were conducted in a conventional three-electrode system. An anodic peak current, indicative of sunitinib malate electrooxidation, was observed around +0.45 V vs. Ag/AgCl reference electrode in 0.1 M PB of pH 7.4. Sensitivity, the limit of detection and method detection limit were determined as 0.386 mu A mu M-1 cm-2 , 0.009 and 0.0108 mu M, respectively. The response exhibited linearity (R2 = 0.990) with sunitinib concentration ranging from 0.08 to 88 mu M with good reproducibility. DPV studies on real samples yielded acceptable recovery values. Electrochemical sensors based on the screenprinted electrode present a promising approach for sunitinib monitoring, offering sensitivity, low limit of detection, and a wide linear range. Since the expected plasma concentration of sunitinib is much higher than the sensor detection range, it can be used for real sample analysis. Here developed methods could simplify and improve therapeutic drug monitoring in colorectal cancer treatment.
C1 [Warrier, Arun; Das Manjulabhai, Pooja; Rajesh, Aiswarya; Shanmughan, Unnimaya; Vijayakumar, Varsha; Gangadharan, Dhanya] APJ Abdul Kalam Technol Univ Thiruvananthapuram, Sahrdaya Coll Engn & Technol, Dept Biotechnol, Trichur, Kerala, India.
   [Raveendran, Jeethu] APJ Abdul Kalam Technol Univ Thiruvananthapuram, Sahrdaya Coll Engn & Technol, Dept Biomed Engn, Trichur, Kerala, India.
RP Gangadharan, D (corresponding author), APJ Abdul Kalam Technol Univ Thiruvananthapuram, Sahrdaya Coll Engn & Technol, Dept Biotechnol, Trichur, Kerala, India.
EM dhanyag@sahrdaya.ac.in
FU Kerala Startup Mission [KSUM/966/2022]; Government of Kerala
   [539/2021/KTU]
FX The authors report funding from the Kerala Startup Mission for the
   financial support provided by IDEAFEST 2022 (KSUM/966/2022 dated
   November 7, 2022) . Ms Pooja Das M. express her sincere thanks to APJ
   Abdul Kalam Kerala Technological University, established by the
   Government of Kerala, for providing financial assistance in the form of
   the Centre for Engineering Research and Development (CERD) PhD
   Fellowship Programme, 2020 (U.O.No. 539/2021/KTU dated 25th March 2021)
   .
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NR 45
TC 0
Z9 0
U1 1
U2 1
PU INT ASSOC PHYSICAL CHEMISTS-IAPC
PI ZAGREB
PA INT ASSOC PHYSICAL CHEMISTS-IAPC, ZAGREB, 00000, CROATIA
SN 1847-9286
J9 J ELECTROCHEM SCI EN
JI J. Electrochem. Sci. Eng.
PY 2024
VL 14
IS 6
BP 803
EP 822
DI 10.5599/jese.2478
EA DEC 2024
PG 20
WC Electrochemistry
WE Emerging Sources Citation Index (ESCI)
SC Electrochemistry
GA Q0K1J
UT WOS:001375219200001
OA gold
DA 2025-01-04
ER

PT J
AU Li, BT
   Li, C
   Guo, MY
   Shang, SH
   Li, XG
   Xie, P
   Sun, XD
   Yu, JM
   Wang, LL
AF Li, Butuo
   Li, Cheng
   Guo, Meiying
   Shang, Shuheng
   Li, Xiaogang
   Xie, Peng
   Sun, Xindong
   Yu, Jinming
   Wang, Linlin
TI Predictive value of LDH kinetics in bevacizumab treatment and survival
   of patients with advanced NSCLC
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE lactate dehydrogenase; bevacizumab; non-small-cell lung cancer;
   mixed-effect model; predictive factor
ID CELL LUNG-CANCER; PROGNOSTIC-FACTORS; PHASE-III; CHEMOTHERAPY; TUMOR;
   IMMUNOTHERAPY; MULTICENTER; DOCETAXEL; NIVOLUMAB; PLACEBO
AB Background: The combination of bevacizumab and chemotherapy is still one of the standard treatments for advanced non-small-cell lung cancer (NSCLC) patients in the new era of targeted therapy. Although a high level of baseline lactate dehydrogenase (LDH) was found to predict survival benefit from bevacizumab in patients with metastatic colorectal cancer, the predictive value of serum level of LDH in NSCLC patients treated with bevacizumab has not been investigated yet. Moreover, dynamic evaluation of serum level of LDH changes may be more informative and promising in predicting patients' prognosis. We thus sought to analyze LDH kinetics and evaluate its predictive role in the response and survival of advanced NSCLC patients treated with bevacizumab.
   Method: We retrospectively collected and analyzed a total of 161 advanced NSCLC patients who had undergone treatment with bevacizumab. Univariate and multivariate logistic regression analyses of serum level of LDH were used for response analyses, and Cox models for both overall survival (OS) and progression-free survival analyses (PFS). Longitudinal analysis of LDH was performed using a mixed-effect regression model.
   Results: On multivariate Cox models, increase of serum level of LDI-I after 4 cycles with bevacizumab (INC4) treatment was shown to be the independent risk factor for OS (hazard ratio =2.17, 95% Cl: 1.21-3.90, P=0.009), and the serum level of LDH after 2 cycles (LDH2) and the increase of LDH after 6 cycles with bevacizumab (INC6) treatment were the predictive factors for PFS (hazard ratio =2.33, 95% CI: 1.38-3.93, P=0.001; hazard ratio =1.96, 95% CI: 1.27-3.03, P=0.002, respectively). Patients with increase of serum level of LDH after 2 cycles of treatment with bevacizumab (INC2) (odds ratio =3.75, 95% CI: 1.83-7.68, P<0.001) were more likely to attain stable disease/progressive disease on multivariate logistic regression analyses, while patients with complete response (CR)/partial response (PR) experienced a reduction of serum level of LDH every 2 cycles (Coef =-0.076, std error =0.017, P<0.001) over time.
   Conclusion: Dynamic changes of LDH were superior to baseline LDH in predicting prognosis of NSCLC patients treated with bevacizumab. Serum level of LDI-I reducing over time was a potential biomarker for patients to achieve good clinical response (CR/PR) to bevacizumab.
C1 [Li, Butuo; Yu, Jinming] Tianjin Med Univ, Dept Radiat Oncol, Tianjin, Peoples R China.
   [Li, Butuo; Yu, Jinming] Tianjin Med Univ, Key Lab Canc Prevent & Therapy, Tianjin, Peoples R China.
   [Li, Butuo; Guo, Meiying; Shang, Shuheng; Xie, Peng; Sun, Xindong; Yu, Jinming; Wang, Linlin] Shandong Univ, Shandong Canc Hosp, Dept Radiat Oncol, Shandong Acad Med Sci, Jiyan Rd 440, Jinan 250117, Shandong, Peoples R China.
   [Li, Cheng] Shandong Univ, Shandong Canc Hosp, Dept Deans Off, Shandong Acad Med Sci, Jinan, Shandong, Peoples R China.
   [Guo, Meiying; Shang, Shuheng] Shandong Univ, Sch Med, Dept Radiat Oncol, Jinan, Shandong, Peoples R China.
   [Li, Xiaogang] Univ Jinan, Sch Med & Life Sci, Dept Radiat Oncol, Shandong Acad Med Sci, Jinan, Shandong, Peoples R China.
C3 Tianjin Medical University; Tianjin Medical University; Shandong
   University; University of Jinan; Shandong First Medical University &
   Shandong Academy of Medical Sciences; University of Jinan; Shandong
   University; Shandong First Medical University & Shandong Academy of
   Medical Sciences; Shandong University; University of Jinan; Shandong
   First Medical University & Shandong Academy of Medical Sciences
RP Wang, LL (corresponding author), Shandong Univ, Shandong Canc Hosp, Dept Radiat Oncol, Shandong Acad Med Sci, Jiyan Rd 440, Jinan 250117, Shandong, Peoples R China.; Yu, JM (corresponding author), Tianjin Med Univ, Qixiangtai Rd 22, Tianjin 300070, Peoples R China.
EM sdyujinming@163.com; wanglinlinatjn@163.com
RI Wang, Linlin/U-9905-2019
OI Li, Xiaogang/0000-0002-2794-4621; Xie, Peng/0000-0002-7235-3230
FU Natural Science Foundation of Shandong Province [ZR2016HM41,
   ZR2015HZ004]; Project of Postdoctoral Innovation of Shandong Province
   [201501010, 201601006]; Project of Postdoctoral Science Foundation of
   China [2016M590640]; National Natural Science Foundation of China
   [81472812]
FX This work was supported by the following grants: Natural Science
   Foundation of Shandong Province (Grant no ZR2016HM41 and ZR2015HZ004),
   the Project of Postdoctoral Innovation of Shandong Province (Grant no
   201501010 and 201601006), the Project of Postdoctoral Science Foundation
   of China (Grant no 2016M590640), and National Natural Science Foundation
   of China (Grant no 81472812).
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NR 32
TC 20
Z9 21
U1 0
U2 6
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6930
J9 ONCOTARGETS THER
JI OncoTargets Ther.
PY 2018
VL 11
BP 6287
EP 6294
DI 10.2147/OTT.S171566
PG 8
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA GW2ND
UT WOS:000446719600003
PM 30310292
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Geissler, F
   Nesic, K
   Kondrashova, O
   Dobrovic, A
   Swisher, EM
   Scott, CL
   Wakefield, MJ
AF Geissler, Franziska
   Nesic, Ksenija
   Kondrashova, Olga
   Dobrovic, Alexander
   Swisher, Elizabeth M.
   Scott, Clare L.
   J. Wakefield, Matthew
TI The role of aberrant DNA methylation in cancer initiation and clinical
   impacts
SO THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
LA English
DT Article
DE BRCA-related cancers; diagnosis; epigenomics; genomics; genomic testing;
   homologous recombination deficiency; oncogenic driver mutations;
   targeted therapy; therapeutic resistance
ID TUMOR-SUPPRESSOR GENES; MISMATCH REPAIR-DEFICIENCY; MLH1 PROMOTER
   METHYLATION; CELL LUNG-CANCER; MICROSATELLITE INSTABILITY;
   COLORECTAL-CANCER; BRCA1 PROMOTER; LYNCH SYNDROME; EPIGENETIC CHANGES;
   SOMATIC MUTATIONS
AB Epigenetic alterations, including aberrant DNA methylation, are now recognized as bone fide hallmarks of cancer, which can contribute to cancer initiation, progression, therapy responses and therapy resistance. Methylation of gene promoters can have a range of impacts on cancer risk, clinical stratification and therapeutic outcomes. We provide several important examples of genes, which can be silenced or activated by promoter methylation and highlight their clinical implications. These include the mismatch DNA repair genes MLH1 and MSH2, homologous recombination DNA repair genes BRCA1 and RAD51C, the TERT oncogene and genes within the P15/P16/RB1/E2F tumour suppressor axis. We also discuss how these methylation changes might occur in the first place - whether in the context of the CpG island methylator phenotype or constitutional DNA methylation. The choice of assay used to measure methylation can have a significant impact on interpretation of methylation states, and some examples where this can influence clinical decision-making are presented. Aberrant DNA methylation patterns in circulating tumour DNA (ctDNA) are also showing great promise in the context of non-invasive cancer detection and monitoring using liquid biopsies; however, caution must be taken in interpreting these results in cases where constitutional methylation may be present. Thus, this review aims to provide researchers and clinicians with a comprehensive summary of this broad, but important subject, illustrating the potentials and pitfalls of assessing aberrant DNA methylation in cancer.
   Silencing genes role in initiation of cancer and clinical impactsGenes can be silenced by molecular tags being placed on them. This is a normal process that controls when and where genes are available to be used. In some cases this silencing can be incorrectly applied to genes involved in preventing cancer, causing cancer initiation and progression. This review discusses the role of one of these tagging processes, DNA methylation and its role in initiation of cancer and implications for treatment.
C1 [Geissler, Franziska; Nesic, Ksenija; Scott, Clare L.] Walter & Eliza Hall Inst Med Res, Parkville, Vic, Australia.
   [Nesic, Ksenija; Scott, Clare L.] Univ Melbourne, Dept Med Biol, Parkville, Vic, Australia.
   [Kondrashova, Olga] QIMR Berghofer Med Res Inst, Brisbane, Qld, Australia.
   [Dobrovic, Alexander] Univ Melbourne, Dept Surg, Austin Hlth, Heidelberg, Vic, Australia.
   [Swisher, Elizabeth M.] Univ Washington, Seattle, WA USA.
   [Scott, Clare L.; J. Wakefield, Matthew] Univ Melbourne, Dept Obstet & Gynaecol, Parkville, Vic, Australia.
   [Scott, Clare L.] Peter MacCallum Canc Ctr, Dept Surg Oncol, Melbourne, Vic, Australia.
   [Scott, Clare L.] Royal Womens Hosp, Parkville, Vic, Australia.
   [Scott, Clare L.] Royal Melbourne Hosp, Parkville, Vic, Australia.
   [J. Wakefield, Matthew] Walter & Eliza Hall Inst Med Res, 1G Royal Parade, Parkville, VIC 3052, Australia.
C3 Walter & Eliza Hall Institute; University of Melbourne; QIMR Berghofer
   Medical Research Institute; Florey Institute of Neuroscience & Mental
   Health; Austin Research Institute; University of Melbourne; University
   of Washington; University of Washington Seattle; University of
   Melbourne; Peter Maccallum Cancer Center; The Royal Women's Hospital;
   Melbourne Health; Royal Melbourne Hospital; Walter & Eliza Hall
   Institute
RP Wakefield, MJ (corresponding author), Univ Melbourne, Dept Obstet & Gynaecol, Parkville, Vic, Australia.; Wakefield, MJ (corresponding author), Walter & Eliza Hall Inst Med Res, 1G Royal Parade, Parkville, VIC 3052, Australia.
EM wakefield@wehi.edu.au
RI Wakefield, Matthew/A-7795-2008
OI Wakefield, Matthew/0000-0001-6624-4698; Geissler,
   Franziska/0000-0003-3568-2008; Nesic, Ksenija/0000-0001-9972-9819
FU Swiss Cancer Research foundation; Swiss Cancer League
   [KFS-5445-08-2021]; AACR-AstraZeneca Ovarian Cancer Research Fellowship;
   NHMRC Emerging Leader 1 Investigator Grant [GNT2008631]; Stafford Fox
   Medical Research Foundation; NHMRC Investigator Grant [GNT2009783]; NIH
   NCI [R01 CA251817, R01 CA237600]
FX The authors disclosed receipt of the following financial support for the
   research, authorship, and/or publication of this article: FG has
   received research support by the Swiss Cancer Research foundation &
   Swiss Cancer League [KFS-5445-08-2021]. KN is supported by
   AACR-AstraZeneca Ovarian Cancer Research Fellowship. OK is supported by
   a NHMRC Emerging Leader 1 Investigator Grant (GNT2008631). MJW and CLS
   received funding support from the Stafford Fox Medical Research
   Foundation. CLS is sup-ported by a NHMRC Investigator Grant
   (GNT2009783). EMS has received funding sup-port from NIH NCI R01
   CA251817 and NIH NCI R01 CA237600.
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NR 198
TC 6
Z9 6
U1 0
U2 4
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1758-8340
EI 1758-8359
J9 THER ADV MED ONCOL
JI Ther. Adv. Med. Oncol.
PY 2024
VL 16
AR 17588359231220511
DI 10.1177/17588359231220511
PG 23
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GI3U4
UT WOS:001152008200001
PM 38293277
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Shrestha, J
   Kim, SW
   Kim, SB
   Oh, YS
   Ki, SH
   Lee, T
   Kim, SB
   Park, T
   Baek, DJ
   Park, EY
AF Shrestha, Jitendra
   Kim, Seong Woong
   Kim, Su-Bin
   Oh, Yoon Sin
   Ki, Sung Hwan
   Lee, Taeho
   Kim, Sang-Bum
   Park, Taeuk
   Baek, Dong Jae
   Park, Eun-Young
TI Determining the Anticancer Activity of Sphingosine Kinase Inhibitors
   Containing Heteroatoms in Their Tail Structure
SO PHARMACEUTICS
LA English
DT Article
DE SK inhibitor; colorectal cancer; S1P; derivative; anticancer agent; PP2A
ID DISCOVERY; CANCER; FTY720; POTENT
AB Sphingosine kinase (SK) enzyme, a central player of sphingolipid rheostat, catalyzes the phosphorylation of sphingosine to the bioactive lipid mediator sphingosine 1 phosphate (S1P), which regulates cancer cell proliferation, migration, differentiation, and angiogenesis through its extracellular five G protein-coupled S1P receptors (S1PR(1-5)). Recently, several research studies on SK inhibitors have taken place in order use them for the development of novel anticancer-targeted therapy. In this study, we designed and synthesized analog derivatives of known SK1 inhibitors, namely RB005 and PF-543, by introducing heteroatoms at their tail structure, as well as investigated their anticancer activities and pharmacokinetic parameters in vitro. Compounds 1-20 of RB005 and PF-543 derivatives containing an aliphatic chain or a tail structure of benzenesulfonyl were synthesized. All compounds of set 1 (1-10) effectively reduced cell viability in both HT29 and HCT116 cells, whereas set 2 derivatives (11-20) showed poor anticancer effect. Compound 10, having the highest cytotoxic effect (48 h, HT29 IC50 = 6.223 mu M, HCT116 IC50 = 8.694 mu M), induced HT29 and HCT116 cell death in a concentration-dependent manner through the mitochondrial apoptotic pathway, which was demonstrated by increased annexin V-FITC level, and increased apoptotic marker cleaved caspase-3 and cleaved PARP. Compound 10 inhibited SK1 by 20%, and, thus, the S1P level decreased by 42%. Unlike the apoptosis efficacy, the SK1 inhibitory effect and selectivity of the PF-543 derivative were superior to that of the RB005 analog. As a result, compounds with an aliphatic chain tail exhibited stronger apoptotic effects. However, this ability was not proportional to the degree of SK inhibition. Compound 10 increased the protein phosphatase 2A (PP2A) activity (1.73 fold) similar to FTY720 (1.65 fold) and RB005 (1.59 fold), whereas compounds 11 and 13 had no effect on PP2A activation. Since the PP2A activity increased in compounds with an aliphatic chain tail, it can be suggested that PP2A activation has an important effect on anticancer and SK inhibitory activities.
C1 [Shrestha, Jitendra; Kim, Seong Woong; Kim, Su-Bin; Baek, Dong Jae; Park, Eun-Young] Mokpo Natl Univ, Coll Pharm, Yeongsan Ro, South Korea.
   [Oh, Yoon Sin] Eulji Univ, Dept Food & Nutr, Seongnam 13135, South Korea.
   [Ki, Sung Hwan] Chosun Univ, Coll Pharm, Gwangju 61452, South Korea.
   [Lee, Taeho] Kyungpook Natl Univ, Res Inst Pharmaceut Sci, Coll Pharm, Daegu 41566, South Korea.
   [Kim, Sang-Bum] Daegu Gyeongbuk Med Innovat Fdn, New Drug Dev Ctr, Daegu 41061, South Korea.
   [Park, Taeuk] Daegu Gyeongbuk Med Innovat Fdn, Lab Anim Ctr, Daegu 41061, South Korea.
C3 Mokpo National University; Eulji University; Chosun University;
   Kyungpook National University (KNU)
RP Baek, DJ; Park, EY (corresponding author), Mokpo Natl Univ, Coll Pharm, Yeongsan Ro, South Korea.
EM shresthasimon2011@gmail.com; 76pey@naver.com; rlatnqls0801@naver.com;
   ysoh@eulji.ac.kr; shki@chosun.ac.kr; tlee@knu.ac.kr;
   ksb2014@dgmif.re.kr; tw3000@dgmif.re.kr; dbaek@mokpo.ac.kr;
   parkey@mokpo.ac.kr
RI , Do Hyang Kim/J-6575-2012; Shrestha, Jitendra/KWU-2275-2024
OI Shrestha, Jitendra/0000-0002-5344-994X; Oh, Yoon
   Sin/0000-0003-3995-4429; Back, Dong Jae/0000-0001-6100-488X
FU Basic Science Research Program through the National Research Foundation
   of Korea (NRF) - Ministry of Science, ICT & Future Planning
   [2020R1A2C1012156, 2020R1F1A1068316]; Mokpo National University (MNU)
   Innovation Support Project
FX This research was supported by the Basic Science Research Program
   through the National Research Foundation of Korea (NRF) funded by the
   Ministry of Science, ICT & Future Planning (2020R1A2C1012156 and
   2020R1F1A1068316). This work was carried out by the Convergence Research
   Laboratory established by the Mokpo National University (MNU) Innovation
   Support Project.
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NR 23
TC 1
Z9 1
U1 0
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1999-4923
J9 PHARMACEUTICS
JI Pharmaceutics
PD JAN
PY 2022
VL 14
IS 1
AR 157
DI 10.3390/pharmaceutics14010157
PG 22
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA YO0VG
UT WOS:000747665600001
PM 35057052
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Miyake, N
   Chikumi, H
   Yamaguchi, K
   Takata, M
   Takata, M
   Okada, K
   Kitaura, T
   Nakamoto, M
   Yamasaki, A
AF Miyake, Naomi
   Chikumi, Hiroki
   Yamaguchi, Kosuke
   Takata, Miyako
   Takata, Miki
   Okada, Kensaku
   Kitaura, Tsuyoshi
   Nakamoto, Masaki
   Yamasaki, Akira
TI Effect of Cetuximab and <i>EGFR</i> Small Interfering RNA Combination
   Treatment in NSCLC Cell Lines with Wild Type <i>EGFR</i> and Use of
   <i>KRAS</i> as a Possible Biomarker for Treatment Responsiveness
SO YONAGO ACTA MEDICA
LA English
DT Article
DE cetuximab; EGFR siRNA; KRAS; non-small cell lung cancer
ID GROWTH-FACTOR RECEPTOR; LUNG-CANCER; PHASE-III; MUTATIONS; APOPTOSIS;
   PTEN; LKB1; SENSITIVITY; PREVALENCE; EXPRESSION
AB Background The epidermal growth factor receptor (EGFR) is a therapeutic target for patients with non-small cell lung cancer (NSCLC). Cetuximab is an anti-EGFR monoclonal antibody that inhibits EGFR signaling and proliferation of colorectal cancer and head and neck cancers. Since only few NSCLC patients benefit from cetuximab therapy, we evaluated a novel combination treatment using cetuximab and EGFR small interfering RNA (siRNA) to strongly suppress EGFR signaling and searched for a biomarker in NSCLC cell lines harboring wild-type EGFR.
   Methods Alterations in EGFR and its downstream genes in five NSCLC cell lines (A549, Lu99, 86-2, Sq19 and Ma10) were assessed through sequencing. The protein expression levels of these molecules were assessed through western blotting. The effect of combination treatment was determined through cell proliferation assay, caspase-3/7 assay, invasion assay, and migration assay.
   Results All cell lines were harboring wild-type EGFR, whereas KRAS, PTEN, TP53 and LKB1 were mutated in A549 and Lu99; Lu99 and Sq19; Lu99, 86-2, Sq19 and Ma10; and A549, 86-2, and Sq19 cell lines, respectively. PTEN was not expressed in Sq19, and LKB1 was not expressed in both A549 and Sq19. TP53 was not expressed in both A549 and Lu99. The combination of cetuximab and EGFR siRNA significantly suppressed cell proliferation in 86-2, Sq19 and Ma10, which express wild-type KRAS. It induced apoptosis in A549, 86-2 and Ma10 cells, which express wild type PTEN. The combination treatment had no effect either on cell invasion nor migration in all cell lines.
   Conclusion EGFR targeted therapy using the combination of cetuximab and EGFR siRNA is effective in NSCLC cell lines harboring wild-type EGFR. Wild-type KRAS may act as a potential biomarker for response to combination treatment by the induction of apoptosis in cells with wild-type PTEN.
C1 [Miyake, Naomi; Yamaguchi, Kosuke; Takata, Miki; Yamasaki, Akira] Tottori Univ, Fac Med, Div Med Oncol & Mol Respirol, Dept Multidisciplinary Internal Med,Sch Med, Yonago, Tottori 6838503, Japan.
   [Chikumi, Hiroki; Okada, Kensaku; Kitaura, Tsuyoshi; Nakamoto, Masaki] Tottori Univ Hosp, Div Infect Dis, Yonago, Tottori 6838504, Japan.
   [Takata, Miyako] Tottori Univ, Fac Med, Dept Pathobiol Sci & Technol, Sch Hlth Sci, Yonago, Tottori 6838503, Japan.
C3 Tottori University; Tottori University; Tottori University
RP Chikumi, H (corresponding author), Tottori Univ Hosp, Div Infect Dis, Yonago, Tottori 6838504, Japan.
EM chikumi@med.tottori-u.ac.jp
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NR 43
TC 4
Z9 5
U1 2
U2 5
PU TOTTORI UNIV MEDICAL PRESS
PI YONAGO
PA 86 NISHI-CHO, YONAGO, TOTTORI-KEN 683-8503, JAPAN
SN 0513-5710
EI 1346-8049
J9 YONAGO ACTA MED
JI Yonago Acta Med.
PD MAR
PY 2019
VL 62
IS 1
BP 85
EP 93
DI 10.33160/yam.2019.03.012
PG 9
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA HS4TX
UT WOS:000463861900012
PM 30962749
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Cui, Y
   Dong, C
   Wu, BQ
   Duan, XC
   Shi, G
   Gong, M
   Wang, TY
AF Cui, Yong
   Dong, Chang
   Wu, Bing-Qun
   Duan, Xin-Chun
   Shi, Guan
   Gong, Min
   Wang, Tian-You
TI Expression of cyclooxygenase-2, vascular endothelial growth factor, and
   epidermal growth factor receptor in Chinese patients with esophageal
   squamous cell carcinoma
SO JOURNAL OF CANCER RESEARCH AND THERAPEUTICS
LA English
DT Article
DE Cyclooxygenase-2; epidermal growth factor receptor; esophageal
   neoplasms; vascular endothelial growth factor
ID LYMPH-NODE METASTASIS; EGFR OVER-EXPRESSION; RANDOMIZED PHASE-II;
   PROGNOSTIC-SIGNIFICANCE; MICROVESSEL DENSITY; COLORECTAL-CANCER;
   ADENOCARCINOMA; SURVIVAL; CHEMORADIOTHERAPY; COX-2
AB Background: Esophageal squamous cell carcinoma (ESCC) is a frequently occurring cancer with poor prognosis despite combined therapeutic strategies. The aim of the current study was to elucidate a further finding on the clinicopathologic significance of immunohistochemical expression of cyclooxygenase-2 (COX-2), vascular endothelial growth factor (VEGF), and epidermal growth factor receptor (EGFR) in Chinese patients with ESCC.
   Methods: Formalin-fixed paraffin-embedded surgically resected tumor samples were obtained from 140 randomly selected Chinese patients with ESCC. Sections were immunohistochemically stained for COX-2, VEGF, and EGFR. The correlations between clinicopathological features and the high expression of COX-2, VEGF, and EGFR were analyzed using the Statistical Package for the Social Sciences 19.0 software (IBM Inc., Chicago, IL, USA).
   Results: In the present study, high expression of COX-2, EGFR, and VEGF was found in 64.3%, 62.1%, and 65.0%, respectively. Results showed that COX-2 overexpression was significantly correlated with degree of differentiation (P = 0.000), and lymph node metastasis (negative/positive, P = 0.002). EGFR and VEGF overexpression was significantly correlated with a differentiated degree, T stage, N stage, and tumor, node, metastases stage.
   Conclusion: High expression of COX-2, EGFR, and VEGF is an unfavorable prognostic factor in ESCC, and could be used as a poor prognosis indicator for the ESCC patients. Targeting therapy to these three targets should be considered to the combined treatment in ESCC.
C1 [Cui, Yong; Dong, Chang; Wu, Bing-Qun; Duan, Xin-Chun; Shi, Guan; Gong, Min; Wang, Tian-You] Capital Med Univ, Dept Thorac Surg, Beijing Friendship Hosp, Beijing, Peoples R China.
C3 Capital Medical University
RP Dong, C (corresponding author), Capital Med Univ, Dept Thorac Surg, Beijing Friendship Hosp, Yongan St, Beijing, Peoples R China.
EM changdongj@aliyun.com
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NR 38
TC 9
Z9 9
U1 0
U2 2
PU MEDKNOW PUBLICATIONS & MEDIA PVT LTD
PI MUMBAI
PA B-9, KANARA BUSINESS CENTRE, OFF LINK RD, GHAKTOPAR-E, MUMBAI, 400075,
   INDIA
SN 0973-1482
EI 1998-4138
J9 J CANCER RES THER
JI J. Canc. Res. Ther.
PD AUG
PY 2015
VL 11
IS 5
SU S
BP C44
EP C48
DI 10.4103/0973-1482.163838
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CQ9SI
UT WOS:000360955000009
PM 26323923
OA gold
DA 2025-01-04
ER

PT J
AU Gu, ZY
   Liu, YK
AF Gu, Zhiyu
   Liu, Yunkun
TI A bibliometric and visualized in oral microbiota and cancer research
   from 2013 to 2022
SO DISCOVER ONCOLOGY
LA English
DT Article
DE Oral microbiota; Cancer; Bibliometric analysis; VOSviewer; WoSCC
ID FUSOBACTERIUM-NUCLEATUM; CARCINOGENESIS; PROGRESSION; HEALTH
AB Numerous studies have highlighted the implication of oral microbiota in various cancers. However, no bibliometric analysis has been conducted on the relationship between oral microbiota and cancer. This bibliometric analysis aimed to identify the research hotspots in oral microbiota and cancer research, as well as predict future research trends. The literature published relating to oral microbiota and cancer was searched from the Web of Science Core Collection database (WoSCC) from 2013 to 2022. VOSviewer or Citespace software was used to perform the bibliometric analysis, focusing on countries, institutions, authors, journals, keywords and references. A total of 1516 publications were included in the analysis. The number of publications related oral microbiota and cancer increased annually, reaching its peak in 2022 with 287 papers. The United States (456) and China (370) were the countries with the most publications and made significant contributions to the field. Sears CL and Zhou XD were the most productive authors. The high frequency of keywords revealed key topics, including cancer (colorectal cancer, oral cancer), oral microbiota (Fusobacterium nucleatum, Porphyromonas gingivalis), and inflammation (periodontal disease). The latest trend keywords were F. nucleatum, dysbiosis, prognosis, tumor microenvironment, gastric microbiota, complications and survival, suggesting a new hotspot in the field of oral microbiota and cancer. Our study provides a comprehensive analysis of oral microbiota and cancer research, revealing an increase in publications in recent years. Future research directions will continue to focus on the diversity of oral microbiota impacted by cancers and the underlying mechanism connecting them, providing new ideas for targeted therapy of tumorigenesis.
C1 [Gu, Zhiyu; Liu, Yunkun] Zunyi Med Univ, Hosp Stomatol, Zunyi 563000, Peoples R China.
C3 Zunyi Medical University
RP Liu, YK (corresponding author), Zunyi Med Univ, Hosp Stomatol, Zunyi 563000, Peoples R China.
EM 121438062@qq.com
FU Doctor Start-up Found Program of Zunyi Medical University [KYJF2020-18]
FX This study was supported by the Doctor Start-up Found Program of Zunyi
   Medical University (KYJF2020-18).
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NR 70
TC 4
Z9 4
U1 9
U2 18
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
EI 2730-6011
J9 DISCOV ONCOL
JI Discov. Oncol.
PD FEB 1
PY 2024
VL 15
IS 1
AR 24
DI 10.1007/s12672-024-00878-5
PG 15
WC Oncology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Endocrinology & Metabolism
GA GP4B5
UT WOS:001153847700001
PM 38302656
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Najafi, M
   Majidpoor, J
   Toolee, H
   Mortezaee, K
AF Najafi, Masoud
   Majidpoor, Jamal
   Toolee, Heidar
   Mortezaee, Keywan
TI The current knowledge concerning solid cancer and therapy
SO JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
LA English
DT Review
DE radiotherapy; surgery; chemotherapy; combination therapy; cancer;
   immunotherapy; solid cancers
ID CELL LUNG-CANCER; NIGHT-SHIFT WORK; OPEN-LABEL; OXIDATIVE STRESS;
   COLORECTAL-CANCER; CLINICAL ACTIVITY; PROSTATE-CANCER; TUMOR
   MICROENVIRONMENT; IMMUNE-RESPONSES; STEM-CELLS
AB Solid cancers comprise a large number of new cases and deaths from cancer each year globally. There are a number of strategies for addressing tumors raised from solid organs including surgery, chemotherapy, radiotherapy, targeted therapy, immunotherapy, combinational therapy, and stem cell and extracellular vesicle (EV) therapy. Surgery, radiotherapy, and chemotherapy are the dominant cures, but are not always effective, in which even in a localized tumor there is a possibility of tumor relapse after surgical resection. Over half of the cancer patients will receive radiotherapy as a part of their therapeutic schedule. Radiotherapy can cause an abscopal response for boosting the activity of the immune system outside the local field of radiation, but it may also cause an unwanted bystander effect, predisposing nonradiated cells into carcinogenesis. In the context of immunotherapy, immune checkpoint inhibition is known as the standard-of-care, but the major concern is in regard with cold cancers that show low responses to such therapy. Stem-cell therapy can be used to send prodrugs toward the tumor area; this strategy, however, has its own predicaments, such as unwanted attraction toward the other sites including healthy tissues and its instability. A substitute to such therapy and quite a novel strategy is to use EVs, by virtue of their stability and potential to cross biological barriers and long-term storage of contents. Combination therapy is the current focus. Despite advances in the field, there are still unmet concerns in the area of effective cancer therapy, raising challenges and opportunities for future investigations.
C1 [Najafi, Masoud] Kermanshah Univ Med Sci, Med Technol Res Ctr, Kermanshah, Iran.
   [Najafi, Masoud] Kermanshah Univ Med Sci, Sch Paramed Sci, Radiol & Nucl Med Dept, Kermanshah, Iran.
   [Majidpoor, Jamal] Gonabad Univ Med Sci, Sch Med, Dept Anat, Gonabad, Iran.
   [Toolee, Heidar] Shahroud Univ Med Sci, Sch Med, Dept Anat, Shahroud, Iran.
   [Mortezaee, Keywan] Kurdistan Univ Med Sci, Canc & Immunol Res Ctr, Res Inst Hlth Dev, Sanandaj 6617713446, Iran.
   [Mortezaee, Keywan] Kurdistan Univ Med Sci, Sch Med, Dept Anat, Sanandaj, Iran.
C3 Kermanshah University of Medical Sciences; Kermanshah University of
   Medical Sciences; Shahroud University Medical Sciences; Kurdistan
   University of Medical Sciences; Kurdistan University of Medical Sciences
RP Mortezaee, K (corresponding author), Kurdistan Univ Med Sci, Canc & Immunol Res Ctr, Res Inst Hlth Dev, Sanandaj 6617713446, Iran.
EM keywan987@yahoo.com
RI Najafi, Masoud/L-8434-2019; majidpoor, jamal/ABM-6221-2022
OI najafi, masoud/0000-0002-6341-9007; Mortezaee,
   Keywan/0000-0003-2004-3465; majidpoor, jamal/0000-0002-9133-2670
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NR 273
TC 73
Z9 76
U1 1
U2 19
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1095-6670
EI 1099-0461
J9 J BIOCHEM MOL TOXIC
JI J. Biochem. Mol. Toxicol.
PD NOV
PY 2021
VL 35
IS 11
AR e22900
DI 10.1002/jbt.22900
EA AUG 2021
PG 26
WC Biochemistry & Molecular Biology; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Toxicology
GA WW1CX
UT WOS:000691221200001
PM 34462987
DA 2025-01-04
ER

PT J
AU Martelli, AM
   Paganelli, F
   Chiarini, F
   Evangelisti, C
   McCubrey, JA
AF Martelli, Alberto M.
   Paganelli, Francesca
   Chiarini, Francesca
   Evangelisti, Camilla
   McCubrey, James A.
TI The Unfolded Protein Response: A Novel Therapeutic Target in Acute
   Leukemias
SO CANCERS
LA English
DT Review
DE survival; apoptosis; genetic anomalies; targeted therapy; prognosis
ID ACUTE PROMYELOCYTIC LEUKEMIA; ACUTE LYMPHOBLASTIC-LEUKEMIA;
   HEMATOPOIETIC STEM-CELLS; ENDOPLASMIC-RETICULUM; ER-STRESS; ARSENIC
   TRIOXIDE; RETINOIC ACID; T-CELL; N-COR; INHIBITOR CX-4945
AB The unfolded protein response (UPR) is an evolutionarily conserved adaptive response triggered by the stress of the endoplasmic reticulum (ER) due, among other causes, to altered cell protein homeostasis (proteostasis). UPR is mediated by three main sensors, protein kinase RNA-like endoplasmic reticulum kinase (PERK), activating transcription factor 6 alpha (ATF6 alpha), and inositol-requiring enzyme-1 alpha (IRE1 alpha). Given that proteostasis is frequently disregulated in cancer, UPR is emerging as a critical signaling network in controlling the survival, selection, and adaptation of a variety of neoplasias, including breast cancer, prostate cancer, colorectal cancer, and glioblastoma. Indeed, cancer cells can escape from the apoptotic pathways elicited by ER stress by switching UPR into a prosurvival mechanism instead of cell death. Although most of the studies on UPR focused on solid tumors, this intricate network plays a critical role in hematological malignancies, and especially in multiple myeloma (MM), where treatment with proteasome inhibitors induce the accumulation of unfolded proteins that severely perturb proteostasis, thereby leading to ER stress, and, eventually, to apoptosis. However, UPR is emerging as a key player also in acute leukemias, where recent evidence points to the likelihood that targeting UPR-driven prosurvival pathways could represent a novel therapeutic strategy. In this review, we focus on the oncogene-specific regulation of individual UPR signaling arms, and we provide an updated outline of the genetic, biochemical, and preclinical therapeutic findings that support UPR as a relevant, novel target in acute leukemias.
C1 [Martelli, Alberto M.; Paganelli, Francesca] Univ Bologna, Dept Biomed & Neuromotor Sci, I-40126 Bologna, Italy.
   [Chiarini, Francesca; Evangelisti, Camilla] CNR, Inst Mol Genet, I-40136 Bologna, Italy.
   [Chiarini, Francesca; Evangelisti, Camilla] IRCCS, Ist Ortoped Rizzoli, I-40136 Bologna, Italy.
   [McCubrey, James A.] East Carolina Univ, Brody Sch Med, Dept Microbiol & Immunol, Greenville, NC 27834 USA.
C3 University of Bologna; Consiglio Nazionale delle Ricerche (CNR);
   Istituto di Genetica Molecolare (IGM-CNR); IRCCS Istituto Ortopedico
   Rizzoli; University of North Carolina; East Carolina University
RP Martelli, AM (corresponding author), Univ Bologna, Dept Biomed & Neuromotor Sci, I-40126 Bologna, Italy.
EM alberto.martelli@unibo.it; francesca.paganell16@studio.unibo.it;
   francesca.chiarini@cnr.it; camilla.evangelisti@cnr.it; mccubreyj@ecu.edu
RI Evangelisti, Camilla/C-6977-2019
OI Evangelisti, Camilla/0000-0003-3531-9540; Paganelli,
   Francesca/0000-0002-8694-2140; Martelli, Alberto
   Maria/0000-0001-5196-7260
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NR 162
TC 26
Z9 28
U1 1
U2 11
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD FEB
PY 2020
VL 12
IS 2
AR 333
DI 10.3390/cancers12020333
PG 24
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KY3ND
UT WOS:000522477300079
PM 32024211
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Li, WJ
   Dong, Q
   Li, L
   Zhang, ZL
   Cai, XL
   Pan, XL
AF Li, Wujie
   Dong, Qing
   Li, Lei
   Zhang, Zhenlei
   Cai, Xiaolan
   Pan, Xinliang
TI Prognostic significance of claudin-1 and cyclin B1 protein expression in
   patients with hypopharyngeal squamous cell carcinoma
SO ONCOLOGY LETTERS
LA English
DT Article
DE hypopharyngeal squamous cell carcinoma; claudin-1; cyclin B1;
   immunohistochemical
ID BREAST-CANCER CELLS; COLORECTAL-CANCER; GASTRIC-CANCER; IN-VIVO;
   OVEREXPRESSION; GROWTH; HEAD; NECK; TUMORIGENESIS; MORTALITY
AB Claudin-l and cyclin B1 are abnormally expressed in certain malignancies, but their expression in hypopharyngeal squamous cell carcinoma (HSCC) has not been reported thus far. Studying the expression levels of claudin-1 and cylin B1 in HSCC tissues and their association with clinical stage, pathological grade and prognosis in patients with HSCC may provide a theoretical basis and guide future research on HSCC targeted therapy. The protein expression levels of the above two biomarkers was immunohistochemically detected in 97 HSCC cases and 90 matched adjacent tissue samples. The correlation between the expression levels of claudin-1 and cylin B1 and the patients' clinical parameters was analyzed via Pearson's chi(2) test, while survival analysis was performed using a log-rank test. The results of the current study revealed that claudin-1 and cyclin B1 were highly expressed in HSCC tissues, and the expression of claudin-1 was associated with tumor differentiation degree and lymph node metastasis, while cyclin B1 expression was associated with tumor differentiation degree. Furthermore, Kaplan-Meier analysis revealed that claudin-1 expression correlated with survival (P=0.003), and the expression levels of claudin-1 and cyclin B1 were observed to be positively correlated, in patients with HSCC. Cyclin B1 and claudin-1 exhibited an elevated expression in HSCC specimens, thus suggesting their use as tumor markers. Therefore, the joint detection of claudin-1 and cyclin B1 may aid to guide cancer therapy and to determine prognosis in HSCC. Furthermore, claudin-1 may be used as an HSCC-monitoring index, and may serve as a therapeutic target.
C1 [Li, Wujie; Cai, Xiaolan; Pan, Xinliang] Shandong Univ, Qilu Hosp, Dept Otolaryngol, 107 West Wenhua Rd, Jinan 250012, Shandong, Peoples R China.
   [Li, Wujie; Zhang, Zhenlei] Taian City Cent Hosp, Dept Otolaryngol, Tai An 271000, Shandong, Peoples R China.
   [Dong, Qing] Taian City Cent Hosp, Dept Pediat, Tai An 271000, Shandong, Peoples R China.
   [Li, Lei] Taian City Cent Hosp, Dept Gastroenterol, Tai An 271000, Shandong, Peoples R China.
C3 Shandong University
RP Pan, XL (corresponding author), Shandong Univ, Qilu Hosp, Dept Otolaryngol, 107 West Wenhua Rd, Jinan 250012, Shandong, Peoples R China.
EM panxinlent@126.com
FU Shandong Provincial Natural Science Foundation (Jinan, China)
   [ZR2013HM107]
FX The present study was supported by the Shandong Provincial Natural
   Science Foundation (Jinan, China; grant no. ZR2013HM107). The authors
   would like to thank all the patients who participated in the study, in
   addition to LetPub (www.letpub.com; Woburn, MA, USA) for the linguistic
   assistance provided during the preparation of the present manuscript.
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PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD MAY
PY 2016
VL 11
IS 5
BP 2995
EP 3002
DI 10.3892/ol.2016.4333
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DJ1TG
UT WOS:000373986400007
PM 27123052
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Petrelli, F
   Cabiddu, M
   Coinu, A
   Borgonovo, K
   Ghilardi, M
   Lonati, V
   Barni, S
AF Petrelli, Fausto
   Cabiddu, Mary
   Coinu, Andrea
   Borgonovo, Karen
   Ghilardi, Mara
   Lonati, Veronica
   Barni, Sandro
TI Prognostic role of lactate dehydrogenase in solid tumors: A systematic
   review and meta-analysis of 76 studies
SO ACTA ONCOLOGICA
LA English
DT Review
ID RENAL-CELL CARCINOMA; RESISTANT PROSTATE-CANCER; METASTATIC
   COLORECTAL-CANCER; PRETREATMENT SERUM-LEVELS; TO-LYMPHOCYTE RATIO;
   LONG-TERM SURVIVAL; NASOPHARYNGEAL CARCINOMA; 1ST-LINE CHEMOTHERAPY;
   TARGETED THERAPY; LDH-A
AB Background. In cancer cells, metabolism is shifted to aerobic glycolysis with lactate production coupled with a higher uptake of glucose as the main energy source. Lactate dehydrogenase (LDH) catalyzes the reduction of pyruvate to form lactate, and serum level is often raised in aggressive cancer and hematological malignancies. We have assessed the prognostic value of LDH in solid tumors.
   Material and methods. A systematic review of electronic databases was conducted to identify publications exploring the association of LDH with clinical outcome in solid tumors. Overall survival (OS) was the primary outcome, and cancer-specific survival (CSS), progression-free survival (PFS), and disease-free survival (DFS) were secondary outcomes. Data from studies reporting a hazard ratio (HR) and 95% confidence interval (CI) were pooled in a meta-analysis. Pooled HRs were computed and weighted using generic inverse-variance and random-effect modeling. All statistical tests were two-sided.
   Results. Seventy-six studies comprising 22 882 patients, mainly with advanced disease, were included in the analysis. Median cut-off of serum LDH was 245 U/L. Overall, higher LDH levels were associated with a HR for OS of 1.7 (95% CI 1.62 - 1.79; p < 0.00001) in 73 studies. The prognostic effect was highest in renal cell, melanoma, gastric, prostate, nasopharyngeal and lung cancers (all p < 0.00001). HRs for PFS was 1.75 (all p < 0.0001).
   Conclusions. A high serum LDH level is associated with a poor survival in solid tumors, in particular melanoma, prostate and renal cell carcinomas, and can be used as a useful and inexpensive prognostic biomarker in metastatic carcinomas.
C1 [Petrelli, Fausto; Cabiddu, Mary; Coinu, Andrea; Borgonovo, Karen; Ghilardi, Mara; Lonati, Veronica; Barni, Sandro] Azienda Osped Treviglio, Dept Oncol, Med Oncol Unit, I-24047 Treviglio, BG, Italy.
RP Petrelli, F (corresponding author), Azienda Osped Treviglio, Dept Oncol, Med Oncol Unit, Piazzale Osped 1, I-24047 Treviglio, BG, Italy.
EM faupe@libero.it
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NR 110
TC 215
Z9 230
U1 2
U2 17
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0284-186X
EI 1651-226X
J9 ACTA ONCOL
JI Acta Oncol.
PY 2015
VL 54
IS 7
BP 961
EP 970
DI 10.3109/0284186X.2015.1043026
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CR4EP
UT WOS:000361284900001
PM 25984930
OA Bronze, Green Submitted
DA 2025-01-04
ER

PT J
AU Hubbard, JM
   Kim, G
   Borad, MJ
   Johnson, E
   Qin, R
   Lensing, J
   Puttabasavaiah, S
   Wright, J
   Erlichman, C
   Grothey, A
AF Hubbard, Joleen M.
   Kim, George
   Borad, Mitesh J.
   Johnson, Elizabeth
   Qin, Rui
   Lensing, Janet
   Puttabasavaiah, Suneetha
   Wright, John
   Erlichman, Charles
   Grothey, Axel
TI Phase I trial of FOLFIRI in combination with sorafenib and bevacizumab
   in patients with advanced gastrointestinal malignancies
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE Colorectal cancer; Systemic therapy; Antiangiogenesis
ID METASTATIC COLORECTAL-CANCER; TARGETED THERAPY; ONCOLOGY-GROUP;
   BREAST-CANCER; GROWTH-FACTOR; FLUOROURACIL; LEUCOVORIN; IRINOTECAN;
   OXALIPLATIN; RESISTANCE
AB Background A previous phase II trial in patients with chemorefractory metastatic colorectal cancer demonstrated a 63 % disease control rate with a combination of bevacizumab and sorafenib. This phase I trial sought to determine the maximum tolerable dose (MTD) of bevacizumab and sorafenib combined with standard cytotoxic therapy for advanced gastrointestinal (GI) cancers. Methods A standard 3 + 3 trial design utilized 3 escalating sorafenib dose levels: (1) 200 mg daily, days 3-7, 10-14; (2) 200 mg twice daily, days 3-6, 10-13; and (3) 200 mg twice daily, days 3-7, 10-14 combined with standard dose FOLFIRI (5-fluouracil, leucovorin, and irinotecan) and bevacizumab (5 mg/kg), repeated every 14 days. Results Fifteen patients were evaluable for safety and response assessment. There were no dose limiting toxicities (DLTs) at dose level 1 or 2. At dose level 3, two patients experienced DLTs (asymptomatic grade 3 hypophosphatemia, grade 3 dehydration and diarrhea). The MTD was determined to be dose level 2: sorafenib 200 mg twice daily, days 3-6, 10-13 combined with FOLFIRI and bevacizumab at standard doses. Four patients had a partial response and 8 had stable disease as best response (disease control rate of 80 %). Three patients with CRC had disease control > 12 months. Conclusions The MTD of this regimen is sorafenib 200 mg twice daily, days 3-6, 10-13 combined with standard doses of FOLFIRI and bevacizumab. Dual antiangiogenic treatment combined with cytotoxic therapy may provide prolonged disease stabilization for select patients with advanced GI malignancies.
C1 [Hubbard, Joleen M.; Lensing, Janet; Puttabasavaiah, Suneetha; Erlichman, Charles; Grothey, Axel] Mayo Clin Rochester, 200 First St SW, Rochester, MN 55905 USA.
   [Kim, George] Univ Florida Hlth Oncol, Jacksonville, FL USA.
   [Borad, Mitesh J.] Mayo Clin Scottsdale, Scottsdale, AZ USA.
   [Johnson, Elizabeth] Mayo Clin Jacksonville, 4500 San Pablo Rd, Jacksonville, FL 32224 USA.
   [Qin, Rui] Regeneron Pharmaceut Inc, Basking Ridge, NJ USA.
   [Wright, John] NCI, Div Canc Treatment, Canc Therapy Evaluat Program, Invest Drug Branch, Bethesda, MD 20892 USA.
C3 Mayo Clinic; State University System of Florida; University of Florida;
   Mayo Clinic; Mayo Clinic Phoenix; Mayo Clinic; Regeneron; National
   Institutes of Health (NIH) - USA; NIH National Cancer Institute (NCI)
RP Hubbard, JM (corresponding author), Mayo Clin Rochester, 200 First St SW, Rochester, MN 55905 USA.
EM hubbard.joleen@mayo.edu
FU CTSA from National Center for Advancing Translational Sciences (NCATS),
   a component of National Institutes of Health (NIH) [UL1 TR000135]; NCI
   [CA69912, CA15083, UL1TR000135]
FX This publication was made possible by CTSA Grant Number UL1 TR000135
   from the National Center for Advancing Translational Sciences (NCATS), a
   component of the National Institutes of Health (NIH). Its contents are
   solely the responsibility of the authors and do not necessarily
   represent the official view of NIH.Supported by NCI Grants CA69912,
   CA15083 and UL1TR000135.
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NR 25
TC 3
Z9 3
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-6997
EI 1573-0646
J9 INVEST NEW DRUG
JI Invest. New Drugs
PD FEB
PY 2016
VL 34
IS 1
BP 96
EP 103
DI 10.1007/s10637-015-0308-5
PG 8
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA DB7VP
UT WOS:000368725100010
PM 26581401
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Caruso, D
   Polici, M
   Zerunian, M
   Pucciarelli, F
   Guido, G
   Polidori, T
   Landolfi, F
   Nicolai, M
   Lucertini, E
   Tarallo, M
   Bracci, B
   Nacci, I
   Rucci, C
   Iannicelli, E
   Laghi, A
AF Caruso, Damiano
   Polici, Michela
   Zerunian, Marta
   Pucciarelli, Francesco
   Guido, Gisella
   Polidori, Tiziano
   Landolfi, Federica
   Nicolai, Matteo
   Lucertini, Elena
   Tarallo, Mariarita
   Bracci, Benedetta
   Nacci, Ilaria
   Rucci, Carlotta
   Iannicelli, Elsa
   Laghi, Andrea
TI Radiomics in Oncology, Part 1: Technical Principles and Gastrointestinal
   Application in CT and MRI
SO CANCERS
LA English
DT Review
DE Radiomics; oncologic imaging; Radiomics technical principles
ID PANCREATIC DUCTAL ADENOCARCINOMA; TEXTURE ANALYSIS; COLORECTAL-CANCER;
   FEATURES; PREDICTION; TUMOR; DIFFERENTIATION; IMAGES
AB Simple Summary
   Part I is an overview aimed to investigate some technical principles and the main fields of radiomic application in gastrointestinal oncologic imaging (CT and MRI) with a focus on diagnosis, prediction prognosis, and assessment of response to therapy in gastrointestinal cancers, describing mostly the results for each pre-eminent tumor. In particular, this paper provides a general description of the main radiomic drawbacks and future challenges, which limit radiomic application in clinical setting as routine. Further investigations need to standardize and validate the Radiomics as a helpful tool in management of oncologic patients. In that context, Radiomics has been playing a relevant role and could be considered as a future imaging landscape.
   Radiomics has been playing a pivotal role in oncological translational imaging, particularly in cancer diagnosis, prediction prognosis, and therapy response assessment. Recently, promising results were achieved in management of cancer patients by extracting mineable high-dimensional data from medical images, supporting clinicians in decision-making process in the new era of target therapy and personalized medicine. Radiomics could provide quantitative data, extracted from medical images, that could reflect microenvironmental tumor heterogeneity, which might be a useful information for treatment tailoring. Thus, it could be helpful to overcome the main limitations of traditional tumor biopsy, often affected by bias in tumor sampling, lack of repeatability and possible procedure complications. This quantitative approach has been widely investigated as a non-invasive and an objective imaging biomarker in cancer patients; however, it is not applied as a clinical routine due to several limitations related to lack of standardization and validation of images acquisition protocols, features segmentation, extraction, processing, and data analysis. This field is in continuous evolution in each type of cancer, and results support the idea that in the future Radiomics might be a reliable application in oncologic imaging. The first part of this review aimed to describe some radiomic technical principles and clinical applications to gastrointestinal oncologic imaging (CT and MRI) with a focus on diagnosis, prediction prognosis, and assessment of response to therapy.
C1 [Caruso, Damiano; Polici, Michela; Zerunian, Marta; Pucciarelli, Francesco; Guido, Gisella; Polidori, Tiziano; Landolfi, Federica; Nicolai, Matteo; Lucertini, Elena; Bracci, Benedetta; Nacci, Ilaria; Rucci, Carlotta; Iannicelli, Elsa; Laghi, Andrea] Sapienza Univ Rome, St Andrea Univ Hosp, Radiol Unit, Dept Med Surg Sci & Translat Med, I-00189 Rome, Italy.
   [Tarallo, Mariarita] Sapienza Univ Rome, Umberto I Univ Hosp, Dept Surg Pietro Valdoni, Viale Policlin 155, I-00161 Rome, Italy.
C3 Sapienza University Rome; Azienda Ospedaliera Sant'Andrea; Sapienza
   University Rome; University Hospital Sapienza Rome
RP Laghi, A (corresponding author), Sapienza Univ Rome, St Andrea Univ Hosp, Radiol Unit, Dept Med Surg Sci & Translat Med, I-00189 Rome, Italy.
EM damiano.caruso@uniroma1.it; michela.polici@uniroma1.it;
   marta.zerunian@uniroma1.it; francesco.pucciarelli@uniroma1.it;
   gisella.guido@uniroma1.it; tiziano.polidori@uniroma1.it;
   federica.l2005@libero.it; matteo.nicolai@uniroma1.it;
   elena.lucertini@uniroma1.it; mariarita.tarallo@uniroma1.it;
   benedetta.bracci@uniroma1.it; ilaria.nacci@uniroma1.it;
   carlotta.rucci@uniroma1.it; elsa.iannicelli@uniroma1.it;
   andrea.laghi@uniroma1.it
RI Guido, Gisella/AAX-6161-2021; Caruso, Damiano/ABK-3390-2022; Laghi,
   Andrea/AAQ-9807-2020; Zerunian, Marta/AAC-9731-2021; Polidori,
   Tiziano/LRC-4269-2024; Landolfi, Federica/P-1134-2016; Laghi,
   Andrea/A-2343-2011
OI Guido, Gisella/0000-0002-0711-2975; Caruso, Damiano/0000-0001-9285-4764;
   Pucciarelli, Francesco/0000-0001-7263-1125; Bracci,
   Benedetta/0000-0002-2017-8493; Landolfi, Federica/0000-0002-2208-2559;
   NACCI, ILARIA/0000-0002-8659-131X; Polici, Michela/0000-0001-7331-6901;
   Zerunian, Marta/0000-0003-4635-7999; Laghi, Andrea/0000-0002-3091-7819;
   Tarallo, Mariarita/0000-0003-3783-4749; Lucertini,
   Elena/0000-0002-5631-2666
FU AIRC (Associazione Italiana per la Ricerca sul Cancro) [IG 2020/24974]
FX This study is funded by AIRC (Associazione Italiana per la Ricerca sul
   Cancro) IG 2020/24974.
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NR 88
TC 35
Z9 35
U1 1
U2 30
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUN
PY 2021
VL 13
IS 11
AR 2522
DI 10.3390/cancers13112522
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SP3ZF
UT WOS:000659609500001
PM 34063937
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Fu, XH
   Ying, JE
   Yang, L
   Fang, WJ
   Han, WD
   Hu, HG
   Zhang, SZ
   Yuan, Y
AF Fu, Xianhua
   Ying, Jieer
   Yang, Liu
   Fang, Weijia
   Han, Weidong
   Hu, Hanguang
   Zhang, Suzhan
   Yuan, Ying
TI Dual targeted therapy with pyrotinib and trastuzumab for HER2-positive
   advanced colorectal cancer: A phase 2 trial
SO CANCER SCIENCE
LA English
DT Article
DE colorectal cancer; human epidermal growth factor receptor 2; pyrotinib;
   RAS mutation; trastuzumab
ID OPEN-LABEL; CAPECITABINE; MULTICENTER; RESISTANCE; LAPATINIB
AB This trial was initiated to evaluate the efficacy and safety of pyrotinib in combination with trastuzumab in patients with human epidermal growth factor receptor 2 (HER2)-positive recurrent/metastatic colorectal cancer (CRC). In this single-arm, open-label, multicenter, phase 2 trial patients with HER2-positive recurrent/metastatic CRC were enrolled and received oral pyrotinib 400 mg once a day plus intravenous trastuzumab 8 mg/kg loading dose followed by 6 mg/kg once every 3 weeks. The primary endpoint was the objective response rate (ORR). Disease control rate (DCR), progression-free survival (PFS), duration of response, and safety were assessed as secondary endpoints. From December 2019 to October 2021, a total of 20 patients were enrolled and 18 of them were evaluable for response. All patients were B-rapidly accelerated fibrosarcoma (BRAF) wild type. Four patients achieved partial response, with an ORR of 22.2% (4/18, 95% confidence interval [CI] 6.4-47.6) and DCR of 61.1% (11/18, 95% CI 35.8-82.7), while the ORR and DCR were 33.3% (4/12, 95% CI 13.8-60.9) and 83.3% (10/12, 95% CI 51.6-97.9), respectively, in RAS wild-type patients. At the time of cut-off day, median follow-up was 10.7 months (range 3.8-13.8). The median PFS was 3.4 months (95% CI 1.8-4.3) in the overall population and 4.3 months (95% CI 3.2-8.5) in the RAS wild-type group. The most common adverse event of grade >= 3 was diarrhea (13/20, 65.0%). Pyrotinib combined with trastuzumab showed promising antitumor activity and a manageable safety profile in patients with RAS/BRAF wild-type HER2-positive advanced CRC.
C1 [Fu, Xianhua; Hu, Hanguang; Yuan, Ying] Zhejiang Univ, Affiliated Hosp 2, Zhejiang Prov Clin Res Ctr CANC, Sch Med,Canc Ctr,Dept Med Oncol,Key Lab Canc Preve, Hangzhou, Zhejiang, Peoples R China.
   [Ying, Jieer] Chinese Acad Sci, Univ Chinese Acad Sci, Zhejiang Canc Hosp, Canc Hosp,Inst Canc & Basic Med IBMC,Dept Hepatopa, Hangzhou, Zhejiang, Peoples R China.
   [Yang, Liu] Hangzhou Med Coll, Zhejiang Prov Peoples Hosp, Peoples Hosp, Dept Oncol, Hangzhou, Zhejiang, Peoples R China.
   [Fang, Weijia] Zhejiang Univ, Affiliated Hosp 1, Sch Med, Dept Med Oncol, Hangzhou, Zhejiang, Peoples R China.
   [Han, Weidong] Zhejiang Univ, Sir Run Run Shaw Hosp, Sch Med, Dept Med Oncol, Hangzhou, Zhejiang, Peoples R China.
   [Zhang, Suzhan] Zhejiang Univ, Affiliated Hosp 2, Zhejiang Prov Clin Res Ctr CANC, Sch Med,Canc Ctr,Canc Inst,Key Lab Canc Prevent &, Hangzhou, Zhejiang, Peoples R China.
   [Zhang, Suzhan] Zhejiang Univ, Affiliated Hosp 2, Zhejiang Prov Clin Res Ctr CANC, Sch Med,Canc Ctr,Dept Colorectal Surg, Hangzhou, Zhejiang, Peoples R China.
   [Zhang, Suzhan; Yuan, Ying] Zhejiang Univ, Affiliated Hosp 2, Sch Med, 88 Jiefang Rd, Hangzhou 310009, Peoples R China.
C3 Zhejiang University; Chinese Academy of Sciences; University of Chinese
   Academy of Sciences, CAS; Zhejiang Cancer Hospital; Hangzhou Medical
   College; Zhejiang Provincial People's Hospital; Zhejiang University;
   Zhejiang University; Zhejiang University; Zhejiang University; Zhejiang
   University
RP Zhang, SZ; Yuan, Y (corresponding author), Zhejiang Univ, Affiliated Hosp 2, Sch Med, 88 Jiefang Rd, Hangzhou 310009, Peoples R China.
EM zrsj@zju.edu.cn; yuanying1999@zju.edu.cn
RI ; Fang, Weijia/AEN-6210-2022
OI Ying, Yuan/0000-0002-3922-9553; Fang, Weijia/0000-0001-9849-347X
FU National Natural Science Foundation of China; Provincial Key R&D Program
   of Zhejiang Province;  [81872481];  [81402365];  [2021C03125]
FX ACKNOWLEDGEMENT This research was funded by the National Natural Science
   Foundation of China (No. 81872481 and No.81402365) and the Provincial
   Key R&D Program of Zhejiang Province (2021C03125).
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NR 29
TC 12
Z9 14
U1 1
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1347-9032
EI 1349-7006
J9 CANCER SCI
JI Cancer Sci.
PD MAR
PY 2023
VL 114
IS 3
BP 1067
EP 1074
DI 10.1111/cas.15660
EA DEC 2022
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA C9MW7
UT WOS:000895726100001
PM 36382603
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Naemi, AA
   Salmanian, AH
   Noormohammadi, Z
   Amani, J
AF Naemi, Azam Almolok
   Salmanian, Ali Hatef
   Noormohammadi, Zahra
   Amani, Jafar
TI A novel EGFR-specific recombinant ricin-panitumumab (scFv) immunotoxin
   against breast and colorectal cancer cell lines;<i> in</i><i> silico</i>
   and<i> in</i><i> vitro</i> analyses
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE Cancer therapy; Epidermal growth factor receptor (EGFR); Immunotoxin
   (IT); Ricin toxin A chain (RTA); Single chain fragment variable (scFv)
ID EPIDERMAL-GROWTH-FACTOR; FACTOR RECEPTOR; PROTEIN-STRUCTURE; TARGETING
   EGFR; DRUG CONJUGATE; IMMUNOGENICITY; INACTIVATION; EXPRESSION;
   PREDICTION; ANTIBODIES
AB The Epidermal Growth Factor Receptor (EGFR) has been of high importance as it is over expressed in a wide diversity of epithelial cancers, promoting cell proliferation and survival pathways. Recombinant immunotoxins (ITs) have emerged as a promising targeted therapy for cancer treatment. In this study, we aimed to investigate the antitumor activity of a novel recombinant immunotoxin designed against EGFR. Using an in silico approach, we confirmed the stability of the RTA-scFv fusion protein. The immunotoxin was successfully cloned and expressed in the pET32a vector, and the purified protein was analyzed by electrophoresis and western blotting. In vitro evaluations were conducted to assess the biological activities of the recombinant proteins (RTA-scFv, RTA, scFv). The novel immunotoxin demonstrated significant anti-proliferative and pro-apoptotic effects against cancer cell lines. The MTT cytotoxicity assay revealed a decrease in cell viability in the treated cancer cell lines. Additionally, Annexin V/Propidium iodide staining followed by flow cytometry analysis showed a significant induction of apoptosis in the cancer cell lines, with half maximal inhibitory concentration (IC50) values of 81.71 nM for MDA-MB-468 and 145.2 nM for HCT116 cells (P < 0.05). Furthermore, the EGFR-specific immunotoxin exhibited non-allergenic properties. The recombinant protein demonstrated high affinity binding to EGFR. Overall, this study presents a promising strategy for the development of recombinant immunotoxins as potential candidates for the treatment of EGFR-expressing cancers.
C1 [Naemi, Azam Almolok; Noormohammadi, Zahra] Islamic Azad Univ, Dept Biol, Sci & Res Branch, Tehran, Iran.
   [Salmanian, Ali Hatef] Natl Inst Genet Engn & Biotechnol NIGEB, Dept Agr Biotechnol, Shahrak E Pajoohesh 15th Km,Tehran Karaj Highway, Tehran, Iran.
   [Amani, Jafar] Green Gene Co, Dept Mol Biol, Tehran, Iran.
C3 Islamic Azad University
RP Salmanian, AH (corresponding author), Natl Inst Genet Engn & Biotechnol NIGEB, Dept Agr Biotechnol, Shahrak E Pajoohesh 15th Km,Tehran Karaj Highway, Tehran, Iran.
EM parinaznaemi@gmail.com; salman@nigeb.ac.ir; z-nouri@srbiau.ac.ir;
   Jafar.amani@gmail.com
RI Amani, Jafar/V-3534-2019; Noormohammadi, Zahra/AAS-6661-2021
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NR 65
TC 1
Z9 1
U1 0
U2 3
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0014-2999
EI 1879-0712
J9 EUR J PHARMACOL
JI Eur. J. Pharmacol.
PD SEP 15
PY 2023
VL 955
AR 175894
DI 10.1016/j.ejphar.2023.175894
EA JUL 2023
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA O4XD4
UT WOS:001043849900001
PM 37429519
DA 2025-01-04
ER

PT J
AU Zou, Q
   Liu, M
   Liu, KW
   Zhang, Y
   North, BJ
   Wang, B
AF Zou, Qiang
   Liu, Meng
   Liu, Kewei
   Zhang, Yi
   North, Brian J. J.
   Wang, Bin
TI E3 ubiquitin ligases in cancer stem cells: key regulators of cancer
   hallmarks and novel therapeutic opportunities
SO CELLULAR ONCOLOGY
LA English
DT Review
DE Cancer stem cells (CSCs); Ubiquitin-proteosome system; E3 ubiquitin
   ligases; Proteolysis-targeting chimera (PROTAC); Molecularly targeted
   therapy
ID TO-MESENCHYMAL TRANSITION; BET INHIBITOR RESISTANCE; COLORECTAL-CANCER;
   PROSTATE-CANCER; DEGRADATION; GLIOBLASTOMA; PROMOTES; PROTEIN; MYC;
   PROLIFERATION
AB BackgroundHuman malignancies are composed of heterogeneous subpopulations of cancer cells with phenotypic and functional diversity. Among them, a unique subset of cancer stem cells (CSCs) has both the capacity for self-renewal and the potential to differentiate and contribute to multiple tumor properties. As such, CSCs are promising cellular targets for effective cancer therapy. At the molecular level, hyper-activation of multiple stemness regulatory signaling pathways and downstream transcription factors play critical roles in controlling CSCs establishment and maintenance. To regulate CSC properties, these stemness pathways are controlled by post-translational modifications including, but not limited to phosphorylation, acetylation, methylation, and ubiquitination.ConclusionIn this review, we focus on E3 ubiquitin ligases and their roles and mechanisms in regulating essential hallmarks of CSCs, such as self-renewal, invasion and metastasis, metabolic reprogramming, immune evasion, and therapeutic resistance. Moreover, we discuss emerging therapeutic approaches to eliminate CSCs through targeting E3 ubiquitin ligases by chemical inhibitors and proteolysis-targeting chimera (PROTACs) which are currently under development at the discovery, preclinical, and clinical stages. Several outstanding issues such as roles for E3 ubiquitin ligases in heterogeneity and phenotypical/functional evolution of CSCs remain to be studied under pathologically and clinically relevant conditions. With the rapid application of functional genomic and proteomic approaches at single cell, spatiotemporal, and even single molecule levels, we anticipate that more specific and precise functions of E3 ubiquitin ligases will be delineated in dictating CSC properties. Rational design and proper translation of these mechanistic understandings may lead to novel therapeutic modalities for cancer procession medicine.
C1 [Zou, Qiang; Zhang, Yi] Chongqing Univ Med Sch, Chongqing Univ Canc Hosp, Dept Hepatobiliary Pancreat Tumor Ctr, Chongqing 400030, Peoples R China.
   [Zou, Qiang; Liu, Meng; Liu, Kewei; Wang, Bin] Third Mil Med Univ, Army Med Univ, Daping Hosp, Dept Gastroenterol, 10 Changjiang Branch Rd, Chongqing 400042, Peoples R China.
   [Zou, Qiang; Liu, Meng; Liu, Kewei; Wang, Bin] Third Mil Med Univ, Army Med Univ, Daping Hosp, Chongqing Key Lab Digest Malignancies, 10 Changjiang Branch Rd, Chongqing 400042, Peoples R China.
   [Liu, Meng] Chongqing Univ Med Sch, Chongqing Univ Canc Hosp, Dept Gastroenterol, Chongqing 400030, Peoples R China.
   [North, Brian J. J.] Creighton Univ Sch Med, Biomed Sci Dept, Omaha, NE 68178 USA.
   [Wang, Bin] Third Mil Med Univ, Army Med Univ, Southwest Hosp, Inst Pathol, Chongqing 400038, Peoples R China.
   [Wang, Bin] Third Mil Med Univ, Army Med Univ, Southwest Hosp, Southwest Canc Ctr, Chongqing 400038, Peoples R China.
   [Wang, Bin] Third Mil Med Univ, Army Med Univ, Southwest Hosp, Key Lab Tumor Immunopathol,Minist Educ China, Chongqing 400038, Peoples R China.
   [Wang, Bin] Jinfeng Lab, Chongqing 401329, Peoples R China.
C3 Chongqing Medical University; Army Medical University; Army Medical
   University; Chongqing Medical University; Creighton University; Army
   Medical University; Army Medical University; Army Medical University
RP Zhang, Y (corresponding author), Chongqing Univ Med Sch, Chongqing Univ Canc Hosp, Dept Hepatobiliary Pancreat Tumor Ctr, Chongqing 400030, Peoples R China.; Wang, B (corresponding author), Third Mil Med Univ, Army Med Univ, Daping Hosp, Dept Gastroenterol, 10 Changjiang Branch Rd, Chongqing 400042, Peoples R China.; Wang, B (corresponding author), Third Mil Med Univ, Army Med Univ, Daping Hosp, Chongqing Key Lab Digest Malignancies, 10 Changjiang Branch Rd, Chongqing 400042, Peoples R China.; North, BJ (corresponding author), Creighton Univ Sch Med, Biomed Sci Dept, Omaha, NE 68178 USA.; Wang, B (corresponding author), Third Mil Med Univ, Army Med Univ, Southwest Hosp, Inst Pathol, Chongqing 400038, Peoples R China.; Wang, B (corresponding author), Third Mil Med Univ, Army Med Univ, Southwest Hosp, Southwest Canc Ctr, Chongqing 400038, Peoples R China.; Wang, B (corresponding author), Third Mil Med Univ, Army Med Univ, Southwest Hosp, Key Lab Tumor Immunopathol,Minist Educ China, Chongqing 400038, Peoples R China.; Wang, B (corresponding author), Jinfeng Lab, Chongqing 401329, Peoples R China.
EM zhangyi9611@163.com; BrianNorth@creighton.edu; wb_tmmu@126.com
RI Liu, Mingyue/GZG-7821-2022; Wang, Bin/W-9917-2019
OI Wang, Bin/0000-0001-5574-1760
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NR 156
TC 8
Z9 8
U1 1
U2 19
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 2211-3428
EI 2211-3436
J9 CELL ONCOL
JI Cell. Oncol.
PD JUN
PY 2023
VL 46
IS 3
BP 545
EP 570
DI 10.1007/s13402-023-00777-x
EA FEB 2023
PG 26
WC Oncology; Cell Biology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology; Pathology
GA G8FT2
UT WOS:000926383000001
PM 36745329
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Brauswetter, D
   Dános, K
   Gurbi, B
   Félegyházi, EF
   Birtalan, E
   Meggyesházi, N
   Krenács, T
   Tamás, L
   Peták, I
AF Brauswetter, Diana
   Danos, Kornel
   Gurbi, Bianka
   Felegyhazi, Eva Fruzsina
   Birtalan, Ede
   Meggyeshazi, Nora
   Krenacs, Tibor
   Tamas, Laszlo
   Petak, Istvan
TI Copy number gain of PIK3CA and MET is associated with poor prognosis in
   head and neck squamous cell carcinoma
SO VIRCHOWS ARCHIV
LA English
DT Article
DE MET; PIK3CA; CNG(copy number gain); Head and neck cancer (HNC)
ID METASTATIC COLORECTAL-CANCER; GROWTH-FACTOR RECEPTOR; LUNG-CANCER;
   HUMAN-PAPILLOMAVIRUS; 1ST-LINE TREATMENT; PRIMARY RESISTANCE; GENE;
   EGFR; AMPLIFICATION; CETUXIMAB
AB The incidence of head and neck squamous cell carcinomas is still growing, and the long-term prognosis of advanced disease remains poor. Only a fraction of head and neck cancers are sensitive to the EGFR-inhibitor cetuximab, which is the only registered targeted therapy available today. In several cancers, gene copy number alterations of MET and PIK3CA have been found to be prognostic and predictive for therapy response. The aim of this study was to systematically analyze in head and neck cancers the pathological characteristics and prognostic significance of copy number changes of MET and PIK3CA genes. MET and PIK3CA copy numbers were analyzed by fluorescence in situ hybridization in tumor samples of 152 patients. Expression of EGFR, p16, and Ki67 was studied by immunohistochemistry. High polysomy of PIK3CA (chromosome 3) was found in 20 % of cases and amplification in 4.5 %. Regarding MET, 35 % of cases showed low or high polysomy of the gene (chromosome 7), while no intra-chromosomal amplification of MET was detected. PIK3CA copy number gain (high polysomy or amplification) was significantly associated with shorter disease-specific survival, larger tumor volume, and lower p16 expression. MET copy number gain (low or high polysomy) in tumors was significantly associated with shorter disease-specific survival and lower level of EGFR. PIK3CA and MET may play an important role in oncogenesis of certain specific subtypes of head and neck cancer. There is an urgent need for the development of novel targeted therapies against these tumors associated with poor prognosis.
C1 [Brauswetter, Diana; Gurbi, Bianka; Felegyhazi, Eva Fruzsina; Petak, Istvan] MTA SE Pathobiochem Res Grp, Tuzolto Str 37-47, H-1094 Budapest, Hungary.
   [Danos, Kornel; Birtalan, Ede; Tamas, Laszlo] Semmelweis Univ, Dept Otorhinolaryngol Head & Neck Surg, Szigony Str 36, H-1083 Budapest, Hungary.
   [Meggyeshazi, Nora; Krenacs, Tibor] Semmelweis Univ, Dept Pathol & Expt Canc Res, Ulloi Str 26, H-1085 Budapest, Hungary.
   [Krenacs, Tibor] MTA SE Tumor Progress Res Grp, Ulloi Str 26, H-1085 Budapest, Hungary.
C3 Semmelweis University; Semmelweis University; Semmelweis University
RP Brauswetter, D (corresponding author), MTA SE Pathobiochem Res Grp, Tuzolto Str 37-47, H-1094 Budapest, Hungary.
EM brauswetter.diana@med.semmelweis-univ.hu
RI Danos, Kornel/JAC-5954-2023; Petak, Istvan/X-3656-2019; Gurbi,
   Bianka/F-4220-2017; Birtalan, Ede/N-2693-2014
OI Gurbi, Bianka/0000-0002-5635-6255; Birtalan, Ede/0000-0002-5699-3545;
   Kornel, Danos/0000-0002-3829-8266
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NR 42
TC 17
Z9 19
U1 0
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0945-6317
EI 1432-2307
J9 VIRCHOWS ARCH
JI Virchows Arch.
PD MAY
PY 2016
VL 468
IS 5
BP 579
EP 587
DI 10.1007/s00428-016-1905-1
PG 9
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA DL5ZX
UT WOS:000375717200007
PM 26832731
DA 2025-01-04
ER

PT J
AU Gao, Q
   Feng, J
   Liu, WC
   Wen, CY
   Wu, YH
   Liao, Q
   Zou, L
   Sui, XB
   Xie, T
   Zhang, JM
   Hu, YC
AF Gao, Quan
   Feng, Jiao
   Liu, Wencheng
   Wen, Chengyong
   Wu, Yihan
   Liao, Qian
   Zou, Liang
   Sui, Xinbing
   Xie, Tian
   Zhang, Jinming
   Hu, Yichen
TI Opportunities and challenges for co-delivery nanomedicines based on
   combination of phytochemicals with chemotherapeutic drugs in cancer
   treatment
SO ADVANCED DRUG DELIVERY REVIEWS
LA English
DT Review
DE Drug combination; Phytochemicals; Drug resistance; Nanosystem; Co
   -delivery
ID HEPATOCELLULAR-CARCINOMA CELLS; NF-KAPPA-B; MESOPOROUS SILICA
   NANOPARTICLES; P-GLYCOPROTEIN EXPRESSION; HUMAN COLORECTAL-CANCER;
   BREAST-CANCER; GASTRIC-CANCER; LUNG-CANCER; MULTIDRUG-RESISTANCE;
   PANCREATIC-CANCER
AB The therapeutic limitations such as insufficient efficacy, drug resistance, metastasis, and undesirable side effects are frequently caused by the long duration monotherapy based on chemotherapeutic drugs. mul-tiple combinational anticancer strategies such as nucleic acids combined with chemotherapeutic agents, chemotherapeutic combinations, chemotherapy and tumor immunotherapy combinations have been embraced, holding great promise to counter these limitations, while still taking including some potential risks.Nowadays, an increasing number of research has manifested the anticancer effects of phytochemicals mediated by modulating cancer cellular events directly as well as the tumor microenvironment. Specifically, these natural compounds exhibited suppression of cancer cell proliferation, apoptosis, migration and invasion of cancer cells, P-glycoprotein inhibition, decreasing vascularization and activa-tion of tumor immunosuppression. Due to the low toxicity and multiple modulation pathways of these phytochemicals, the combination of chemotherapeutic agents with natural compounds acts as a novel approach to cancer therapy to increase the efficiency of cancer treatments as well as reduce the adverse consequences. In order to achieve the maximized combination advantages of small-molecule chemother-apeutic drugs and natural compounds, a variety of functional nano-scaled drug delivery systems, such as liposomes, host-guest supramolecules, supramolecules, dendrimers, micelles and inorganic systems have been developed for dual/multiple drug co-delivery. These co-delivery nanomedicines can improve pharmacokinetic behavior, tumor accumulation capacity, and achieve tumor site-targeting delivery. In that way, the improved antitumor effects through multiple-target therapy and reduced side effects by decreasing dose can be implemented. Here, we present the synergistic anticancer outcomes and the related mechanisms of the combination of phytochemicals with small-molecule anticancer drugs. We also focus on illustrating the design concept, and action mechanisms of nanosystems with co-delivery of drugs to synergistically improve anticancer efficacy. In addition, the challenges and prospects of how these insights can be translated into clinical benefits are discussed.(c) 2022 Published by Elsevier B.V.
C1 [Gao, Quan; Feng, Jiao; Liu, Wencheng; Wen, Chengyong; Sui, Xinbing; Xie, Tian] Hangzhou Normal Univ, Affiliated Hosp, Sch Pharm, Hangzhou 311121, Zhejiang, Peoples R China.
   [Gao, Quan; Feng, Jiao; Liu, Wencheng; Wen, Chengyong; Sui, Xinbing; Xie, Tian] Hangzhou Normal Univ, Affiliated Hosp, Dept Med Oncol, Hangzhou 311121, Zhejiang, Peoples R China.
   [Gao, Quan; Feng, Jiao; Liu, Wencheng; Wen, Chengyong; Sui, Xinbing; Xie, Tian] Hangzhou Normal Univ, Key Lab Elemene Class Anticanc Chinese Med, Hangzhou 311121, Zhejiang, Peoples R China.
   [Gao, Quan; Feng, Jiao; Liu, Wencheng; Wen, Chengyong; Sui, Xinbing; Xie, Tian] Hangzhou Normal Univ, Engn Lab Dev & Applicat Tradit Chinese Med, Hangzhou 311121, Zhejiang, Peoples R China.
   [Gao, Quan; Feng, Jiao; Liu, Wencheng; Wen, Chengyong; Sui, Xinbing; Xie, Tian] Hangzhou Normal Univ, Collaborat Innovat Ctr Tradit Chinese Med Zhejiang, Hangzhou 311121, Zhejiang, Peoples R China.
   [Wu, Yihan; Liao, Qian; Zhang, Jinming] Chengdu Univ Tradit Chinese Med, Coll Pharm, State Key Lab Southwestern Chinese Med Resources, Chengdu 611137, Peoples R China.
   [Hu, Yichen] Chengdu Univ, Key Lab Coarse Cereal Proc, Minist Agr & Rural Affairs, 2025 Cheng Luo Rd, Chengdu 610106, Sichuan, Peoples R China.
C3 Hangzhou Normal University; Hangzhou Normal University; Hangzhou Normal
   University; Hangzhou Normal University; Hangzhou Normal University;
   Chengdu University of Traditional Chinese Medicine; Ministry of
   Agriculture & Rural Affairs; Chengdu University
RP Sui, XB; Xie, T (corresponding author), Hangzhou Normal Univ, Affiliated Hosp, Sch Pharm, Hangzhou 311121, Zhejiang, Peoples R China.; Sui, XB; Xie, T (corresponding author), Hangzhou Normal Univ, Affiliated Hosp, Dept Med Oncol, Hangzhou 311121, Zhejiang, Peoples R China.; Zhang, JM (corresponding author), Chengdu Univ Tradit Chinese Med, Coll Pharm, State Key Lab Southwestern Chinese Med Resources, Chengdu 611137, Peoples R China.; Hu, YC (corresponding author), Chengdu Univ, Key Lab Coarse Cereal Proc, Minist Agr & Rural Affairs, 2025 Cheng Luo Rd, Chengdu 610106, Sichuan, Peoples R China.
EM xbs@hznu.edu.cn; hzzju@hznu.edu.cn; cdutcmzjm@126.com;
   huyichen0323@126.com
RI Liu, Wen-Cheng/AGI-3519-2022; meng, meng/KHW-8303-2024; Xie,
   Tian/LUA-1225-2024; Sui, Xinbing/ADE-9174-2022
OI Sui, Xinbing/0000-0001-7330-0467
FU National Natural Science Foundation of China [81874380, 82022075,
   81973662]; Zhejiang Provincial Nat- ural Science Foundation of China for
   Distinguished Young Scholars [LR18H160001]; Sichuan Provincial Natural
   Science Foundation for Distinguished Young Scholars [2019JDJQ0049];
   Zhejiang Provincial Natural Science Foundation of China [LQ21H160038];
   Zhejiang Province Science and Technology Project of TCM [2019ZZ016]
FX This work was financially funded by the grants National Natural Science
   Foundation of China (No. 81874380 and 82022075 to Xin- bing Sui, No.
   81973662 to Jinming Zhang) , Zhejiang Provincial Nat- ural Science
   Foundation of China for Distinguished Young Scholars (No. LR18H160001,
   to Xinbing Sui) , Sichuan Provincial Natural Science Foundation for
   Distinguished Young Scholars (No. 2019JDJQ0049, to Jinming Zhang) ,
   Zhejiang Provincial Natural Science Foundation of China (LQ21H160038, to
   Jiao Feng) , and Zhe- jiang Province Science and Technology Project of
   TCM (No. 2019ZZ016, to Xinbing Sui) .
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NR 271
TC 124
Z9 125
U1 59
U2 287
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0169-409X
EI 1872-8294
J9 ADV DRUG DELIVER REV
JI Adv. Drug Deliv. Rev.
PD SEP
PY 2022
VL 188
AR 114445
DI 10.1016/j.addr.2022.114445
EA JUL 2022
PG 30
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 4M5MH
UT WOS:000853367300007
PM 35820601
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Lu, N
   Guan, X
   Zhu, JG
   Li, Y
   Zhang, JP
AF Lu, Na
   Guan, Xiao
   Zhu, Jianguo
   Li, Yuan
   Zhang, Jianping
TI A Contrast-Enhanced CT-Based Deep Learning System for Preoperative
   Prediction of Colorectal Cancer Staging and RAS Mutation
SO CANCERS
LA English
DT Article
DE colorectal cancer; stage; RAS status; deep learning; convolutional
   neural networks; transformer
ID LYMPH-NODE METASTASIS; RADIOMIC FEATURES; ARTIFICIAL-INTELLIGENCE;
   TARGETED THERAPY; PROGNOSIS; DIAGNOSIS; ADENOCARCINOMA; IDENTIFICATION;
   NOMOGRAM; FOLFIRI
AB Simple Summary This study explored the role of CT-based deep learning in detecting colorectal cancer tumor location and preoperatively predicting the stage and RAS gene mutation status of colorectal cancer patients. The deep learning model we built achieved excellent performance. The detection network based on Yolov7 realized the detection and preoperative staging of colorectal cancer with an average mean accuracy of 0.98 in the validation cohort. The vision transformer-based prediction network achieved accurate prediction of preoperative RAS in colorectal cancer patients, achieving an area under the receiver operating characteristic curve (AUC) of 0.9591 and 0.9554 in the test cohort and the validation cohort, respectively. This study also explored the clinical applications of deep learning models. Based on the proposed detection network and prediction network, we built a deep learning system for clinicians who do not understand deep learning.Abstract Purpose: This study aimed to build a deep learning system using enhanced computed tomography (CT) portal-phase images for predicting colorectal cancer patients' preoperative staging and RAS gene mutation status. Methods: The contrast-enhanced CT image dataset comprises the CT portal-phase images from a retrospective cohort of 231 colorectal cancer patients. The deep learning system was developed via migration learning for colorectal cancer detection, staging, and RAS gene mutation status prediction. This study used pre-trained Yolov7, vision transformer (VIT), swin transformer (SWT), EfficientNetV2, and ConvNeXt. 4620, and contrast-enhanced CT images and annotated tumor bounding boxes were included in the tumor identification and staging dataset. A total of 19,700 contrast-enhanced CT images comprise the RAS gene mutation status prediction dataset. Results: In the validation cohort, the Yolov7-based detection model detected and staged tumors with a mean accuracy precision (IoU = 0.5) (mAP_0.5) of 0.98. The area under the receiver operating characteristic curve (AUC) in the test set and validation set for the VIT-based prediction model in predicting the mutation status of the RAS genes was 0.9591 and 0.9554, respectively. The detection network and prediction network of the deep learning system demonstrated great performance in explaining contrast-enhanced CT images. Conclusion: In this study, a deep learning system was created based on the foundation of contrast-enhanced CT portal-phase imaging to preoperatively predict the stage and RAS mutation status of colorectal cancer patients. This system will help clinicians choose the best treatment option to increase colorectal cancer patients' chances of survival and quality of life.
C1 [Lu, Na; Guan, Xiao; Zhang, Jianping] Nanjing Med Univ, Dept Gen Surg, Affiliated Hosp 2, 121 Jiangjiayuan Rd, Nanjing 210011, Peoples R China.
   [Zhu, Jianguo] Nanjing Med Univ, Dept Radiol, Affiliated Hosp 2, Nanjing 210011, Peoples R China.
   [Li, Yuan] Nanjing Med Univ, Sch Publ Hlth, Key Lab Modern Toxicol, Minist Educ, Nanjing 211166, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University; Nanjing Medical
   University
RP Zhang, JP (corresponding author), Nanjing Med Univ, Dept Gen Surg, Affiliated Hosp 2, 121 Jiangjiayuan Rd, Nanjing 210011, Peoples R China.
EM n2248457306@163.com; xiaoguan@stu.njmu.edu.cn; zhujianguo@njmu.edu.cn;
   liyuan@njmu.edu.cn; drzhangjp@njmu.edu.cn
FU The authors thanked all colleagues who contributed to this work.
FX The authors thanked all colleagues who contributed to this work.
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NR 74
TC 1
Z9 1
U1 5
U2 13
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD SEP
PY 2023
VL 15
IS 18
AR 4497
DI 10.3390/cancers15184497
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA S5EI5
UT WOS:001071393400001
PM 37760468
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Goricar, K
   Dolzan, V
   Lenassi, M
AF Goricar, Katja
   Dolzan, Vita
   Lenassi, Metka
TI Extracellular Vesicles: A Novel Tool Facilitating Personalized Medicine
   and Pharmacogenomics in Oncology
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE extracellular vesicle; pharmacogenomics; liquid biopsy; cancer;
   biomarker; personalized medicine
ID CELL-FREE DNA; METASTATIC BREAST-CANCER; DOUBLE-STRANDED DNA;
   COLORECTAL-CANCER; LIQUID BIOPSY; CIRCULATING EXOSOMES; PROTEOMIC
   ANALYSIS; LEUKEMIA-CELLS; SERUM EXOSOMES; MUTANT KRAS
AB Biomarkers that can guide cancer therapy based on patients' individual cancer molecular signature can enable a more effective treatment with fewer adverse events. Data on actionable somatic mutations and germline genetic variants, studied by personalized medicine and pharmacogenomics, can be obtained from tumor tissue or blood samples. As tissue biopsy cannot reflect the heterogeneity of the tumor or its temporal changes, liquid biopsy is a promising alternative approach. In recent years, extracellular vesicles (EVs) have emerged as a potential source of biomarkers in liquid biopsy. EVs are a heterogeneous population of membrane bound particles, which are released from all cells and accumulate into body fluids. They contain various proteins, lipids, nucleic acids (miRNA, mRNA, and DNA) and metabolites. In cancer, EV biomolecular composition and concentration are changed. Tumor EVs can promote the remodeling of the tumor microenvironment and pre-metastatic niche formation, and contribute to transfer of oncogenic potential or drug resistance during chemotherapy. This makes them a promising source of minimally invasive biomarkers. A limited number of clinical studies investigated EVs to monitor cancer progression, tumor evolution or drug resistance and several putative EV-bound protein and RNA biomarkers were identified. This review is focused on EVs as novel biomarker source for personalized medicine and pharmacogenomics in oncology. As several pharmacogenes and genes associated with targeted therapy, chemotherapy or hormonal therapy were already detected in EVs, they might be used for fine-tuning personalized cancer treatment.
C1 [Goricar, Katja; Dolzan, Vita; Lenassi, Metka] Univ Ljubljana, Inst Biochem & Mol Genet, Fac Med, Ljubljana, Slovenia.
C3 University of Ljubljana
RP Lenassi, M (corresponding author), Univ Ljubljana, Inst Biochem & Mol Genet, Fac Med, Ljubljana, Slovenia.
EM metka.lenassi@mf.uni-lj.si
FU Slovenian Research Agency (ARRS) [P1-0170, J3-9255, J3-1753]
FX This work was financially supported by the Slovenian Research Agency
   (ARRS Grant Nos. P1-0170, J3-9255, and J3-1753).
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NR 204
TC 17
Z9 17
U1 0
U2 11
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD APR 30
PY 2021
VL 12
AR 671298
DI 10.3389/fphar.2021.671298
PG 16
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA SB5BK
UT WOS:000650009300001
PM 33995103
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Tan, WL
   Luo, X
   Li, WD
   Zhong, JY
   Cao, J
   Zhu, SC
   Chen, XQ
   Zhou, R
   Shang, CZ
   Chen, YJ
AF Tan, Wenliang
   Luo, Xuan
   Li, Wenda
   Zhong, Jinyi
   Cao, Jun
   Zhu, Sicong
   Chen, Xianqing
   Zhou, Rui
   Shang, Changzhen
   Chen, Yajin
TI TNF-α is a potential therapeutic target to overcome sorafenib resistance
   in hepatocellular carcinoma
SO EBIOMEDICINE
LA English
DT Article
DE Hepatocellular carcinoma; Sorafenib resistance; TNF-alpha; Ulinastatin;
   Combination treatment
ID EPITHELIAL-MESENCHYMAL TRANSITION; NECROSIS-FACTOR-ALPHA; NF-KAPPA-B;
   GROWTH-FACTOR; COLORECTAL-CANCER; BREAST-CANCER; INHIBITION; EXPRESSION;
   PATHWAY; MATRIX-METALLOPROTEINASE-9
AB Background: The role of tumor necrosis factor alpha (TNF-alpha) in targeted therapy for hepatocellular carcinoma (HCC) remains largely unknown. The current study aimed to clarify the mechanistic effects of targeting TNF-alpha to overcome sorafenib resistance in HCC.
   Methods: A correlation of TNF-alpha expression with the prognosis was analyzed in 62 HCC patients who underwent surgical resection and subsequent received adjuvant sorafenib treatment. The relation of TNF-alpha expression and sorafenib sensitivity was determined in different HCC cell lines. The combined therapeutic effects of sorafenib and ulinastatin, which could inhibit TNF-alpha expression, on HCC were examined in vitro and in vivo.
   Findings: High TNF-alpha expression was correlated with poor outcomes in HCC patients who received adjuvant sorafenib after surgery. In vitro experiments showed that TNF-alpha promotes HCC cell resistant to sorafenib through inducing epithelial-mesenchymal transition (EMT). Notably, the current study revealed that sorafenib has no significant influence on the expression and secretion of TNF-alpha, and sorafenib had limited effectiveness on reversing EMT in HCC cells with high TNF-alpha expression. Inhibiting the expression of TNF-alpha with ulinastatin significantly enhanced the anti-tumor effect of sorafenib on HCC cells with high expression of TNF-alpha in vitro and in vivo.
   Interpretation: Our findings indicate that TNF-alpha may serve as a novel predictor of sorafenib sensitivity in HCC patients. Sorafenib combined with ulinastatin may improve the effectiveness of treatment of HCC in patients with high expression of TNF-alpha. (C) 2018 The Authors. Published by Elsevier B.V.
C1 [Tan, Wenliang; Luo, Xuan; Li, Wenda; Cao, Jun; Zhu, Sicong; Chen, Xianqing; Zhou, Rui; Shang, Changzhen; Chen, Yajin] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Guangdong Prov Key Lab Malignant Tumor Epigenet &, Guangzhou, Guangdong, Peoples R China.
   [Tan, Wenliang; Luo, Xuan; Li, Wenda; Zhong, Jinyi; Cao, Jun; Chen, Xianqing; Zhou, Rui; Shang, Changzhen; Chen, Yajin] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Hepatobiliary Surg, Guangzhou 510120, Guangdong, Peoples R China.
   [Zhu, Sicong] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Surg Intens Care Unit, Guangzhou, Guangdong, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen University
RP Shang, CZ; Chen, YJ (corresponding author), Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Hepatobiliary Surg, Guangzhou 510120, Guangdong, Peoples R China.
EM shangcz_sysu@163.com; cyj0509@126.com
RI Cao, Jun/AAK-7312-2021; xianqing, chen/C-7474-2012; Li,
   Wenda/LKL-1246-2024; zhou, rui/KZT-9353-2024; Tan,
   Wenliang/LDE-8488-2024
OI shang, chang zhen/0000-0003-4629-7682
FU National Natural Science Foundation of China [81572398, 81672419];
   Science and Technology Planning Project of Guangdong Province
   [2017A010105003, 2015A050502023, 2016A020216010]; Natural Science
   Foundation of Guangdong Province [2014A030313061, 2013B021800101]
FX This work was supported by grants from the National Natural Science
   Foundation of China (no. 81572398; no. 81672419), the Science and
   Technology Planning Project of Guangdong Province (no. 2017A010105003;
   no. 2015A050502023; no. 2016A020216010), the Natural Science Foundation
   of Guangdong Province (no. 2014A030313061; no. 2013B021800101). These
   funding sources had no role in the study design, data collection, data
   analysis, interpretation, or writing of this manuscript.
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NR 40
TC 76
Z9 81
U1 2
U2 20
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2352-3964
J9 EBIOMEDICINE
JI EBioMedicine
PD FEB
PY 2019
VL 40
BP 446
EP 456
DI 10.1016/j.ebiom.2018.12.047
PG 11
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA HO1UO
UT WOS:000460696900055
PM 30594557
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kim, IU
   Sung, IS
   Sim, JJ
   Park, M
   Jeong, KY
   Kim, HM
AF Kim, In Un
   Sung, In Sung
   Sim, Jae Jun
   Park, Minhee
   Jeong, Keun-Yeong
   Kim, Hwan Mook
TI Antitumor Effect of Calcium-Mediated Destabilization of Epithelial
   Growth Factor Receptor on Non-Small Cell Lung Carcinoma
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE non-small-cell lung carcinoma; epithelial growth factor receptor; Src;
   alpha-tubulin; calcium; calpain
ID COLORECTAL-CANCER CELLS; TARGETED THERAPY; ENDOCYTOSIS; CALPAIN;
   PROTEIN; EGFR; PHOSPHORYLATION; INACTIVATION; TRAFFICKING; KINASE
AB Despite the development of numerous therapeutics targeting the epithelial growth factor receptor (EGFR) for non-small cell lung carcinoma (NSCLC), the application of these drugs is limited because of drug resistance. Here, we investigated the antitumor effect of calcium-mediated degradation of EGFR pathway-associated proteins on NSCLC. First, lactate calcium salt (LCS) was utilized for calcium supplementation. Src, alpha-tubulin and EGFR levels were measured after LSC treatment, and the proteins were visualized by immunocytochemistry. Calpeptin was used to confirm the calcium-mediated effect of LCS on NSCLC. Nuclear expression of c-Myc and cyclin D1 was determined to understand the underlying mechanism of signal inhibition following EGFR and Src destabilization. The colony formation assay and a xenograft animal model were used to confirm the in vitro and in vivo antitumor effects, respectively. LCS supplementation reduced Src and alpha-tubulin expression in NSCLC cells. EGFR was destabilized because of proteolysis of Src and alpha-tubulin. c-Myc and cyclin D1 expression levels were also reduced following the decrease in the transcriptional co-activation of EGFR and Src. Clonogenic ability and tumor growth were significantly inhibited by LSC treatment-induced EGFR destabilization. These results suggest that other than specifically targeting EGFR, proteolysis of associated molecules such as Src or alpha-tubulin may effectively exert an antitumor effect on NSCLC via EGFR destabilization. Therefore, LCS is expected to be a good candidate for developing novel anti-NSCLC therapeutics overcoming chemoresistance.
C1 [Kim, In Un; Sung, In Sung; Sim, Jae Jun; Kim, Hwan Mook] Gachon Univ, Gachon Inst Pharmaceut Sci, Incheon 21936, South Korea.
   [Park, Minhee; Jeong, Keun-Yeong] Metimedi Pharmaceut Co R&D Div, 263 Cent Ro, Incheon 22006, South Korea.
C3 Gachon University
RP Kim, HM (corresponding author), Gachon Univ, Gachon Inst Pharmaceut Sci, Incheon 21936, South Korea.
EM kiminun5@naver.com; sltjd0114@naver.com; genesis0804@hanmail.net;
   pmh1880@hanmail.net; alvirus@naver.com; hwanmook@gachon.ac.kr
RI ; Jeong, Keun-Yeong/B-8845-2015
OI PARK, MINHEE/0000-0002-2513-2080; Jeong, Keun-Yeong/0000-0002-4933-3493
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NR 37
TC 3
Z9 4
U1 0
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD APR
PY 2018
VL 19
IS 4
AR 1158
DI 10.3390/ijms19041158
PG 16
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA GJ0XU
UT WOS:000434978700237
PM 29641465
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Golan, T
   Milella, M
   Ackerstein, A
   Berger, R
AF Golan, Talia
   Milella, Michele
   Ackerstein, Aliza
   Berger, Ranaan
TI The changing face of clinical trials in the personalized medicine and
   immuno-oncology era: report from the international congress on clinical
   trials in Oncology & Hemato-Oncology (ICTO 2017)
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Article
DE Oncology; Hematology; Clinical trials; Immuno-oncology; Targeted
   therapy; Personalized medicine; Biostatistics; Endpoints; Methodology
ID ACUTE PROMYELOCYTIC LEUKEMIA; CELL LUNG-CANCER; ACUTE
   LYMPHOBLASTIC-LEUKEMIA; PROGRESSION-FREE SURVIVAL; CHRONIC
   MYELOID-LEUKEMIA; CIRCULATING TUMOR DNA; END-POINTS; STATISTICAL
   CHALLENGES; COLORECTAL-CANCER; PANCREATIC-CANCER
AB In the past decade, the oncology community has witnessed major advances in the understanding of cancer biology and major breakthroughs in several different therapeutic areas, from solid tumors to hematological malignancies; moreover, the advent of effective immunotherapy approaches, such as immune-checkpoint blockade, is revolutionizing treatment algorithms in almost all oncology disease areas. As knowledge evolves and new weapons emerge in the "war against cancer", clinical and translational research need to adapt to a rapidly changing environment to effectively translate novel concepts into sustainable and accessible therapeutic options for cancer patients.
   With this in mind, translational cancer researchers, oncology professionals, treatment experts, CRO and industry leaders, as well as patient representatives gathered in London, 16-17 March 2017, for The International Congress on Clinical Trials in Oncology and Hemato-Oncology (ICTO2017), to discuss the changing face of oncology clinical trials in the new era of personalized medicine and immuno-oncology. A wide range of topics, including clinical trial design in immuno-oncology, biomarker-oriented drug development paths, statistical design and endpoint selection, challenges in the design and conduct of personalized medicine clinical trials, risk-based monitoring, financing and reimbursement, as well as best operational practices, were discussed in an open, highly interactive format, favoring networking among all relevant stakeholders. The most relevant data, approaches and issues emerged and discussed during the conference are summarized in this report.
C1 [Golan, Talia; Ackerstein, Aliza; Berger, Ranaan] Sheba Med Ctr, Oncol Inst, Emek HaEla St 1, Ramat Gan, Israel.
   [Golan, Talia; Berger, Ranaan] Tel Aviv Univ, Sackler Fac Med, Tel Aviv, Israel.
   [Milella, Michele] Regina Elena Inst Canc Res, Div Med Oncol 1, Via Elio Chianesi 53, I-00144 Rome, Italy.
C3 Chaim Sheba Medical Center; Tel Aviv University; IRCCS Istituti
   Fisioterapici Ospitalieri (IFO); IRCCS Regina Elena
RP Milella, M (corresponding author), Regina Elena Inst Canc Res, Div Med Oncol 1, Via Elio Chianesi 53, I-00144 Rome, Italy.
EM michele.milella@ifo.gov.it
RI Milella, Michele/ABH-8606-2020
OI Milella, Michele/0000-0002-3826-5237
FU Italian Association for Cancer Research (AIRC) [IG18622, 9979]
FX This work was funded in part through grants from the Italian Association
   for Cancer Research (AIRC, IG18622 and 5x1000 Molecular Clinical
   Oncology Extension Program 9979, to M.M.).
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NR 70
TC 11
Z9 14
U1 1
U2 20
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1756-9966
J9 J EXP CLIN CANC RES
JI J. Exp. Clin. Cancer Res.
PD DEC 28
PY 2017
VL 36
AR 192
DI 10.1186/s13046-017-0668-0
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FR0FM
UT WOS:000418736800001
PM 29282151
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Loomans, HA
   Andl, CD
AF Loomans, Holli A.
   Andl, Claudia D.
TI Activin receptor-like kinases: a diverse family playing an important
   role in cancer
SO AMERICAN JOURNAL OF CANCER RESEARCH
LA English
DT Review
DE TGF-beta; Activin; BMP; targeted therapy
ID GROWTH-FACTOR-BETA; BONE MORPHOGENETIC PROTEIN; TGF-BETA;
   COLORECTAL-CANCER; SERINE/THREONINE KINASE; JUVENILE POLYPOSIS;
   UP-REGULATION; I RECEPTORS; MICROSATELLITE INSTABILITY; TROPHOBLAST
   INVASION
AB The role and function of the members of the TGF beta superfamily has been a substantial area of research focus for the last several decades. During that time, it has become apparent that aberrations in TGF beta family signaling, whether through the BMP, Activin, or TGF beta arms of the pathway, can result in tumorigenesis or contribute to its progression. Downstream signaling regulates cellular growth under normal physiological conditions yet induces diverse processes during carcinogenesis, ranging from epithelial-to-mesenchymal transition to cell migration and invasion to angiogenesis. Due to these observations, the question has been raised how to utilize and target components of these signaling pathways in cancer therapy. Given that these cascades include both ligands and receptors, there are multiple levels at which to interfere. Activin receptor-like kinases (ALKs) are a group of seven type I receptors responsible for TGF beta family signal transduction and are utilized by many ligands within the superfamily. The challenge lies in specifically targeting the often-overlapping functional effects of BMP, Activin, or TGF beta signaling during cancer progression. This review focuses on the characteristic function of the individual receptors within each subfamily and their recognized roles in cancer. We next explore the clinical utility of therapeutically targeting ALKs as some have shown partial responses in Phase I clinical trials but disappointing outcomes when used in Phase II studies. Finally, we discuss the challenges and future directions of this body of work.
C1 [Loomans, Holli A.] Vanderbilt Univ, Dept Canc Biol, 221 Kirkland Hall, Nashville, TN 37235 USA.
   [Andl, Claudia D.] Univ Cent Florida, Coll Med, Burnett Sch Biomed Sci, 4110 Libra Dr,Bldg 20,BMS 223, Orlando, FL 32816 USA.
C3 Vanderbilt University; State University System of Florida; University of
   Central Florida
RP Andl, CD (corresponding author), Univ Cent Florida, Coll Med, Burnett Sch Biomed Sci, 4110 Libra Dr,Bldg 20,BMS 223, Orlando, FL 32816 USA.
EM claudia.andl@ucf.edu
OI Loomans-Kropp, Holli/0000-0002-9681-8725
FU National Institute of Health [DK094900, DK091491, T32-CA0095193-26,
   F31-DE025477-01A1, VICTR VR16470]
FX This work was supported by grants from the National Institute of Health
   (DK094900, DK091491 to CDA; T32-CA0095193-26, F31-DE025477-01A1, VICTR
   VR16470 to HAL).
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NR 136
TC 34
Z9 37
U1 0
U2 4
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 2156-6976
J9 AM J CANCER RES
JI Am. J. Cancer Res.
PY 2016
VL 6
IS 11
BP 2431
EP 2447
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EF8PO
UT WOS:000390591500003
PM 27904762
DA 2025-01-04
ER

PT J
AU He, XB
   Zhang, Y
   Ma, YX
   Zhou, T
   Zhang, JW
   Hong, SD
   Sheng, J
   Zhang, ZH
   Yang, YP
   Huang, Y
   Zhang, L
   Zhao, HY
AF He, Xiaobo
   Zhang, Yang
   Ma, Yuxiang
   Zhou, Ting
   Zhang, Jianwei
   Hong, Shaodong
   Sheng, Jin
   Zhang, Zhonghan
   Yang, Yunpeng
   Huang, Yan
   Zhang, Li
   Zhao, Hongyun
TI Optimal tumor shrinkage predicts long-term outcome in advanced nonsmall
   cell lung cancer (NSCLC) treated with target therapy Result from 3
   clinical trials of advanced NSCLC by 1 institution
SO MEDICINE
LA English
DT Article
DE advanced nonsmall cell lung cancer; EGFR-TKIs; prognostic factor;
   RECIST; tumor shrinkage
ID COLORECTAL-CANCER; NEVER-SMOKERS; CHEMOTHERAPY; GEFITINIB; GUIDELINES;
   EPIDEMIOLOGY; ANGIOGENESIS; MUTATIONS; EVALUATE
AB Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are used as standard therapies for advanced nonsmall cell \ lung cancer (NSCLC) patients with EGFR mutation positive. Because these targeted therapies could cause tumor necrosis and shrinkage, the purpose of the study is to search for a value of optimal tumor shrinkage as an appropriate indicator of outcome for advanced NSCLC.
   A total of 88 NSCLC enrollees of 3 clinical trials (IRESSA registration clinical trial, TRUST study and ZD6474 study), who received Gefitinib (250 mg, QD), Erlotinib (150 mg, CD), and ZD6474 (100 mg, QD), respectively, during December 2003 and October 2007, were retrospectively analyzed. The response evaluation criteria in solid tumors (RECIST) were used to identify responders, who had complete response (CR) or partial responses (PR) and nonresponders who had stable disease (SD) or progressive disease (PD). Receiver operating characteristics (ROC) analysis was used to find the optimal tumor shrinkage as an indicator for tumor therapeutic outcome. Univariate and multivariate Cox regression analyses were performed to compare the progression-free survival (PFS) and overall survival (OS) between responders and nonresponders stratified based on radiologic criteria.
   Among the 88 NSCLC patients, 26 were responders and 62 were nonresponders based on RECIST 1.0. ROC indicated that 8.32% tumor diameter shrinkage in the sum of the longest tumor diameter (SLD) was the cutoff point of tumor shrinkage outcomes, resulting in 16 responders (>= 8.32%) and 12 nonresponders (>= 8.32%). Univariate and multivariate Cox regression analyses indicated that (1) the responders (>= 8.32%) and nonresponders(>=- 8.32%) were significantly different in median PFS (13.40 vs 1.17 months, P >= 0.001) and OS (19.80 vs 7.90 months, P < 0.001) and (2) 8.32% in SLD could be used as the optimal threshold for PFS (hazard ratio [HR], 8.11, 95% CI, 3.75 to 17.51, P < 0.001) and OS (HR, 2.36, 95% CI, 1.41 to 3.96, P=0.001).
   However, 8.32% tumor diameter shrinkage is validated as a reliable outcome predictor of advanced NSCLC patients receiving EGFR-TKIs therapies and may provide a practical measure to guide therapeutic decisions.
C1 [He, Xiaobo; Zhang, Yang; Ma, Yuxiang; Zhou, Ting; Zhang, Jianwei; Hong, Shaodong; Sheng, Jin; Zhang, Zhonghan; Yang, Yunpeng; Huang, Yan; Zhang, Li; Zhao, Hongyun] Sun Yat Sen Univ, Ctr Canc, Dept Med Oncol, Guangzhou, Guangdong, Peoples R China.
   [He, Xiaobo; Zhang, Yang; Ma, Yuxiang; Zhou, Ting; Zhang, Jianwei; Hong, Shaodong; Sheng, Jin; Zhang, Zhonghan; Yang, Yunpeng; Huang, Yan; Zhang, Li; Zhao, Hongyun] State Key Lab Oncol South China, Guangzhou, Guangdong, Peoples R China.
C3 Sun Yat Sen University; State Key Lab Oncology South China
RP Zhang, L (corresponding author), Sun Yat Sen Univ, Ctr Canc, Dept Med Oncol, Guangzhou, Guangdong, Peoples R China.; Zhao, HY (corresponding author), Sun Yat Sen Univ, Ctr Canc, State Key Lab Oncol South China, Guangzhou, Guangdong, Peoples R China.
EM zhangli6@mail.sysu.edu.cn; zhaohy@sysucc.org.cn
RI zhou, ting/KMX-1693-2024; Zhang, Jianwei/ABU-2767-2022
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NR 28
TC 9
Z9 9
U1 0
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD AUG
PY 2016
VL 95
IS 31
AR e4176
DI 10.1097/MD.0000000000004176
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA DS4ZI
UT WOS:000380789800007
PM 27495021
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhang, MY
   Zhang, RJ
   Jiang, HJ
   Jiang, H
   Xu, HL
   Pan, WB
   Wang, YQ
   Li, X
AF Zhang, Ming-Yu
   Zhang, Rong-Jun
   Jiang, Hui-Jie
   Jiang, Hao
   Xu, Hai-Long
   Pan, Wen-Bin
   Wang, Yi-Qiao
   Li, Xin
TI <SUP>18</SUP>F-fluoromisonidazole positron emission tomography may be
   applicable in the evaluation of colorectal cancer liver metastasis
SO HEPATOBILIARY & PANCREATIC DISEASES INTERNATIONAL
LA English
DT Article
DE F-18-FMISO; Positron emission tomography; Colorectal liver metastases;
   Heterogeneity
ID IMAGING TUMOR HYPOXIA; F-18 FLUOROMISONIDAZOLE; TARGETED THERAPY;
   HETEROGENEITY; EXPRESSION; MICROENVIRONMENT; EPIDEMIOLOGY; RADIOTHERAPY;
   RESISTANCE
AB Background: Positron emission tomography (PET) imaging is a non-invasive functional imaging method used to reflect tumor spatial information, and to provide biological characteristics of tumor progression. The aim of this study was to focus on the application of F-18-fluoromisonidazole (FMISO) PET quantitative parameter of maximum standardized uptake value (SUVmax) ratio to detect the liver metastatic potential of human colorectal cancer (CRC) in mice.
   Methods: Colorectal liver metastases (CRLM) xenograft models were established by injecting tumor cells (LoVo, HT29 and HCT116) into spleen of mice, tumor-bearing xenograft models were established by subcutaneously injecting tumor cells in the right left flank of mice. Wound healing assays were performed to examine the ability of cell migration in vitro. F-18-FMISO uptake in CRC cell lines was measured by cellular uptake assay. F-18-FMISO-based micro-PET imaging of CRLM and tumor-bearing mice was performed and quantified by tumor-to-liver SUVmax ratio. The correlation between the F-18-FMISO SUVmax ratio, liver metastases number, hypoxia-induced factor 1 alpha(HIF-1 alpha) and serum starvation-induced glucose transporter 1 (GLUT-1) was evaluated using Pearson correlation analysis.
   Results: Compared with HT29 and HCT116, LoVo-CRLM mice had significantly higher liver metastases ratio and shorter median survival time. LoVo cells exhibited stronger migration capacity and higher radiotracer uptake compared with HT29 and HCT116 in in vitro. Moreover, F-18-FMISO SUVmax ratio was significantly higher in both LoVo-CRLM model and LoVo-bearing tumor model compared to models established using HT29 and HCT116. In addition, Pearson correlation analysis revealed a significant correlation between F-18-FMISO SUVmax ratio of CRLM mice and number of liver metastases larger than 0.5 cm, as well as between F-18-FMISO SUVmax ratio and HIF-1 alpha or GLUT-1 expression in tumor-bearing tissues.
   Conclusions: F-18-FMISO parameter of SUVmax ratio may provide useful tumor biological information in mice with CRLM, thus allowing for better prediction of CRLM and yielding useful radioactive markers for predicting liver metastasis potential in CRC. (C) 2019 First Affiliated Hospital, Zhejiang University School of Medicine in China. Published by Elsevier B.V. All rights reserved.
C1 [Zhang, Ming-Yu; Jiang, Hui-Jie; Jiang, Hao; Xu, Hai-Long; Pan, Wen-Bin; Wang, Yi-Qiao; Li, Xin] Harbin Med Univ, Affiliated Hosp 2, Dept Radiol, Harbin 150086, Heilongjiang, Peoples R China.
   [Zhang, Rong-Jun] Jiangsu Inst Nucl Med, Jiangsu Key Lab Mol Nucl Med, Minist Hlth, Key Lab Nucl Med, Wuxi 214063, Peoples R China.
C3 Harbin Medical University
RP Jiang, HJ (corresponding author), Harbin Med Univ, Affiliated Hosp 2, Dept Radiol, Harbin 150086, Heilongjiang, Peoples R China.
EM jhjemail@163.com
RI jiang, hui/KYP-5273-2024; Zhang, mingyu/HGB-1069-2022
FU National Natural Science Foundation of China [81471736, 81671760
   and81873910]; Scientific Research Transformation Special Fund of
   Heilongjiang Academy of Medical Sciences [2018415]; Scientific Research
   Project of Health and Family Planning Commission of Heilongjiang
   Province [CR201807]
FX This study was supported by grants from the National Natural Science
   Foundation of China (81471736, 81671760 and81873910), Scientific
   Research Transformation Special Fund of Heilongjiang Academy of Medical
   Sciences (2018415), Scientific Research Project of Health and Family
   Planning Commission of Heilongjiang Province (CR201807).
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NR 34
TC 5
Z9 5
U1 1
U2 4
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1499-3872
EI 2352-9377
J9 HEPATOB PANCREAT DIS
JI Hepatob. Pancreatic. Dis. Int.
PD APR
PY 2019
VL 18
IS 2
BP 164
EP 172
DI 10.1016/j.hbpd.2019.02.008
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HU2NE
UT WOS:000465107200010
PM 30850340
DA 2025-01-04
ER

PT J
AU Ahmad, R
   Singh, JK
   Wunnava, A
   Al-Obeed, O
   Abdulla, M
   Srivastava, SK
AF Ahmad, Rehan
   Singh, Jaikee Kumar
   Wunnava, Amoolya
   Al-Obeed, Omar
   Abdulla, Maha
   Srivastava, Sandeep Kumar
TI Emerging trends in colorectal cancer: Dysregulated signaling pathways
   (Review)
SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
LA English
DT Review
DE colorectal cancer; signaling pathways; mutations; metastasis; targeted
   therapy
ID ISLAND METHYLATOR PHENOTYPE; COMPREHENSIVE MOLECULAR CHARACTERIZATION;
   DOSE-RESPONSE METAANALYSIS; ENDOTHELIAL GROWTH-FACTOR; VISCERAL
   ADIPOSE-TISSUE; BODY-MASS INDEX; COLON-CANCER; MICROSATELLITE
   INSTABILITY; C-MET; TUMOR-SUPPRESSOR
AB Colorectal cancer (CRC) is the third most frequently detected type of cancer, and the second most common cause of cancer-related mortality globally. The American Cancer Society predicted that approximately 147,950 individuals would be diagnosed with CRC, out of which 53,200 individuals would succumb to the disease in the USA alone in 2020. CRC-related mortality ranks third among both males and females in the USA. CRC arises from 3 major pathways: i) The adenoma-carcinoma sequence; ii) serrated pathway; and iii) the inflammatory pathway. The majority of cases of CRC are sporadic and result from risk factors, such as a sedentary lifestyle, obesity, processed diets, alcohol consumption and smoking. CRC is also a common preventable cancer. With widespread CRC screening, the incidence and mortality from CRC have decreased in developed countries. However, over the past few decades, CRC cases and mortality have been on the rise in young adults (age, <50 years). In addition, CRC cases are increasing in developing countries with a low gross domestic product (GDP) due to lifestyle changes. CRC is an etiologically heterogeneous disease classified by tumor location and alterations in global gene expression. Accumulating genetic and epigenetic perturbations and aberrations over time in tumor suppressor genes, oncogenes and DNA mismatch repair genes could be a precursor to the onset of colorectal cancer. CRC can be divided as sporadic, familial, and inherited depending on the origin of the mutation. Germline mutations in APC and MLH1 have been proven to play an etiological role, resulting in the predisposition of individuals to CRC. Genetic alterations cause the dysregulation of signaling pathways leading to drug resistance, the inhibition of apoptosis and the induction of proliferation, invasion and migration, resulting in CRC development and metastasis. Timely detection and effective precision therapies based on the present knowledge of CRC is essential for successful treatment and patient survival. The present review presents the CRC incidence, risk factors, dysregulated signaling pathways and targeted therapies.
C1 [Ahmad, Rehan; Al-Obeed, Omar; Abdulla, Maha] King Saud Univ, Coll Med, Dept Surg, Colorectal Res Chair, Riyadh 11472, Saudi Arabia.
   [Singh, Jaikee Kumar; Wunnava, Amoolya; Srivastava, Sandeep Kumar] Manipal Univ Jaipur, Dept Biosci, Jaipur 303007, Rajasthan, India.
C3 King Saud University; Manipal University Jaipur
RP Srivastava, SK (corresponding author), Manipal Univ Jaipur, Dept Biosci, Jaipur 303007, Rajasthan, India.
EM sandeepkumar.srivastava@jaipur.manipal.edu
RI srivastava, sandeep/ABH-3565-2022; Singh, Jaikee Kumar/GPS-4553-2022
OI Singh, Jaikee Kumar/0000-0003-0850-0950; Srivastava, Sandeep
   Kumar/0000-0002-7138-1387; SRIVASTAVA, SANDEEP/0000-0003-4484-0223;
   Ahmad, Rehan/0000-0003-2612-2818
FU King Saud University
FX The authors are grateful to the Deanship of Scientific Research, King
   Saud University for funding through the Vice Deanship of Scientific
   Research Chairs.
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NR 286
TC 85
Z9 90
U1 5
U2 39
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1107-3756
EI 1791-244X
J9 INT J MOL MED
JI Int. J. Mol. Med.
PD MAR
PY 2021
VL 47
IS 3
AR 14
DI 10.3892/ijmm.2021.4847
PG 25
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA PY4WV
UT WOS:000612047400001
PM 33655327
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Shan, JQ
   Li, XY
   Sun, RQ
   Yao, Y
   Sun, Y
   Kuang, Q
   Dai, XL
   Sun, YL
AF Shan, Junqi
   Li, Xinyu
   Sun, Runqi
   Yao, Yao
   Sun, Yan
   Kuang, Qin
   Dai, Xianling
   Sun, Yanlai
TI Palmitoyltransferase ZDHHC6 promotes colon tumorigenesis by targeting
   PPARγ-driven lipid biosynthesis via regulating lipidome metabolic
   reprogramming
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Article
DE Colorectal cancer (CRC); ZDHHC6; PPAR gamma; Palmitoylation; Lysosomal
   degradation
ID COLORECTAL-CANCER; PALMITOYLATION; UBIQUITINATION; EXPRESSION; DELTA
AB BackgroundThe failure of proper recognition of the intricate nature of pathophysiology in colorectal cancer (CRC) has a substantial effect on the progress of developing novel medications and targeted therapy approaches. Imbalances in the processes of lipid oxidation and biosynthesis of fatty acids are significant risk factors for the development of CRC. Therapeutic intervention that specifically targets the peroxisome proliferator-activated receptor gamma (PPAR gamma) and its downstream response element, in response to lipid metabolism, has been found to promote the growth of tumors and has shown significant clinical advantages in cancer patients.MethodsClinical CRC samples and extensive in vitro and in vivo experiments were carried out to determine the role of ZDHHC6 and its downstream targets via a series of biochemical assays, molecular analysis approaches and lipid metabolomics assay, etc.ResultsTo study the effect of ZDHHC6 on the progression of CRC and identify whether ZDHHC6 is a palmitoyltransferase that regulates fatty acid synthesis, which directly palmitoylates and stabilizes PPAR gamma, and this stabilization in turn activates the ACLY transcription-related metabolic pathway. In this study, we demonstrate that PPAR gamma undergoes palmitoylation in its DNA binding domain (DBD) section. This lipid-related modification enhances the stability of PPAR gamma protein by preventing its destabilization. As a result, palmitoylated PPAR gamma inhibits its degradation induced by the lysosome and facilitates its translocation into the nucleus. In addition, we have identified zinc finger-aspartate-histidine-cysteine 6 (ZDHHC6) as a crucial controller of fatty acid biosynthesis. ZDHHC6 directly interacts with and adds palmitoyl groups to stabilize PPAR gamma at the Cys-313 site within the DBD domain of PPAR gamma. Consequently, this palmitoylation leads to an increase in the expression of ATP citrate lyase (ACLY). Furthermore, our findings reveals that ZDHHC6 actively stimulates the production of fatty acids and plays a role in the development of colorectal cancer. However, we have observed a significant reduction in the cancer-causing effects when the expression of ZDHHC6 is inhibited in in vivo trials. Significantly, in CRC, there is a strong positive correlation between the high expression of ZDHHC6 and the expression of PPAR gamma. Moreover, this high expression of ZDHHC6 is connected with the severity of CRC and is indicative of a poor prognosis.ConclusionsWe have discovered a mechanism in which lipid biosynthesis is controlled by ZDHHC6 and includes the signaling of PPAR gamma-ACLY in the advancement of CRC. This finding provides a justification for targeting lipid synthesis by blocking ZDHHC6 as a potential therapeutic approach.
C1 [Shan, Junqi; Yao, Yao; Sun, Yanlai] Shandong First Med Univ, Shandong Acad Med Sci, Shandong Canc Hosp & Inst, Dept Surg Oncol, Jinan 250117, Shandong, Peoples R China.
   [Li, Xinyu] Shandong Second Med Univ, Sch Clin Med, Weifang 261000, Shandong, Peoples R China.
   [Sun, Runqi] Jining Med Univ, Sch Clin Med, Jining 272000, Shandong, Peoples R China.
   [Sun, Yan; Kuang, Qin; Dai, Xianling] Chongqing Univ, Coll Bioengn, Key Lab Biorheol Sci & Technol, Minist Educ, Chongqing 400030, Peoples R China.
C3 Shandong First Medical University & Shandong Academy of Medical
   Sciences; University of Jinan; Shandong Second Medical University;
   Jining Medical University; Chongqing University
RP Sun, YL (corresponding author), Shandong First Med Univ, Shandong Acad Med Sci, Shandong Canc Hosp & Inst, Dept Surg Oncol, Jinan 250117, Shandong, Peoples R China.
EM ylsun@sdfmu.edu.cn
FU Start-up fund of Shandong Cancer Hospital [2020PYA05]; National Science
   Foundation of Shandong Province [ZR2020MH254]; Science and Technology
   Program of Jinan [202134062]
FX This work was supported by (1) the Start-up fund of Shandong Cancer
   Hospital (NO. 2020PYA05); (2) the National Science Foundation of
   Shandong Province (NO. ZR2020MH254) and (3) the Science and Technology
   Program of Jinan (NO. 202134062).
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NR 61
TC 2
Z9 2
U1 8
U2 8
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1756-9966
J9 J EXP CLIN CANC RES
JI J. Exp. Clin. Cancer Res.
PD AUG 16
PY 2024
VL 43
IS 1
AR 227
DI 10.1186/s13046-024-03154-0
PG 27
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA C7P5I
UT WOS:001291254800001
PM 39148124
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Krebs, MG
   Renehan, AG
   Backen, A
   Gollins, S
   Chau, I
   Hasan, J
   Valle, JW
   Morris, K
   Beech, J
   Ashcroft, L
   Saunders, MP
   Dive, C
AF Krebs, Matthew G.
   Renehan, Andrew G.
   Backen, Alison
   Gollins, Simon
   Chau, Ian
   Hasan, Jurjees
   Valle, Juan W.
   Morris, Karen
   Beech, Janette
   Ashcroft, Linda
   Saunders, Mark P.
   Dive, Caroline
TI Circulating Tumor Cell Enumeration in a Phase II Trial of a Four-Drug
   Regimen in Advanced Colorectal Cancer
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE Biomarker; Cetuximab; Cell Search; Circulating tumor cells; Colorectal
   cancer
ID 1ST-LINE TREATMENT; INFUSIONAL FLUOROURACIL; PROGNOSTIC-SIGNIFICANCE;
   DISEASE PROGRESSION; ACQUIRED-RESISTANCE; IRINOTECAN FOLFIRI;
   PERIPHERAL-BLOOD; ORAL LEUCOVORIN; OXALIPLATIN; SURVIVAL
AB Circulating tumor cells (CTCs) are strongly prognostic in advanced colorectal cancer but have not yet been used to guide therapy. In the present phase II study of a 4-drug regimen, we sought to determine whether patients with high or low CTCs would benefit the most. Compared with historical controls, patients with high CTCs survived longer than expected; however, patients with low CTCs gained no extra benefit. Our data require validation from prospective CTC-guided randomized trials.
   Background: Multidrug regimens are active against advanced colorectal cancer (ACRC). However, the increased toxicity requires the use of biomarkers to select the patients who will derive the most benefit. We assessed circulating tumor cells (CTCs) as a prognostic biomarker in patients treated with a 4-drug regimen. Patients and Methods: A single-arm phase II trial (Erbitux Study of CPT11, Oxaliplatin, UFToral Targeted-therapy [eSCOUT]) was undertaken in patients with previously untreated KRAS wild-type ACRC using a regimen of irinotecan, oxaliplatin, and tegafur-uracil with leucovorin and cetuximab. Baseline CTCs were enumerated using CellSearch. The endpoints were an objective response rate (ORR) and overall survival (OS). We modeled our results and compared them with those modeled for the ;capecitabine, oxaliplatin, bevacizumab +/- cetuximab (CAIRO2) trial, stratifying patients a priori into low (< 3) and high (>= 3) CTC groups. Results: For 48 eligible patients, the best ORR from the 4-drug regimen was 71%, with a disease control rate of 98%. The median OS for patients with a high and low CTC count was 18.7 and 22.3 months (log-rank test, P =.038), respectively. In our modeled data, for patients with a low CTC count, no differences were found between the median OS in the eSCOUT trial and that in the CAIRO2 trial (22.2 vs. 22.0 months). However, for the high CTC group, a clinically relevant improvement was seen in median OS (eSCOUT vs. CAIR02, 18.7 vs. 13.7 months; P =.001). Conclusion: These data are hypothesis generating for patients with ACRC, stratification by CTC count can identify those who might benefit the most from an intensive 4-drug regimen, avoiding high-toxicity regimens in low CTC groups. This hypothesis warrants validation in a phase III biomarker-driven trial.
C1 [Krebs, Matthew G.; Renehan, Andrew G.; Backen, Alison; Morris, Karen; Dive, Caroline] Canc Res UK Manchester Inst, Clin & Expt Pharmacol, Manchester, Lancs, England.
   [Krebs, Matthew G.; Hasan, Jurjees; Valle, Juan W.; Beech, Janette; Ashcroft, Linda; Saunders, Mark P.] Christie NHS Fdn Trust, Manchester M20 4BX, Lancs, England.
   [Krebs, Matthew G.; Renehan, Andrew G.; Valle, Juan W.] Univ Manchester, Inst Canc Sci, Manchester, Lancs, England.
   [Gollins, Simon] North Wales Canc Treatment Ctr, Rhyl, Clwyd, Wales.
   [Chau, Ian] Royal Marsden Hosp, London SW3 6JJ, England.
C3 Cancer Research UK; Christie NHS Foundation Trust; University of
   Manchester; Royal Marsden NHS Foundation Trust
RP Saunders, MP (corresponding author), Christie NHS Fdn Trust, Wilmslow Rd, Manchester M20 4BX, Lancs, England.
EM mark.saunders@christie.nhs.uk
RI Chau, Ian/ABC-2023-2020; Valle, Juan/J-3571-2015; Renehan,
   Andrew/K-5992-2015
OI Krebs, Matthew/0000-0001-7540-3064; Valle, Juan/0000-0002-1999-0863;
   Dive, Caroline/0000-0002-1726-8850; Renehan, Andrew/0000-0003-4309-4396;
   Chau, Ian/0000-0003-0286-8703
FU Merck Serono; National Health Service; Christie Charitable Trust; Cancer
   Research UK; Clinical and Experimental Pharmacology group
   [C5759/A12328]; Manchester Experimental Cancer Medicines Centre
   [C1467/A15578]
FX We would like to thank Merck Serono for providing cetuximab and
   supporting funds for management of this trial; Gareth Adaway and
   Willemijn Spoor for data management; and Lisa Miles for trial
   co-ordination. We thank the trial nurses involved at all 3 recruiting
   sites for their dedicated work. I.C. would like to acknowledge the
   National Health Service funding to the National Institute for Health
   Research Biomedical Research Centre. M.K., M.S., and C.D. acknowledge
   the Manchester Experimental Cancer Medicines Centre. We also thank our
   patients for their participation. The present study was funded in part
   by Merck Serono, the Christie Charitable Trust, Cancer Research UK core
   funding to the Cancer Research UK Manchester Institute, the Clinical and
   Experimental Pharmacology group (grant C5759/A12328), and the Manchester
   Experimental Cancer Medicines Centre (grant C1467/A15578).
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NR 45
TC 45
Z9 50
U1 0
U2 12
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1533-0028
EI 1938-0674
J9 CLIN COLORECTAL CANC
JI Clin. Colorectal Canc.
PD JUN
PY 2015
VL 14
IS 2
BP 115
EP 122
DI 10.1016/j.clcc.2014.12.006
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CJ0HY
UT WOS:000355157600007
PM 25680623
DA 2025-01-04
ER

PT J
AU Pellini, B
   Pejovic, N
   Feng, WJ
   Earland, N
   Harris, PK
   Usmani, A
   Szymanski, JJ
   Qaium, F
   Mudd, J
   Petty, M
   Jiang, YQ
   Singh, A
   Maher, CA
   Henke, LE
   Park, H
   Ciorba, MA
   Kim, H
   Mutch, MG
   Pedersen, KS
   Tan, BR
   Hawkins, WG
   Fields, RC
   Chaudhuri, AA
AF Pellini, Bruna
   Pejovic, Nadja
   Feng, Wenjia
   Earland, Noah
   Harris, Peter K.
   Usmani, Abul
   Szymanski, Jeffrey J.
   Qaium, Faridi
   Mudd, Jacqueline
   Petty, Marvin
   Jiang, Yuqiu
   Singh, Ashla
   Maher, Christopher A.
   Henke, Lauren E.
   Park, Haeseong
   Ciorba, Matthew A.
   Kim, Hyun
   Mutch, Matthew G.
   Pedersen, Katrina S.
   Tan, Benjamin R.
   Hawkins, William G.
   Fields, Ryan C.
   Chaudhuri, Aadel A.
TI ctDNA MRD Detection and Personalized Oncogenomic Analysis in
   Oligometastatic Colorectal Cancer From Plasma and Urine
SO JCO PRECISION ONCOLOGY
LA English
DT Article
ID CIRCULATING TUMOR DNA; PULMONARY METASTASIS; CLONAL HEMATOPOIESIS;
   HEPATIC RESECTION; LIVER METASTASES; RESIDUAL DISEASE; POOLED ANALYSIS;
   LUNG-CANCER; THERAPY; OUTCOMES
AB PURPOSE We hypothesized that circulating tumor DNA (ctDNA) molecular residual disease (MRD) analysis without prior mutational knowledge could be performed after neoadjuvant chemotherapy to assess oligometastatic colorectal cancer (CRC) treated surgically with curative intent. We also investigated urine as an alternative analyte for ctDNA MRD detection in this nongenitourinary setting.
   PATIENTS AND METHODS We applied AVENIO targeted next-generation sequencing to plasma, tumor, and urine samples acquired on the day of curative-intent surgery from 24 prospectively enrolled patients with oligometastatic CRC. Age-related clonal hematopoiesis was accounted for by removing variants also present in white blood cells. Plasma and urine ctDNA MRD were correlated with tumor cells detected in the surgical specimen, and adjuvant treatment strategies were proposed based on ctDNA-inferred tumor mutational burden (iTMB) and targetable alterations.
   RESULTS Seventy-one percent of patients were treated with neoadjuvant chemotherapy. Tumor-naive plasma ctDNA analysis detected MRD at a median level of 0.62% with 95% sensitivity and 100% specificity, and 94% and 77% sensitivity when only considering patients treated with neoadjuvant chemotherapy and putative driver mutations, respectively. In urine, ctDNA MRD detection specificity remained high at 100%, but sensitivity decreased to 64% with median levels being 11-fold lower than in plasma (P < .0001). Personalized ctDNA MRD oncogenomic analysis revealed 81% of patients might have been candidates for adjuvant immunotherapy based on high iTMB or targeted therapy based on actionable PIK3CA mutations.
   CONCLUSION Tumor-naive plasma ctDNA analysis can sensitively and specifically detect MRD in patients with oligometastatic CRC after neoadjuvant chemotherapy. Urine-based ctDNA MRD detection is also feasible; however, it is less sensitive than plasma because of significantly lower levels. Oligometastatic patients with detectable MRD may benefit from additional personalized treatment based on ctDNA-derived oncogenomic profiling. (C) 2021 by American Society of Clinical Oncology
C1 [Pellini, Bruna] H Lee Moffitt Canc Ctr & Res Inst, Dept Thorac Oncol, Tampa, FL USA.
   [Pellini, Bruna] Univ S Florida, Morsani Coll Med, Dept Oncol Sci, Tampa, FL USA.
   [Pejovic, Nadja; Feng, Wenjia; Earland, Noah; Harris, Peter K.; Usmani, Abul; Szymanski, Jeffrey J.; Qaium, Faridi; Henke, Lauren E.; Chaudhuri, Aadel A.] Washington Univ, Sch Med, Dept Radiat Oncol, Div Canc Biol, St Louis, MO USA.
   [Mudd, Jacqueline; Petty, Marvin] Washington Univ, Sch Med, Dept Surg, Sect Surg Oncol, St Louis, MO USA.
   [Jiang, Yuqiu; Singh, Ashla] Roche Sequencing Solut, Pleasanton, CA USA.
   [Maher, Christopher A.; Park, Haeseong; Pedersen, Katrina S.; Tan, Benjamin R.] Washington Univ, Sch Med, Dept Med, Div Oncol, St Louis, MO 63110 USA.
   [Maher, Christopher A.; Chaudhuri, Aadel A.] Washington Univ, Sch Med, Dept Biomed Engn, St Louis, MO USA.
   [Maher, Christopher A.; Henke, Lauren E.; Park, Haeseong; Ciorba, Matthew A.; Kim, Hyun; Mutch, Matthew G.; Pedersen, Katrina S.; Tan, Benjamin R.; Hawkins, William G.; Fields, Ryan C.; Chaudhuri, Aadel A.] Barnes Jewish Hosp, Siteman Canc Ctr, St Louis, MO 63110 USA.
   [Maher, Christopher A.; Henke, Lauren E.; Park, Haeseong; Ciorba, Matthew A.; Kim, Hyun; Mutch, Matthew G.; Pedersen, Katrina S.; Tan, Benjamin R.; Hawkins, William G.; Fields, Ryan C.; Chaudhuri, Aadel A.] Washington Univ, Sch Med, St Louis, MO USA.
   [Maher, Christopher A.] Washington Univ, Sch Med, McDonnell Genome Inst, St Louis, MO USA.
   [Ciorba, Matthew A.] Washington Univ, Sch Med, Dept Med, Div Gastroenterol, St Louis, MO 63110 USA.
   [Mutch, Matthew G.] Washington Univ, Sch Med, Dept Surg, Sect Colon & Rectal Surg, St Louis, MO 63110 USA.
   [Hawkins, William G.] Washington Univ, Sch Med, Dept Surg, Sect Hepatobiliary Pancreat & Gastrointestinal Su, St Louis, MO 63110 USA.
   [Chaudhuri, Aadel A.] Washington Univ, Sch Med, Dept Genet, St Louis, MO 63110 USA.
   [Chaudhuri, Aadel A.] Washington Univ, Dept Comp Sci & Engn, St Louis, MO 63110 USA.
C3 H Lee Moffitt Cancer Center & Research Institute; State University
   System of Florida; University of South Florida; Washington University
   (WUSTL); Washington University (WUSTL); Washington University (WUSTL);
   Washington University (WUSTL); Siteman Cancer Center; Washington
   University (WUSTL); Barnes-Jewish Hospital; Washington University
   (WUSTL); Washington University (WUSTL); Washington University (WUSTL);
   Washington University (WUSTL); Washington University (WUSTL); Washington
   University (WUSTL); Washington University (WUSTL)
RP Chaudhuri, AA (corresponding author), Dept Radiat Oncol, 4511 Forest Pk Ave, St Louis, MO 63108 USA.
EM aadel@wustl.edu
RI Park, Haeseong/AAL-7982-2021; Usmani, Abul/J-3756-2019; Pedersen,
   Katrina/KBA-8737-2024; Sen Chaudhuri, Arka/GLN-3613-2022; JIANG,
   YUQIU/C-7806-2014
OI Pellini, Bruna/0000-0003-0898-0202; Usmani, Abul/0000-0001-5485-7323;
   Pedersen, Katrina/0000-0003-2793-6901; Szymanski,
   Jeffrey/0000-0002-8005-701X; Earland, Noah/0000-0003-0170-407X; Feng,
   Wenjia/0000-0002-6320-3927
FU National Cancer Institute of the National Institutes of Health
   [K08CA238711]; NCI [P50CA196510]; Cancer Research Foundation Young
   Investigator Award; V Foundation V Scholar Award; American Surgical
   Association Foundation Fellowship; American Cancer Society Institutional
   Review Grant; Society of Surgical Oncology James Ewing Foundation
   Clinical Investigator Award; Sidney Kimmel Translational Science Scholar
   Award; David Riebel Cancer Research Fund; National Cancer Institute
   [K08CA238711] Funding Source: NIH RePORTER
FX Supported by the National Cancer Institute of the National Institutes of
   Health under award number K08CA238711 (A.A.C.), the NCI P50CA196510
   Career Enhancement Program (A.A.C., W.G.H.), the Cancer Research
   Foundation Young Investigator Award (A.A.C.), the V Foundation V Scholar
   Award (A.A.C.), the American Surgical Association Foundation Fellowship
   (R.C.F.), the American Cancer Society Institutional Review Grant
   (R.C.F.), the Society of Surgical Oncology James Ewing Foundation
   Clinical Investigator Award (R.C.F.), the Sidney Kimmel Translational
   Science Scholar Award (R.C.F.), and the David Riebel Cancer Research
   Fund (R.C.F).
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NR 49
TC 35
Z9 35
U1 0
U2 16
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
EI 2473-4284
J9 JCO PRECIS ONCOL
JI JCO Precis. Oncol.
PD FEB 12
PY 2021
VL 5
BP 378
EP 388
DI 10.1200/PO.20.00276
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RH9TV
UT WOS:000636554900001
PM 34250420
OA Bronze, Green Published
DA 2025-01-04
ER

PT J
AU Tang, XM
   Chen, H
   Li, Q
   Song, YL
   Zhang, SP
   Xu, XS
   Xu, YW
   Chen, SL
AF Tang, Xue-miao
   Chen, Hao
   Li, Qing
   Song, Yiling
   Zhang, Shuping
   Xu, Xiao-Shuan
   Xu, Yiwei
   Chen, Shulin
TI A ssessment of the cardiac safety between cetuximab and panitumumab as
   single therapy in Chinese chemotherapy-refractory mCRC
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE cetuximab; panitumumab; targeted therapy; colorectal cancer; toxicity;
   cardiac safety
ID METASTATIC COLORECTAL-CANCER; GROWTH-FACTOR RECEPTOR; WILD-TYPE KRAS;
   MONOCLONAL-ANTIBODIES; ST DEPRESSION; QT INTERVAL; DE-POINTES;
   OPEN-LABEL; ONCOLOGY; CARDIOTOXICITY
AB Objective: The cardiac safety of cetuximab and panitumumab, particularly as single agents, has not been investigated extensively. This trial was designed to specifically evaluate the cardiac safety of cetuximab and panitumumab as single therapy in Chinese chemotherapy-refractory metastatic colorectal cancer (mCRC) patients.
   Patients and methods: Sixty-one patients received cetuximab at an initial dose of 400 mg/m2 intravenously over 120 minutes on day 1 (week 1), followed by a maintenance dose of 250 mg/m2 intravenously over 60 minutes on day 1 of each 7-day cycle. Forty-three patients received panitumumab at a dose of 6 mg/kg intravenously every 14 days. Routine laboratory tests and electrocardiogram (ECG) were performed at baseline, during therapy and after the treatment (4th and 10th months). The incidence of elevation of troponin I ultra (TNI Ultra), abnormal ECGs, cardiac events and noncardiac adverse events (AEs) were recorded and analyzed.
   Results: The incidence of elevation of TNI Ultra between the two groups had no significance (p= 0.681), and TNI Ultra+ was observed more frequently in patients with metastases to more than three organs and they received fourth or above lines of chemotherapy. The most frequent abnormal ECG manifestations were nonspecific ST changes and QTc prolongation in the two groups. At 10 months after treatment, most of the abnormal ECG manifestations were reversed. The most common cardiac AEs of cetuximab and panitumumab included palpitations, dyspnea, chest pain and arrhythmias requiring treatment. Most of the events were mild and transient. The incidence of cardiac AEs had no significant difference between the two groups. Rash was still the most common noncardiac AE in both groups.
   Conclusion: Cetuximab and panitumumab showed favorable cardiac safety as single agents for Chinese chemotherapy-refractory mCRC patients. But monitoring for cardiac AEs is still necessary throughout the entire treatment process.
C1 [Tang, Xue-miao; Li, Qing] Sun Yat Sen Univ, Ctr Canc, Dept Ultrasound & Electrocardiogram, Guangzhou, Guangdong, Peoples R China.
   [Tang, Xue-miao; Chen, Hao; Li, Qing; Song, Yiling; Zhang, Shuping; Chen, Shulin] Sun Yat Sen Univ, Ctr Canc, State Key Lab Oncol South China, Collaborat Innovat Ctr Canc Med, Guangzhou, Guangdong, Peoples R China.
   [Chen, Hao; Song, Yiling; Zhang, Shuping; Chen, Shulin] Sun Yat Sen Univ, Ctr Canc, Dept Clin Lab, 651 Dongfeng Rd East, Guangzhou 510060, Guangdong, Peoples R China.
   [Xu, Xiao-Shuan] Guangdong Med Univ, Sch Lab Med, Guangzhou, Guangdong, Peoples R China.
   [Xu, Yiwei] Shantou Univ, Coll Med, Canc Hosp, Dept Clin Lab, Shantou, Guangdong, Peoples R China.
   [Xu, Yiwei] Shantou Univ, Coll Med, Key Lab Mol Biol High Canc Incidence Coastal Chao, Shantou, Guangdong, Peoples R China.
C3 Sun Yat Sen University; State Key Lab Oncology South China; Sun Yat Sen
   University; Sun Yat Sen University; Guangdong Medical University;
   Shantou University; Shantou University
RP Chen, SL (corresponding author), Sun Yat Sen Univ, Ctr Canc, Dept Clin Lab, 651 Dongfeng Rd East, Guangzhou 510060, Guangdong, Peoples R China.; Xu, YW (corresponding author), Shantou Univ, Coll Med, Key Lab Mol Biol High Canc Incidence Coastal Chao, Dept Clin Lab,Canc Hosp, 22 Xinling Rd, Shantou 515041, Guangdong, Peoples R China.
EM yiwei512@126.com; chenshl@sysucc.org.cn
RI Chen, Shulin/GXG-9029-2022; hao, chen/ISB-3213-2023
FU Guangdong Medical Research Foundation [A2016156]
FX This work was supported by the Guangdong Medical Research Foundation
   (A2016156).
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NR 23
TC 4
Z9 4
U1 0
U2 2
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6930
J9 ONCOTARGETS THER
JI OncoTargets Ther.
PY 2018
VL 11
BP 123
EP 129
DI 10.2147/OTT.S149716
PG 7
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA FR5FX
UT WOS:000419093400001
PM 29343971
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Hermawan, A
   Putri, H
AF Hermawan, Adam
   Putri, Herwandhani
TI Computational analysis of G-protein-coupled receptor kinase family
   members as potential targets for colorectal cancer therapy
SO EGYPTIAN JOURNAL OF MEDICAL HUMAN GENETICS
LA English
DT Article
DE G-protein-coupled receptor kinase; Colorectal cancer; Computational
   analysis; Targeted therapy
ID GENE-EXPRESSION; DOWN-REGULATION; 6 GRK6; PROGRESSION; METASTASIS;
   MICROARRAY; INVASION; DATABASE
AB Background G-protein-coupled receptor (GPCR) kinases (GRKs) interact with ligand-activated GPCR, causing intracellular phosphorylation and interfering with the intracellular signal transduction associated with the development of cancer. Colorectal cancer (CRC) is a fast-growing disease, and its molecular mechanism involves various regulatory proteins, including kinases. However, the GRK mechanism in CRC has not been explored. Methods We used an integrated computational approach to investigate the potential of GRK family members as targeted proteins in CRC. The GRK expression levels in tumor and normal tissues, colon adenocarcinoma samples, and metastatic colon adenocarcinoma were analyzed using ONCOMINE, GEPIA, and UALCAN, as well as TNM plots. Genetic changes in the GRK family genes were investigated using cBioportal. The prognostic value related to the gene expression of the GRK family was examined using GEPIA and UALCAN. Co-expression analysis of the GRK family was conducted using COXPRESdb. Association analysis of the Gene Ontology, KEGG pathway enrichment, and drug-gene analyses were performed using the over-representation analysis (ORA) in WebGestalt. Results GRK2, GRK3, and GRK5 mRNA levels increased significantly in patients with CRC and metastatic CRC. Genetic changes were detected in patients with CRC, including GRK7 (1.1%), GRK2 (1.7%), GRK4 (2.3%), GRK5 (2.5%), GRK6 (2.5%), GRK3 (2.9%), and GRK1 (4%). CRC patients with low mRNA of GRK7 levels had better disease-free and overall survival than those with high GRK7 levels. Hierarchical clustering analysis revealed significant positive correlations between GRK5 and GRK2 and between GRK2 and GRK6. KEGG pathway enrichment analysis showed that the gene network (GN) regulated several cellular pathways, such as the morphine addiction signaling and chemokine signaling pathways in cancer. The drug-gene association analysis indicated that the GN was associated with several drugs, including reboxetine, pindolol, beta-blocking agents, and protein kinase inhibitors. Conclusion No research has been conducted on the relation of GRK1 and GRK7 to cancer, particularly CRC. In this work, genes GRK2, GRK3, GRK5, and GRK6 were found to be oncogenes in CRC. Although inhibitors against GRK2, GRK5, and GRK6 have previously been developed, further research, particularly preclinical and clinical studies, is needed before these agents may be used to treat CRC.
C1 [Hermawan, Adam] Univ Gadjah Mada Sekip Utara II, Dept Pharmaceut Chem, Lab Macromol Engn, Fac Pharm, Yogyakarta 55281, Indonesia.
   [Hermawan, Adam; Putri, Herwandhani] Univ Gadjah Mada Sekip Utara II, Fac Pharm, Canc Chemoprevent Res Ctr, Yogyakarta 55281, Indonesia.
RP Hermawan, A (corresponding author), Univ Gadjah Mada Sekip Utara II, Dept Pharmaceut Chem, Lab Macromol Engn, Fac Pharm, Yogyakarta 55281, Indonesia.; Hermawan, A (corresponding author), Univ Gadjah Mada Sekip Utara II, Fac Pharm, Canc Chemoprevent Res Ctr, Yogyakarta 55281, Indonesia.
EM adam_apt@ugm.ac.id
RI Hermawan, Adam/E-9236-2012
OI Hermawan, Adam/0000-0001-5851-3691
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NR 68
TC 0
Z9 0
U1 0
U2 5
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 1110-8630
EI 2090-2441
J9 EGYPTIAN J MED HUMAN
JI Egypt. J. Med. Human Genet.
PD SEP 11
PY 2022
VL 23
IS 1
AR 137
DI 10.1186/s43042-022-00349-y
PG 17
WC Genetics & Heredity
WE Emerging Sources Citation Index (ESCI)
SC Genetics & Heredity
GA 4L3GM
UT WOS:000852519600001
OA gold
DA 2025-01-04
ER

PT J
AU Chuang, J
   Wang, CK
   Guo, YM
   Valenzuela, V
   Wu, J
   Fakih, M
AF Chuang, Jeremy
   Wang, Chongkai
   Guo, Yuming
   Valenzuela, Valerie
   Wu, Jun
   Fakih, Marwan
TI <i>MAP2K1</i> Mutations in Advanced Colorectal Cancer Predict Poor
   Response to Anti-EGFR Therapy and to Vertical Targeting of <i>MAPK</i>
   Pathway
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE Metastatic colorectal cancer; Molecular profiling; Next-generation
   sequencing; Precision medicine; Targeted therapy
ID MEK; RESISTANCE; PANITUMUMAB; TRAMETINIB; CETUXIMAB; EVOLUTION; BVD-523;
   BRAF
AB MAP2K1 is a rare oncogenic mutation with clinical and therapeutic implications that have yet to be explored in colorectal cancer. While targeting the MAPK signaling pathway has demonstrated antitumor efficacy in mouse xenograft models, colorectal cancer patients that harbor this mutation are predicted to have a poor response to EGFR inhibitors with or without MEK, BRAF, or ERK inhibition. Our study suggests colorectal cancer patients harboring MAP2K1 mutation may not benefit from anti-EGFR therapy.
   Background: MAP2K1 mutations, otherwise known as MEK mutations, are rare oncogenic alterations that have been implicated in MAPK pathway activation. The impact of MAP2K1 mutations in colorectal cancer on EGFR antibody response has not been characterized. Patients and Methods: Antitumor activity was assessed in mouse xenograft models with SW48 cell lines harboring MAP2K1 mutation, and protein expression of the RAS signaling pathway was studied by Western blot analysis. We retrospectively identified patients with MAP2K1-mutated metastatic colorectal cancer patients treated at City of Hope Comprehensive Cancer Center between 2015 and 2020 using next-generation sequencing. Patients' tumor characteristics, treatment response, and outcome are described. Additional patients with the MAP2K1 mutation were identified from The Cancer Genome Atlas and Memorial Sloan Kettering Cancer Center oncogenomic databases. Results: Antitumor activity in mouse xenograft models demonstrated efficacy with combination therapy with EGFR and MEK inhibition with either BRAF or ERK inhibitors. Five patients treated at City of Hope between 2015 and 2020 harbored a MAP2K1 mutation at a frequency of 1%. APC and TP53 were common coalterations. All disease was RAS and BRAF wild type, except 1 case that harbored a concurrent KRAS mutation. Four RAS/BRAF wild-type MAP2K1-mutated patients was treated with anti-EGFR, anti-EGFR thorn MEK and BRAF inhibitors, and anti-EGFR thorn ERK inhibitors. All 4 patients experienced disease progression. Conclusion: MAP2K1 mutation in colorectal cancer is associated with poor response to EGFR inhibition. EGFR inhibition with or without MEK, BRAF, or ERK inhibitors did not result in any clinical benefit in our limited experience. (C) 2020 Elsevier Inc. All rights reserved.
C1 [Chuang, Jeremy; Wang, Chongkai; Fakih, Marwan] City Hope Comprehens Canc Ctr, Dept Med Oncol & Therapeut Res, 1500 E Duane Rd, Duarte, CA 91010 USA.
   [Guo, Yuming; Valenzuela, Valerie; Wu, Jun] City Hope Comprehens Canc Ctr, Div Comparat Med, Duarte, CA 91010 USA.
C3 City of Hope; City of Hope
RP Fakih, M (corresponding author), City Hope Comprehens Canc Ctr, Dept Med Oncol & Therapeut Res, 1500 E Duane Rd, Duarte, CA 91010 USA.
EM mfakih@coh.org
RI Guo, Yuming/AAH-1124-2021; Wu, Jian/H-9404-2019
OI Guo, Yuming/0000-0001-8732-3213; Wu, Jun/0000-0003-1834-9596; Fakih,
   Marwan/0000-0002-6554-5488
CR Arcila ME, 2015, CLIN CANCER RES, V21, P1935, DOI 10.1158/1078-0432.CCR-14-2124
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NR 22
TC 12
Z9 14
U1 0
U2 5
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1533-0028
EI 1938-0674
J9 CLIN COLORECTAL CANC
JI Clin. Colorectal Canc.
PD MAR
PY 2021
VL 20
IS 1
BP 72
EP 78
DI 10.1016/j.clcc.2020.12.003
EA MAR 2021
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RX7BL
UT WOS:000647374800015
PM 33436306
OA Bronze
DA 2025-01-04
ER

PT J
AU Ciardiello, F
   Ciardiello, D
   Martini, G
   Napolitano, S
   Tabernero, J
   Cervantes, A
AF Ciardiello, Fortunato
   Ciardiello, Davide
   Martini, Giulia
   Napolitano, Stefania
   Tabernero, Josep
   Cervantes, Andres
TI Clinical management of metastatic colorectal cancer in the era of
   precision medicine
SO CA-A CANCER JOURNAL FOR CLINICIANS
LA English
DT Article
DE immunotherapy; metastatic colorectal cancer; molecular target therapy;
   precision medicine; tumor molecular profiling
ID FOLFIRI PLUS CETUXIMAB; CONSENSUS MOLECULAR SUBTYPES; ISLAND METHYLATOR
   PHENOTYPE; PHASE-II TRIAL; WILD-TYPE KRAS; CIRCULATING TUMOR DNA;
   ANTI-EGFR ANTIBODIES; OPEN-LABEL; MICROSATELLITE INSTABILITY; 1ST-LINE
   TREATMENT
AB Colorectal cancer (CRC) represents approximately 10% of all cancers and is the second most common cause of cancer deaths. Initial clinical presentation as metastatic CRC (mCRC) occurs in approximately 20% of patients. Moreover, up to 50% of patients with localized disease eventually develop metastases. Appropriate clinical management of these patients is still a challenging medical issue. Major efforts have been made to unveil the molecular landscape of mCRC. This has resulted in the identification of several druggable tumor molecular targets with the aim of developing personalized treatments for each patient. This review summarizes the improvements in the clinical management of patients with mCRC in the emerging era of precision medicine. In fact, molecular stratification, on which the current treatment algorithm for mCRC is based, although it does not completely represent the complexity of this disease, has been the first significant step toward clinically informative genetic profiling for implementing more effective therapeutic approaches. This has resulted in a clinically relevant increase in mCRC disease control and patient survival. The next steps in the clinical management of mCRC will be to integrate the comprehensive knowledge of tumor gene alterations, of tumor and microenvironment gene and protein expression profiling, of host immune competence as well as the application of the resulting dynamic changes to a precision medicine-based continuum of care for each patient. This approach could result in the identification of individual prognostic and predictive parameters, which could help the clinician in choosing the most appropriate therapeutic program(s) throughout the entire disease journey for each patient with mCRC. CA Cancer J Clin. 2022;72:000-000.
C1 [Ciardiello, Fortunato; Ciardiello, Davide; Martini, Giulia; Napolitano, Stefania] Univ Campania Luigi Vanvitelli, Dept Precis Med, Div Med Oncol, Via S Pansini 5, I-80131 Naples, Italy.
   [Ciardiello, Davide] IRCCS Fdn Home Relief Suffering, Div Med Oncol, San Giovanni Rotondo, Italy.
   [Tabernero, Josep] Vall dHebron Hosp Campus, Med Oncol Dept, Barcelona, Spain.
   [Tabernero, Josep] Univ Vic, Inst Oncol, Cent Univ Catalonia, Barcelona, Spain.
   [Tabernero, Josep] Biomed Res Ctr Canc, Oncol Inst Barcelona Quironsalud, Barcelona, Spain.
   [Cervantes, Andres] Univ Valencia, Inst Invest Sanitaria Valencia, Med Oncol Dept, Biomed Res Inst, Valencia, Spain.
   [Cervantes, Andres] Carlos III Inst Hlth, Biomed Res Ctr Canc, Madrid, Spain.
C3 Universita della Campania Vanvitelli; Universitat de Vic - Universitat
   Central de Catalunya (UVic-UCC); University of Valencia; Instituto de
   Salud Carlos III
RP Ciardiello, F (corresponding author), Univ Campania Luigi Vanvitelli, Dept Precis Med, Div Med Oncol, Via S Pansini 5, I-80131 Naples, Italy.
EM fortunato.ciardiello@unicampania.it
RI Martini, Giulia/AIB-8246-2022; Ciardiello, Davide/AAC-4613-2022;
   Napolitano, Stefania/AIB-9708-2022; Cervantes, Andres/J-8713-2013
OI Cervantes, Andres/0000-0003-3806-3691; MARTINI,
   Giulia/0000-0003-4093-2681
FU Regione Campania (I-Cure Research Project Cup) [21C17000030007];
   Instituto de Salud Carlos III [PI18/01909, PI21/00689]
FX Fortunato Ciardiello was supported by a grant from Regione Campania
   (I-Cure Research Project Cup 21C17000030007). Andres Cervantes was
   supported by grants from the Instituto de Salud Carlos III (PI18/01909
   and PI21/00689). Fortunato Ciardiello reports institutional research
   grants from Amgen, Merck KGaA, Merck Sharp & Dohme, Pfizer, Pierre
   Fabre, Roche, and Servier; and service on advisory boards for Bayer,
   Merck KGaA, Merck Sharp & Dohme, Pierre Fabre, Roche, and Servier
   outside the submitted work. Davide Ciardiello reports a travel grant
   from Sanofi outside the submitted work. Stefania Napolitano reports
   honoraria from Bristol Myers Squibb and Novartis outside the submitted
   work. Josep Tabernero reports advisory board or scientific consultancy
   fees from Array Biopharma, AstraZeneca, Avvinity, Bayer, Boehringer
   Ingelheim, Chugai, Daiichi--Sankyo, Roche, Genentech, HalioDX SAS,
   Hutchison MediPharma International, Ikena Oncology, Inspirna Inc, IQVIA,
   Lilly, Menarini, Merck KGaA, Merus, Merck Sharp & Dohme, Mirati,
   Neophore, Novartis, Ona Therapeutics, Orion Biotechnology, Peptomyc,
   Pfizer, Pierre Fabre, Samsung Bioepis, Sanofi, Seattle Genetics,
   Scandion Oncology, Servier, SotioBiotech, Taiho, Tessa Therapeutics, and
   TheraMyc outside the submitted work. Andres Cervantes reports
   institutional research grants from Genentech, Merck KGaA, Bristol Myers
   Squibb, Merck Sharp & Dohme, Roche, Beigene, Bayer, Servier, Lilly,
   Novartis, Takeda, Astellas, Takeda, and Fibrogen; and honoraria or
   speaker's fees from Amgen, Merck KGaA, Roche, Bayer, Servier, and Pierre
   Fabre outside the submitted work. Giulia Martini reports no conflicts of
   interest.
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NR 217
TC 270
Z9 287
U1 21
U2 128
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-9235
EI 1542-4863
J9 CA-CANCER J CLIN
JI CA-Cancer J. Clin.
PD JUL
PY 2022
VL 72
IS 4
BP 372
EP 401
DI 10.3322/caac.21728
EA APR 2022
PG 30
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3D8WG
UT WOS:000787357900001
PM 35472088
OA gold
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Wu, HM
   Deng, M
   Xue, DW
   Guo, RK
   Zhang, CY
   Gao, JQ
   Li, HY
AF Wu, Huiming
   Deng, Min
   Xue, Dingwen
   Guo, Renkai
   Zhang, Chenyu
   Gao, Jiaqi
   Li, Huiyu
TI PD-1/PD-L1 inhibitors for early and middle stage microsatellite
   high-instability and stable colorectal cancer: a review
SO INTERNATIONAL JOURNAL OF COLORECTAL DISEASE
LA English
DT Review
DE Programmed cell death receptor 1; Programmed cell death ligand 1;
   Microsatellite high-instability; Microsatellite stable; Colorectal
   cancer
ID IMMUNITY; COMBINATION
AB Background Programmed cell death receptor 1 (PD-1) and programmed cell death ligand 1 (PD-L1) are important immune checkpoint molecules that contribute to tumor immune evasion. However, the main treatment modalities for patients with early and intermediate stage colorectal cancer (CRC) are surgery, and the role of PD-1/PD-L1 inhibitors in these patients is not yet clear. Therefore, this study aims to review the treatment progress of PD-1/PD-L1 inhibitors for early- and intermediate-stage microsatellite high-instability (MSI-H) and stable (MSS) colorectal cancer, in order to provide more options for patients with early- and intermediate-stage colorectal cancer.Materials and methods A scoping review of clinical trial registries (Clinicaltrials.gov and EU clinical trial registers) and PubMed/Medline database of trials on PD-1/PD-L1 Inhibitors for early and middle-stage MSI-H and MSS CRC was done up to March 2024.Results A total of 19 trials related to early to mid-stage MSH-I or MSS CRC were included. Among them, 6 trials are in recruiting status, 3 trials are in active, not recruiting status, 3 trials are completed, 1 trial is terminated, and 1 trial is unknown. Of these, 9 trials involve MSI-H type CRC, and 10 trials involve MSS type CRC. Preclinical phase I/II trials are predominant, with only 3 clinical phase III trials. In trials related to MSI-H type CRC, 4 studies involve PD-1/PD-L1 inhibitors combined with neoadjuvant therapy, and 5 studies involve combination therapy. In trials related to MSS type CRC, 3 studies involve PD-1/PD-L1 inhibitors combined with targeted therapy, 2 studies involve PD-1/PD-L1 inhibitors combined with chemotherapy, 1 study involves PD-1/PD-L1 inhibitor combined immunotherapy, 1 study involves PD-1/PD-L1 inhibitors combined with bacterial therapy, and 3 studies involve PD-1/PD-L1 inhibitors combined with comprehensive therapy. As for primary outcome measures, 4 trials select pathological complete response rates, 3 trials select progression-free survival rate, 3 trials select objective response rate, 3 trials select overall survival rate, 4 trials select disease-free survival rate, 1 trial selects clinical complete response rate, and 1 trial selects percentage of participants with a dose-limiting toxicity.Conclusion For early- and middle-stage MSI-H and MSS CRC, PD-1/PD-L1 inhibitors have shown some therapeutic efficacy, as evidenced by phase I/II studies. However, contemporary trial designs exhibit heterogeneity, with relatively few inclusion criteria, the use of various drug combinations and regimens, and significant variations in reported endpoints. Nevertheless, more double-arm, multicenter, randomized controlled trials are still needed to confirm the efficacy of immunotherapy.
C1 [Wu, Huiming; Deng, Min; Xue, Dingwen; Guo, Renkai; Zhang, Chenyu; Gao, Jiaqi; Li, Huiyu] Shanxi Med Univ, Shanxi Bethune Hosp, Tongji Shanxi Hosp, Shanxi Acad Med Sci,Hosp 3,Dept Gen Surg, Taiyuan, Peoples R China.
C3 Shanxi Medical University
RP Li, HY (corresponding author), Shanxi Med Univ, Shanxi Bethune Hosp, Tongji Shanxi Hosp, Shanxi Acad Med Sci,Hosp 3,Dept Gen Surg, Taiyuan, Peoples R China.
EM wuhuiming@sxmu.edu.cn; lihuiyu1978@sxmu.edu.cn
RI Wu, Huiming/JNS-5059-2023; Guo, Renkai/LVR-3315-2024; GAO,
   JIAQI/KHZ-7357-2024
OI Wu, Huiming/0000-0001-6717-9867
FU Key Research and Development (R&D) Projects of Shanxi Province
FX No Statement Available
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NR 41
TC 0
Z9 0
U1 3
U2 3
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0179-1958
EI 1432-1262
J9 INT J COLORECTAL DIS
JI Int. J. Colorectal Dis.
PD MAY 29
PY 2024
VL 39
IS 1
AR 83
DI 10.1007/s00384-024-04654-3
PG 10
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA SO1M5
UT WOS:001235301300002
PM 38809459
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Miao, ZW
   Gu, MJ
   Yan, J
   Lu, LD
   Xu, Y
   Ning, LQ
   Xu, Y
AF Miao, Zhiwei
   Gu, Mingjia
   Yan, Jing
   Lu, Lidan
   Xu, Yan
   Ning, Liqin
   Xu, Yi
TI Dual-targeted colon-based integrated micelle drug delivery system for
   treatment of ulcerative colitis
SO JOURNAL OF DRUG TARGETING
LA English
DT Article
DE Inflammatory bowel disease; Emodin; Eu-CS-Man-Ps-P(HEMA-DMAM); EMO-QDs;
   pH sensitive; targeted therapy
ID INFLAMMATORY-BOWEL-DISEASE; EVIDENCE-BASED CONSENSUS; POLYMERIC
   MICELLES; COLORECTAL-CANCER; IN-VITRO; EMODIN; NANOPARTICLES;
   ABSORPTION; METHOTREXATE; NANOCARRIER
AB Emodin (EMO) is an active ingredient of Chinese traditional medicine with the potential to reportedly treat ulcerative colitis (UC). However, the solubility of EMO in water is poor coupled with low oral bioavailability, whilst existing conventional oral preparations of the drug lack targeting ability. Thus, this work sought to design and fabricate a mannose modified colon targeted micelle drug delivery system comprising quantum dots (QDs) and EMO to obtain Eu-CS-Man-Ps-P(HEMA-DMAM)/EMO-QDs, which exhibited stable physicochemical properties, smaller average sized droplets (226.22 +/- 1.83 nm), better polydispersity (PDI = 0.060 +/- 0.005), negative zeta-potential (-19.19 +/- 0.89 mV) and high efficiency of encapsulation (95.14 +/- 0.23%). We observed Eu-CS-Man-Ps-P(HEMA-DMAM)/EMO-QDs to be an effective approach for the improvement of EMO solubility in an aqueous medium with an increased oral bioavailability (3.23 times higher than native drug) of the drug. Besides, the micelle could increase the retention and release of EMO in colonic ulcers through multi-stage targeting, improve oral bioavailability, regulate the expression of inflammatory factors and repair damaged tissues, which helped us to achieve the design goal of integrated diagnosis and treatment of UC. Conclusively, the therapeutic effect of EMO was enhanced through an integrated micelle, which exhibited good prospects in improving solubility and oral biological availability.
C1 [Miao, Zhiwei; Xu, Yan] Nanjing Univ Chinese Med, Zhangjiagang TCM Hosp, Dept Gastroenterol, Zhangjiagang, Peoples R China.
   [Gu, Mingjia] Nanjing Univ Chinese Med, Changshu Hosp, Dept Nephrol, Changshu, Peoples R China.
   [Yan, Jing] Nanjing Univ Chinese Med, Clin Med Coll 1, Key Lab Metab Dis Chinese Med, Nanjing, Peoples R China.
   [Lu, Lidan] Nanjing Univ Chinese Med, Changshu Hosp, Dept Gynaecol, Changshu, Peoples R China.
   [Ning, Liqin; Xu, Yi] Nanjing Univ Chinese Med, Affiliated Hosp, Dept Gastroenterol, 155 Hanzhong Rd, Nanjing 210029, Peoples R China.
C3 Nanjing University of Chinese Medicine; Nanjing University of Chinese
   Medicine; Nanjing University of Chinese Medicine; Nanjing University of
   Chinese Medicine; Nanjing University of Chinese Medicine
RP Ning, LQ; Xu, Y (corresponding author), Nanjing Univ Chinese Med, Affiliated Hosp, Dept Gastroenterol, 155 Hanzhong Rd, Nanjing 210029, Peoples R China.
EM xuyi_jshtcm@outlook.com
RI Gu, Mingjia/GPX-1198-2022; Miao, Zhiwei/AFA-9607-2022
OI Gu, Mingjia/0000-0001-9677-8279; Miao, Zhiwei/0000-0003-2540-5517
FU National Natural Science Foundation of China [82104792]; Natural Science
   Foundation of Nanjing University of Chinese Medicine [XZR2020059];
   Natural Science Foundation of Jiangsu Province [BK20181235, BK20210134];
   Suzhou science and technology project [SYS2020056].]
FX This work was supported by the [Funding Agency National Natural Science
   Foundation of China] under Grant [number 82104792]; [Funding Agency
   Natural Science Foundation of Nanjing University of Chinese Medicine]
   under Grant [number XZR2020059]; [Funding Agency Natural Science
   Foundation of Jiangsu Province] under Grant [number BK20181235];
   [Funding Agency Natural Science Foundation of Jiangsu Province] under
   Grant [number BK20210134]; and [Funding Agency Suzhou science and
   technology project] under Grant [number SYS2020056].
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NR 72
TC 7
Z9 8
U1 1
U2 50
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1061-186X
EI 1029-2330
J9 J DRUG TARGET
JI J. Drug Target.
PD JUL 3
PY 2022
VL 30
IS 6
BP 657
EP 672
DI 10.1080/1061186X.2022.2052887
EA MAR 2022
PG 16
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 2C3SI
UT WOS:000770257100001
PM 35285362
DA 2025-01-04
ER

PT J
AU Hao, HX
   Jiang, XM
   Cong, F
AF Hao, Huai-Xiang
   Jiang, Xiaomo
   Cong, Feng
TI Control of Wnt Receptor Turnover by R-spondin-ZNRF3/RNF43 Signaling
   Module and Its Dysregulation in Cancer
SO CANCERS
LA English
DT Review
DE Wnt signaling pathway; targeted therapy; RNF43; ZNRF3; R-spondin;
   Frizzled
ID R-SPONDIN RECOGNITION; MOUSE MAMMARY-TUMORS; WNT/BETA-CATENIN;
   COLORECTAL-CANCER; IDENTIFIES GENES; STRUCTURAL BASIS; LGR5; MUTATIONS;
   RNF43; GROWTH
AB Aberrant activation of the Wnt/beta-catenin pathway is frequently found in various cancers, often through mutations of downstream components. Inhibiting beta-catenin signaling in tumors with downstream pathway mutations remains challenging, due to a lack of favorable targets. On the other hand, targeting upstream components of the Wnt pathway is rather straightforward. However, it is difficult to identify tumors addicted to autocrine or paracrine Wnt signaling. Discovery of the R-spondin-ZNRF3/RNF43 signaling module and its genetic alterations in cancers represents a breakthrough in this area. Membrane E3 ligase ZNRF3 and RNF43 are critical negative feedback regulators of the Wnt pathway, which function through promoting ubiquitination and degradation of Wnt receptors. R-spondin proteins (RSPO1-4) serve as natural antagonists of ZNRF3/RNF43. To maintain strong and sustained Wnt/beta-catenin signaling, cancers need to overcome ZNRF3/RNF43-mediated feedback inhibition. Indeed, mutations of RNF43/ZNRF3 and recurrent translocations of RSPO2/RSPO3 have recently been identified in various cancers. Significantly, genetic alterations in RNF43/ZNRF3/RSPO2/RSPO3 have shown promise as predictive biomarkers in pre-clinical models for the efficacy of upstream Wnt inhibitors. In this review, we will discuss the biology of the R-spondin-ZNRF3/RNF43 signaling module, cancer-associated alterations of this signaling module, and their value as biomarkers to identify Wnt-addicted tumors.
C1 [Hao, Huai-Xiang; Jiang, Xiaomo; Cong, Feng] Novartis Inst Biomed Res, 181 Massachusetts Ave, Cambridge, MA 02139 USA.
C3 Novartis; Novartis USA
RP Cong, F (corresponding author), Novartis Inst Biomed Res, 181 Massachusetts Ave, Cambridge, MA 02139 USA.
EM huaixiang.hao@novartis.com; feng.cong@novartis.com
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NR 72
TC 125
Z9 133
U1 1
U2 17
PU MDPI AG
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 2072-6694
J9 CANCERS
JI Cancers
PD JUN
PY 2016
VL 8
IS 6
AR 54
DI 10.3390/cancers8060054
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EO7RZ
UT WOS:000396889100001
PM 27338477
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Surugiu, R
   Vintilescu, SB
   Sandu, RE
   Pirscoveanu, D
   Pirici, D
   Neagoe, CD
   Matei, D
   Aldea, M
   Dumitra, GG
   Stepan, MD
   Genunche-Dumitrescu, AV
AF Surugiu, Roxana
   Vintilescu, Stefanita Bianca
   Sandu, Raluca Elena
   Pirscoveanu, Denisa
   Pirici, Daniel
   Neagoe, Carmen Daniela
   Matei, Daniela
   Aldea, Madalina
   Dumitra, Gheorghe Gindrovel
   Stepan, Mioara Desdemona
   Genunche-Dumitrescu, Amelia Valentina
TI Nephrotic syndrome as a possible indicator of colonic cancer: A case
   report
SO BIOMEDICAL REPORTS
LA English
DT Article
DE nephrotic syndrome; colonic cancer; paraneoplastic syndrome
ID GLOMERULAR-DISEASES; CELL CARCINOMA; NEPHROPATHY; ASSOCIATION;
   MALIGNANCY
AB The concept of paraneoplastic syndromes encompasses a spectrum of indirect clinical manifestations caused by secretion of bioactive products by malignant cells. Paraneoplastic glomerulopathy represent a distinct clinical entity where nephrotic syndrome can arise as a manifestation of underlying malignancies, particularly solid tumors. Membranous nephropathy is notably associated with such malignancies, highlighting the intricate relationship between nephrotic syndrome and cancer. The present study reports the case of a 44-year-old Caucasian male, smoker (22 pack-years) and chronic ethanol consumer who presented in the Emergency County Hospital of Craiova in March 2018 with abdominal distension, genital and leg edema and no prior medical history. Laboratory tests revealed inflammatory syndrome (erythrocyte sedimentation rate=110 mm/h, fibrinogen, 150 mg/dl, high levels of C reactive protein=6.87 mg/dl), as well as hypoproteinemia (total protein levels=3.90 g/l), hypertriglyceridemia=213 mg/dl, hypercholesterolemia=475 mg/dl, total urinary protein excretion of 12,500 mg/24 h and normal levels of urea (38 mg/dl) and creatinine (0.90 mg/dl). After meeting the diagnostic criteria for nephrotic syndrome (edema, proteinuria, hypoalbuminemia, and hyperlipidemia, it was investigated whether the syndrome was primary or secondary in origin. Notably, an unexplained inflammatory syndrome in conjunction with elevated tumor marker levels (carbohydrate antigen 19-9, 82.47 U/ml; Carcinoembryonic antigen-CEA=9.46 ng/ml) prompted a thorough imagistic investigation, using computer tomography. A polyp was discovered during colonoscopy, prompting a biopsy. The presence of adenocarcinoma was confirmed by histopathological analysis. The only clinical manifestation of the colonic malignancy was the symptomatic presentation of nephrotic syndrome, which led to early detection of the underlying cancer. Paraneoplastic nephropathy connects kidney disease with systemic cancer, showing that renal symptoms may aid in diagnosing hidden malignancies. Nephrotic syndrome, especially membranous nephropathy, is associated with various solid tumors. The present case demonstrated that paraneoplastic syndrome, though rare, may lead to early cancer detection. Ongoing research is essential for improving understanding, targeted therapy and patient management.
C1 [Surugiu, Roxana; Sandu, Raluca Elena] Univ Med & Pharm Craiova, Dept Biochem, St Petru Rares, Craiova 200433, Romania.
   [Vintilescu, Stefanita Bianca; Stepan, Mioara Desdemona] Univ Med & Pharm Craiova, Dept Infant Care Pediat Neonatol, St Petru Rares, Craiova 200433, Romania.
   [Sandu, Raluca Elena; Pirscoveanu, Denisa] Univ Med & Pharm Craiova, Dept Neurol, St Petru Rares, Craiova 200433, Romania.
   [Pirici, Daniel] Univ Med & Pharm Craiova, Dept Pathol, St Petru Rares, Craiova 200433, Romania.
   [Neagoe, Carmen Daniela; Genunche-Dumitrescu, Amelia Valentina] Univ Med & Pharm Craiova, Dept Internal Med, St Petru Rares, Craiova 200433, Romania.
   [Matei, Daniela] Univ Med & Pharm Craiova, Dept Phys Med & Rehabil, Craiova 200433, Romania.
   [Aldea, Madalina] Univ Med & Pharm Craiova, Dept Psychiat, Craiova 200433, Romania.
   [Dumitra, Gheorghe Gindrovel] Univ Med & Pharm Craiova, Dept Family Med, 2-4 Petru Rares St, Craiova 200349, Romania.
C3 University of Medicine & Pharmacy of Craiova; University of Medicine &
   Pharmacy of Craiova; University of Medicine & Pharmacy of Craiova;
   University of Medicine & Pharmacy of Craiova; University of Medicine &
   Pharmacy of Craiova; University of Medicine & Pharmacy of Craiova;
   University of Medicine & Pharmacy of Craiova; University of Medicine &
   Pharmacy of Craiova
RP Dumitra, GG (corresponding author), Univ Med & Pharm Craiova, Dept Family Med, 2-4 Petru Rares St, Craiova 200349, Romania.; Stepan, MD (corresponding author), Univ Med & Pharm Craiova, Dept Infant Care Pediat Neonatol, St Petru Rares,2-4 Petru Rares St, Craiova 200433, Romania.
EM gindrovel.dumitra@umfcv.ro; desdemona.stepan@umfcv.ro
RI Dumitra, Gindrovel/AAA-4025-2021; Surugiu, Roxana/AAA-1991-2021; MATEI,
   DANIELA/KQT-9410-2024; STEPAN, DESDEMONA/GZH-1533-2022; Dumitra,
   Gindrovel/T-5989-2018
OI Dumitra, Gindrovel/0000-0002-8982-9645
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NR 43
TC 0
Z9 0
U1 3
U2 3
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 2049-9434
EI 2049-9442
J9 BIOMED REP
JI Biomed. Rep.
PD NOV
PY 2024
VL 21
IS 5
AR 170
DI 10.3892/br.2024.1858
PG 8
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA H1X0J
UT WOS:001321424900001
PM 39345954
OA gold
DA 2025-01-04
ER

PT J
AU Oliveira, DM
   Grillone, K
   Mignogna, C
   De Falco, V
   Laudanna, C
   Biamonte, F
   Locane, R
   Corcione, F
   Fabozzi, M
   Sacco, R
   Viglietto, G
   Malanga, D
   Rizzuto, A
AF Oliveira, Duarte Mendes
   Grillone, Katia
   Mignogna, Chiara
   De Falco, Valentina
   Laudanna, Carmelo
   Biamonte, Flavia
   Locane, Rosa
   Corcione, Francesco
   Fabozzi, Massimiliano
   Sacco, Rosario
   Viglietto, Giuseppe
   Malanga, Donatella
   Rizzuto, Antonia
TI Next-generation sequencing analysis of receptor-type tyrosine kinase
   genes in surgically resected colon cancer: identification of
   gain-of-function mutations in the RET proto-oncogene
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Article
DE Next-generation sequencing; Receptor-type tyrosine kinases; Colon
   cancer; RET proto-oncogene
ID HUMAN-BREAST; ACTIVATION; ASSOCIATION; RESISTANCE; LEUKEMIA; TUMORS
AB Background: Improvement in genetic characterization of Colon Cancer (CC) patients is required to propose new potential targets, since surgical resection coupled to chemotherapy, presents several limits such as cancer recurrence and drug resistance. Targeted therapies have more efficacy and less toxicity than standard treatments. One of the most relevant cancer-specific actionable targets are receptor tyrosine kinases (RTKs) whose role in CC need to be better investigated.
   Methods: We have analysed 37 CC patients using the Ion AmpliSeq (TM) Comprehensive Cancer Panel (CCP). We have confirmed the somatic nature of RET variants through Sanger sequencing and assessed RET activation status and protein expression by immunofluorescence and western-blot analyses. We have used RET mutant expression vectors to evaluate the effect of selected mutations in HEK293 cells by performing proliferation, migration and clonogenic assays.
   Results: Among the 409 cancer-related genes included in the CCP we have focused on the RTKs. Overall, we have observed 101 different potentially damaging variants distributed across 31 RTK genes in 28 patients. The most frequently mutated RTKs were FLT4, ROS1, EPH7, ERBB2, EGFR, RET, FGFR3 and FGFR4. In particular, we have identified 4 different somatic variants in 10% of CC patients in RET proto-oncogene. Among them, we have demonstrated that the G533C variant was able to activate RET by promoting dimer formation and enhancing Y1062 phosphorylation. Moreover, we have demonstrated that RET G533C variant was able to stimulate anchorage-dependent proliferation, migration and clonogenic cell survival. Notably, the effects induced by the RET G533C variant were abolished by vandetanib.
   Conclusions: The discovery of pathogenic variants across RTK genes in 75% of the CC patients under analysis, suggests a previously underestimated role for RTKs in CC development. The identification of a gain-of-function RET mutation in CC highlights the potential use of RET in targeted therapy.
C1 [Oliveira, Duarte Mendes; Grillone, Katia; Laudanna, Carmelo; Biamonte, Flavia; Viglietto, Giuseppe; Malanga, Donatella] Magna Graecia Univ Catanzaro, Dept Expt & Clin Med, Campus Salvatore Venuta Viale Europa, I-88100 Catanzaro, Italy.
   [Mignogna, Chiara] Magna Graecia Univ Catanzaro, Dept Hlth Sci, Campus Salvatore Venuta Viale Europa, I-88100 Catanzaro, Italy.
   [Locane, Rosa; Sacco, Rosario; Rizzuto, Antonia] Magna Graecia Univ Catanzaro, Dept Med & Surg Sci, Campus Salvatore Venuta Viale Europa, I-88100 Catanzaro, Italy.
   [De Falco, Valentina] Univ Federico II, Dept Mol Med & Med Biotechnol, Naples, Italy.
   [Corcione, Francesco; Fabozzi, Massimiliano] Azienda Osped Colli, UOC Chirurg Gen, Naples, Italy.
C3 Magna Graecia University of Catanzaro; Magna Graecia University of
   Catanzaro; Magna Graecia University of Catanzaro; University of Naples
   Federico II
RP Viglietto, G; Malanga, D (corresponding author), Magna Graecia Univ Catanzaro, Dept Expt & Clin Med, Campus Salvatore Venuta Viale Europa, I-88100 Catanzaro, Italy.
EM viglietto@unicz.it; malanga@unicz.it
RI Biamonte, Flavia/AAC-4934-2019; Maione, Francesco/HLG-5940-2023;
   Malanga, Donatella/J-4877-2018; Fabozzi, Massimiliano/AAE-6037-2022;
   Viglietto, Giuseppe/AAC-2852-2019; Rizzuto, Antonia/GVT-4842-2022; DE
   FALCO, VALENTINA/C-2061-2015; Mignogna, Chiara/IQR-8127-2023
OI Mendes Oliveira, Duarte/0000-0003-3922-3060; Malanga,
   Donatella/0000-0002-0491-7698; Rizzuto, Antonia/0000-0003-4359-4702;
   Fabozzi, MD, PhD, FACS, Massimiliano/0000-0001-5102-0210; Biamonte,
   Flavia/0000-0003-3248-3863; DE FALCO, VALENTINA/0000-0002-8972-7921;
   Mignogna, Chiara/0000-0001-5576-4946; LAUDANNA,
   Carmelo/0000-0002-0397-6020
FU Centro di Genomica Funzionale e Patologia Molecolare of University Magna
   Graecia of Catanzaro;  [PON01_02782]
FX This work was supported by Centro di Genomica Funzionale e Patologia
   Molecolare of University Magna Graecia of Catanzaro and by PON01_02782
   to GV.
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NR 38
TC 15
Z9 19
U1 1
U2 10
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1756-9966
J9 J EXP CLIN CANC RES
JI J. Exp. Clin. Cancer Res.
PD APR 17
PY 2018
VL 37
AR 84
DI 10.1186/s13046-018-0746-y
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GD0KI
UT WOS:000430189300001
PM 29665843
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Sugita, Y
   Yamashita, K
   Fujita, M
   Saito, M
   Yamada, K
   Agawa, K
   Watanabe, A
   Fukuoka, E
   Hasegawa, H
   Kanaji, S
   Oshikiri, T
   Matsuda, T
   Nakamura, T
   Suzuki, S
   Kakeji, Y
AF Sugita, Yutaka
   Yamashita, Kimihiro
   Fujita, Mitsugu
   Saito, Masafumi
   Yamada, Kota
   Agawa, Kyosuke
   Watanabe, Akihiro
   Fukuoka, Eiji
   Hasegawa, Hiroshi
   Kanaji, Shingo
   Oshikiri, Taro
   Matsuda, Takeru
   Nakamura, Tetsu
   Suzuki, Satoshi
   Kakeji, Yoshihiro
TI CD244<SUP>+</SUP> polymorphonuclear myeloid-derived suppressor cells
   reflect the status of peritoneal dissemination in a colon cancer mouse
   model
SO ONCOLOGY REPORTS
LA English
DT Article
DE myeloid-derived suppressor cell; polymorphonuclear myeloid-derived
   suppressor cell; neutrophil; CD244; peritoneal dissemination; colon
   cancer
ID COLORECTAL-CANCER; G-CSF; CARCINOEMBRYONIC ANTIGEN; TUMOR
   MICROENVIRONMENT; STIMULATING FACTOR; CARCINOMATOSIS; CHEMOTHERAPY;
   NEUTROPHILS; PROGNOSIS; THERAPY
AB Despite the recent development of chemotherapeutic agents, the prognosis of colorectal cancer (CRC) patients with peritoneal dissemination (PD) remains poor. The tumor immune microenvironment (TIME) has drawn attention as a key contributing factor of tumor progression. Of TIME components, myeloid-derived suppressor cells (MDSCs) are considered to play a responsible role in the immunosuppressive characteristics of the TIME. MDSCs are classified into two major subsets: Monocytic MDSCs (M-MDSCs) and polymorphonuclear MDSCs (PMN-MDSCs). Therefore, we hypothesize that MDSCs would play important roles in the PD-relevant TIME and PD progression. To address this hypothesis, we established PD mouse models. As the PD nodules consisted scarcely of immune cells, we focused on the peritoneal cavity, but not PD nodule, to evaluate the PD-relevant TIME. As a result, intraperitoneal PMN-MDSCs were found to be substantially increased in association with PD progression. Based on these results, we phenotypically and functionally verified the usefulness of CD244 for identifying PMN-MDSCs. In addition, the concentrations of interleukin (IL)-6 and granulocyte-colony stimulating factor (G-CSF) were significantly increased in the peritoneal cavity, both of which were produced by the tumors and thought to contribute to the increases in the PMN-MDSCs. In vivo depletion of the PMN-MDSCs by anti-Ly6G monoclonal antibody (mAb) significantly inhibited the PD progression and reverted CD4(+) and CD8(+) T cells in the peritoneal cavity and the peripheral blood. Collectively, these results suggest that the targeted therapy for PMN-MDSCs would provide not only new therapeutic value but also a novel strategy to synergize with T-cell-based immunotherapy for CRC-derived PD.
C1 [Sugita, Yutaka; Yamashita, Kimihiro; Fujita, Mitsugu; Yamada, Kota; Agawa, Kyosuke; Watanabe, Akihiro; Hasegawa, Hiroshi; Kanaji, Shingo; Oshikiri, Taro; Matsuda, Takeru; Nakamura, Tetsu; Kakeji, Yoshihiro] Kobe Univ, Grad Sch Med, Dept Surg, Div Gastrointestinal Surg, Kobe, Hyogo 6500017, Japan.
   [Fujita, Mitsugu] Kindai Univ, Fac Med, Ctr Med Educ & Clin Training, 377-2 Ohno Higashi, Osaka 5898511, Japan.
   [Saito, Masafumi] Kobe Univ, Grad Sch Med, Dept Disaster & Emergency & Crit Care Med, Kobe, Hyogo 6500017, Japan.
   [Fukuoka, Eiji] Hyogo Canc Ctr, Dept Gastroenterol Surg, Akashi, Hyogo 6738558, Japan.
   [Suzuki, Satoshi] Kobe Univ, Grad Sch Med, Dept Social Community Med & Hlth Sci, Div Community Med & Med Network, Kobe, Hyogo 6500017, Japan.
C3 Kobe University; Kindai University (Kinki University); Kobe University;
   Hyogo Cancer Center; Kobe University
RP Fujita, M (corresponding author), Kindai Univ, Fac Med, Ctr Med Educ & Clin Training, 377-2 Ohno Higashi, Osaka 5898511, Japan.; Yamashita, K (corresponding author), Kobe Univ, Grad Sch Med, Dept Surg, Div Gastrointestinal Surg,Chuo Ku, 7-5-2 Kusunoki Cho, Kobe, Hyogo 6500017, Japan.
EM kiyama@med.kobe-u.ac.jp; mfujita47@gmail.com
RI Yamashita, Kimihiro/J-4396-2014; Nakamura, Tetsu/W-3864-2019; Fujita,
   Mitsugu/A-6690-2009
OI Fujita, Mitsugu/0000-0002-0000-9879
FU JSPS KAKENHI [20K17650]; Grants-in-Aid for Scientific Research
   [20K17650, 20K09008] Funding Source: KAKEN
FX This work was supported by JSPS KAKENHI (grant no. 20K17650).
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NR 55
TC 7
Z9 7
U1 2
U2 7
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1021-335X
EI 1791-2431
J9 ONCOL REP
JI Oncol. Rep.
PD JUN
PY 2021
VL 45
IS 6
AR 106
DI 10.3892/or.2021.8057
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RT4OW
UT WOS:000644441400001
PM 33907826
OA Green Accepted, Green Published, Green Submitted, hybrid
DA 2025-01-04
ER

PT J
AU Tian, YF
   Huang, CJ
   Liu, CY
   Yang, SH
   Hung, CS
   Lin, KY
   Lai, CL
   Chang, CC
AF Tian, Yu-Feng
   Huang, Chi-Jung
   Liu, Chih-Yi
   Yang, Shung-Haur
   Hung, Chih-Sheng
   Lin, Kai-Yuan
   Lai, Ching-Long
   Chang, Chun-Chao
TI MicroRNA-24 alleviates colorectal cancer progression via a rs28382740
   single nucleotide polymorphism in the long noncoding region of X-linked
   inhibitor of apoptosis protein
SO ONCOLOGY LETTERS
LA English
DT Article
DE recurrent CRC; XIAP; rs28382740 SNP; miR-24
ID DOWN-REGULATION; THERAPEUTIC TARGETS; POOR-PROGNOSIS; XIAP; EXPRESSION;
   PLASMA; GENE; CARCINOGENESIS; SENSITIVITY; RECURRENCE
AB Colorectal cancer (CRC) is one of the most prevalent malignant diseases worldwide. Recurrence is associated with the poor survival of patients with CRC. Targeted therapy and precision medicine for recurrent CRC may improve the clinical outcome. Therefore, finding biomarkers that can detect CRC early, assess its prognosis and survival, and predict its treatment response is key to improving the clinical prognosis. The aim of this study was to assess CRC recurrence by analyzing molecular differences using postoperative specimens. Whole-exome sequencing was first used to evaluate the molecular differences in CRC tissues from patients with recurrent disease, and the results were then verified with tissue array methods. The regulation of single nucleotide polymorphisms (SNPs) in long noncoding regions of interest was analyzed in the presence of target microRNAs (miRs) using luciferase assays. The results demonstrated that in patients with recurrent CRC, the G allele was mainly detected at the rs28382740 SNP in the 3 '-untranslated region of the X-linked inhibitor of apoptosis (XIAP)-encoding gene. From the tissue arrays, 60% (3/5) of patients with the G allele of the rs28382740 SNP were diagnosed with CRC recurrence, whilst only 10% (1/10) of patients without the G allele had recurrent CRC (P=0.077). Furthermore, XIAP levels were high in non-CRC (50%; 2/4) and CRC (75%; 3/4) tissues of patients with recurrent disease and CRC (54.5%; 6/11) tissues of patients without recurrent disease. However, but only 9.1% (1/11) of non-CRC tissues of nonrecurrent patients had significantly high XIAP expression levels (P=0.022). Using a luciferase assay, it was demonstrated that miR-24s (miR-24-1-5p and miR-24-2-5p) targeting the rs28382740 SNP reduced XIAP levels in CRC cells with rs28382740 SNP genotype G. These results indicate that apoptosis-related proteins, such as XIAP, may be therapeutic targets or biomarkers for tumor development. The data from the present study support an inhibitory effect of miR-24s on XIAP expression. However, this inhibitory potency depends on the rs28382740 SNP genotype and may alleviate CRC progression by regulating the expression of XIAP.
C1 [Tian, Yu-Feng] Chi Mei Med Ctr, Dept Surg, Tainan, Taiwan.
   [Huang, Chi-Jung] Natl Def Med Ctr, Dept Biochem, Taipei 114201, Taiwan.
   [Huang, Chi-Jung] Cathay Gen Hosp, Dept Med Res, Taipei 106438, Taiwan.
   [Liu, Chih-Yi] Sijhih Cathay Gen Hosp, Dept Pathol, New Taipei 221037, Taiwan.
   [Liu, Chih-Yi; Hung, Chih-Sheng] Fu Jen Catholic Univ, Coll Med, Sch Med, New Taipei 242062, Taiwan.
   [Yang, Shung-Haur] Natl Yang Ming Chiao Tung Univ Hosp, Dept Colorectal Surg, Yilan, Taiwan.
   [Yang, Shung-Haur] Yang Ming Chiao Tung Univ, Sch Med, Taipei 112304, Taiwan.
   [Yang, Shung-Haur] Taipei Vet Gen Hosp, Dept Surg, Div Colon & Rectal Surg, Taipei 112201, Taiwan.
   [Hung, Chih-Sheng] Cathay Gen Hosp, Dept Internal Med, Div Gastroenterol, Taipei 106438, Taiwan.
   [Lin, Kai-Yuan] Chi Mei Med Ctr, Dept Med Res, Tainan, Taiwan.
   [Lai, Ching-Long] Chang Gung Univ Sci & Technol, Dept Nursing, Div Basic Med Sci, Taoyuan City 333324, Taiwan.
   [Lai, Ching-Long] Chang Gung Univ Sci & Technol, Res Ctr Chinese Herbal Med, Taoyuan City 333324, Taiwan.
   [Chang, Chun-Chao] Taipei Med Univ Hosp, Dept Internal Med, Div Gastroenterol & Hepatol, 252 Wuxing St, Taipei 110301, Taiwan.
   [Chang, Chun-Chao] Taipei Med Univ, Coll Med, Sch Med, Div Gastroenterol & Hepatol,Dept Internal Med, Taipei 110301, Taiwan.
C3 Chi Mei Hospital; National Defense Medical Center; Cathay General
   Hospital; Cathay General Hospital; Fu Jen Catholic University; Taipei
   Veterans General Hospital; Cathay General Hospital; Chi Mei Hospital;
   Taipei Medical University Hospital
RP Chang, CC (corresponding author), Taipei Med Univ Hosp, Dept Internal Med, Div Gastroenterol & Hepatol, 252 Wuxing St, Taipei 110301, Taiwan.
EM chunchao@tmu.edu.tw
RI Chan, Chun-Hsiang/JWO-8978-2024
FU Chi Mei Medical Center and Taipei Medical University
FX Not applicable.
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NR 84
TC 0
Z9 0
U1 0
U2 0
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD DEC
PY 2024
VL 28
IS 6
AR 591
DI 10.3892/ol.2024.14724
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA I8M6E
UT WOS:001332744800001
PM 39417038
OA gold
DA 2025-01-04
ER

PT J
AU Ortendahl, JD
   Carter, GC
   Thakkar, SG
   Bognar, K
   Hall, DW
   Abdou, Y
AF Ortendahl, Jesse D.
   Carter, Gebra Cuyun
   Thakkar, Snehal G.
   Bognar, Katalin
   Hall, David W.
   Abdou, Yara
TI Value of next generation sequencing (NGS) testing in advanced cancer
   patients
SO JOURNAL OF MEDICAL ECONOMICS
LA English
DT Article
DE Oncology; genomic testing; diagnostics; costs; comparative
   effectiveness; I18; I1; I; C50; C5; C
ID PEMBROLIZUMAB PLUS CHEMOTHERAPY; METASTATIC COLORECTAL-CANCER;
   BREAST-CANCER; BUDGET IMPACT; BEVACIZUMAB; ELIGIBILITY; SURVIVAL;
   OLAPARIB; MUTATION
AB ObjectiveThe availability of targeted therapies for oncology patients is increasing. Available genomic tests to identify treatment-eligible patients include single gene tests and gene panel tests, including the whole-exome, whole-transcriptome OncoExTra test. We assessed the costs and clinical benefits of test choice.MethodsA Microsoft Excel-based model was developed to evaluate test choice in patients with advanced/metastatic non-small cell lung cancer (NSCLC), breast, prostate, and colorectal cancer. Treatment pathways were based on NCCN guidelines and medical expert opinion. Inputs were derived from published literature. Annual economic results and lifetime clinical results with OncoExTra testing were projected per-tested-patient and compared with single gene testing and no testing. Separately, results were estimated for a US health plan without the OncoExTra test and with its use in 5% of patients.ResultsCompared with no genomic testing, OncoExTra test use increased costs by $4,915 per patient; however, 82%-92% of individuals across tumour types were identified as eligible for targeted therapy or a clinical trial. Compared with single gene testing, OncoExTra test use decreased costs by $9,966 per-patient-tested while increasing use of approved or investigational targeted therapies by 20%. When considering a hypothetical health plan with 1 million members, 858 patients were eligible for genomic testing. Using the OncoExTra test in 5% of those eligible, per-member per-month costs decreased by $0.003, ranging from cost-savings of $0.026 in NSCLC patients to a $0.009 increase in prostate cancer patients. Cost-savings were driven by reduced treatment costs with increased clinical trial enrolment and reduced direct and indirect medical costs associated with targeted treatments.LimitationsLimitations include the required simplifications in modelling complex conditions that may not fully reflect evolving real-world testing and treatment patterns.ConclusionsCompared to single-gene testing, results indicate that using next generation sequencing test such as OncoExTra identified more actionable alterations, leading to improved outcomes and reduced costs.
C1 [Ortendahl, Jesse D.; Bognar, Katalin] Partnership Hlth Analyt Res PHAR LLC, Beverly Hills, CA USA.
   [Carter, Gebra Cuyun; Thakkar, Snehal G.; Hall, David W.] Exact Sci Corp, Madison, WI USA.
   [Abdou, Yara] UNC Hlth Care, Chapel Hill, NC USA.
   [Carter, Gebra Cuyun] Exact Sci Corp, 5505 Endeavor Lane, Madison, WI 53719 USA.
C3 Partnership HealthPlan
RP Carter, GC (corresponding author), Exact Sci Corp, 5505 Endeavor Lane, Madison, WI 53719 USA.
EM gcuyuncarter@exactsciences.com
RI Abdou, Yara/L-6069-2019
OI Abdou, Yara/0000-0002-4827-8613; Bognar, Katalin/0000-0001-8357-8569;
   Hall, David/0000-0001-7708-6656; Cuyun Carter,
   Gebra/0000-0002-6549-0069; Ortendahl, Jesse/0009-0002-6808-8267
FU Exact Sciences Corporation
FX None stated.
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NR 77
TC 1
Z9 1
U1 3
U2 9
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1369-6998
EI 1941-837X
J9 J MED ECON
JI J. Med. Econ.
PD DEC 31
PY 2024
VL 27
IS 1
BP 519
EP 530
DI 10.1080/13696998.2024.2329009
PG 12
WC Economics; Health Care Sciences & Services; Health Policy & Services;
   Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Business & Economics; Health Care Sciences & Services; General &
   Internal Medicine
GA MU1Q6
UT WOS:001196061500001
PM 38466204
OA gold
DA 2025-01-04
ER

PT J
AU Le Roy, B
   Tixier, L
   Pereira, B
   Sauvanet, P
   Buc, E
   Pétorin, C
   Déchelotte, P
   Pezet, D
   Balayssac, D
AF Le Roy, Bertrand
   Tixier, Lucie
   Pereira, Bruno
   Sauvanet, Pierre
   Buc, Emmanuel
   Petorin, Caroline
   Dechelotte, Pierre
   Pezet, Denis
   Balayssac, David
TI Assessment of the Relation between the Expression of Oxaliplatin
   Transporters in Colorectal Cancer and Response to FOLFOX-4 Adjuvant
   Chemotherapy: A Case Control Study
SO PLOS ONE
LA English
DT Article
ID ORGANIC CATION TRANSPORTERS; 1ST-LINE TREATMENT; 3 SLC22A3;
   FLUOROURACIL; LEUCOVORIN; IRINOTECAN; SURVIVAL; PREDICTOR; MEMBRANE;
   OCT1
AB Background
   Adjuvant chemotherapy for colorectal cancer is mainly based on the combination of 5-fluorouracil, folinic acid and oxaliplatin (FOLFOX-4). The pharmacological target of oxaliplatin remains intracellular and therefore dependent on its entry into cells. The intracellular distribution of oxaliplatin is mediated by organic cation transporters 1, 2 and 3 (OCT1, 2 and 3), copper transporter 1 (CTR1) and ATPase Cu2+ transporting beta polypeptide (ATP7B) and may modulate the efficacy of oxaliplatin-based chemotherapy. The aim of this study was to perform a retrospective study to assess the relation between the expression of oxaliplatin transporters in colorectal cancer before chemotherapy and the response to FOLFOX-4 adjuvant chemotherapy in responder and non-responder patients.
   Methods
   This retrospective study was conducted at a single center (University Hospital of ClermontFerrand, France). The target population was patients with resectable colorectal cancer operated between 2006 and 2013. Inclusion criteria were defined for the responder patients as no cancer recurrence 3 years after the end of chemotherapy, and for the non-responder patients as cancer recurrence within 1 year. Other inclusion criteria were stages IIb-IV cancers, first-line adjuvant FOLFOX-4 chemotherapy, and the availability of resected primary tumor samples. Exclusion criteria were preoperative chemotherapy and/or radiotherapy, a targeted therapy, other anticancer drugs, cancer recurrence between the first and the third year after the end of chemotherapy and follow-up < 3 years. Immunostaining of oxaliplatin transporters (OCT1, 2, 3, CTR1 and ATP7B) and Ki-67 was assessed in tumor samples.
   Results
   Retrospectively, 31 patients have been selected according to inclusion and exclusion criteria (15 responders and 16 non-responders). Before FOLFOX-4 regimen, OCT3 expression was significantly lower in responder patients compared to non-responders (p<0.001). According to multivariate analysis, OCT3 remains an independent criterion for adjuvant FOLFOX chemotherapy response (p = 0.039). No significant relation is reported between chemotherapy response and the expression of OCT1 (p = 0.49), OCT2 (p = 0.09), CTR1 (p = 0.45), ATP7B (p = 0.94) and Ki-67 (p = 0.34) in tumors.
   Conclusions
   High expression of OCT3 could be an independent factor related to resistance to FOLFOX-4 chemotherapy.
C1 [Le Roy, Bertrand; Sauvanet, Pierre; Buc, Emmanuel; Petorin, Caroline; Pezet, Denis] CHU Clermont Ferrand, Serv Chirurg & Oncol Digest, F-63003 Clermont Ferrand, France.
   [Tixier, Lucie; Dechelotte, Pierre] CHU Clermont Ferrand, Serv Anatomopathol, F-63003 Clermont Ferrand, France.
   [Pereira, Bruno; Balayssac, David] CHU Clermont Ferrand, Delegat Rech Clin & Innovat, F-63003 Clermont Ferrand, France.
   [Sauvanet, Pierre; Buc, Emmanuel; Pezet, Denis] INRA, INSERM, UdA U1071, USC 2018,M2iSH, F-63001 Clermont Ferrand, France.
   [Dechelotte, Pierre] Univ Auvergne, R2D2, EA 7281, F-63001 Clermont Ferrand, France.
   [Balayssac, David] INSERM, U1107, Neurodol, F-63001 Clermont Ferrand, France.
C3 CHU Clermont Ferrand; CHU Clermont Ferrand; CHU Clermont Ferrand;
   Institut National de la Sante et de la Recherche Medicale (Inserm);
   INRAE; Universite Clermont Auvergne (UCA); Institut National de la Sante
   et de la Recherche Medicale (Inserm)
RP Balayssac, D (corresponding author), CHU Clermont Ferrand, Delegat Rech Clin & Innovat, F-63003 Clermont Ferrand, France.; Balayssac, D (corresponding author), INSERM, U1107, Neurodol, F-63001 Clermont Ferrand, France.
EM dbalayssac@chu-clermontferrand.fr
RI Pereira, Bruno/JTT-9628-2023; Buc, Emmanuel/JEP-6444-2023; Balayssac,
   David/K-2265-2015; Pezet, Denis/I-4423-2017
OI Le Roy, Bertrand/0000-0002-4668-9275; Pereira,
   Bruno/0000-0003-3778-7161; Balayssac, David/0000-0002-6126-6588; Tixier,
   Lucie/0000-0002-1325-3141
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NR 33
TC 11
Z9 12
U1 0
U2 10
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD FEB 9
PY 2016
VL 11
IS 2
AR e0148739
DI 10.1371/journal.pone.0148739
PG 12
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA DD6MN
UT WOS:000370038400072
PM 26859833
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Tardito, S
   Matis, S
   Zocchi, MR
   Benelli, R
   Poggi, A
AF Tardito, Samuele
   Matis, Serena
   Zocchi, Maria Raffaella
   Benelli, Roberto
   Poggi, Alessandro
TI Epidermal Growth Factor Receptor Targeting in Colorectal Carcinoma:
   Antibodies and Patient-Derived Organoids as a Smart Model to Study
   Therapy Resistance
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE organoids; EGFR; therapeutic antibodies; colorectal cancer; drug
   resistance
ID DRUG CONJUGATES DESIGN; ANTI-EGFR THERAPY; GENE COPY NUMBER; CELL
   LUNG-CANCER; MONOCLONAL-ANTIBODIES; CETUXIMAB RESISTANCE; MUTATION
   STATUS; HUMAN COLON; IN-VITRO; ACTIVATION
AB Colorectal cancer (CRC) is the second leading cause of cancer-related death worldwide. Therefore, the need for new therapeutic strategies is still a challenge. Surgery and chemotherapy represent the first-line interventions; nevertheless, the prognosis for metastatic CRC (mCRC) patients remains unacceptable. An important step towards targeted therapy came from the inhibition of the epidermal growth factor receptor (EGFR) pathway, by the anti-EGFR antibody, Cetuximab, or by specific tyrosine kinase inhibitors (TKI). Cetuximab, a mouse-human chimeric monoclonal antibody (mAb), binds to the extracellular domain of EGFR thus impairing EGFR-mediated signaling and reducing cell proliferation. TKI can affect the EGFR biochemical pathway at different steps along the signaling cascade. Apart from Cetuximab, other anti-EGFR mAbs have been developed, such as Panitumumab. Both antibodies have been approved for the treatment of KRAS-NRAS wild type mCRC, alone or in combination with chemotherapy. These antibodies display strong differences in activating the host immune system against CRC, due to their different immunoglobulin isotypes. Although anti-EGFR antibodies are efficient, drug resistance occurs with high frequency. Resistant tumor cell populations can either already be present before therapy or develop later by biochemical adaptations or new genomic mutations in the EGFR pathway. Numerous efforts have been made to improve the efficacy of the anti-EGFR mAbs or to find new agents that are able to block downstream EGFR signaling cascade molecules. Indeed, we examined the importance of analyzing the anti-EGFR antibody-drug conjugates (ADC) developed to overcome resistance and/or stimulate the tumor host's immunity against CRC growth. Also, patient-derived CRC organoid cultures represent a useful and feasible in vitro model to study tumor behavior and therapy response. Organoids can reflect tumor genetic heterogeneity found in the tissue of origin, representing a unique tool for personalized medicine. Thus, CRC-derived organoid cultures are a smart model for studying the tumor microenvironment and for the preclinical assay of anti-EGFR drugs.
C1 [Tardito, Samuele] Childrens Natl Hosp, Ctr Canc & Immunol Res, Washington, DC 20010 USA.
   [Matis, Serena; Benelli, Roberto; Poggi, Alessandro] IRCCS Osped Policlin San Martino, Mol Oncol & Angiogenesis Unit, I-16132 Genoa, Italy.
   [Zocchi, Maria Raffaella] IRCCS Sci Inst San Raffaele, Dept Immunol Transplant & Infect Dis, I-20132 Milan, Italy.
C3 Children's National Health System
RP Benelli, R; Poggi, A (corresponding author), IRCCS Osped Policlin San Martino, Mol Oncol & Angiogenesis Unit, I-16132 Genoa, Italy.
EM samuele.tardito@childrensnational.org; serena.matis@hsanmartino.it;
   marazocchi55@gmail.com; roberto.benelli@hsanmartino.it;
   alessandro.poggi@hsanmartino.it
RI Benelli, Roberto/AAF-3143-2019; Poggi, Alessandro/K-6664-2016
OI Poggi, Alessandro/0000-0002-1860-430X; Benelli,
   Roberto/0000-0002-9769-0954
FU Ministero della salute; Associazione Italiana per la Ricerca sul Cancro
   [AIRC IG 21648]; Compagnia di San Paolo [ROL 32567]
FX This research was funded by Ministero della salute Ricerca Corrente
   (2022-2024, to R.B. and S.M.), Associazione Italiana per la Ricerca sul
   Cancro (AIRC IG 21648, to A.P.) and Compagnia di San Paolo (ROL 32567 to
   AP).
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NR 211
TC 2
Z9 2
U1 8
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JUL
PY 2024
VL 25
IS 13
AR 7131
DI 10.3390/ijms25137131
PG 26
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA YI9X6
UT WOS:001267990500001
PM 39000238
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Abadi, ZMA
   Asl, DH
   Rahmani, B
   Peimani, A
   Dodaran, MS
   Rad, FS
AF Abadi, Z. M. Abbas
   Asl, D. Hamedi
   Rahmani, B.
   Peimani, A.
   Dodaran, M. Soleimani
   Rad, F. Samiee
TI THE CLINICOPATHOLOGIC FEATURES OF COLORECTAL ADENOCARCINOMA WITH RESPECT
   TO MISMATCH REPAIR GENES AND KRAS STATUS: A RETROSPECTIVE STUDY
SO WORLD CANCER RESEARCH JOURNAL
LA English
DT Article
DE Clinicopathologic; MMR; KRAS; CRC
ID MICROSATELLITE INSTABILITY; RAS MUTATIONS; CANCER; CARCINOMA;
   IMMUNOHISTOCHEMISTRY; EXPRESSION; PROGNOSIS; SURVIVAL; IMPACT
AB Objective: KRAS and mismatch repair genes are two important molecular markers used in determining prognosis and probability of response to the targeted therapy in patients with colorectal cancer. In this study, the expression status of mismatch repair genes was investigated along with mutation in KRAS gene, and clinicopathologic features were also evaluated in these tumors.
   Patients and Methods: Clinical and pathological data were collected from 153 known cases of colorectal adenocarcinoma. Expression status of mismatch repair genes was assessed using immunohistochemistry (IHC) technique. Mutation in codons 12 and 13 of KRAS gene was evaluated using pyrosequencing technique. Relationship between clinical and pathologic features of the patients with status of MMR and KRAS markers was also investigated.
   Results: A total of 16.3% of tumors lacked expression at least in one of MLH1, MSH2, MSH6, and PMS2 proteins. KRAS was found to be mutated in 37.9% of the patients. Tumors were classified into four categories: dMMR + wild type KRAS (12.4%), dMMR + mutated KRAS (3.9%), pMMR + wild type KRAS (49.6%), and pMMR + mutated KRAS (33.9%). The dMMR tumors mostly had features, such as female gender, proximal location, mucinous production, increased number of lymph nodes, Signet ring cell, and vascular invasion. Compared to pMMR + wild type tumors, pMMR + mutated KRAS tumors were more associated with female gender, proximal location, mucinous component, and lymph node metastasis.
   Conclusions: Results of this study indicated a relationship between MMR status and presence of mutated KRAS with clinicopathologic features of colorectal tumors. Knowledge about these markers along with pathological features can help us to predict metastatic progression and prognosis of the disease.
C1 [Abadi, Z. M. Abbas; Rahmani, B.] Qazvin Univ Med Sci, Fac Med Sci, Dept Mol Med, Qazvin, Iran.
   [Asl, D. Hamedi; Dodaran, M. Soleimani] Dept Pathol & Mol Med, Mehr Lab, Hashtgerd, Iran.
   [Peimani, A.] Qazvin Univ Med Sci, Med Microbiol Res Ctr, Qazvin, Iran.
   [Rad, F. Samiee] Qazvin Univ Med Sci, Dept Pathol, Qazvin, Iran.
C3 Qazvin University of Medical Sciences (QUMS); Qazvin University of
   Medical Sciences (QUMS); Qazvin University of Medical Sciences (QUMS)
RP Rad, FS (corresponding author), Qazvin Univ Med Sci, Dept Pathol, Qazvin, Iran.
EM fsamieerad@gmail.com
FU  [14003016]
FX This work was supported by Grant-in-Aid for Scientific Research of
   Qazvin University of Medical Scienc-es (NO.14003016)
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NR 47
TC 1
Z9 1
U1 0
U2 2
PU VERDUCI PUBLISHER
PI ROME
PA VIA GREGORIO VII, ROME, 186-00165, ITALY
SN 2372-3416
J9 WORLD CANCER RES J
JI World Cancer Res. J.
PY 2021
VL 8
AR e1850
PG 11
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA QE4PM
UT WOS:000616189400001
DA 2025-01-04
ER

PT J
AU Hassibian, S
   Taghdisi, SM
   Jamshidi, Z
   Samie, A
   Nameghi, MA
   Shayan, M
   Farrokhi, N
   Alibolandi, M
   Ramezani, M
   Dehnavi, SM
   Abnous, K
AF Hassibian, Sepideh
   Taghdisi, Seyed Mohammad
   Jamshidi, Zahra
   Samie, Ali
   Nameghi, Morteza Alinezhad
   Shayan, Mersedeh
   Farrokhi, Naser
   Alibolandi, Mona
   Ramezani, Mohammad
   Dehnavi, Seyed Mohsen
   Abnous, Khalil
TI Surface modification of hollow gold nanoparticles conducted by
   incorporating cancer cell membrane and AS1411 aptamer, aiming to achieve
   a dual-targeted therapy for colorectal cancer
SO INTERNATIONAL JOURNAL OF PHARMACEUTICS
LA English
DT Article
DE Colon cancer cell membrane; Homologous targeting; Hollow gold NPs;
   Biomimetic nanoparticle; Photothermal therapy
AB Due to its inherent membrane structure, a nanostructure enveloped by an active cell membrane possesses distinctive characteristics such as prolonged presence in the bloodstream, precise identification capabilities, and evasion of immune responses. This research involved the production of biomimetic nanoparticles, specifically hollow gold nanoparticles (HGNPs) loaded with methotrexate (MTX), which were further coated with cancer cell membrane. These nanoparticles were then adorned with AS1411 aptamer to serve as a targeting agent (Apt-CCMHG@MTX). The nanoplatform demonstrated precise targeting towards cancer cells due to its dual-targeting characteristic (AS1411 aptamer and C26 cancer cell membrane), exhibiting uniformity in distribution. It also displayed a desirable response to photothermal stimulation, controlled release of drugs, and exceptional properties for fluorescence imaging. The system was composed of spherical HGNPs measuring 51.33 +/- 5.70 nm in diameter, which were effectively loaded with MTX using a physical absorption method. The encapsulation efficiency achieved was recorded at 79.54 %, while the loading efficiency reached 38.21 %. The targeted formulation demonstrated a noteworthy mortality of approximately 45 % in the nucleolin positive cell line, C26, as determined by in vitro cytotoxicity assays. As a result of the functionalization process applied to the homologous binding adhesion molecules found in cancer cell membranes and targeting ability of AS1411 aptamer, AptCCM-HG@MTX demonstrated a substantial enhancement in targeting tumors and facilitating cellular uptake during in vivo experiments. Furthermore, under NIR radiation the photothermal effect exhibited by Apt-CCMHG@MTX in the tumor area was notably robust due to the distinctive attributes of HGNPs. The conclusions obtained from this study have the potential to assist in adopting a bioinspired strategy that will significantly improve the effective management of MTX and therapy for individuals with colorectal cancer.
C1 [Hassibian, Sepideh; Farrokhi, Naser; Dehnavi, Seyed Mohsen] Shahid Beheshti Univ, Fac Life Sci & Biotechnol, Dept Cell & Mol Biol, POB 1983969411, Tehran, Iran.
   [Taghdisi, Seyed Mohammad; Samie, Ali] Mashhad Univ Med Sci, Pharmaceut Technol Inst, Targeted Drug Delivery Res Ctr, Mashhad, Iran.
   [Taghdisi, Seyed Mohammad] Mashhad Univ Med Sci, Sch Pharm, Dept Pharmaceut Biotechnol, Mashhad, Iran.
   [Jamshidi, Zahra; Samie, Ali; Shayan, Mersedeh] Mashhad Univ Med Sci, Sch Pharm, Dept Med Chem, Mashhad, Iran.
   [Nameghi, Morteza Alinezhad] Mashhad Univ Med Sci, Sch Pharm, Mashhad, Iran.
   [Alibolandi, Mona; Ramezani, Mohammad; Abnous, Khalil] Mashhad Univ Med Sci, Pharmaceut Technol Inst, Pharmaceut Res Ctr, Mashhad, Iran.
   [Abnous, Khalil] Mashhad Univ Med Sci, Pharmaceut Res Ctr, Sch Pharm, Dept Med Chem, Mashhad, Iran.
C3 Shahid Beheshti University; Mashhad University of Medical Sciences;
   Mashhad University of Medical Sciences; Mashhad University of Medical
   Sciences; Mashhad University of Medical Sciences; Mashhad University of
   Medical Sciences; Mashhad University of Medical Sciences
RP Dehnavi, SM (corresponding author), Shahid Beheshti Univ, Fac Life Sci & Biotechnol, Dept Cell & Mol Biol, POB 1983969411, Tehran, Iran.; Abnous, K (corresponding author), Mashhad Univ Med Sci, Pharmaceut Res Ctr, Sch Pharm, Dept Med Chem, Mashhad, Iran.
EM mo_dehnavi@sbu.ac.ir; abnouskh@mums.ac.ir
RI jamshidi, zahra/HGE-8146-2022; abnous, Khalil/R-8103-2017; Alinezhad
   Nameghi, Morteza/IWM-2392-2023; Dehnavi, Seyed Mohsen/GRJ-8899-2022;
   Taghdisi, Seyed Mohammad/F-6694-2017
OI Samie, Dr. Ali/0000-0002-4388-0461; Taghdisi, Seyed
   Mohammad/0000-0001-9836-2189; Hassibian, Sepideh/0000-0001-9104-4372
FU Mashhad University of Medical Sciences [4020234]
FX Financial support of this study was provided by Mashhad University of
   Medical Sciences (grant number: 4020234) .
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NR 29
TC 6
Z9 6
U1 4
U2 6
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0378-5173
EI 1873-3476
J9 INT J PHARMACEUT
JI Int. J. Pharm.
PD APR 25
PY 2024
VL 655
AR 124036
DI 10.1016/j.ijpharm.2024.124036
EA MAR 2024
PG 10
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA QB1Z8
UT WOS:001218342500001
PM 38522491
DA 2025-01-04
ER

PT J
AU He, M
   Li, XD
   Wang, ZW
   Sun, H
   Fan, J
AF He, Miao
   Li, Xiao-dong
   Wang, Zi-wei
   Sun, Hao
   Fan, Jing
TI A Retrospective Observational Study of Hyperthermic Intraperitoneal
   Chemotherapy for Gastric Cancer and Colorectal Cancer From a Single
   Center in the Recent 5 years
SO CANCER CONTROL
LA English
DT Article
DE HIPEC; gastric cancer; colorectal cancer; PFS
ID CYTOREDUCTIVE SURGERY; PERITONEAL METASTASES; 1ST-LINE BEVACIZUMAB;
   HIPEC; S-1
AB ObjectiveTo retrospectively analyze the effect of hyperthermic intraperitoneal chemotherapy (HIPEC) on the progression free survival (PFS) of advanced gastric cancer (GC) and colorectal cancer (CRC).MethodWe retrospectively collected all the HIPEC data of GC and CRC in the Chongqing University Cancer Hospital from August 2018 to April 2023. Data were extracted from inpatient records and outpatient examination records. The IBM SPSS statistics 23.0 software was used to analyze the data. We mainly compared the PFS of HIPEC cases with that of non-HIPEC cases (both from our center and from the literature). PFS was analyzed with the Kaplan-Meier method. Log Rank (Mantel Cox), Breslow (Generalized Wilcoxon), and Tarone-Ware were used for univariate analyses.ResultA total of 342 HIPEC cases were analyzed in this study. Stage IV GC and CRC accounted for 48.5% of the total number of cases. Abdominal pain and distension (47.4%) were the most common side effects from HIPEC. Serious complications were rare (1.8%, including bleeding, perforation, obstruction, and death). The PFS and disease-free survival (DFS) of abdominal malignancy treated with HIPEC were significantly associated with the TNM stage, but not HIPEC numbers nor HIPEC drugs. In stage IV HIPEC cases, adding adjuvant chemotherapy after HIPEC resulted in better PFS. In addition, the association between peritoneal carcinomatosis index (PCI) and PFS of stage IV HIPEC cases was close to significant. Compared with the 33 stage IV (with peritoneal metastases) GC cases without HIPEC in our center from the last 15 years, the PFS of the 56 stage GC cases with HIPEC was not improved significantly (median PFS: 6 +/- 2.92 months vs 7 +/- 1.63 months for with vs without HIPEC in stage IV GC, respectively; P >= 0.05). Compared with the 58 stage IV (with peritoneal metastases) CRC cases without HIPEC in our center from the last 15 years, the PFS of the 86 stage IV CRC cases with HIPEC was not improved significantly either (median PFS: 7 +/- 1.68 months vs 7 +/- 0.62 months for with vs without HIPEC in stage IV CRC, respectively; P >= 0.05). When comparing our HIPEC data with the non-HIPEC data reported by other scholars for the PFS of advanced GC and CRC, the negative results were similar.ConclusionThe PFS/DFS of HIPEC cases was associated with the TNM stage, but not with the HIPEC numbers or HIPEC drugs. PCI may be related to the PFS of stage IV HIPEC cases. Adding chemotherapy or targeted therapy after HIPEC may improve the PFS of stage IV cases. HIPEC did not significantly improve the PFS of stage IV GC or CRC cases in our center.
C1 [He, Miao; Li, Xiao-dong; Sun, Hao] Chongqing Univ, Chongqing Key Lab Translat Res Canc Metastasis & I, Canc Hosp, Chongqing 400030, Peoples R China.
   [Wang, Zi-wei] Chongqing Med Univ, Affiliated Hosp 1, Dept Gen Surg, Chongqing, Peoples R China.
   [Fan, Jing] Chongqing Med Univ, Affiliated Hosp 1, Dept Crit Care Med, Chongqing 400016, Peoples R China.
C3 Chongqing University; Chongqing Medical University; Chongqing Medical
   University
RP Sun, H (corresponding author), Chongqing Univ, Chongqing Key Lab Translat Res Canc Metastasis & I, Canc Hosp, Chongqing 400030, Peoples R China.; Fan, J (corresponding author), Chongqing Med Univ, Affiliated Hosp 1, Dept Crit Care Med, Chongqing 400016, Peoples R China.
EM Sunhao68@sina.com
OI he, miao/0009-0001-5753-0681
FU Scientific and Technological Research Program of Chongqing Municipal
   Education Commission
FX Authors agree on the order of attribution. FAN Jing and SUN Hao are the
   co-corresponding authors of this article. We thank LI Xiao-dong for
   providing detailed data records. We thank Professor WANG Zi-wei for his
   guidance on the analysis of this study.
CR Akturk Esen S, 2023, ONCOLOGY-BASEL, V101, P321, DOI 10.1159/000528609
   Allievi N, 2023, UPDATES SURG, V75, P159, DOI 10.1007/s13304-022-01399-y
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   Demircan NC, 2019, J BUON, V24, P1494
   Filis P, 2022, ESMO OPEN, V7, DOI 10.1016/j.esmoop.2022.100586
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   Yamada Y, 2015, ANN ONCOL, V26, P141, DOI 10.1093/annonc/mdu472
NR 20
TC 0
Z9 0
U1 2
U2 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1073-2748
EI 1526-2359
J9 CANCER CONTROL
JI Cancer Control
PD SEP
PY 2024
VL 31
AR 10732748241284535
DI 10.1177/10732748241284535
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA G6M3N
UT WOS:001317752500001
PM 39292867
OA gold
DA 2025-01-04
ER

PT J
AU Froelich, MF
   Heinemann, V
   Sommer, WH
   Holch, JW
   Schoeppe, F
   Hesse, N
   Baumann, AB
   Kunz, WG
   Reiser, MF
   Ricke, J
   D'Anastasi, M
   Stintzing, S
   Modest, DP
   Kazmierczak, PM
   Hofmann, FO
AF Froelich, Matthias F.
   Heinemann, Volker
   Sommer, Wieland H.
   Holch, Julian W.
   Schoeppe, Franziska
   Hesse, Nina
   Baumann, Alena B.
   Kunz, Wolfgang G.
   Reiser, Maximilian F.
   Ricke, Jens
   D'Anastasi, Melvin
   Stintzing, Sebastian
   Modest, Dominik P.
   Kazmierczak, Philipp M.
   Hofmann, Felix O.
TI CT attenuation of liver metastases before targeted therapy is a
   prognostic factor of overall survival in colorectal cancer patients.
   Results from the randomised, open-label FIRE-3/AIO KRK0306 trial
SO EUROPEAN RADIOLOGY
LA English
DT Article
DE Colorectal neoplasms; Neoplasm metastasis; Prognosis; Chemotherapy;
   Liver
ID RESPONSE EVALUATION; 1ST-LINE TREATMENT; RAS MUTATIONS; CRITERIA;
   BEVACIZUMAB; PREDICTORS; MORTALITY
AB ObjectivesTo assess the prognostic value of pre-therapeutic computed tomography (CT) attenuation of liver metastases for overall survival (OS) in metastatic colorectal cancer (mCRC).MethodsIn the open-label, randomised, prospective phase-III FIRE-3 trial, patients with histologically confirmed mCRC received fluorouracil (5-FU), leucovorin and irinotecan (FOLFIRI) with either cetuximab or bevacizumab. Participating patients gave written informed consent prior to study entry. In CT at baseline (portal venous phase, slice thickness 5 mm), mean attenuation [Hounsfield units (HU)] of liver metastases was retrospectively assessed by semi-automated volumetry. Its prognostic influence on OS was analysed in Kaplan-Meier-analysis and Cox proportional hazard regression and an optimal threshold was determined.ResultsIn FIRE-3, 592 patients were enrolled between 2007 and 2012. Among the 347 patients eligible for liver volumetry, median baseline CT attenuation of liver metastases was 59.67 HU [interquartile range (IQR), 49.13, 68.85]. Increased attenuation was associated with longer OS {per 10 HU: hazard ratio (HR), 0.85 [95% confidence interval (CI), 0.78, 0.93], p < 0.001}. The optimised threshold (61.62 HU) was a strong predictor for increased OS [median, 21.3 vs 30.6 months; HR, 0.61 (95% CI, 0.47, 0.80), p < 0.001]. Multivariate regression controlling for correlated and further prognostic factors confirmed this [HR, 0.60 (95% CI, 0.45, 0.81), p = 0.001]. Furthermore, mean attenuation 61.62 HU was significantly associated with increased early tumour shrinkage (p = 0.002) and increased depth of response (p = 0.012).ConclusionsIncreased mean baseline CT attenuation of liver metastases may identify mCRC patients with prolonged OS and better tumour response.Key Points center dot In colorectal cancer, increased attenuation of liver metastases in baseline computed tomography is a prognostic factor for prolonged OS (p < 0.001).center dot A threshold of 61.62 HU was determined as optimal cut-off to identify patients with prolonged OS (p < 0.001), early tumour shrinkage (p = 0.002) and increased depth of response (p = 0.012).
C1 [Froelich, Matthias F.; Sommer, Wieland H.; Schoeppe, Franziska; Hesse, Nina; Baumann, Alena B.; Kunz, Wolfgang G.; Reiser, Maximilian F.; Ricke, Jens; D'Anastasi, Melvin; Kazmierczak, Philipp M.; Hofmann, Felix O.] Ludwig Maximilians Univ Munchen, Univ Hosp, Dept Radiol, Marchioninistr 15, D-81377 Munich, Germany.
   [Heinemann, Volker; Holch, Julian W.; Stintzing, Sebastian; Modest, Dominik P.] Ludwig Maximilians Univ Munchen, Univ Hosp Grosshadern, Comprehens Canc Ctr Munich, Dept Internal Med 3, Marchioninistr 15, D-81377 Munich, Germany.
   [Heinemann, Volker; Holch, Julian W.; Stintzing, Sebastian; Modest, Dominik P.] German Canc Consortium DKTK, Partner Site Munich, Heidelberg, Germany.
   [Heinemann, Volker; Holch, Julian W.; Stintzing, Sebastian; Modest, Dominik P.] German Canc Res Ctr, Heidelberg, Germany.
C3 University of Munich; University of Munich; Helmholtz Association;
   German Cancer Research Center (DKFZ); Helmholtz Association; German
   Cancer Research Center (DKFZ)
RP Sommer, WH (corresponding author), Ludwig Maximilians Univ Munchen, Univ Hosp, Dept Radiol, Marchioninistr 15, D-81377 Munich, Germany.
EM wieland.sommer@icloud.com
RI Modest, Dominik Paul/AAW-9756-2021; Froelich, Matthias/AAG-9109-2020;
   Stintzing, Sebastian/I-4538-2016
OI Froelich, Matthias/0000-0001-8501-2147; D'Anastasi,
   Melvin/0000-0002-4778-5939; Galie, Franziska/0000-0002-1950-0844;
   Stintzing, Sebastian/0000-0002-3297-5801
FU University Hospital Grosshadern, Ludwig-Maximilians-University of
   Munich; Merck Serono GmbH, an affiliate of Merck KGaA, Darmstadt,
   Germany; Pfizer Pharma GmbH, Karlsruhe, Germany; German Consortium of
   Translational Cancer Research, Heidelberg, Germany
FX The FIRE-3 study was sponsored by University Hospital Grosshadern,
   Ludwig-Maximilians-University of Munich and received financial support
   from Merck Serono GmbH, an affiliate of Merck KGaA, Darmstadt, Germany,
   Pfizer Pharma GmbH, Karlsruhe, Germany and the German Consortium of
   Translational Cancer Research, Heidelberg, Germany.
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NR 26
TC 20
Z9 23
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0938-7994
EI 1432-1084
J9 EUR RADIOL
JI Eur. Radiol.
PD DEC
PY 2018
VL 28
IS 12
BP 5284
EP 5292
DI 10.1007/s00330-018-5454-7
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA HB8PT
UT WOS:000451353500041
PM 29882070
DA 2025-01-04
ER

PT J
AU Lu, L
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   Chan, KM
   Cho, CH
AF Lu, Lan
   Li, Zhi Jie
   Li, Long Fei
   Wu, William Ka Kei
   Shen, Jing
   Zhang, Lin
   Chan, Ruby Lok Yi
   Yu, Le
   Liu, Ya Wei
   Ren, Shun Xiang
   Chan, Kam Ming
   Cho, Chi Hin
TI Vascular-targeted TNFα improves tumor blood vessel function and enhances
   antitumor immunity and chemotherapy in colorectal cancer
SO JOURNAL OF CONTROLLED RELEASE
LA English
DT Article
DE Vascular targeting peptide; TNF alpha; Colorectal cancer; Drug delivery;
   Antitumor therapy
ID NECROSIS-FACTOR-ALPHA; ISOLATED LIMB PERFUSION; ADVANCED SOLID TUMORS;
   DRUG-DELIVERY; NGR-HTNF; IMMUNOTHERAPEUTIC PROPERTIES; PHAGE DISPLAY;
   IN-VITRO; COMBINATION; DOXORUBICIN
AB Delivery and penetration of chemotherapeutic drugs into neoplasm through the tumor vasculature are essential mechanisms to enhance the efficiency of chemotherapy. "Vascular targeting" strategy focuses on promoting the infiltration of chemotherapeutic drugs into neoplastic tissues. In this study, we achieved a targeted therapy by coupling tumor necrosis factor a (TNF alpha) with TCP-1, a novel vascular-targeting peptide, in an orthotopic colorectal cancer model in mice. High dose of TCP-1-conjugated TNF alpha (TCP-1/TNF alpha: 5 mu g/mouse) displayed potent antitumor activity by inducing apoptosis and reducingmicrovessel number in tumors than unconjugated TNF alpha, with no evidence of increased toxicity. In the combined therapy, the antitumor action of 5-fluorouracil (5-FU) was potentiated when the mice were pretreated with a low dose of TNF alpha (1 ng/mouse) and to a greater extent by the same concentration of TCP-1/TNF alpha. In this regard, TCP-1/TNF alpha combined with 5-FU synergistically inhibited the tumor growth, induced apoptosis and reduced cell proliferation. More importantly, TCP-1/TNF alpha normalized the tumor vasculature and facilitated the infiltration of immune cells to neoplasm as well as attenuated the immunosuppressing effects of TNFa in bone marrow and spleen. At the same time, TCP-1/TNF alpha significantly improved 5-FU absorption into the tumor mass. Taken together, these findings underscore the therapeutic potential of TCP-1 as a drug carrier in cancer therapy. TCP-1 is a novel vascular-targeting peptide and appears to be a promising agent for drug delivery. TCP-1 fused with TNF alpha holds great promise for colorectal cancer therapy. (C) 2015 Elsevier B.V. All rights reserved.
C1 [Lu, Lan] Chengdu Univ, Sichuan Ind Inst Antibiot, Chengdu, Peoples R China.
   [Lu, Lan; Li, Zhi Jie; Li, Long Fei; Shen, Jing; Zhang, Lin; Chan, Ruby Lok Yi; Ren, Shun Xiang; Chan, Kam Ming; Cho, Chi Hin] Chinese Univ Hong Kong, Fac Med, Sch Biomed Sci, Shatin, Hong Kong, Peoples R China.
   [Wu, William Ka Kei] Chinese Univ Hong Kong, Dept Anaesthesia & Intens Care, Shatin, Hong Kong, Peoples R China.
   [Yu, Le] Southern Med Univ, Sch Pharm, Guangzhou, Guangdong, Peoples R China.
   [Liu, Ya Wei] Southern Med Univ, Nanfang Hosp, Dept Neurosurg, Guangzhou, Guangdong, Peoples R China.
C3 Chengdu University; Chinese University of Hong Kong; Chinese University
   of Hong Kong; Southern Medical University - China; Southern Medical
   University - China
RP Li, ZJ (corresponding author), Chinese Univ Hong Kong, Sch Biomed Sci, Shatin, Hong Kong, Peoples R China.
EM jackylizhijie@gmail.com; chcho@cuhk.edu.hk
RI Chan, K/AAH-4084-2019; Cho, Chi/C-6543-2014; LI, ZHIJIE/HJG-6926-2022;
   ZHANG, Lin/O-9109-2015; Wu, William K.K./A-3277-2009
OI Wu, William K.K./0000-0002-5662-5240; Zhang, Lin/0000-0003-1634-3780;
   LI, Longfei/0009-0000-7872-2175
FU Innovation and Technology Fund from the Innovation and Technology
   Commission [ITS/212/12]; General Research Fund from the Hong Kong
   Research Grant Council [CUHK 463613]; National Natural Science
   Foundation of China [81473269]
FX The authors would like to thank the following granting agents: the
   Innovation and Technology Fund from the Innovation and Technology
   Commission (Grant No.: ITS/212/12) and the General Research Fund from
   the Hong Kong Research Grant Council (Grant No.: CUHK 463613), for their
   generous support of this project. The financial support from the
   National Natural Science Foundation of China (Grant No.: 81473269) is
   also appreciated.
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NR 60
TC 30
Z9 34
U1 3
U2 48
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-3659
EI 1873-4995
J9 J CONTROL RELEASE
JI J. Control. Release
PD JUL 28
PY 2015
VL 210
BP 134
EP 146
DI 10.1016/j.jconrel.2015.05.282
PG 13
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA CK5CC
UT WOS:000356238700015
PM 26003042
DA 2025-01-04
ER

PT J
AU Unseld, M
   Mader, R
   Baumann, L
   Veraar, C
   Wrba, F
   Waneck, F
   Kieler, M
   Bianconi, D
   Berger, W
   Sibilia, M
   Müllauer, L
   Zielinski, C
   Prager, GW
AF Unseld, Matthias
   Mader, Robert
   Baumann, Lukas
   Veraar, Clarence
   Wrba, Fritz
   Waneck, Fredrik
   Kieler, Markus
   Bianconi, Daniela
   Berger, Walter
   Sibilia, Maria
   Muellauer, Leonhard
   Zielinski, Christoph
   Prager, Gerald W.
TI Feasibility of personalized treatment concepts in gastrointestinal
   malignancies: Sub-group results of prospective clinical phase II trial
   EXACT
SO CHINESE JOURNAL OF CANCER RESEARCH
LA English
DT Article
DE Personalized medicine; gastrointestinal malignancies; prospective trial;
   next generations sequencing
ID COLORECTAL-CANCER; TARGETED THERAPY; PRECISION MEDICINE; KRAS;
   MULTICENTER; MUTATIONS; TUMORS; BRAF
AB Objective: Advances in high-throughput genomic profiling and the development of new targeted therapies improve patient's survival. In gastrointestinal (GI) malignancies, the concept of personalized medicine (PM) was not investigated so far. The aim of this prospective study was to evaluate the efficacy of a personalized treatment in GI patients who failed standard treatment.
   Methods: Out of the original prospective clinical phase II EXACT trial, 21 (38%) GI cancer patients who had no further treatment options were identified. A molecular profile (MP) via a 50 gene next generation sequencing (NGS) panel in combination with immunohistochemistry (IHC) was conducted using real-time biopsy tumor material.
   Results were discussed by a multidisciplinary team (MDT) to translate the individual MP in an experimental treatment. Results: Of the 55 patients originally included in the EXACT trial, 21 (38%) suffered from GI malignancies. The final analysis showed that 15 (71%) patients had experienced a longer progression-free survival (PFS) upon experimental targeted treatment (124 d, quartiles 70/193 d), when compared with the PFS achieved by the previous conventional therapy (62 d, quartiles 55/83 d) (P=0.014). Thirteen (62%) patients receiving targeted treatment experienced a disease control according to Response Evaluation Criteria in Solid Tumors (RECIST). Median overall survival (OS) from the start of experimental therapy to time of censoring or death was 193 d (quartiles 115/374 d).
   Conclusions: PM was not investigated in GI malignancies so far in a prospective trial. This study shows that treatment based on real-time molecular tumor profiling led to a superior clinical benefit, and survival as well as response was significantly improved when compared with previous standard medications.
C1 [Unseld, Matthias; Mader, Robert; Veraar, Clarence; Kieler, Markus; Bianconi, Daniela; Zielinski, Christoph; Prager, Gerald W.] Med Univ Vienna, Div Oncol, Dept Med 1, A-1090 Vienna, Austria.
   [Unseld, Matthias; Mader, Robert; Veraar, Clarence; Wrba, Fritz; Waneck, Fredrik; Kieler, Markus; Bianconi, Daniela; Berger, Walter; Sibilia, Maria; Muellauer, Leonhard; Zielinski, Christoph; Prager, Gerald W.] Med Univ Vienna, Gen Hosp, Comprehens Canc Ctr, A-1090 Vienna, Austria.
   [Baumann, Lukas] Med Univ Vienna, Dept Med Stat, A-1090 Vienna, Austria.
   [Wrba, Fritz; Muellauer, Leonhard] Med Univ Vienna, Clin Inst Pathol, A-1090 Vienna, Austria.
   [Waneck, Fredrik] Med Univ Vienna, Dept Intervent Radiol, A-1090 Vienna, Austria.
   [Berger, Walter; Sibilia, Maria] Med Univ Vienna, Inst Canc Res, Dept Med 1, A-1090 Vienna, Austria.
C3 Medical University of Vienna; Medical University of Vienna; Medical
   University of Vienna; Medical University of Vienna; Medical University
   of Vienna; Medical University of Vienna
RP Prager, GW (corresponding author), Med Univ Vienna, Comprehens Canc Ctr, Dept Med 1, Div Oncol, A-1090 Vienna, Austria.
EM gerald.prager@meduniwien.ac.at
RI Kieler, Markus/AAF-4612-2020; Berger, Walter/AFQ-9733-2022; Prager,
   Gerald/AAS-8674-2021; Mullauer, Leonhard/GSN-9884-2022
OI Baumann, Lukas/0000-0001-7931-7470; Kieler, Markus/0000-0002-4082-5731;
   Mader, Robert/0000-0003-3017-8240; Mullauer,
   Leonhard/0000-0002-3399-078X; Sibilia, Maria/0000-0001-6129-5613
FU Medical University of Vienna
FX The study was supported by the Medical University of Vienna.
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NR 18
TC 2
Z9 2
U1 0
U2 2
PU CHINESE JOURNAL CANCER RESEARCH CO
PI BEIJING
PA LTD PEKING U CANCER HOSP & INST, NO 52, FUCHENG RD, HAIDIAN, BEIJING,
   100142, PEOPLES R CHINA
SN 1000-9604
EI 1993-0631
J9 CHINESE J CANCER RES
JI Chin. J. Cancer Res.
PD OCT
PY 2018
VL 30
IS 5
BP 508
EP 515
DI 10.21147/j.issn.1000-9604.2018.05.04
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GY7TX
UT WOS:000448819200004
PM 30510362
OA Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Seligmann, JF
   Elliott, F
   Richman, SD
   Jacobs, B
   Hemmings, G
   Brown, S
   Barrett, JH
   Tejpar, S
   Quirke, P
   Seymour, MT
AF Seligmann, Jenny F.
   Elliott, Faye
   Richman, Susan D.
   Jacobs, Bart
   Hemmings, Gemma
   Brown, Sarah
   Barrett, Jennifer H.
   Tejpar, Sabine
   Quirke, Philip
   Seymour, Matthew T.
TI Combined Epiregulin and Amphiregulin Expression Levels as a Predictive
   Biomarker for Panitumumab Therapy Benefit or Lack of Benefit in Patients
   With RAS Wild-Type Advanced Colorectal Cancer
SO JAMA ONCOLOGY
LA English
DT Article
ID RANDOMIZED PHASE-III; EGFR LIGANDS; GENE-EXPRESSION; PLUS CETUXIMAB;
   CELL-LINE; IRINOTECAN; FLUOROURACIL; MUTATIONS; LEUCOVORIN; CARCINOMA
AB IMPORTANCE RAS wild-type (wt) status is necessary but not sufficient for response to anti-epidermal growth factor receptor (EGFR) agents in advanced colorectal cancer (aCRC). RNA expression of EGFR ligands epiregulin (EREG) and amphiregulin (AREG) may correlate with EGFR-targeted therapy efficacy in aCRC, so may represent a much-needed additional predictive marker for these drugs.
   OBJECTIVE To examine a novel ligand model in a randomized clinical trial of panitumumab, irinotecan, and ciclosporin in colorectal cancer (PICCOLO) with with the a priori hypothesis that high tumor expression of either AREG or EREG would predict panitumumab therapy benefit in RAS-wt patients; and low expression, lack of efficacy.
   DESIGN, SETTING, AND PARTICIPANTS Prospectively planned retrospective biomarker study from the PICCOLO trial, which tested the addition of panitumumab to irinotecan therapy in patients with KRAS wt aCRC who experienced failure with prior fluoropyrimidine treatment. The analysis was conducted between 2012 and 2014. A predefined dichotomous model classified tumors as "high expressor" (either EREG or AREG in top tertile for messenger RNA level) or "low expressor" (neither EREG nor AREG in top tertile). Ligand expression was assessed as a prognostic and predictive biomarker. Expression of AREG/EREG and RAS and BRAF mutations were assessed in archival tumor tissue.
   MAIN OUTCOMES AND MEASURES Primary end point was progression-free survival (PFS); secondary end points were response rate and overall survival (OS).
   RESULTS Of the 696 PICCOLO trial patients in the irinotecan-vs-irinotecan with panitumumab randomization, 331 had sufficient tumor tissue available and measurement of ligand expression was successful in 323. High ligand expression was not prognostic for OS (hazard ratio [HR], 0.79 [95% CI, 0.58-1.09]; P =.15) or PFS (HR, 0.93 [95% CI, 0.68-1.27]; P =.64). The primary population had RAS wt aCRC (n = 220); for RAS wt patients with high ligand expression, median (interquartile range [IQR]) PFS was 8.3 [4.0-11.0] months (irinotecan with panitumumab) vs 4.4 [2.8-6.7] months (irinotecan alone); HR, 0.38 [95% CI, 0.24-0.61]; P <.001). In RAS wt patients with low ligand expression, median (IQR) PFS was 3.2 [2.7-8.1] months (irinotecan with panitumumab) vs 4.0 [2.7-7.5] months (irinotecan); HR, 0.93 [95% CI, 0.64-1.37]; P =.73; interaction test results were significant [P =.01]). Less marked effects were seen for response rate (interaction P =.17) and OS (interaction P =.11).
   CONCLUSIONS AND RELEVANCE High ligand expression is a predictive marker for panitumumab therapy benefit on PFS in RAS wt patients; conversely, patients with low ligand expression gained no benefit. The current "opt-in" strategy for anti-EGFR therapy in all patients with RAS wt aCRC should be questioned. Expression of EREG/AREG is a useful biomarker for anti-EGFR therapy; optimization for clinical use is indicated.
C1 [Seligmann, Jenny F.; Elliott, Faye; Richman, Susan D.; Hemmings, Gemma; Barrett, Jennifer H.; Quirke, Philip; Seymour, Matthew T.] Univ Leeds, St Jamess Univ Hosp, Leeds Inst Canc & Pathol, Leeds, W Yorkshire, England.
   [Jacobs, Bart; Tejpar, Sabine] Univ Hosp Gasthuisberg, Digest Oncol Unit, Herestr 49, B-3000 Louvain, Belgium.
   [Brown, Sarah] Univ Leeds, Clin Trials Res Unit, Leeds, W Yorkshire, England.
C3 Saint James's University Hospital; University of Leeds; KU Leuven;
   University Hospital Leuven; University of Leeds
RP Seymour, MT (corresponding author), St James Univ Hosp, St Jamess Inst Oncol, Beckett St, Leeds LS9 7FT, W Yorkshire, England.
EM matt.seymour@nihr.ac.uk
RI Quirke, Philip/AAI-1362-2019; Seligmann, Jenny/AAC-2030-2022
OI Quirke, Philip/0000-0002-3597-5444; Seymour,
   Matthew/0000-0002-2441-9629; Richman, Susan/0000-0003-3993-5041; Brown,
   Sarah/0000-0002-7975-7537
FU Cancer Research UK (CRUK); Yorkshire Cancer Research; Fund for
   Scientific Research Flanders (FWO-Vlaanderen); CRUK; Amgen Inc.;
   National Institute for Health Research (NIHR) Cancer Research Network;
   Amgen; NIHR/CRUK Experimental Cancer Medicine Centre
FX This study was supported by Cancer Research UK (CRUK) and Yorkshire
   Cancer Research. Dr Tejpar is supported by the Fund for Scientific
   Research Flanders (FWO-Vlaanderen). The PICCOLO trial was developed
   through the National Cancer Research Institute Colorectal Clinical
   Studies Group, funded by CRUK and supported by an unrestricted
   educational grant from Amgen Inc. It was conducted within the UK
   National Health Service with the support of the National Institute for
   Health Research (NIHR) Cancer Research Network. Molecular testing for
   RAS and BRAF mutations was supported by Amgen, NIHR/CRUK Experimental
   Cancer Medicine Centre, and Yorkshire Cancer Research.
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NR 31
TC 70
Z9 71
U1 0
U2 9
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2374-2437
EI 2374-2445
J9 JAMA ONCOL
JI JAMA Oncol.
PD MAY
PY 2016
VL 2
IS 5
BP 633
EP 642
DI 10.1001/jamaoncol.2015.6065
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DW5KS
UT WOS:000383684300015
PM 26867820
OA Bronze
DA 2025-01-04
ER

PT J
AU Shen, CJ
   Chan, RH
   Lin, BW
   Li, NC
   Huang, YH
   Chang, WC
   Chen, BK
AF Shen, Chih-Jie
   Chan, Ren-Hao
   Lin, Bo-Wen
   Li, Nien-Chi
   Huang, Ying-Hsuan
   Chang, Wen-Chang
   Chen, Ben-Kuen
TI Oleic acid-induced metastasis of KRAS/p53-mutant colorectal cancer
   relies on concurrent KRAS activation and IL-8 expression bypassing EGFR
   activation
SO THERANOSTICS
LA English
DT Article
DE multigene mutant CRC; oleic acid; IL-8; KRAS activation; metastasis
ID INFLAMMATORY-BOWEL-DISEASE; BREAST-CANCER; INTERLEUKIN-8; MUTATIONS;
   GROWTH; RAS; ANGIOGENESIS; CHEMOTHERAPY; MIGRATION; SURVIVAL
AB Background: Multigene mutations in colorectal cancer (CRC), including KRAS, BRAF, and p53, afford high metastatic ability and resistance to EGFR-targeting therapy. Understanding the molecular mechanisms regulating anti-EGFR-resistant CRC metastasis can improve CRC therapy. This study aimed to investigate the effects of IL-8 and the activation of KRAS on reactive oxygen species (ROS) production and metastasis of hyperlipidemia-associated CRC harboring mutations of KRAS and p53.
   Methods: The cytokine array analysis determined the up-expression of secreted factors, including IL-8. The clinical relevance of the relationship between IL-8 and angiopoietin-like 4 (ANGPTL4) was examined in CRC patients from National Cheng Kung University Hospital and TCGA dataset. Expressions of IL-8, ANGPTL4, NADPH oxidase 4 (NOX4), and epithelial-mesenchymal transition (EMT) markers in free fatty acids (FFAs)-treated KRAS/p53 mutant CRC cells were determined. The hyperlipidemia-triggered metastatic ability of CRC cells under treatments of antioxidants, statin, and cetuximab or knockdown of IL-8, KRAS, and EGFR was evaluated in vitro and in vivo. In addition, the effects of antioxidants and depletion of IL-8 and KRAS on the correlation between ROS production and hyperlipidemia-promoted CRC metastasis were also clarified.
   Results: In this study, we found that free fatty acids promoted KRAS/p53-mutant but not single-mutant or non-mutant CRC cell metastasis. IL-8, the most abundant secreted factor in KRAS/p53-mutant cells, was correlated with the upregulation of NOX4 expression and ROS production under oleic acid (OA)-treated conditions. In addition, the metastasis of KRAS/p53-mutant CRC relies on the ANGPTL4/IL-8/NOX4 axis and the activation of KRAS. The antioxidants and inactivation of KRAS also inhibited OA-induced EMT and metastasis. Although KRAS mediated EGF- and OA-promoted CRC cell invasion, the inhibition of EGFR did not affect OA-induced ANGPTL4/IL-8/NOX4 axis and CRC metastasis. The high-fat diet mice fed with vitamin E and statin or in IL-8-depleted cells significantly inhibited tumor extravasation and metastatic lung growth of CRC.
   Conclusion: The antioxidants, statins, and targeting IL- 8 may provide better outcomes for treating metastatic CRC that harbors multigene mutations and anti-EGFR resistance.
C1 [Shen, Chih-Jie; Chang, Wen-Chang] Taipei Med Univ, Grad Inst Med Sci, Coll Med, Taipei 110, Taiwan.
   [Chan, Ren-Hao; Lin, Bo-Wen] Natl Cheng Kung Univ, Natl Cheng Kung Univ Hosp, Div Colorectal Surg, Dept Surg, Tainan 701, Taiwan.
   [Li, Nien-Chi; Huang, Ying-Hsuan; Chen, Ben-Kuen] Natl Cheng Kung Univ, Dept Pharmacol, Coll Med, Tainan 701, Taiwan.
C3 Taipei Medical University; National Cheng Kung University; National
   Cheng Kung University Hospital; National Cheng Kung University
RP Chang, WC (corresponding author), Taipei Med Univ, Grad Inst Med Sci, Coll Med, Taipei 110, Taiwan.; Chen, BK (corresponding author), Natl Cheng Kung Univ, Dept Pharmacol, Coll Med, Tainan 701, Taiwan.
EM wcchang@tmu.edu.tw; bkchen58@mail.ncku.edu
RI Chan, Ren-Hao/GPW-6295-2022; Shen, Chih-Jie/JHU-1108-2023
OI SHEN, CHIH-JIE/0000-0001-7392-056X
FU National Science and Technology Council of Taiwan [MOST
   109-2320-B-006-040, MOST 110-2320-B-006-034-MY3, MOST
   111-2320-B-006-016]
FX This work was supported by the National Science and Technology Council
   of Taiwan [Grant MOST 109-2320-B-006-040; MOST 110-2320-B-006-034-MY3
   and MOST 111-2320-B-006-016]. We thank the Research Center of Clinical
   Medicine, National Cheng Kung University Hospital, for providing cell
   lines and helping authenticate the cells by short tandem repeat (STR)
   analysis. We thank the Taiwan Mouse Clinic, Academia Sinica and Taiwan
   Animal Consortium for the technical support in Optical image:
   Luminescence (vivo) -mice (NCKU).
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NR 48
TC 1
Z9 1
U1 0
U2 3
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1838-7640
J9 THERANOSTICS
JI Theranostics
PY 2023
VL 13
IS 13
BP 4650
EP 4666
DI 10.7150/thno.85855
PG 17
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA U6MO0
UT WOS:001085926200021
PM 37649607
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Shen, H
   Decollogne, S
   Dilda, PJ
   Hau, E
   Chung, SA
   Luk, PP
   Hogg, PJ
   McDonald, KL
AF Shen, Han
   Decollogne, Stephanie
   Dilda, Pierre J.
   Hau, Eric
   Chung, Sylvia A.
   Luk, Peter P.
   Hogg, Philip J.
   McDonald, Kerrie L.
TI Dual-targeting of aberrant glucose metabolism in glioblastoma
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Article
DE Cancer; Metabolism; PENAO; Dichloroacetate; Apoptosis
ID DICHLOROACETATE INDUCES APOPTOSIS; COLORECTAL-CANCER CELLS; IN-VIVO;
   MITOCHONDRIAL-FUNCTION; GLYCOLYTIC INHIBITORS; GROWTH; TUMORS;
   PHENOTYPE; OXIDATION; CYCLE
AB Background: Glioblastoma (GBM) is the most common and malignant primary brain tumor. In contrast to some other tumor types, aberrant glucose metabolism is an important component of GBM growth and chemoresistance. Recent studies of human orthotopic GBM in mice and in situ demonstrated GBM cells rely on both glycolysis and mitochondrial oxidation for glucose catabolism. These observations suggest that the homeostasis of energy metabolism of GBM cells might be further disturbed by dual-inhibition of glucose metabolism. The present study aimed to evaluate the efficacy and the mechanisms of dual-targeting therapy in GBM cells.
   Methods: Representative GBM cells (immortalized GBM cell lines and patient-derived GBM cells) and non-cancerous cells were treated with 4-(N-(S-penicillaminylacetyl) amino) phenylarsonous acid (PENAO), an in-house designed novel arsenic-based mitochondrial toxin, in combination with dichloroacetate (DCA), a pyruvate dehydrogenase kinase inhibitor. The efficacy of this combinatorial therapy was evaluated by MTS assay, clonogenic surviving assay and apoptotic assays. The underlying mechanisms of this dual-targeting treatment were unraveled by using mitochondrial membrane potential measurements, cytosol/mitochondrial ROS detection, western blotting, extracellular flux assay and mass spectrometry.
   Results: As monotherapies, both PENAO and DCA induced proliferation arrest in a panel of GBM cell lines and primary isolates. PENAO inhibited oxygen consumption, induced oxidative stress and depolarized mitochondrial membrane potential, which in turn activated mitochondria-mediated apoptosis. By combining DCA with PENAO, the two drugs worked synergistically to inhibit cell proliferation (but had no significant effect on non-cancerous cells), impair the clonogenicity, and induce mitochondria-mediated apoptosis. An oxidative stress of mitochondrial origin takes a prominent place in the mechanism by which the combination of PENAO and DCA induces cell death. Additionally, PENAO-induced oxidative damage was enhanced by DCA through glycolytic inhibition which in turn diminished acid production induced by PENAO. Moreover, DCA treatment also led to an alteration in the multidrug resistance (MDR) phenotype of GBM cells, thereby leading to an increased cytosolic accumulation of PENAO.
   Conclusions: The findings of this study shed a new light with respect to the dual-targeting of glucose metabolism in GBM cells and the innovative combination of PENAO and DCA shows promise in expanding GBM therapies.
C1 [Shen, Han; Hau, Eric; Chung, Sylvia A.; McDonald, Kerrie L.] Univ New S Wales, Lowy Canc Res Ctr, Adult Canc Program, Cure Brain Canc Neurooncol Grp, Sydney, NSW 2052, Australia.
   [Shen, Han; Decollogne, Stephanie; Dilda, Pierre J.; Hau, Eric; Chung, Sylvia A.; Luk, Peter P.; Hogg, Philip J.; McDonald, Kerrie L.] Univ New S Wales, Prince Wales Clin Sch, Sydney, NSW 2052, Australia.
   [Decollogne, Stephanie; Dilda, Pierre J.; Luk, Peter P.; Hogg, Philip J.] Univ New S Wales, Lowy Canc Res Ctr, Adult Canc Program, Tumour Metab Grp, Sydney, NSW 2052, Australia.
   [Hau, Eric] St George Hosp, Canc Care Ctr, Kogarah, NSW 2217, Australia.
C3 University of New South Wales Sydney; University of New South Wales
   Sydney; University of New South Wales Sydney; St George Hospital
RP McDonald, KL (corresponding author), Univ New S Wales, Lowy Canc Res Ctr, Adult Canc Program, Cure Brain Canc Neurooncol Grp, Sydney, NSW 2052, Australia.
EM k.mcdonald@unsw.edu.au
RI Shen, Han/AAA-6883-2021
OI Shen, Han/0000-0003-2435-2150; Hogg, Philip/0000-0001-6486-2863; Luk,
   Peter P/0000-0001-8779-4461
FU Cure Brain Cancer Foundation; Olle Fund for Brain Cancer Research;
   Cancer Council NSW; National Health and Medical Council
FX This study was supported by the Cure Brain Cancer Foundation, the Olle
   Fund for Brain Cancer Research, the Cancer Council NSW and the National
   Health and Medical Council.
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NR 54
TC 43
Z9 46
U1 1
U2 29
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1756-9966
J9 J EXP CLIN CANC RES
JI J. Exp. Clin. Cancer Res.
PD FEB 5
PY 2015
VL 34
AR 14
DI 10.1186/s13046-015-0130-0
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CA7XO
UT WOS:000349130900001
PM 25652202
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Rovers, KP
   Bakkers, C
   van Erning, FN
   Burger, JWA
   Nienhuijs, SW
   Simkens, GAAM
   Creemers, GJM
   Hemmer, PHJ
   Punt, CJA
   Lemmens, VEPP
   Tanis, PJ
   de Hingh, IHJT
AF Rovers, Koen P.
   Bakkers, Checca
   van Erning, Felice N.
   Burger, Jacobus W. A.
   Nienhuijs, Simon W.
   Simkens, Geert A. A. M.
   Creemers, Geert-Jan M.
   Hemmer, Patrick H. J.
   Punt, Cornelis J. A.
   Lemmens, Valery E. P. P.
   Tanis, Pieter J.
   de Hingh, Ignace H. J. T.
TI Adjuvant Systemic Chemotherapy vs Active Surveillance Following Up-front
   Resection of Isolated Synchronous Colorectal Peritoneal Metastases
SO JAMA ONCOLOGY
LA English
DT Article
ID HYPERTHERMIC INTRAPERITONEAL CHEMOTHERAPY; III COLON-CANCER;
   CYTOREDUCTIVE SURGERY; OPEN-LABEL; PLUS OXALIPLATIN; LIVER METASTASES;
   PROPENSITY-SCORE; PHASE-III; CARCINOMATOSIS; ORIGIN
AB Key PointsQuestionIs adjuvant systemic chemotherapy associated with improved overall survival compared with active surveillance in patients undergoing up-front resection of isolated synchronous colorectal peritoneal metastases? FindingsIn this Dutch nationwide propensity score-matched cohort study including 393 patients, adjuvant systemic chemotherapy was associated with improved overall survival (median, 39 months) compared with active surveillance (median, 25 months). This difference in survival rates was statistically significant. MeaningIn this study, adjuvant systemic chemotherapy was associated with improved overall survival following up-front resection of isolated synchronous colorectal peritoneal metastases; however, randomized trials are needed to address the influence of potential residual confounding and allocation bias on this association.
   ImportanceTo date, there are no data on the value of adjuvant systemic chemotherapy following up-front resection of isolated synchronous colorectal peritoneal metastases. ObjectiveTo assess the association between adjuvant systemic chemotherapy and overall survival following up-front resection of isolated synchronous colorectal peritoneal metastases. Design, Setting, and ParticipantsIn this population-based, observational cohort study using nationwide data from the Netherlands Cancer Registry (diagnoses between January 1, 2005, and December 31, 2017; follow-up until January 31, 2019), 393 patients with isolated synchronous colorectal peritoneal metastases who were alive 3 months after up-front complete cytoreductive surgery with hyperthermic intraperitoneal chemotherapy were included. Patients allocated to the adjuvant systemic chemotherapy group were matched (1:1) with those allocated to the active surveillance group by propensity scores based on patient-, tumor-, and treatment-level covariates. ExposuresAdjuvant systemic chemotherapy, defined as systemic chemotherapy without targeted therapy, starting within 3 months postoperatively. Main Outcomes and MeasuresOverall survival was compared between matched groups using Cox proportional hazards regression analysis adjusted for residual imbalance. A landmark analysis was performed by excluding patients who died within 6 months postoperatively. A sensitivity analysis was performed to adjust for unmeasured confounding by major postoperative morbidity. ResultsOf 393 patients (mean [SD] age, 61 [10] years; 181 [46%] men), 172 patients (44%) were allocated to the adjuvant systemic chemotherapy group. After propensity score matching of 142 patients in the adjuvant systemic chemotherapy group with 142 patients in the active surveillance group, adjuvant systemic chemotherapy was associated with improved overall survival compared with active surveillance (median, 39.2 [interquartile range, 21.1-111.1] months vs 24.8 [interquartile range, 15.0-58.4] months; adjusted hazard ratio [aHR], 0.66; 95% CI, 0.49-0.88; P=.006), which remained consistent after excluding patients who died within 6 months postoperatively (aHR, 0.68; 95% CI, 0.50-0.93; P=.02) and after adjustment for major postoperative morbidity (aHR, 0.71; 95% CI, 0.53-0.95). Conclusions and RelevanceFindings of this study suggest that in patients undergoing up-front resection of isolated synchronous colorectal peritoneal metastases, adjuvant systemic chemotherapy appeared to be associated with improved overall survival. Although randomized trials are needed to address the influence of potential residual confounding and allocation bias on this association, results of this study may be used for clinical decision-making in this patient group for whom no data are available.
   This cohort study compares survival with adjuvant systemic chemotherapy vs active surveillance in patients with up-front resection of isolated synchronous colorectal peritoneal metastases.
C1 [Rovers, Koen P.; Bakkers, Checca; Burger, Jacobus W. A.; Nienhuijs, Simon W.; Simkens, Geert A. A. M.; de Hingh, Ignace H. J. T.] Catharina Canc Inst, Dept Surg, Michelangelolaan 2, NL-5623 EJ Eindhoven, Netherlands.
   [van Erning, Felice N.; Lemmens, Valery E. P. P.; de Hingh, Ignace H. J. T.] Netherlands Comprehens Canc Org, Dept Res, Utrecht, Netherlands.
   [Creemers, Geert-Jan M.] Catharina Canc Inst, Dept Med Oncol, Eindhoven, Netherlands.
   [Hemmer, Patrick H. J.] Univ Med Ctr Groningen, Dept Surg, Groningen, Netherlands.
   [Punt, Cornelis J. A.] Univ Amsterdam, Canc Ctr Amsterdam, Amsterdam Univ Med Ctr, Dept Med Oncol, Amsterdam, Netherlands.
   [Lemmens, Valery E. P. P.] Erasmus Univ, Med Ctr, Dept Publ Hlth, Rotterdam, Netherlands.
   [Tanis, Pieter J.] Univ Amsterdam, Canc Ctr Amsterdam, Amsterdam Univ Med Ctr, Dept Surg, Amsterdam, Netherlands.
   [de Hingh, Ignace H. J. T.] Maastricht Univ, GROW Sch Oncol & Dev Biol, Maastricht, Netherlands.
C3 University of Groningen; University of Amsterdam; Vrije Universiteit
   Amsterdam; Erasmus University Rotterdam; Erasmus MC; University of
   Amsterdam; Vrije Universiteit Amsterdam; Maastricht University
RP de Hingh, IHJT (corresponding author), Catharina Canc Inst, Dept Surg, Michelangelolaan 2, NL-5623 EJ Eindhoven, Netherlands.
EM ignace.d.hingh@catharinaziekenhuis.nl
RI Nienhuijs, Simon/H-7505-2019; Rovers, Koen/AGQ-5109-2022; Tanis,
   Pieter/U-2827-2019
OI Tanis, Pieter/0000-0002-3146-3310
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NR 53
TC 30
Z9 31
U1 0
U2 5
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2374-2437
EI 2374-2445
J9 JAMA ONCOL
JI JAMA Oncol.
PD AUG
PY 2020
VL 6
IS 8
AR e202701
DI 10.1001/jamaoncol.2020.2701
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OC2IO
UT WOS:000578984000001
PM 32672798
OA Green Published
DA 2025-01-04
ER

PT J
AU Watanabe, J
   Muro, K
   Shitara, K
   Yamazaki, K
   Shiozawa, M
   Ohori, H
   Takashima, A
   Yokota, M
   Makiyama, A
   Akazawa, N
   Ojima, H
   Yuasa, Y
   Miwa, K
   Yasui, H
   Oki, E
   Sato, T
   Naitoh, T
   Komatsu, Y
   Kato, T
   Hihara, M
   Soeda, J
   Misumi, T
   Yamamoto, K
   Akagi, K
   Ochiai, A
   Uetake, H
   Tsuchihara, K
   Yoshino, T
AF Watanabe, Jun
   Muro, Kei
   Shitara, Kohei
   Yamazaki, Kentaro
   Shiozawa, Manabu
   Ohori, Hisatsugu
   Takashima, Atsuo
   Yokota, Mitsuru
   Makiyama, Akitaka
   Akazawa, Naoya
   Ojima, Hitoshi
   Yuasa, Yasuhiro
   Miwa, Keisuke
   Yasui, Hirofumi
   Oki, Eiji
   Sato, Takeo
   Naitoh, Takeshi
   Komatsu, Yoshito
   Kato, Takeshi
   Hihara, Masamitsu
   Soeda, Junpei
   Misumi, Toshihiro
   Yamamoto, Kouji
   Akagi, Kiwamu
   Ochiai, Atsushi
   Uetake, Hiroyuki
   Tsuchihara, Katsuya
   Yoshino, Takayuki
TI Panitumumab vs Bevacizumab Added to Standard First-line Chemotherapy and
   Overall Survival Among Patients With RAS Wild-type, Left-Sided
   Metastatic Colorectal Cancer A Randomized Clinical Trial
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID FOLFIRI PLUS BEVACIZUMAB; TUMOR SHRINKAGE ETS; JAPANESE SOCIETY;
   OPEN-LABEL; PHASE-III; CETUXIMAB; FIRE-3; COLON; RECURRENCE; MUTATIONS
AB Importance For patients with RAS wild-type metastatic colorectal cancer, adding anti-epidermal growth factor receptor (anti-EGFR) or anti-vascular endothelial growth factor (anti-VEGF) monoclonal antibodies to first-line doublet chemotherapy is routine, but the optimal targeted therapy has not been defined.Objective To evaluate the effect of adding panitumumab (an anti-EGFR monoclonal antibody) vs bevacizumab (an anti-VEGF monoclonal antibody) to standard first-line chemotherapy for treatment of RAS wild-type, left-sided, metastatic colorectal cancer.Design, Setting, and Participants Randomized, open-label, phase 3 clinical trial at 197 sites in Japan in May 2015-January 2022 among 823 patients with chemotherapy-naive RAS wild-type, unresectable metastatic colorectal cancer (final follow-up, January 14, 2022).Interventions Panitumumab (n = 411) or bevacizumab (n = 412) plus modified fluorouracil, l-leucovorin, and oxaliplatin (mFOLFOX6) every 14 days.Main Outcomes and Measures The primary end point, overall survival, was tested first in participants with left-sided tumors, then in the overall population. Secondary end points were progression-free survival, response rate, duration of response, and curative (defined as R0 status) resection rate.Results In the as-treated population (n = 802; median age, 66 years; 282 [35.2%] women), 604 (75.3%) had left-sided tumors. Median follow-up was 61 months. Median overall survival was 37.9 months with panitumumab vs 34.3 months with bevacizumab in participants with left-sided tumors (hazard ratio [HR] for death, 0.82; 95.798% CI, 0.68-0.99; P = .03) and 36.2 vs 31.3 months, respectively, in the overall population (HR, 0.84; 95% CI, 0.72-0.98; P = .03). Median progression-free survival for panitumumab vs bevacizumab was 13.1 vs 11.9 months, respectively, for those with left-sided tumors (HR, 1.00; 95% CI, 0.83-1.20) and 12.2 vs 11.4 months overall (HR, 1.05; 95% CI, 0.90-1.24). Response rates with panitumumab vs bevacizumab were 80.2% vs 68.6%, respectively, for left-sided tumors (difference, 11.2%; 95% CI, 4.4%-17.9%) and 74.9% vs 67.3% overall (difference, 7.7%; 95% CI, 1.5%-13.8%). Median duration of response with panitumumab vs bevacizumab was 13.1 vs 11.2 months for left-sided tumors (HR, 0.86; 95% CI, 0.70-1.10) and 11.9 vs 10.7 months overall (HR, 0.89; 95% CI, 0.74-1.06). Curative resection rates with panitumumab vs bevacizumab were 18.3% vs 11.6% for left-sided tumors; (difference, 6.6%; 95% CI, 1.0%-12.3%) and 16.5% vs 10.9% overall (difference, 5.6%; 95% CI, 1.0%-10.3%). Common treatment-emergent adverse events were acneiform rash (panitumumab: 74.8%; bevacizumab: 3.2%), peripheral sensory neuropathy (panitumumab: 70.8%; bevacizumab: 73.7%), and stomatitis (panitumumab: 61.6%; bevacizumab: 40.5%).Conclusions and Relevance Among patients with RAS wild-type metastatic colorectal cancer, adding panitumumab, compared with bevacizumab, to standard first-line chemotherapy significantly improved overall survival in those with left-sided tumors and in the overall population.
C1 [Watanabe, Jun] Yokohama City Univ, Gastroenterol Ctr, Dept Surg, Med Ctr, Yokohama, Japan.
   [Muro, Kei] Aichi Canc Ctr Hosp, Dept Clin Oncol, Nagoya, Japan.
   [Shitara, Kohei; Yoshino, Takayuki] Natl Canc Ctr Hosp East, Dept Gastroenterol & Gastrointestinal Oncol, Kashiwa, Japan.
   [Shitara, Kohei] Nagoya Univ, Dept Immunol, Grad Sch Med, Nagoya, Aichi, Japan.
   [Yamazaki, Kentaro; Yasui, Hirofumi] Shizuoka Canc Ctr, Div Gastrointestinal Oncol, Nagaizumi, Shizuoka, Japan.
   [Shiozawa, Manabu] Kanagawa Canc Ctr, Div Gastrointestinal Surg, Yokohama, Kanagawa, Japan.
   [Ohori, Hisatsugu] Japanese Red Cross Ishinomaki Hosp, Div Med Oncol, Ishinomaki, Miyagi, Japan.
   [Takashima, Atsuo] Natl Canc Ctr, Dept Gastrointestinal Med Oncol, Tokyo, Japan.
   [Yokota, Mitsuru] Kurashiki Cent Hosp, Dept Gen Surg, Kurashiki, Okayama, Japan.
   [Makiyama, Akitaka] Japan Community Healthcare Org, Dept Hematol Oncol, Fukuoka, Japan.
   [Akazawa, Naoya] Sendai Open Hosp, Sendai City Med Ctr, Dept Gastrointestinal Surg, Sendai, Miyagi, Japan.
   [Ojima, Hitoshi] Gunma Prefectural Canc Ctr, Dept Gastroenterol Surg, Ota, Gunma, Japan.
   [Yuasa, Yasuhiro] Japanese Red Cross Tokushima Hosp, Dept Gastroenterol Surg, Komatsushima, Tokushima, Japan.
   [Miwa, Keisuke] Kurume Univ Hosp, Dept Canc Multimodel Therapy Ctr, Fukuoka, Japan.
   [Oki, Eiji] Kyushu Univ, Grad Sch Med Sci, Dept Surg & Sci, Fukuoka, Japan.
   [Sato, Takeo] Kitasato Univ, Res & Dev Ctr Med Educ, Dept Clin Skills Educ, Sch Med, Sagamihara, Japan.
   [Naitoh, Takeshi] Kitasato Univ, Dept Lower Gastrointestinal Surg, Sch Med, Sagamihara, Japan.
   [Komatsu, Yoshito] Hokkaido Univ Hosp, Div Canc Chemotherapy, Canc Ctr, Sapporo, Japan.
   [Kato, Takeshi] Natl Hosp Org Osaka Natl Hosp, Dept Surg, Osaka, Japan.
   [Hihara, Masamitsu; Soeda, Junpei] Takeda Pharmaceut Co Ltd, Japan Oncol Business Unit, Japan Med Affairs, Tokyo, Japan.
   [Misumi, Toshihiro; Yamamoto, Kouji] Yokohama City Univ, Dept Biostat, Sch Med, Yokohama, Japan.
   [Akagi, Kiwamu] Saitama Canc Ctr, Div Mol Diag & Canc Prevent, Saitama, Japan.
   [Ochiai, Atsushi] Natl Canc Ctr, Exploratory Oncol Res & Clin Trial Ctr, Pathol Div, Chiba, Japan.
   [Ochiai, Atsushi] Tokyo Univ Sci, Res Inst Biomed Sci, Tokyo, Japan.
   [Uetake, Hiroyuki] Natl Hosp Org, Disaster Med Ctr, Tokyo, Japan.
   [Yoshino, Takayuki] Natl Canc Ctr, Exploratory Oncol Res & Clin Trial Ctr, Div Translat Informat, Chiba, Japan.
   [Yoshino, Takayuki] Natl Canc Ctr Hosp East, Dept Gastroenterol & Gastrointestinal Oncol, 6-5-1 Kashiwanoha, Kashiwa 2778577, Japan.
C3 Yokohama City University; Aichi Cancer Center; National Cancer Center -
   Japan; Nagoya University; Shizuoka Cancer Center; Kanagawa Prefectural
   Cancer Center; National Cancer Center - Japan; Kurashiki Central
   Hospital; Kurume University; Kyushu University; Kitasato University;
   Kitasato University; Hokkaido University; Osaka National Hospital;
   Takeda Pharmaceutical Company Ltd; Yokohama City University; National
   Cancer Center - Japan; Tokyo University of Science; National Cancer
   Center - Japan; National Cancer Center - Japan
RP Yoshino, T (corresponding author), Natl Canc Ctr Hosp East, Dept Gastroenterol & Gastrointestinal Oncol, Kashiwa, Japan.; Yoshino, T (corresponding author), Natl Canc Ctr Hosp East, Dept Gastroenterol & Gastrointestinal Oncol, 6-5-1 Kashiwanoha, Kashiwa 2778577, Japan.
EM tyoshino@east.ncc.go.jp
RI Soeda, Jumpei/JAC-0196-2023; Oki, Eiji/AFO-6423-2022; Naitoh,
   Takeshi/K-1693-2014; Uetake, Hiroyuki/AAC-2669-2020; Shitara,
   Kohei/AAA-3877-2021; Makiyama, Akitaka/AAU-7256-2020
OI Soeda, Junpei/0000-0003-3753-0999; Tsuchihara,
   Katsuya/0000-0001-7507-2349
FU Takeda Pharmaceutical Company Limited
FX This study was funded by Takeda Pharmaceutical Company Limited.
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NR 40
TC 96
Z9 98
U1 4
U2 15
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD APR 18
PY 2023
VL 329
IS 15
BP 1271
EP 1282
DI 10.1001/jama.2023.4428
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA J3FC1
UT WOS:001008491200016
PM 37071094
OA Bronze, Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Ackermann, A
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   Friedrichs, N
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AF Ackermann, Anne
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   Bon, Dimitra
   Friedrichs, Nicolaus
   Bankov, Katrin
   Wild, Peter
   Plotz, Guido
   Zeuzem, Stefan
   Herrmann, Eva
   Hansmann, Martin-Leo
   Brieger, Angela
TI Downregulation of SPTAN1 is related to MLH1 deficiency and metastasis in
   colorectal cancer
SO PLOS ONE
LA English
DT Article
ID MICROSATELLITE INSTABILITY; ALPHA-SPECTRIN; CLINICOPATHOLOGICAL
   FEATURES; E-CADHERIN; FODRIN; DNA; CARCINOMA; COMPLEX; SYSTEM
AB Introduction
   Colorectal cancers (CRCs) deficient in the DNA mismatch repair protein MutL homolog 1 (MLH1) display distinct clinicopathological features and require a different therapeutic approach compared to CRCs with MLH1 proficiency. However, the molecular basis of this fundamental difference remains elusive. Here, we report that MLH1-deficient CRCs exhibit reduced levels of the cytoskeletal scaffolding protein non-erythroid spectrin alpha II (SPTAN1), and that tumor progression and metastasis of CRCs correlate with SPTAN1 levels.
   Methods and results
   To investigate the link between MLH1 and SPTAN1 in cancer progression, a cohort of 189 patients with CRC was analyzed by immunohistochemistry. Compared with the surrounding normal mucosa, SPTAN1 expression was reduced in MLH1-deficient CRCs, whereas MLH1-proficient CRCs showed a significant upregulation of SPTAN1. Overall, we identified a strong correlation between MLH1 status and SPTAN1 expression. When comparing TNM classification and SPTAN1 levels, we found higher SPTAN1 levels in stage I CRCs, while stages II to IV showed a gradual reduction of SPTAN1 expression. In addition, SPTAN1 expression was lower in metastatic compared with non-metastatic CRCs. Knockdown of SPTAN1 in CRC cell lines demonstrated decreased cell viability, impaired cellular mobility and reduced cell-cell contact formation, indicating that SPTAN1 plays an important role in cell growth and cell attachment. The observed weakened cell-cell contact of SPTAN1 knockdown cells might indicate that tumor cells expressing low levels of SPTAN1 detach from their primary tumor and metastasize more easily.
   Conclusion
   Taken together, we demonstrate that MLH1 deficiency, low SPTAN1 expression, and tumor progression and metastasis are in close relation. We conclude that SPTAN1 is a candidate molecule explaining the tumor progression and metastasis of MLH1-deficient CRCs. The detailed analysis of SPTAN1 is now mandatory to substantiate its relevance and its potential value as a candidate protein for targeted therapy, and as a predictive marker of cancer aggressiveness.
C1 [Ackermann, Anne; Schrecker, Christopher; Plotz, Guido; Zeuzem, Stefan; Brieger, Angela] Univ Clin Frankfurt, Biomed Res Lab, Med Clin 1, Frankfurt, Germany.
   [Bon, Dimitra; Herrmann, Eva] Goethe Univ, Inst Biostat & Math Modelling, Frankfurt, Germany.
   [Friedrichs, Nicolaus] Univ Cologne, Sch Med, Inst Pathol, Cologne, Germany.
   [Bankov, Katrin; Wild, Peter; Hansmann, Martin-Leo] Univ Hosp Frankfurt, Dr Senckenberg Inst Pathol, Frankfurt, Germany.
C3 Goethe University Frankfurt; University of Cologne; Goethe University
   Frankfurt; Goethe University Frankfurt Hospital
RP Brieger, A (corresponding author), Univ Clin Frankfurt, Biomed Res Lab, Med Clin 1, Frankfurt, Germany.
EM a.brieger@em.uni-frankfurt.de
RI Plotz, Guido/K-8446-2012; Herrmann, Eva/E-8215-2010; Zeuzem,
   Stefan/AAE-7435-2019
OI Plotz, Guido/0000-0001-5314-9739; Wild, Peter
   Johannes/0000-0002-1017-3744; Herrmann, Eva/0000-0002-0662-6675; Bankov,
   Katrin/0009-0005-4033-4966
FU Wilhelm Sander Foundation [2014.169.1]; Nachlasse Maria Christine Held
   und Erika Hecker (E.V.); University Clinic Frankfurt
FX This work was supported by Wilhelm Sander Foundation (2014.169.1),
   Nachlasse Maria Christine Held und Erika Hecker (E.V.), and
   institutional funds of the University Clinic Frankfurt. The funders had
   no role in study design, data collection and analysis, decision to
   publish, or preparation of the manuscript.
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NR 43
TC 23
Z9 26
U1 0
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAR 11
PY 2019
VL 14
IS 3
AR e0213411
DI 10.1371/journal.pone.0213411
PG 19
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA HO6HL
UT WOS:000461030300037
PM 30856214
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Sun, LN
   Fang, Y
   Wang, X
   Han, YN
   Du, F
   Li, CX
   Hu, HY
   Liu, H
   Liu, Q
   Wang, J
   Liang, JR
   Chen, P
   Yang, HB
   Nie, YZ
   Wu, KC
   Fang, DM
   Coffey, RJ
   Lu, YY
   Zhao, XD
AF Sun, Lina
   Fang, Ying
   Wang, Xin
   Han, Yanan
   Du, Feng
   Li, Cunxi
   Hu, Huaying
   Liu, Hao
   Liu, Qi
   Wang, Jing
   Liang, Junrong
   Chen, Ping
   Yang, Hongbin
   Nie, Yongzhan
   Wu, Kaichun
   Fang, Daiming
   Coffey, Robert J.
   Lu, Yuanyuan
   Zhao, Xiaodi
TI miR-302a Inhibits Metastasis and Cetuximab Resistance in Colorectal
   Cancer by Targeting NFIB and CD44
SO THERANOSTICS
LA English
DT Article
DE miRNA; colorectal cancer; metastasis; targeted therapy; drug resistance
ID CELL-PROLIFERATION; STEM-CELLS; INVASION; MICRORNA-302A; PROMOTES;
   EXPRESSION; MIGRATION; DIFFERENTIATION; PROGNOSIS; APOPTOSIS
AB Introduction: Metastasis and drug resistance contribute substantially to the poor prognosis of colorectal cancer (CRC) patients. However, the epigenetic regulatory mechanisms by which CRC develops metastatic and drug-resistant characteristics remain unclear. This study aimed to investigate the role of miR-302a in the metastasis and molecular-targeted drug resistance of CRC and elucidate the underlying molecular mechanisms.
   Methods: miR-302a expression in CRC cell lines and patient tissue microarrays was analyzed by qPCR and fluorescence in situ hybridization. The roles of miR-302a in metastasis and cetuximab (CTX) resistance were evaluated both in vitro and in vivo. Bioinformatic prediction algorithms and luciferase reporter assays were performed to identify the miR-302a binding regions in the NFIB and CD44 3'-UTRs. A chromatin immunoprecipitation assay was performed to examine NFIB occupancy in the ITGA6 promoter region. Immunoblotting was performed to identify the EGFR-mediated pathways altered by miR-302a.
   Results: miR-302a expression was frequently reduced in CRC cells and tissues, especially in CTX-resistant cells and patient-derived xenografts. The decreased miR-302a levels correlated with poor overall CRC patient survival. miR-302a overexpression inhibited metastasis and restored CTX responsiveness in CRC cells, whereas miR-302a silencing exerted the opposite effects. NFIB and CD44 were identified as novel targets of miR-302a. miR-302a inhibited the metastasis-promoting effect of NFIB that physiologically activates ITGA6 transcription. miR-302a restored CTX responsiveness by suppressing CD44-induced cancer stem cell-like properties and EGFR-mediated MAPK and AKT signaling. These results are consistent with clinical observations indicating that miR-302a expression is inversely correlated with the expression of its targets in CRC specimens.
   Conclusions: Our findings show that miR-302a acts as a multifaceted regulator of CRC metastasis and CTX resistance by targeting NFIB and CD44, respectively. Our study implicates miR-302a as a candidate prognostic predictor and a therapeutic agent in CRC.
C1 [Sun, Lina; Fang, Ying; Han, Yanan; Yang, Hongbin] Xi An Jiao Tong Univ, Affiliated Childrens Hosp, Xian 710003, Shaanxi, Peoples R China.
   [Sun, Lina; Wang, Xin; Du, Feng; Liu, Hao; Liang, Junrong; Chen, Ping; Nie, Yongzhan; Wu, Kaichun; Fang, Daiming; Lu, Yuanyuan; Zhao, Xiaodi] Fourth Mil Med Univ, Natl Clin Res Ctr Digest Dis, State Key Lab Canc Biol, Xian 710032, Shaanxi, Peoples R China.
   [Sun, Lina; Wang, Xin; Du, Feng; Liu, Hao; Liang, Junrong; Chen, Ping; Nie, Yongzhan; Wu, Kaichun; Fang, Daiming; Lu, Yuanyuan; Zhao, Xiaodi] Fourth Mil Med Univ, Xijing Hosp Digest Dis, Xian 710032, Shaanxi, Peoples R China.
   [Wang, Xin; Liang, Junrong; Chen, Ping] Fourth Mil Med Univ, Tangdu Hosp, Dept Gastroenterol, Xian 710038, Shaanxi, Peoples R China.
   [Li, Cunxi; Hu, Huaying] Beijing Jiaen Hosp, Jiaen Genet Lab, Beijing 100191, Peoples R China.
   [Hu, Huaying] Xiamen Univ, Sch Med, Xiamen 361002, Fujian, Peoples R China.
   [Liu, Qi; Wang, Jing] Vanderbilt Univ, Dept Biomed Informat, Med Ctr, Nashville, TN 37232 USA.
   [Liu, Qi; Wang, Jing] Vanderbilt Univ, Ctr Quantitat Sci, Med Ctr, Nashville, TN 37232 USA.
   [Coffey, Robert J.] Vanderbilt Univ, Dept Med, Med Ctr, Nashville, TN 37232 USA.
   [Coffey, Robert J.] Dept Vet Affairs Med Ctr, Nashville, TN 37212 USA.
   [Zhao, Xiaodi] Natl Inst Biol Sci, Beijing 102206, Peoples R China.
C3 Xi'an Jiaotong University; Air Force Military Medical University; Air
   Force Military Medical University; Air Force Military Medical
   University; Xiamen University; Vanderbilt University; Vanderbilt
   University; Vanderbilt University; US Department of Veterans Affairs;
   Veterans Health Administration (VHA); VA Tennessee Valley Healthcare
   System; National Institute of Biological Sciences, Beijing
RP Wang, X (corresponding author), Fourth Mil Med Univ, Natl Clin Res Ctr Digest Dis, State Key Lab Canc Biol, Xian 710032, Shaanxi, Peoples R China.; Wang, X (corresponding author), Fourth Mil Med Univ, Xijing Hosp Digest Dis, Xian 710032, Shaanxi, Peoples R China.; Wang, X (corresponding author), Fourth Mil Med Univ, Tangdu Hosp, Dept Gastroenterol, Xian 710038, Shaanxi, Peoples R China.
EM wangx@fmmu.edu.cn; luyuandreamer@aliyun.com; leedyzhao@fmmu.edu.cn
RI zhao, xd/HJX-9525-2023; Li, Cunxi/B-2924-2011; Liu, Qi/KLZ-9389-2024;
   Wan, Chunhua/ABD-8426-2021; Lu, Yuanyuan/JAA-9312-2023; du,
   feng/KTH-9559-2024; Wang, Jing/AGT-2656-2022; Li, Xianzhi/IUO-5698-2023
OI Du, Feng/0000-0001-9886-5317; hu, huaying/0000-0002-3933-1451; Wu,
   Kaichun/0000-0002-0699-9666; Wang, Jing/0000-0003-2775-9001; Sun,
   Lina/0000-0003-1268-7033; , Junrong/0000-0001-7096-978X; Lu,
   Yuanyuan/0000-0003-0194-8074
FU National Science Fund for Excellent Young Scholars [81822031]; National
   Natural Science Foundation of China [81602641, 81972224, 81673038,
   81572929, 81871913]; National Institutes of Health [U19CA179514];
   National Key R&D Program of China [2018YFC1313101, 2017YFC0908200];
   Young Elite Scientists Sponsorship Program by CAST [2017QNRC001]; China
   Postdoctoral Science Foundation
FX This study was supported by the National Science Fund for Excellent
   Young Scholars (No. 81822031) and National Natural Science Foundation of
   China (Nos. 81602641, 81972224, 81673038, 81572929 and 81871913),
   National Institutes of Health (U19CA179514), National Key R&D Program of
   China (2018YFC1313101; 2017YFC0908200), Young Elite Scientists
   Sponsorship Program by CAST (2017QNRC001), and China Postdoctoral
   Science Foundation.
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NR 50
TC 61
Z9 66
U1 1
U2 14
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1838-7640
J9 THERANOSTICS
JI Theranostics
PY 2019
VL 9
IS 26
BP 8409
EP 8425
DI 10.7150/thno.36605
PG 17
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA JH5TI
UT WOS:000492831200030
PM 31754405
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Shen, L
   Liu, M
   Liu, W
   Cui, J
   Li, CZ
AF Shen, Liang
   Liu, Ming
   Liu, Wei
   Cui, Jing
   Li, Changzhong
TI Bioinformatics analysis of RNA sequencing data reveals multiple key
   genes in uterine corpus endometrial carcinoma
SO ONCOLOGY LETTERS
LA English
DT Article
DE uterine corpus endometrial carcinoma; differentially expressed genes;
   gene co-expression network; small molecule drugs
ID ESCULETIN INDUCES APOPTOSIS; COLON-CANCER CELLS; PROGNOSTIC MARKER;
   EXPRESSION; PATHWAY; METASTASIS; INVASION; ARREST
AB In the present study, the RNA sequencing (RNA-seq) data of uterine corpus endometrial carcinoma (UCEC) samples were collected and analyzed using bioinformatics tools to identify potential genes associated with the development of UCEC. UCEC RNA-seq data were downloaded from The Cancer Genome Atlas database. Differential analysis was performed using edgeR software. A false discovery rate <0.01 and Ilog2(fold change)I>1 were set as the cut-off criteria to screen for differentially expressed genes (DEGs). Differential gene co-expression analysis was performed using R/EBcoexpress package in R. DEGs in the gene co-expression network were subjected to Gene Ontology analysis using the Database for Annotation, Visualization and Integration Discovery. Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis was also performed on the DEGs using KOBAS 2.0 software. The ConnectivityMap database was used to identify novel drug candidates. A total of 3,742 DEGs were identified among the 552 UCEC samples and 35 normal controls, and comprised 2,580 upregulated and 1,162 downregulated genes. A gene co-expression network consisting of 129 DEGs and 368 edges was constructed. Genes were associated with the cell cycle and the tumor protein p53 signaling pathway. Three modules were identified, in which genes were associated with the mitotic cell cycle, nuclear division and the M phase of the mitotic cell cycle. Multiple key hub genes were identified, including cell division cycle 20, cyclin B2, non-SMC condensin I complex subunit H, BUB1 mitotic checkpoint serine/threonine kinase, cell division cycle associated 8, maternal embryonic leucine zipper kinase, MYB proto-oncogene like 2, TPX2, microtubule nucleation factor and non-SMC condensin I complex subunit G. In addition, the small molecule drug esculetin was implicated in the suppression of UCEC progression. Overall, the present study identified multiple key genes in UCEC and clinically relevant small molecule agents, thereby improving our understanding of UCEC and expanding perspectives on targeted therapy for this type of cancer.
C1 [Shen, Liang; Liu, Ming; Liu, Wei; Li, Changzhong] Shandong Univ, Shandong Prov Hosp, Dept Gynecol, 324 Jingwuweiqi St, Jinan 250021, Shandong, Peoples R China.
   [Cui, Jing] Jinan Stomatol Hosp, Dept Oral Surg, Jinan 250021, Shandong, Peoples R China.
C3 Shandong University; Shandong First Medical University & Shandong
   Academy of Medical Sciences
RP Li, CZ (corresponding author), Shandong Univ, Shandong Prov Hosp, Dept Gynecol, 324 Jingwuweiqi St, Jinan 250021, Shandong, Peoples R China.
EM shenlang007@163.com
OI Li, Changzhong/0000-0001-5654-1031
FU National Natural Science Foundation of China [81671434]
FX The present study was supported by the National Natural Science
   Foundation of China (grant no. 81671434).
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NR 46
TC 18
Z9 20
U1 0
U2 9
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD JAN
PY 2018
VL 15
IS 1
BP 205
EP 212
DI 10.3892/ol.2017.7346
PN A
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FX5UB
UT WOS:000426144800027
PM 29387216
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Ramaswamy, A
   Ostwal, V
   Pande, N
   Sharma, A
   Patil, S
   Thippeswamy, R
   Ghadyalpatil, N
   Roy, R
   Peshwe, H
   Poladia, B
   Rajamanickam, D
   Rangarajan, B
   Reddy, PRN
   Pandita, V
   Mukherjee, A
   Thoke, A
   Sarkar, A
   Satish, CT
   Shashidara, H
   Banavali, SD
AF Ramaswamy, Anant
   Ostwal, Vikas
   Pande, Nikhil
   Sharma, Atul
   Patil, Shekar
   Thippeswamy, Ravi
   Ghadyalpatil, Nikhil
   Roy, Rakesh
   Peshwe, Harish
   Poladia, Bhavesh
   Rajamanickam, Deepan
   Rangarajan, Bharat
   Reddy, P. R. Neelesh
   Pandita, Vimal
   Mukherjee, Ashis
   Thoke, Aniket
   Sarkar, Abhijit
   Satish, C. T.
   Shashidara, H.
   Banavali, S. D.
TI Practice patterns and outcomes with the use of regorafenib in metastatic
   colorectal cancer: Results from the Regorafenib in Metastatic colorectal
   cancer - An Indian exploratory analysis study
SO SOUTH ASIAN JOURNAL OF CANCER
LA English
DT Article
DE Colorectal cancer; India; REgorafenib in metastatic colorectal cancer -
   An Indian eXploratory analysis study; regorafenib
ID THERAPY; CARE
AB Background: Regorafenib is considered a standard of care as third-line therapy in metastatic colorectal cancers (mCRCs). Materials and Methods: The study was based on a computerized clinical data form sent to oncologists across the country for entry of anonymized patient data. The data entry form was conceived and generated by the coordinating center's (Tata Memorial Hospital) gastrointestinal medical oncologists and disseminated through personal contacts at academic conferences as well as through E-mail to various oncologists across India. Results: A total of 19 physicians contributed data resulting in 80 patients receiving regorafenib who were available for the evaluation of practice patterns. The median age was 55 years (range: 24-75). Majority had received oxaliplatin-based (97.5%), irinotecan-based (87.5%), and targeted therapy (65%), previously. Patients were primarily started on reduced doses of regorafenib upfront (160 mg - 28.8%, 120 mg - 58.8%, and 80 mg - 12.5%). The median duration of treatment (treatment duration) with regorafenib was 3.1 months (range: 0.5-18), while the median progression free survival was 3.48 months (range: 2.6-4.3). Forty-five percent of patients required dose modifications due to toxicities, and the most common were (all grades) hand-foot syndrome (68.8%), fatigue (46.3%), mucositis (37.6%), and diarrhea (31.3%). Conclusions: Majority of physicians in this collaborative study from India used a lower dose of regorafenib at the outset in patients with mCRC. Despite a lower dose, there was a significant requirement for dose reduction. Duration of treatment with regorafenib as an efficacy end point in this study is similar to available data from other regions as it is the side effect profile.
C1 [Ramaswamy, Anant; Ostwal, Vikas; Pande, Nikhil; Banavali, S. D.] Tata Mem Hosp, Dept Med Oncol, Mumbai, Maharashtra, India.
   [Sharma, Atul] AIIMS, Dr BRA IRCH, Dept Med Oncol, New Delhi, India.
   [Patil, Shekar; Satish, C. T.; Shashidara, H.] HCG, Dept Med Oncol, Bengaluru, Karnataka, India.
   [Thippeswamy, Ravi] Sri Shankara Canc Hosp, Dept Med Oncol, Bengaluru, Karnataka, India.
   [Reddy, P. R. Neelesh] Columbia Asia Hosp, Dept Med Oncol, Bengaluru, Karnataka, India.
   [Ghadyalpatil, Nikhil] Yashoda Canc Inst, Dept Med Oncol, Hyderabad, Telangana, India.
   [Roy, Rakesh] Saroj Gupta Canc Ctr & Res Inst, Kolkata, W Bengal, India.
   [Mukherjee, Ashis] Netaji Subhash Chandra Bose Canc Res Inst, Dept Oncol, Kolkata, W Bengal, India.
   [Sarkar, Abhijit] Saroj Gupta Canc Ctr & Res Inst, Kolkata, W Bengal, India.
   [Thoke, Aniket] Sanjeevani CBCC USA Canc Hosp, Dept Oncol, Raipur, Chhattisgarh, India.
   [Peshwe, Harish] Healthway Hosp, Dept Gastroenterol & Hepatol, Panaji, Goa, India.
   [Poladia, Bhavesh; Rajamanickam, Deepan] Thangam Canc Ctr, Namakkal, Tamil Nadu, India.
   [Rangarajan, Bharat] Kovai Med Ctr & Hosp, Coimbatore, Tamil Nadu, India.
   [Pandita, Vimal] Max Superspecial Hosp, Dept Med Oncol, Dehra Dun, Uttarakhand, India.
C3 Tata Memorial Centre (TMC); Tata Memorial Hospital; All India Institute
   of Medical Sciences (AIIMS) New Delhi; DR. B.R.A. Institute Rotary
   Cancer Hospital
RP Ostwal, V (corresponding author), Tata Mem Hosp, Dept Med Oncol, Mumbai, Maharashtra, India.
EM dr.vikas.ostwal@gmail.com
RI Sharma, Atul/ISS-2723-2023
CR [Anonymous], J CLIN ONCOL S
   Chew MH, 2010, INT J COLORECTAL DIS, V25, P1221, DOI 10.1007/s00384-010-1033-3
   Ghosh J, 2011, INDIAN J CANCER, V48, P391, DOI 10.4103/0019-509X.92245
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   Meeting Library, REG DOS OPT STUD RED
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NR 14
TC 3
Z9 3
U1 0
U2 1
PU WOLTERS KLUWER MEDKNOW PUBLICATIONS
PI MUMBAI
PA WOLTERS KLUWER INDIA PVT LTD , A-202, 2ND FLR, QUBE, C T S  NO 1498A-2
   VILLAGE MAROL, ANDHERI EAST, MUMBAI, 400059, INDIA
SN 2278-330X
EI 2278-4306
J9 SOUTH ASIAN J CANCER
JI South Asian J. Cancer
PD JAN-MAR
PY 2019
VL 8
IS 1
BP 22
EP +
DI 10.4103/sajc.sajc_173_18
PG 5
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA HH7SC
UT WOS:000455929800004
PM 30766846
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Bu, YW
   Li, XN
   He, YC
   Huang, CF
   Shen, Y
   Cao, Y
   Huang, D
   Cai, CA
   Wang, YH
   Wang, ZQ
   Liao, DF
   Cao, DL
AF Bu, Yiwen
   Li, Xiaoning
   He, Yingchun
   Huang, Chenfei
   Shen, Yi
   Cao, Yu
   Huang, Dan
   Cai, Chuan
   Wang, Yuhong
   Wang, Ziqi
   Liao, Duan-Fang
   Cao, Deliang
TI A phosphomimetic mutant of RelA/p65 at Ser536 induces apoptosis and
   senescence: An implication for tumor-suppressive role of Ser536
   phosphorylation
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE NF-kappa B; RelA/p65; phosphomimetic mutation; Ser536 phosphorylation;
   apoptosis; senescence; tumor suppressor
ID NF-KAPPA-B; GENE-EXPRESSION; COLORECTAL-CARCINOMA; SIGNALING PATHWAY;
   CANCER; P65; ACTIVATION; KINASE; IKK; CONTRIBUTES
AB Hundreds of NF-kappa B inhibitors have been developed for cancer therapy, but their clinical efficacy is unsatisfactory. Here we show that the phosphorylation activation at Ser536 of RelA/p65 protein, a main subunit in the NF-kappa B family, may play a tumor-suppressive role. In normal colon mucosa, RelA/p65 phosphorylation at Ser536 was increasingly increased with the maturation and apoptotic shedding of epithelial cells, but the phosphorylation at Ser536 was decreased in colon cancer. In colon (HCT116 p53 wt and p53 -/-), breast (MCF7), and prostate (LNCaP and DU145) cancer cells, a phosphomimetic mutation of RelA/p65 at Ser536 (named p65/S536D) triggered dramatic apoptosis through affecting expression of a wide range of cell death/survival genes, such as Bim, Puma, Noxa, Bcl-2 and survivin. In HCT116 cells, p65/S536D mutant upregulated Fas, insulted mitochondrial membrane potential, and triggered cleavage and activation of caspase-3, 7, 8 and 9. A FasL neutralizing antibody (NOK1) prevented cell death induced by the p65/S536D. A pan inhibitor of caspases, Z-VAD-FMK (20 mu M), blocked caspase-mediated mitochondrial membrane depolarization. This p65/S536D also triggered senescence in HCT116 cells through a p16-dependent pathway, but not in MFC7 due to lack of p16. Intratumoral delivery of the p65/S536D effectively suppressed tumor growth in nude mice. Together our data suggest that the phosphorylation of RelA/p65 at Ser536 may confer it a tumor-suppressive role by inducing apoptosis and senescence, highlighting the importance of discriminating the function and active status of individual active sites in RelA/p65 when NF-kappa B inhibitors are considered for targeted therapy of cancer.
C1 [Bu, Yiwen; Li, Xiaoning; He, Yingchun; Huang, Chenfei; Shen, Yi; Cao, Yu; Cao, Deliang] So Illinois Univ, Sch Med, Simmons Canc Inst, Dept Med Microbiol Immunol & Cell Biol, 913 N Rutledge St, Springfield, IL 62794 USA.
   [He, Yingchun; Huang, Dan; Cai, Chuan; Wang, Yuhong; Wang, Ziqi; Liao, Duan-Fang; Cao, Deliang] Hunan Univ Chinese Med, Div Stem Cell Regulat & Applicat, State Key Lab Chinese Med Powder & Med Innovat Hu, Changsha 410208, Hunan, Peoples R China.
C3 Southern Illinois University System; Southern Illinois University; Hunan
   University of Chinese Medicine
RP Cao, DL (corresponding author), So Illinois Univ, Sch Med, Simmons Canc Inst, Dept Med Microbiol Immunol & Cell Biol, 913 N Rutledge St, Springfield, IL 62794 USA.; Liao, DF (corresponding author), Hunan Univ Chinese Med, Div Stem Cell Regulat & Applicat, State Key Lab Chinese Med Powder & Med Innovat Hu, Changsha 410208, Hunan, Peoples R China.
EM dfliao66@aliyun.com; dcao@siumed.edu
RI wang, ziqi/IQS-5011-2023; Cao, Yu/L-6743-2014; Shen, Yi/A-2031-2016; Bu,
   Yiwen/D-2203-2016
OI Huang, Dan/0000-0003-4221-574X
FU National Natural Science Foundation of China [81272918, 81472465]
FX Grant sponsor: National Natural Science Foundation of China; Grant
   numbers: 81272918 and 81472465 (D.C.)
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NR 49
TC 29
Z9 34
U1 0
U2 14
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD MAR 1
PY 2016
VL 138
IS 5
BP 1186
EP 1198
DI 10.1002/ijc.29852
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DC4BL
UT WOS:000369164700016
PM 26375985
OA Bronze
DA 2025-01-04
ER

PT J
AU Hess, LM
   Smith, D
   Cui, ZLL
   Montejano, L
   Liepa, AM
   Schelman, W
   Bowman, L
AF Hess, Lisa M.
   Smith, David
   Cui, Zhanglin L.
   Montejano, Leslie
   Liepa, Astra M.
   Schelman, William
   Bowman, Lee
TI The relationship between Eastern Cooperative Oncology Group performance
   status and healthcare resource utilization among patients with advanced
   or metastatic colorectal, lung or gastric cancer
SO JOURNAL OF DRUG ASSESSMENT
LA English
DT Article
DE Colorectal cancer; lung cancer; gastric cancer; performance status;
   retrospective study; electronic medical record; chemotherapy; biologic;
   targeted therapy; comorbid conditions
AB Aims: The ability of a patient to receive anti-cancer treatment depends on a variety of factors, including performance status (PS), which is typically measured using the Eastern Cooperative Oncology Group (ECOG) scale. This study hypothesized that there would be a strong and positive correlation between ECOG PS values and healthcare resource utilization (HCRU) and a strong and negative correlation with the use of anti-cancer therapy.
   Materials and methods: Patients with colorectal, lung or gastric cancer were included in this retrospective analysis of administrative claims data linked to electronic medical records (EMR). All-cause HCRU (hospitalization/inpatient care, emergency room visits, systemic anti-cancer therapy, radiation therapy, outpatient physician visits, hospice, home health care and key supportive care treatments such as anti-emetics, hematopoietic treatments, transfusions, and durable medical equipment) was evaluated by baseline ECOG PS value and PS over time. Adjusted multivariable regression analysis was used to assess the relationship between baseline ECOG PS and HCRU. Regression analyses were conducted to explore the relationship between other baseline variables and HCRU.
   Results: There were 1311 patients included in this study. There was low correlation between PS and any HCRU variable or receipt of anti-cancer therapy (correlation coefficients all <0.10). In regression analyses, the proportion of patients with poor PS (PS = 2+) who were hospitalized was not significantly different from those with good PS (PS = 0/1) (28.9% versus 19.3%, p = .07).
   Limitations: The low rate of reporting of PS and the small sample size of patient groups in this study.
   Conclusions: There is very little evidence of a relationship between ECOG PS and HCRU, ECOG PS, or anti-cancer therapy in this study, in part due to low rates of and lack of variability in reported PS. There is some evidence that baseline comorbidities were significantly associated with HCRU and should be accounted for in future research evaluating HCRU.
C1 [Hess, Lisa M.; Cui, Zhanglin L.; Liepa, Astra M.; Schelman, William; Bowman, Lee] Eli Lilly & Co, Indianapolis, IN 46285 USA.
   [Smith, David; Montejano, Leslie] IBM Watson Hlth, Cambridge, MA USA.
C3 Eli Lilly
RP Hess, LM (corresponding author), Eli Lilly & Co, Indianapolis, IN 46285 USA.
EM Hess_lisa_m@lilly.com
OI Montejano, Leslie/0000-0002-4542-7257
FU Eli Lilly and Company
FX This study was supported by Eli Lilly and Company.
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NR 14
TC 4
Z9 4
U1 0
U2 51
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1369-9474
EI 2155-6660
J9 J DRUG ASSESS
JI J. Drug Assess.
PD JAN 15
PY 2021
VL 10
IS 1
BP 10
EP 17
DI 10.1080/21556660.2020.1851504
PG 8
WC Pharmacology & Pharmacy
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA PG5WP
UT WOS:000599805800001
PM 33403155
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Nair, KG
   Kamath, SD
   Chowattukunnel, N
   Krishnamurthi, SS
AF Nair, Kanika G.
   Kamath, Suneel D.
   Chowattukunnel, Nivan
   Krishnamurthi, Smitha S.
TI Preoperative Strategies for Locally Advanced Colon Cancer
SO CURRENT TREATMENT OPTIONS IN ONCOLOGY
LA English
DT Review
DE Colon cancer; Neoadjuvant; Preoperative; Mismatch repair; Microsatellite
   instability; Microsatellite stable
ID MISMATCH REPAIR STATUS; ADJUVANT CHEMOTHERAPY; DURATION; BLOCKADE
AB Neoadjuvant chemotherapy is safe for patients with locally advanced colon cancer (LACC). The FOxTROT trial demonstrated a reduction in residual and recurrent cancer at 2 years with neoadjuvant chemotherapy for patients with cT3-4 LACC. Preoperative chemotherapy should be avoided, if possible, for patients with dMMR LACC, as over 50% of dMMR cancers have no pathologic response. Early universal testing of MMR status is critical to selecting the appropriate neoadjuvant therapy. Concerns about CT staging of LACC have limited uptake of neoadjuvant chemotherapy, as approximately 25% of patients with cT3-T4 cancer on CT have low-risk stage II disease. Development of CT criteria for malignant nodes should reduce the risk of over-staging. A multidisciplinary approach is needed to identify patients for neoadjuvant therapy. Neoadjuvant immunotherapy is safe and results in dramatic pathologic responses in patients with dMMR LACC. Longer follow-up is needed to determine if the exceptionally high pathologic response rates observed will translate into long-term remission. Remarkably, neoadjuvant immunotherapy has been found to cause major pathologic responses in a subset of patients with pMMR LACC, indicating the potential to cure more patients with this common cancer. Patients with cT4 LACC, whether stage II or III, have a substantial risk of recurrence despite adjuvant fluoropyrimidine plus oxaliplatin chemotherapy. We recommend neoadjuvant systemic therapy for all patients with cT4b LACC (dMMR and pMMR). Features of T4b disease are routinely reported by radiology. We use three cycles of FOLFOX chemotherapy for patients with cT4b pMMR LACC, due to the high rate of compliance and improvement in residual and recurrent disease. Patients with cT4b dMMR LACC should receive neoadjuvant immunotherapy, if there are no contraindications. Clinical trials of neoadjuvant therapy for LACC are of great interest and should provide training for radiologists to identify eligible patients. Results are anticipated from multiple ongoing trials of neoadjuvant chemotherapy, immunotherapy, and targeted therapy for pMMR LACC and immunotherapy for dMMR LACC.
C1 [Nair, Kanika G.; Kamath, Suneel D.; Chowattukunnel, Nivan; Krishnamurthi, Smitha S.] Cleveland Clin, Taussig Canc Ctr, Dept Hematol Oncol, 9500 Euclid Ave, Cleveland, OH 44195 USA.
C3 Cleveland Clinic Foundation
RP Krishnamurthi, SS (corresponding author), Cleveland Clin, Taussig Canc Ctr, Dept Hematol Oncol, 9500 Euclid Ave, Cleveland, OH 44195 USA.
EM krishns3@ccf.org
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NR 30
TC 3
Z9 3
U1 2
U2 3
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1527-2729
EI 1534-6277
J9 CURR TREAT OPTION ON
JI Curr. Treat. Options Oncol.
PD MAR
PY 2024
VL 25
IS 3
BP 376
EP 388
DI 10.1007/s11864-024-01184-6
EA FEB 2024
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IR2M0
UT WOS:001160405500001
PM 38349502
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Vangala, D
   Ladigan, S
   Liffers, ST
   Noseir, S
   Maghnouj, A
   Götze, TM
   Verdoodt, B
   Klein-Scory, S
   Godfrey, L
   Zowada, MK
   Huerta, M
   Edelstein, DL
   de Villarreal, JM
   Marqués, M
   Kumbrink, J
   Jung, AD
   Schiergens, T
   Werner, J
   Heinemann, V
   Stintzing, S
   Lindoerfer, D
   Mansmann, U
   Pohl, M
   Teschendorf, C
   Bernhardt, C
   Wolters, H
   Stern, J
   Usta, S
   Viebahn, R
   Admard, J
   Casadei, N
   Fröhling, S
   Ball, CR
   Siveke, JT
   Glimm, H
   Tannapfel, A
   Schmiegel, W
   Hahn, SA
AF Vangala, Deepak
   Ladigan, Swetlana
   Liffers, Sven T.
   Noseir, Soha
   Maghnouj, Abdelouahid
   Gotze, Tina-Maria
   Verdoodt, Berlinda
   Klein-Scory, Susanne
   Godfrey, Laura
   Zowada, Martina K.
   Huerta, Mario
   Edelstein, Daniel L.
   de Villarreal, Jaime Martinez
   Marques, Miriam
   Kumbrink, Jorg
   Jung, Andreas
   Schiergens, Tobias
   Werner, Jens
   Heinemann, Volker
   Stintzing, Sebastian
   Lindoerfer, Doris
   Mansmann, Ulrich
   Pohl, Michael
   Teschendorf, Christian
   Bernhardt, Christiane
   Wolters, Heiner
   Stern, Josef
   Usta, Selami
   Viebahn, Richard
   Admard, Jacob
   Casadei, Nicolas
   Frohling, Stefan
   Ball, Claudia R.
   Siveke, Jens T.
   Glimm, Hanno
   Tannapfel, Andrea
   Schmiegel, Wolff
   Hahn, Stephan A.
TI Secondary resistance to anti-EGFR therapy by transcriptional
   reprogramming in patient-derived colorectal cancer models
SO GENOME MEDICINE
LA English
DT Article
DE Anti-EGFR; PDX; Secondary resistance; Targeted treatment;
   Transcriptional reprogramming
ID ACQUIRED-RESISTANCE; EXTRACELLULAR DOMAIN; SIGNALING PATHWAYS; GENOMIC
   LANDSCAPE; LUNG-CANCER; PHASE-II; CELL; CETUXIMAB; GROWTH; EXPRESSION
AB Background The development of secondary resistance (SR) in metastatic colorectal cancer (mCRC) treated with anti-epidermal growth factor receptor (anti-EGFR) antibodies is not fully understood at the molecular level. Here we tested in vivo selection of anti-EGFR SR tumors in CRC patient-derived xenograft (PDX) models as a strategy for a molecular dissection of SR mechanisms. Methods We analyzed 21 KRAS, NRAS, BRAF, and PI3K wildtype CRC patient-derived xenograft (PDX) models for their anti-EGFR sensitivity. Furthermore, 31 anti-EGFR SR tumors were generated via chronic in vivo treatment with cetuximab. A multi-omics approach was employed to address molecular primary and secondary resistance mechanisms. Gene set enrichment analyses were used to uncover SR pathways. Targeted therapy of SR PDX models was applied to validate selected SR pathways. Results In vivo anti-EGFR SR could be established with high efficiency. Chronic anti-EGFR treatment of CRC PDX tumors induced parallel evolution of multiple resistant lesions with independent molecular SR mechanisms. Mutations in driver genes explained SR development in a subgroup of CRC PDX models, only. Transcriptional reprogramming inducing anti-EGFR SR was discovered as a common mechanism in CRC PDX models frequently leading to RAS signaling pathway activation. We identified cAMP and STAT3 signaling activation, as well as paracrine and autocrine signaling via growth factors as novel anti-EGFR secondary resistance mechanisms. Secondary resistant xenograft tumors could successfully be treated by addressing identified transcriptional changes by tailored targeted therapies. Conclusions Our study demonstrates that SR PDX tumors provide a unique platform to study molecular SR mechanisms and allow testing of multiple treatments for efficient targeting of SR mechanisms, not possible in the patient. Importantly, it suggests that the development of anti-EGFR tolerant cells via transcriptional reprogramming as a cause of anti-EGFR SR in CRC is likely more prevalent than previously anticipated. It emphasizes the need for analyses of SR tumor tissues at a multi-omics level for a comprehensive molecular understanding of anti-EGFR SR in CRC.
C1 [Vangala, Deepak; Ladigan, Swetlana; Noseir, Soha; Maghnouj, Abdelouahid; Gotze, Tina-Maria; Hahn, Stephan A.] Ruhr Univ Bochum, Fac Med, Dept Mol GI Oncol, D-44780 Bochum, Germany.
   [Vangala, Deepak; Ladigan, Swetlana; Klein-Scory, Susanne; Pohl, Michael; Schmiegel, Wolff; Hahn, Stephan A.] Ruhr Univ Bochum, Knappschaftskrankenhaus, Dept Internal Med, Bochum, Germany.
   [Liffers, Sven T.; Verdoodt, Berlinda; Tannapfel, Andrea] Ruhr Univ Bochum, Inst Pathol, Bochum, Germany.
   [Liffers, Sven T.] Univ Hosp Essen, Div Solid Tumor Translat Oncol, West German Canc Ctr, Essen, Germany.
   [Godfrey, Laura; Siveke, Jens T.] Univ Hosp Essen, Bridge Inst Expt Tumor Therapy, West German Canc Ctr, Essen, Germany.
   [Godfrey, Laura; Siveke, Jens T.] German Canc Consortium DKTK, Div Solid Tumor Translat Oncol, Partner Site Essen, Heidelberg, Germany.
   [Godfrey, Laura; Zowada, Martina K.; Huerta, Mario; Ball, Claudia R.; Siveke, Jens T.; Glimm, Hanno] DKFZ, German Canc Res Ctr, Heidelberg, Germany.
   [Zowada, Martina K.; Huerta, Mario; Ball, Claudia R.; Glimm, Hanno] NCT Heidelberg, Translat Funct Canc Genom, Heidelberg, Germany.
   [Zowada, Martina K.] Heidelberg Univ, Fac Biosci, Heidelberg, Germany.
   [Huerta, Mario; Ball, Claudia R.; Glimm, Hanno] Natl Ctr Tumor Dis NCT, Dept Translat Med Oncol, Dresden, Germany.
   [Huerta, Mario; Ball, Claudia R.; Glimm, Hanno] German Canc Res Ctr, Dresden, Germany.
   [Edelstein, Daniel L.] Sysmex Inost Inc, Med Sci Affairs, Baltimore, MD USA.
   [de Villarreal, Jaime Martinez; Marques, Miriam] Spanish Natl Canc Res Ctr CNIO, Epithelial Carcinogenesis Grp, Madrid, Spain.
   [de Villarreal, Jaime Martinez; Marques, Miriam] CIBERONC, Madrid, Spain.
   [Kumbrink, Jorg; Jung, Andreas] Ludwig Maximilian Univ LMU, Inst Pathol, Munich, Germany.
   [Kumbrink, Jorg; Jung, Andreas] German Canc Consortium DKTK, Partner Site Munich, Munich, Germany.
   [Schiergens, Tobias; Werner, Jens] Ludwig Maximilians Univ Munchen, Univ Hosp, Dept Gen Visceral & Transplantat Surg, Munich, Germany.
   [Heinemann, Volker] Ludwig Maximilians Univ Munchen, Univ Hosp, Dept Med 3, Munich, Germany.
   [Stintzing, Sebastian] Charite Univ Med Berlin, Dept Hematol Oncol & Tumor Immunol CCM, Berlin, Germany.
   [Lindoerfer, Doris; Mansmann, Ulrich] Ludwig Maximilians Univ Munchen, Inst Med Informat Proc Biometry & Epidemiol, Munich, Germany.
   [Teschendorf, Christian; Bernhardt, Christiane] St Josefs Hosp, Dept Internal Med, Dortmund, Germany.
   [Wolters, Heiner; Stern, Josef; Usta, Selami] St Josef Hosp, Dept Visceral & Gen Surg, Dortmund, Germany.
   [Viebahn, Richard] Ruhr Univ Bochum, Dept Surg, Knappschaftskrankenhaus, Bochum, Germany.
   [Admard, Jacob; Casadei, Nicolas] Univ Tubingen, Inst Med Genet & Appl Genom, Tubingen, Germany.
   [Frohling, Stefan] German Canc Consortium DKTK, Heidelberg, Germany.
   [Frohling, Stefan] NCT Heidelberg, Dept Translat Med Oncol, Heidelberg, Germany.
   [Frohling, Stefan] German Canc Res Ctr, Heidelberg, Germany.
   [Ball, Claudia R.; Glimm, Hanno] NCT Dresden, Ctr Personalized Oncol, Dresden, Germany.
   [Ball, Claudia R.; Glimm, Hanno] Tech Univ Dresden, Univ Hosp Carl Gustav Carus Dresden, Dresden, Germany.
   [Ball, Claudia R.; Glimm, Hanno] German Canc Consortium DKTK, Dresden, Germany.
C3 Ruhr University Bochum; Ruhr University Bochum; Ruhr University Bochum;
   University of Duisburg Essen; University of Duisburg Essen; Helmholtz
   Association; German Cancer Research Center (DKFZ); Helmholtz
   Association; German Cancer Research Center (DKFZ); Helmholtz
   Association; German Cancer Research Center (DKFZ); Ruprecht Karls
   University Heidelberg; Ruprecht Karls University Heidelberg; Helmholtz
   Association; German Cancer Research Center (DKFZ); Ruprecht Karls
   University Heidelberg; Helmholtz Association; German Cancer Research
   Center (DKFZ); Centro Nacional de Investigaciones Oncologicas (CNIO);
   CIBER - Centro de Investigacion Biomedica en Red; CIBERONC; University
   of Munich; Helmholtz Association; German Cancer Research Center (DKFZ);
   University of Munich; University of Munich; Berlin Institute of Health;
   Free University of Berlin; Humboldt University of Berlin; Charite
   Universitatsmedizin Berlin; University of Munich; Ruhr University
   Bochum; Eberhard Karls University of Tubingen; Helmholtz Association;
   German Cancer Research Center (DKFZ); Helmholtz Association; German
   Cancer Research Center (DKFZ); Ruprecht Karls University Heidelberg;
   Helmholtz Association; German Cancer Research Center (DKFZ); Technische
   Universitat Dresden; Carl Gustav Carus University Hospital; Helmholtz
   Association; German Cancer Research Center (DKFZ)
RP Hahn, SA (corresponding author), Ruhr Univ Bochum, Fac Med, Dept Mol GI Oncol, D-44780 Bochum, Germany.; Hahn, SA (corresponding author), Ruhr Univ Bochum, Knappschaftskrankenhaus, Dept Internal Med, Bochum, Germany.
EM stephan.hahn@rub.de
RI Siveke, Jens/AAQ-6170-2021; Marqués, Miriam/AAN-6642-2020; Casadei,
   Nicolas/H-3283-2019; Vangala, Deepak/AAV-5780-2021; Klein-Scory,
   Susanne/JMB-0127-2023; Stintzing, Sebastian/I-4538-2016; Hahn,
   Stephan/E-3880-2010
OI Stintzing, Sebastian/0000-0002-3297-5801; Lindoerfer,
   Doris/0000-0003-3078-0856; Godfrey, Laura/0000-0003-2393-9881; Ball,
   Claudia/0000-0002-1749-3791; Martinez Villarreal,
   Jaime/0000-0002-3003-7766; Zowada, Martina/0000-0002-4231-1021; Admard,
   Jakob/0000-0003-0466-582X; Marques, Miriam/0000-0003-1550-3033; Hahn,
   Stephan/0000-0003-0855-9741; Klein-Scory, Susanne/0000-0003-1930-3354
FU German Cancer Aid [70112505, 70113834, 70111971]; Ministry of Science,
   North Rhine-Westphalia, Germany (PURE/PRODI); German Cancer Consortium
   (DKTK); German Research Foundation (DFG) [SI1549/3-1, KFO337]; German
   Cancer Research Center-Heidelberg Center for Personalized Oncology
   (DKFZ-HIPO); Molecular Diagnostics Program of the National Center for
   Tumor Diseases (NCT) in Heidelberg; Projekt DEAL
FX The work was supported by grants from the German Cancer Aid (70111971)
   to A. Jung, J. Werner, V. Heinemann, S. Stintzing, U. Mansmann, A.
   Tannapfel., C.R. Ball, S. Frohling, H. Glimm, S.A. Hahn, and W.
   Schmiegel and from the Ministry of Science, North Rhine-Westphalia,
   Germany (PURE/PRODI) to W. Schmiegel. J.T. Siveke is supported by
   funding from the German Cancer Consortium (DKTK), the German Cancer Aid
   (grant no. 70112505 (PIPAC) and grant no. 70113834 (PREDICT-PACA)), and
   the German Research Foundation (DFG) through grant SI1549/3-1 (Clinical
   Research Unity KFO337). This work was supported by the German Cancer
   Research Center-Heidelberg Center for Personalized Oncology (DKFZ-HIPO)
   and the Molecular Diagnostics Program of the National Center for Tumor
   Diseases (NCT) in Heidelberg. Open Access funding enabled and organized
   by Projekt DEAL.
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NR 101
TC 11
Z9 11
U1 0
U2 3
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1756-994X
J9 GENOME MED
JI Genome Med.
PD JUL 16
PY 2021
VL 13
IS 1
AR 116
DI 10.1186/s13073-021-00926-7
PG 25
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA TM2GY
UT WOS:000675371100001
PM 34271981
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhao, R
   Yin, FX
   Fredimoses, M
   Zhao, JH
   Fu, XR
   Xu, BB
   Liang, MR
   Chen, HY
   Liu, KD
   Lei, MJ
   Laster, KV
   Li, Z
   Kundu, JK
   Dong, ZG
   Lee, MH
AF Zhao, Ran
   Yin, Fanxiang
   Fredimoses, Mangaladoss
   Zhao, Jianhua
   Fu, Xiaorong
   Xu, Beibei
   Liang, Mengrui
   Chen, Hanyong
   Liu, Kangdong
   Lei, Mingjuan
   Laster, Kyle Vaughn
   Li, Zhi
   Kundu, Joydeb Kumar
   Dong, Zigang
   Lee, Mee-Hyun
TI Targeting FGFR1 by β,β-dimethylacrylalkannin suppresses the
   proliferation of colorectal cancer in cellular and xenograft models
SO PHYTOMEDICINE
LA English
DT Article
DE FGFR1; beta-dimethylacrylalkannin ( beta; beta-DMAA); Colorectal cancer;
   Targeted therapy; PDX mouse model; Kinase activity
ID GROWTH-FACTOR RECEPTOR; THERAPEUTIC TARGET; COLON-CANCER; LUNG-CANCER;
   EXPRESSION; STATISTICS; PATIENT; ADENOCARCINOMA; IDENTIFICATION;
   PAZOPANIB
AB Background: Colorectal cancer (CRC) continues to be a major global health challenge, ranking as a top cause of cancer-related mortality. Alarmingly, the five-year survival rate for CRC patients hovers around a mere 10-30 %. The disruption of fibroblast growth factor receptor (FGFRs) signaling pathways is significantly implicated in the onset and advancement of CRC, presenting a promising target for therapeutic intervention in CRC management. Further investigation is essential to comprehensively elucidate FGFR1 ' s function in CRC and to create potent therapies that specifically target FGFR1. Purpose: This study aims to demonstrate the oncogenic role of FGFR1 in colorectal cancer and to explore the potential of fl,fl-dimethylacrylalkannin (fl,fl-DMAA) as a therapeutic option to inhibit FGFR1. Methods: In this research, we employed a comprehensive suite of techniques including tissue array, kinase profiling, computational docking, knockdown assay to predict and explore the inhibitor of FGFR1. Furthermore, we utilized kinase assay, pull-down, cell proliferation tests, and Patient derived xenograft (PDX) mouse models to further investigate a novel FGFR1 inhibitor and its impact on the growth of CRC. Results: In our research, we discovered that FGFR1 protein is markedly upregulated in colorectal cancer tissues, suggesting a significant role in regulating cellular proliferation, particularly in patients with colorectal cancer. Furthermore, we conducted a computational docking, kinase profiling analysis, simulation and identified that fl,fl-DMAA could directly bind with FGFR1 within ATP binding pocket domain. Cell-based assays confirmed that fl,fl-DMAA effectively inhibited the proliferation of colon cancer cells and also triggered cell cycle arrest, apoptosis, and altered FGFR1-mediated signaling pathways. Moreover, fl,fl-DMAA effectively attenuated the development of PDX tumors in mice that were FGFR1-positive, with no notable toxicity observed. In summary, our study highlights the pivotal role of FGFR1 in colorectal cancer, suggesting that inhibiting FGFR1 activity could be a promising strategy for therapeutic intervention. We present strong evidence that targeting FGFR1 with fl,fl-DMAA is a viable approach for the management of colorectal cancer. Given its low toxicity and high efficacy, fl,fl-DMAA, as an FGFR1 inhibitor, warrants further investigation in clinical settings for the treatment of FGFR1positive tumors.
C1 [Zhao, Ran; Yin, Fanxiang; Zhao, Jianhua; Fu, Xiaorong; Xu, Beibei; Liang, Mengrui; Liu, Kangdong; Dong, Zigang; Lee, Mee-Hyun] Zhengzhou Univ, Sch Basic Med Sci, Dept Pathophysiol, Zhengzhou 450001, Peoples R China.
   [Zhao, Ran; Yin, Fanxiang; Fredimoses, Mangaladoss; Zhao, Jianhua; Fu, Xiaorong; Xu, Beibei; Liang, Mengrui; Lei, Mingjuan; Laster, Kyle Vaughn; Dong, Zigang; Lee, Mee-Hyun] China US Henan Hormel Canc Inst, Zhengzhou 450000, Peoples R China.
   [Zhao, Ran; Dong, Zigang] Tianjian Lab Adv Biomed Sci, Zhengzhou 450000, Peoples R China.
   [Yin, Fanxiang] Zhengzhou Univ, Affiliated Hosp 1, Translat Med Ctr, Zhengzhou 450000, Peoples R China.
   [Chen, Hanyong] Univ Minnesota, Hormel Inst, Austin, MN 55912 USA.
   [Liu, Kangdong; Lee, Mee-Hyun] Collaborat Innovat Ctr Henan Prov Canc Chemopreven, Zhengzhou 450000, Peoples R China.
   [Li, Zhi] Zhengzhou Univ, Affiliated Tumor Hosp, Dept Gen Surg, Zhengzhou 450000, Peoples R China.
   [Kundu, Joydeb Kumar] Univ Alberta, Li Ka Shing Appl Virol Inst, Edmonton, AB T6G 2R3, Canada.
   [Lee, Mee-Hyun] Dongshin Univ, Coll Korean Med, Naju 58245, South Korea.
C3 Zhengzhou University; Zhengzhou University; University of Minnesota
   System; Zhengzhou University; University of Alberta; Dongshin University
RP Dong, ZG; Lee, MH (corresponding author), Zhengzhou Univ, Sch Basic Med Sci, Dept Pathophysiol, Zhengzhou 450001, Peoples R China.; Dong, ZG; Lee, MH (corresponding author), China US Henan Hormel Canc Inst, Zhengzhou 450000, Peoples R China.; Dong, ZG (corresponding author), Tianjian Lab Adv Biomed Sci, Zhengzhou 450000, Peoples R China.; Lee, MH (corresponding author), Collaborat Innovat Ctr Henan Prov Canc Chemopreven, Zhengzhou 450000, Peoples R China.; Lee, MH (corresponding author), Dongshin Univ, Coll Korean Med, Naju 58245, South Korea.
EM dongzg@zzu.edu.cn; mhyun_lee@hanmail.net
RI Zhao, Jianhua/HSB-9267-2023; xu, beibei/ABB-5313-2021
FU Scientific and Technological Project in Henan Province [222102310104];
   China Postdoctoral Science Foundation Funded Project [2023M743180];
   Henan Medical Science and Technology Joint Building Program
   [LHGJ20210322]; Natural Science Foundation of Henan [222300420391];
   National Research Foundation of Korea (NRF) - Ministry of Science and
   ICT [2022R1A5A2029546]
FX This work was supported by grant funding from the Scientific and
   Technological Project in Henan Province (no. 222102310104), China
   Postdoctoral Science Foundation Funded Project (No. 2023M743180), the
   Henan Medical Science and Technology Joint Building Program (No.
   LHGJ20210322), Natural Science Foundation of Henan (222300420391) and
   the National Research Foundation of Korea (NRF), funded by the Ministry
   of Science and ICT (No. 2022R1A5A2029546).
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NR 55
TC 1
Z9 1
U1 2
U2 2
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0944-7113
EI 1618-095X
J9 PHYTOMEDICINE
JI Phytomedicine
PD JUL
PY 2024
VL 129
AR 155612
DI 10.1016/j.phymed.2024.155612
EA APR 2024
PG 16
WC Plant Sciences; Chemistry, Medicinal; Integrative & Complementary
   Medicine; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Plant Sciences; Pharmacology & Pharmacy; Integrative & Complementary
   Medicine
GA SH2L2
UT WOS:001233497700001
PM 38669968
OA hybrid
DA 2025-01-04
ER

PT J
AU Nunes, L
   Aasebo, K
   Mathot, L
   Ljungström, V
   Edqvist, PH
   Sundström, M
   Dragomir, A
   Pfeiffer, P
   Ameur, A
   Ponten, F
   Mezheyeuski, A
   Sorbye, H
   Sjöblom, T
   Glimelius, B
AF Nunes, Luis
   Aasebo, Kristine
   Mathot, Lucy
   Ljungstrom, Viktor
   Edqvist, Per-Henrik
   Sundstrom, Magnus
   Dragomir, Anca
   Pfeiffer, Per
   Ameur, Adam
   Ponten, Fredrik
   Mezheyeuski, Artur
   Sorbye, Halfdan
   Sjoblom, Tobias
   Glimelius, Bengt
TI Molecular characterization of a large unselected cohort of metastatic
   colorectal cancers in relation to primary tumor location, rare
   metastatic sites and prognosis
SO ACTA ONCOLOGICA
LA English
DT Article
ID PHASE-III TRIAL; BRAF MUTATION; MICROSATELLITE INSTABILITY; 1ST-LINE
   TREATMENT; PREDICTIVE-VALUE; SURVIVAL; FLUOROURACIL; CHEMOTHERAPY;
   POPULATION; LEUCOVORIN
AB Background: We have reported that BRAF V600E mutations and microsatellite instability-high (MSI-H) are more prevalent in a population-based cohort of metastatic colorectal cancer (mCRC) patients than has been reported from clinical trials or hospital-based patient groups. The aim was to explore if other mutations in mCRC differ in prevalence between these cohorts in relation to mismatch repair status and primary tumor location and if presence of bone or brain metastases is associated with any mutations. Material and methods: A population-based cohort of 798 mCRC patients from three regions in Scandinavia was used. Forty-four cancer related genes were investigated in a custom designed Ampliseq hotspot panel. Differences in survival were analyzed using the Kaplan-Meier estimator and the Cox regression analysis. Results: Determination of mutations was possible in 449/501 patients for 40/44 genes. Besides BRAF V600E, seen in 19% of the tumors, none of the other mutations appeared more prevalent than in trial cohorts. BRAF V600E and MSI-H, seen in 8%, were associated with poor prognosis as was right-sided primary tumor location (39%) when compared to left-sided and rectum together; however, in a multivariable regression, only the BRAF mutation retained its statistical significance. No other mutations were associated with poor prognosis. ERBB2 alterations were more common if bone metastases were present at diagnosis (17% vs. 4%, p = .011). No association was found for brain metastases. Fifty-two percent had an alteration that is treatable with an FDA-approved targeted therapy, chiefly by EGFR-inhibitor for RAS wild-type and a check-point inhibitor for MSI-H tumors. Conclusions: Right-sided tumor location, BRAF V600E mutations, but no other investigated mutation, and MSI-H are more commonly seen in an unselected cohort than is reported from clinical patient cohorts, likely because they indicate poor prognosis. Half of the patients have a tumor that is treatable with an already FDA-approved targeted drug for mCRC.
C1 [Nunes, Luis; Ljungstrom, Viktor; Edqvist, Per-Henrik; Sundstrom, Magnus; Dragomir, Anca; Ameur, Adam; Ponten, Fredrik; Mezheyeuski, Artur; Sjoblom, Tobias; Glimelius, Bengt] Uppsala Univ, Sci Life Lab, Dept Immunol Genet & Pathol, Dag Hammarskjolds Vag 20, SE-75185 Uppsala, Sweden.
   [Aasebo, Kristine; Sorbye, Halfdan] Univ Bergen, Dept Clin Sci, Bergen, Norway.
   [Dragomir, Anca] Uppsala Univ Hosp, Dept Pathol, Uppsala, Sweden.
   [Pfeiffer, Per] Odense Univ Hosp, Dept Oncol, Odense, Denmark.
   [Sorbye, Halfdan] Haukeland Hosp, Dept Oncol, Bergen, Norway.
C3 Uppsala University; University of Bergen; Uppsala University; Uppsala
   University Hospital; University of Southern Denmark; Odense University
   Hospital; University of Bergen; Haukeland University Hospital
RP Nunes, L (corresponding author), Uppsala Univ, Sci Life Lab, Dept Immunol Genet & Pathol, Dag Hammarskjolds Vag 20, SE-75185 Uppsala, Sweden.
EM luis.nunes@igp.uu.se
RI Mathot, Lucy/AAF-1463-2020; Dragomir, Anca/IAM-4024-2023; Nunes,
   Luís/AAF-4265-2021; Mezheyeuski, Artur/AAA-1217-2020; Ameur,
   Adam/E-6207-2011
OI Dragomir, Anca/0000-0003-2777-8114; Mezheyeuski,
   Artur/0000-0002-4394-2634; Nunes, Luis/0000-0002-3391-1607; Ameur,
   Adam/0000-0001-6085-6749; Ponten, Fredrik/0000-0003-0703-3940; Mathot,
   Lucy/0000-0002-2990-2038; Aasebo, Kristine/0000-0003-3575-5588;
   Pfeiffer, Per/0000-0002-2925-0586
FU Swedish Cancer Society [CAN 2016/447, CAN 2018/1165]
FX This work was supported by the Swedish Cancer Society under Grant CAN
   2016/447 and CAN 2018/1165.
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NR 39
TC 22
Z9 22
U1 1
U2 3
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0284-186X
EI 1651-226X
J9 ACTA ONCOL
JI Acta Oncol.
PD APR 2
PY 2020
VL 59
IS 4
BP 417
EP 426
DI 10.1080/0284186X.2019.1711169
EA JAN 2020
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KS3UF
UT WOS:000506548200001
PM 31924107
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Cui, HL
   Yu, QQ
   Xu, QM
   Lin, C
   Zhang, L
   Ye, W
   Yang, YF
   Tian, SJ
   Zhou, YL
   Sun, RZ
   Meng, YS
   Yao, NN
   Wang, HZ
   Cao, FL
   Liu, ML
   Ma, JF
   Liao, C
   Sun, RF
AF Cui, Huilin
   Yu, Qianqian
   Xu, Qumiao
   Lin, Chen
   Zhang, Long
   Ye, Wei
   Yang, Yifei
   Tian, Sijia
   Zhou, Yilu
   Sun, Runzhe
   Meng, Yongsheng
   Yao, Ningning
   Wang, Haizhen
   Cao, Feilin
   Liu, Meilin
   Ma, Jinfeng
   Liao, Cheng
   Sun, Ruifang
TI EGFR and MUC1 as dual-TAA drug targets for lung cancer and colorectal
   cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE EGFR; MUC1; TAA; LUAD; CRC
ID GROWTH-FACTOR RECEPTOR; EXPRESSION; THERAPY; ANTIBODY
AB Background Epidermal growth factor receptor (EGFR) is a key protein in cellular signaling that is overexpressed in many human cancers, making it a compelling therapeutic target. On-target severe skin toxicity has limited its clinical application. Dual-targeting therapy represents a novel approach to overcome the challenges of EGFR-targeted therapies.Methods A single-cell tumor-normal RNA transcriptomic meta-atlas of lung adenocarcinoma (LUAD) and normal lung tissues was constructed from published data. Tumor associated antigens (TAAs) were screened from the genes which were expressed on cell surface and could distinguish cancer cells from normal cells. Expression of MUC1 and EGFR in tumors and normal tissues was detected by immunohistochemistry (IHC), bulk transcriptomic and single-cell transcriptomic analyses. RNA cut-off values were calculated using paired analysis of RNA sequencing and IHC in patient-derived tumor xenograft samples. They were used to estimate the abundance of EGFR- and MUC-positive subjects in The Cancer Genome Atlas Program (TCGA) database. Survival analysis of EGFR and MUC1 expression was carried out using the transcription and clinical data from TCGA.Results A candidate TAA target, transmembrane glycoprotein mucin 1 (MUC1), showed strong expression in cancer cells and low expression in normal cells. Single-cell analysis suggested EGFR and MUC1 together had better tumor specificity than the combination of EGFR with other drug targets. IHC data confirmed that EGFR and MUC1 were highly expressed on LUAD and colorectal cancer (CRC) clinical samples but not on various normal tissues. Notably, co-expression of EGFR and MUC1 was observed in 98.4% (n=64) of patients with LUAD and in 91.6% (n=83) of patients with CRC. It was estimated that EGFR and MUC1 were expressed in 97.5% of LUAD samples in the TCGA dataset. Besides, high expression of EGFR and MUC1 was significantly associated with poor prognosis of LUAD and CRC patients.Conclusions Single-cell RNA, bulk RNA and IHC data demonstrated the high expression levels and co-expression patterns of EGFR and MUC1 in tumors but not normal tissues. Therefore, it is a promising TAA combination for therapeutic targeting which could enhance on-tumor efficacy while reducing off-tumor toxicity.
C1 [Cui, Huilin] Shanxi Med Univ, Dept Histol & Embryol, Taiyuan, Shanxi, Peoples R China.
   [Yu, Qianqian; Meng, Yongsheng; Wang, Haizhen; Cao, Feilin; Liu, Meilin; Sun, Ruifang] Shanxi Med Univ, Dept Tumor Biobank,Shanxi Prov Canc Hosp, Shanxi Hosp Affiliated Canc Hosp, Chinese Acad Med Sci,Canc Hosp, Taiyuan, Peoples R China.
   [Xu, Qumiao; Lin, Chen; Zhang, Long; Ye, Wei; Yang, Yifei; Tian, Sijia; Zhou, Yilu; Liao, Cheng] Shanghai Shengdi Med Co Ltd, Dept Translat Med, Shanghai, Peoples R China.
   [Sun, Runzhe] Shanxi Med Univ, Sch Basic Med, Jinzhong, Peoples R China.
   [Yao, Ningning] Shanxi Med Univ, Dept Radiobiol,Shanxi Prov Canc Hosp, Shanxi Hosp Affiliated Canc Hosp, Chinese Acad Med Sci,Canc Hosp, Taiyuan, Peoples R China.
   [Ma, Jinfeng] Shanxi Med Univ, Shanxi Prov Canc Hosp,Canc Hosp, Shanxi Hosp Affiliated Canc Hosp, Chinese Acad Med Sci,Dept Hepatobiliary & Pancreat, Taiyuan, Peoples R China.
C3 Shanxi Medical University; Shanxi Medical University; Chinese Academy of
   Medical Sciences - Peking Union Medical College; Shanxi Medical
   University; Shanxi Medical University; Chinese Academy of Medical
   Sciences - Peking Union Medical College; Chinese Academy of Medical
   Sciences - Peking Union Medical College; Shanxi Medical University
RP Sun, RF (corresponding author), Shanxi Med Univ, Dept Tumor Biobank,Shanxi Prov Canc Hosp, Shanxi Hosp Affiliated Canc Hosp, Chinese Acad Med Sci,Canc Hosp, Taiyuan, Peoples R China.; Liao, C (corresponding author), Shanghai Shengdi Med Co Ltd, Dept Translat Med, Shanghai, Peoples R China.
EM cheng.liao@hengrui.com; sunruifang@sxmu.edu.cn
RI yu, qianqian/AGQ-3260-2022; YANG, Yifei/HKN-6975-2023
FU Central Government Funds for Guiding Local Scientific and Technological
   Development [YDZJSX2022B014]; Project of Shanxi Provincial Key Research
   and Development Program [201803D421054]
FX The author(s) declare financial support was received for the research,
   authorship, and/or publication of this article. This work was supported
   by Central Government Funds for Guiding Local Scientific and
   Technological Development (YDZJSX2022B014) and the Project of Shanxi
   Provincial Key Research and Development Program (201803D421054) in
   China.
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NR 58
TC 0
Z9 0
U1 0
U2 0
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD NOV 27
PY 2024
VL 14
AR 1433033
DI 10.3389/fonc.2024.1433033
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA O8A7C
UT WOS:001373293600001
PM 39664199
OA gold
DA 2025-01-04
ER

PT J
AU Li, J
   Li, XM
   Dong, NN
   Yan, S
   Jing, C
   Ma, TH
   Li, W
   Zhang, CH
   Cai, Y
   Deng, W
AF Li, Jun
   Li, Xiaomo
   Dong, Ningning
   Yan, Shu
   Jing, Chao
   Ma, Tonghui
   Li, Wei
   Zhang, Chenghai
   Cai, Yi
   Deng, Wei
TI Driver and targetable alterations in Chinese patients with small bowel
   carcinoma
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Article
DE Small bowel adenocarcinoma; Driver alterations; Targetable alterations;
   Precision therapy; Next-generation sequencing
ID LYNCH SYNDROME; CANCER; INHIBITION; DIFFERENTIATION; MUTATIONS;
   VARIANTS; GENOMICS; SOX9; MDM2
AB PurposeSmall bowel carcinoma (SBA) is a rare gastrointestinal cancer with a poor prognosis. Recent genomic profiling studies revealed that the landscape of molecular alterations in SBA was distinct from colorectal cancer (CRC) and gastric cancer (GC). To explore driver and targetable alterations in SBA, we performed next-generation sequencing in 107 Chinese SBA patients.MethodsDNA from paraffin-embedded SBA samples and the corresponding peripheral blood control samples were analyzed through a next-generation sequencing panel. Somatic alterations including point mutations, indels, copy number alterations, gene fusions as well as pathogenic germline variants were characterized.ResultsMore than half of SBA cases carried KRAS mutations, including canonical (G12, G12, Q61) and atypical mutations (A146, L19, and K117). To our best knowledge, this was the first report of rare driver alterations including KRAS A146V/L19F, PIK3CA N345K/G364R/Q546E, and ZKSCAN1-MET fusion in SBA. Compared to KRAS-mutant patients, alternative activating alterations were enriched in KRAS wild-type patients, and some of them are targetable. Among BRAF-mutated SBA patients, class 1/2 BRAF mutants were mutually exclusive with RAS mutations, but class 3 BRAF mutants were not. Activating ERBB2 alternations, including amplification and activating mutations, represent the most common targetable alternation in this SBA cohort. Of note, the spectrums of BRAF and PIK3CA mutations in this Chinese SBA cohort were distinct from those of a European SBA cohort. Patients with three druggable mutations (PIK3CA, MAP2K1, KRAS G12C) had a high prevalence of concurring drivers, which may interfere with the clinical efficacy of single-target therapy.ConclusionTaken together, our work provided a comprehensive analysis of driver and targetable alterations in SBA, which can facilitate the practice of precision oncology in this challenging disease.
C1 [Li, Jun; Jing, Chao; Deng, Wei] Capital Med Univ, Beijing Friendship Hosp, Natl Clin Res Ctr Digest Dis, Beijing Digest Dis Ctr,Dept Gen Surg, Beijing, Peoples R China.
   [Li, Xiaomo; Ma, Tonghui; Li, Wei] Hangzhou Jichenjunchuang Med Lab Co Ltd, Hangzhou, Peoples R China.
   [Dong, Ningning] Capital Med Univ, Beijing Friendship Hosp, Natl Clin Res Ctr Digest Dis, Beijing Digest Dis Ctr,Dept Gastroenterol,Beijing, Beijing, Peoples R China.
   [Yan, Shu] Beijing Aerosp Gen Hosp, Dept Anorectal Surg, Beijing, Peoples R China.
   [Zhang, Chenghai] Peking Univ, Canc Hosp & Inst, Dept Gastrointestinal Surg 4, Key Lab Carcinogenesis & Translat Res,Minist Educ, Beijing, Peoples R China.
C3 Capital Medical University; Capital Medical University; Peking
   University
RP Deng, W (corresponding author), Capital Med Univ, Beijing Friendship Hosp, Natl Clin Res Ctr Digest Dis, Beijing Digest Dis Ctr,Dept Gen Surg, Beijing, Peoples R China.; Zhang, CH (corresponding author), Peking Univ, Canc Hosp & Inst, Dept Gastrointestinal Surg 4, Key Lab Carcinogenesis & Translat Res,Minist Educ, Beijing, Peoples R China.
EM drchenghaizhang@163.com; yicai108@gmail.com; dengweiwei@126.com
RI Li, Bing/GSN-3295-2022; Jing, Chao/JNS-7360-2023; Dong,
   Ningning/HGT-8491-2022; Ma, Tonghui/AAE-1874-2022
OI Ma, Tonghui/0000-0002-5414-0522
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NR 52
TC 2
Z9 2
U1 2
U2 5
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0171-5216
EI 1432-1335
J9 J CANCER RES CLIN
JI J. Cancer Res. Clin. Oncol.
PD AUG
PY 2023
VL 149
IS 9
BP 6139
EP 6150
DI 10.1007/s00432-022-04521-0
EA JAN 2023
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA U4PM3
UT WOS:000919048500001
PM 36680582
DA 2025-01-04
ER

PT J
AU Tawara, M
   Suzuki, H
   Goto, N
   Tanaka, T
   Kaneko, MK
   Kato, Y
AF Tawara, Mayuki
   Suzuki, Hiroyuki
   Goto, Nohara
   Tanaka, Tomohiro
   Kaneko, Mika K. K.
   Kato, Yukinari
TI A Novel Anti-CD44 Variant 9 Monoclonal Antibody C<sub>44</sub>Mab-1 Was
   Developed for Immunohistochemical Analyses against Colorectal Cancers
SO CURRENT ISSUES IN MOLECULAR BIOLOGY
LA English
DT Article
DE CD44; CD44v9; monoclonal antibody; colorectal cancer
ID PODOPLANIN ANTIBODY; BIVATUZUMAB MERTANSINE; GASTRIC-CANCER; STEM-CELLS;
   PA TAG; CD44; EXPRESSION; BIOMARKER; ISOFORMS; ADHESION
AB Cluster of differentiation 44 (CD44) is a type I transmembrane glycoprotein and has been shown to be a cell surface marker of cancer stem-like cells in various cancers. In particular, the splicing variants of CD44 (CD44v) are overexpressed in cancers and play critical roles in cancer stemness, invasiveness, and resistance to chemotherapy and radiotherapy. Therefore, the understanding of the function of each CD44v is indispensable for CD44-targeting therapy. CD44v9 contains the variant 9-encoded region, and its expression predicts poor prognosis in patients with various cancers. CD44v9 plays critical roles in the malignant progression of tumors. Therefore, CD44v9 is a promising target for cancer diagnosis and therapy. Here, we developed sensitive and specific monoclonal antibodies (mAbs) against CD44 by immunizing mice with CD44v3-10-overexpressed Chinese hamster ovary-K1 (CHO/CD44v3-10) cells. We first determined their critical epitopes using enzyme-linked immunosorbent assay and characterized their applications as flow cytometry, western blotting, and immunohistochemistry. One of the established clones, C(44)Mab-1 (IgG(1), kappa), reacted with a peptide of the variant 9-encoded region, indicating that C(44)Mab-1 recognizes CD44v9. C(44)Mab-1 could recognize CHO/CD44v3-10 cells or colorectal cancer cell lines (COLO201 and COLO205) in flow cytometric analysis. The apparent dissociation constant (K-D) of C(44)Mab-1 for CHO/CD44v3-10, COLO201, and COLO205 was 2.5 x 10(-8) M, 3.3 x 10(-8) M, and 6.5 x 10(-8) M, respectively. Furthermore, C(44)Mab-1 was able to detect the CD44v3-10 in western blotting and the endogenous CD44v9 in immunohistochemistry using colorectal cancer tissues. These results indicated that C(44)Mab-1 is useful for detecting CD44v9 not only in flow cytometry or western blotting but also in immunohistochemistry against colorectal cancers.
C1 [Tawara, Mayuki; Suzuki, Hiroyuki; Goto, Nohara; Tanaka, Tomohiro; Kaneko, Mika K. K.; Kato, Yukinari] Tohoku Univ, Grad Sch Med, Dept Mol Pharmaco, 2-1 Seiryo Machi,Aoba Ku, Sendai 9808575, Japan.
   [Kaneko, Mika K. K.; Kato, Yukinari] Tohoku Univ, Grad Sch Med, Dept Antibody Drug Dev, 2-1 Seiryo Machi,Aoba Ku, Sendai 9808575, Japan.
C3 Tohoku University; Tohoku University
RP Suzuki, H; Kato, Y (corresponding author), Tohoku Univ, Grad Sch Med, Dept Mol Pharmaco, 2-1 Seiryo Machi,Aoba Ku, Sendai 9808575, Japan.; Kato, Y (corresponding author), Tohoku Univ, Grad Sch Med, Dept Antibody Drug Dev, 2-1 Seiryo Machi,Aoba Ku, Sendai 9808575, Japan.
EM tawara.mayuki.p8@dc.tohoku.ac.jp; hiroyuki.suzuki.b4@tohoku.ac.jp;
   s1930550@s.tsukuba.ac.jp; tomohiro.tanaka.b5@tohoku.ac.jp;
   mika@med.tohoku.ac.jp; yukinari.kato.e6@tohoku.ac.jp
OI K. Kaneko, Mika/0000-0002-4158-9208; Suzuki,
   Hiroyuki/0000-0003-2646-5132; Kato, Yukinari/0000-0001-5385-8201
FU Japan Agency for Medical Research and Development (AMED) [JP22ama121008,
   JP22am0401013, JP22bm1004001, JP22ck0106730, JP21am0101078]; Japan
   Society for the Promotion of Science (JSPS) [21K20789, 22K06995,
   21K07168, 22K07224]
FX This research was supported in part by Japan Agency for Medical Research
   and Development (AMED) under Grant Numbers JP22ama121008 (to Y.K.),
   JP22am0401013 (to Y.K.), JP22bm1004001 (to Y.K.), JP22ck0106730 (to
   Y.K.), and JP21am0101078 (to Y.K.) and by the Japan Society for the
   Promotion of Science (JSPS) Grants-in-Aid for Scientific Research
   (KAKENHI) under Grant Numbers 21K20789 (to T.T.), 22K06995 (to H.S.),
   21K07168 (to M.K.K.), and 22K07224 (to Y.K.).
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NR 84
TC 9
Z9 11
U1 0
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1467-3037
EI 1467-3045
J9 CURR ISSUES MOL BIOL
JI Curr. Issues Mol. Biol.
PD APR
PY 2023
VL 45
IS 4
BP 3658
EP 3673
DI 10.3390/cimb45040238
PG 16
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA F0JW3
UT WOS:000979305900001
PM 37185762
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Chen, TH
   Wang, ZX
   Zhou, WD
   Chong, ZC
   Meric-Bernstam, F
   Mills, GB
   Chen, K
AF Chen, Tenghui
   Wang, Zixing
   Zhou, Wanding
   Chong, Zechen
   Meric-Bernstam, Funda
   Mills, Gordon B.
   Chen, Ken
TI Hotspot mutations delineating diverse mutational signatures and
   biological utilities across cancer types
SO BMC GENOMICS
LA English
DT Article; Proceedings Paper
CT 5th Variant-Interpretation-Special-Interest-Group Meeting (VarI-SIG)
   held at the Joint ISMB/ECCB Meeting
CY JUL 11, 2015
CL Dublin, IRELAND
SP Variant Interpretat Special Interest Grp, ISMB, ECCB
ID PATHWAY INHIBITORS; DRUG-SENSITIVITY; PI3K PATHWAY; TUMOR TYPES; GENES;
   DISCOVERY; RESOURCE; PIK3CA; IDENTIFICATION; EXPRESSION
AB Background: An important step towards personalizing cancer treatment is to integrate heterogeneous evidences to catalog mutational hotspots that are biologically and therapeutically relevant and thus represent where targeted therapy would likely be beneficial. However, existing methods do not sufficiently delineate varying functionality of individual mutations within the same genes.
   Results: We observed a large discordancy of mutation rates across different mutation subtypes and tumor types, and nominated 702 hotspot mutations in 549 genes in the Catalog of Somatic Mutations in Cancer (COSMIC) by considering context specific mutation characteristics such as genes, cancer types, mutation rates, mutation subtypes and sequence contexts. We observed that hotspot mutations were highly prevalent in Non CpG-island C/G transition and transversion sequence contexts in 10 tumor types, and specific insertion hotspot mutations were enriched in breast cancer and deletion hotspot mutations in colorectal cancer. We found that the hotspot mutations nominated by our approach were significantly more conserved than non-hotspot mutations in the corresponding cancer genes. We also examined the biological significance and pharmacogenomics properties of these hotspot mutations using data in the Cancer Genome Atlas (TCGA) and the Cancer Cell-Line Encyclopedia (CCLE), and found that 53 hotspot mutations are independently associated with diverse functional evidences in 1) mRNA and protein expression, 2) pathway activity, or 3) drug sensitivity and 82 were highly enriched in specific tumor types. We highlighted the distinct functional indications of hotspot mutations under different contexts and nominated novel hotspot mutations such as MAP3K4 A1199 deletion, NR1H2 Q175 insertion, and GATA3 P409 insertion as potential biomarkers or drug targets.
   Conclusion: We identified a set of hotspot mutations across 17 tumor types by considering the background mutation rate variations among genes, tumor subtypes, mutation subtypes, and sequence contexts. We illustrated the common and distinct mutational signatures of hotspot mutations among different tumor types and investigated their variable functional relevance under different contexts, which could potentially serve as a resource for explicitly selecting targets for diagnosis, drug development, and patient management.
C1 [Chen, Tenghui; Wang, Zixing; Zhou, Wanding; Chong, Zechen; Chen, Ken] Univ Texas MD Anderson Canc Ctr, Dept Bioinformat & Computat Biol, Houston, TX 77030 USA.
   [Meric-Bernstam, Funda] Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapy, Houston, TX 77030 USA.
   [Mills, Gordon B.] Univ Texas MD Anderson Canc Ctr, Dept Syst Biol, Houston, TX 77030 USA.
   [Meric-Bernstam, Funda; Mills, Gordon B.] Univ Texas MD Anderson Canc Ctr, Inst Personalized Canc Therapy, Houston, TX 77030 USA.
   [Chen, Tenghui; Mills, Gordon B.; Chen, Ken] Univ Texas Houston, Grad Sch Biomed Sci, Biostat Bioinformat & Syst Biol Program, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; University of
   Texas System; UTMD Anderson Cancer Center; University of Texas System;
   UTMD Anderson Cancer Center; University of Texas System; UTMD Anderson
   Cancer Center; University of Texas System; University of Texas Health
   Science Center Houston
RP Chen, K (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Bioinformat & Computat Biol, Houston, TX 77030 USA.; Chen, K (corresponding author), Univ Texas Houston, Grad Sch Biomed Sci, Biostat Bioinformat & Syst Biol Program, Houston, TX 77030 USA.
EM KChen3@mdanderson.org
RI Chen, Ken/AAU-1432-2021; Mills, Gordon/L-5416-2014; Meric-Bernstam,
   Funda/JRZ-1866-2023; Zhou, Wanding/K-3709-2016
OI Zhou, Wanding/0000-0001-9126-1932; Chen, Ken/0000-0003-4013-5279
FU NCATS NIH HHS [UL1 TR000371] Funding Source: Medline; NCI NIH HHS [U54
   CA112970, P30 CA016672, U24 CA143883, P50 CA083639, P50 CA098258, R01
   CA172652, U01 CA168394] Funding Source: Medline; NHGRI NIH HHS [U41
   HG007497] Funding Source: Medline
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NR 44
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Z9 26
U1 0
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PY 2016
VL 17
SU 2
AR 394
DI 10.1186/s12864-016-2727-x
PG 14
WC Biotechnology & Applied Microbiology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA DQ0NK
UT WOS:000378896000002
PM 27356755
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Fischer, LE
   Stintzing, S
   von Weikersthal, LF
   Modest, DP
   Decker, T
   Kiani, A
   Kaiser, F
   Al-Batran, SE
   Heintges, T
   Lerchenmüller, C
   Kahl, C
   Seipelt, G
   Kullmann, F
   Stauch, M
   Scheithauer, W
   Giessen-Jung, C
   Uhlig, J
   Peuser, B
   Denzlinger, C
   Stahler, A
   Weiss, L
   Heinrich, K
   Held, S
   Jung, A
   Kirchner, T
   Heinemann, V
AF Fischer, Laura E.
   Stintzing, Sebastian
   von Weikersthal, Ludwig Fischer
   Modest, Dominik P.
   Decker, Thomas
   Kiani, Alexander
   Kaiser, Florian
   Al-Batran, Salah-Eddin
   Heintges, Tobias
   Lerchenmueller, Christian
   Kahl, Christoph
   Seipelt, Gernot
   Kullmann, Frank
   Stauch, Martina
   Scheithauer, Werner
   Giessen-Jung, Clemens
   Uhlig, Jens
   Peuser, Bettina
   Denzlinger, Claudio
   Stahler, Arndt
   Weiss, Lena
   Heinrich, Kathrin
   Held, Swantje
   Jung, Andreas
   Kirchner, Thomas
   Heinemann, Volker
TI Efficacy of FOLFIRI plus cetuximab vs FOLFIRI plus bevacizumab in
   1st-line treatment of older patients with <i>RAS</i> wild-type
   metastatic colorectal cancer: an analysis of the randomised trial FIRE-3
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
ID ELDERLY-PATIENTS; OPEN-LABEL; TUMOR CHARACTERISTICS; SUBGROUP ANALYSIS;
   CHEMOTHERAPY; KRAS; CAPECITABINE; PROGNOSIS; SURVIVAL; OPTIONS
AB Background The evidence on the efficacy of anticancer therapy is limited in older patients with metastatic colorectal cancer (mCRC). This retrospective analysis of phase III FIRE-3 trial assesses the efficacy of FOLFIRI plus either cetuximab or bevacizumab according to the patients' age and sidedness of primary tumour. Methods The study endpoints overall response rate (ORR), progression-free survival (PFS) and overall survival (OS) were compared between younger (<65 years) and older (>= 65 years) patients, followed by stratification according to primary tumour sidedness. ORR was compared using Fisher ' s exact test, OS and PFS were estimated by the Kaplan-Meier method and compared using the log-rank test. Univariate Cox regression analyses assessed hazard ratios and 95% confidence intervals for OS and PFS. Results Overall, older patients with RAS WT tumours had a significantly shorter OS when compared to younger patients (25.9 months vs 29.3 months, HR 1.29; P = 0.02). Also the proportion of right-sided tumours was significantly greater in older patients (27.1% vs 17.9%; P = 0.029). Secondary resection rates were numerically higher in younger patients (25.4% vs. 17.6%, P = 0.068) than in older patients. This was primarily seen in the Cetuximab arm, where older patients underwent less likely resection (13.1% vs. 26%; P = 0.02). Older patients with left-sided tumours showed only a trend towards greater efficacy of cetuximab (HR 0.86; P = 0.38). In patients with right-sided primary tumours, older patients did not appear to benefit from cetuximab in contrast to younger patients (>= 65 years: 16.6 months vs 23.6 months, HR 1.1; P = 0.87; P = 0.31). Conclusions In FIRE-3, OS was generally shorter in older patients in comparison to younger patients. This could be explained by the overrepresentation of right-sided tumours and a lower secondary resection rate in older patients. The efficacy of targeted therapy was dependent on tumour sidedness in older patients with RAS WT mCRC.
C1 [Fischer, Laura E.; Giessen-Jung, Clemens; Weiss, Lena; Heinrich, Kathrin; Heinemann, Volker] LMU Univ Hosp Munich, Dept Med 3, Munich, Germany.
   [Stintzing, Sebastian; Modest, Dominik P.; Stahler, Arndt] Charite Univ Med Berlin, Berlin, Germany.
   [Stintzing, Sebastian; Modest, Dominik P.; Stahler, Arndt] Free Univ Berlin, Berlin, Germany.
   [Stintzing, Sebastian; Modest, Dominik P.; Stahler, Arndt] Humboldt Univ, Dept Hematol Oncol & Canc Immunol, Campus Mitte, Berlin, Germany.
   [von Weikersthal, Ludwig Fischer] Gesundheitszentrum St Marien, Amberg, Germany.
   [Decker, Thomas] Onclg Practice, Ravensburg, Germany.
   [Kiani, Alexander] Klinikum Bayreuth GmbH, Bayreuth, Germany.
   [Kaiser, Florian] Onclg Praxis, Landshut, Germany.
   [Al-Batran, Salah-Eddin] Krankenhaus Nordwest Univ, Ctr Canc, Inst Clin Canc Res, Frankfurt, Germany.
   [Heintges, Tobias] Rheinlandklinikum Neuss, Lukaskrankenhaus, Neuss, Germany.
   [Lerchenmueller, Christian] Onclg Practice, Munster, Germany.
   [Kahl, Christoph] Klinikum Magdeburg gGmbH, Dept Hematol Oncol & Palliat Care, Magdeburg, Germany.
   [Kahl, Christoph] Rostock Univ Med Ctr, Clin Hematol Oncol & Palliat Care 3, Dept Internal Med, Rostock, Germany.
   [Seipelt, Gernot] Onclg Practice, Bad Soden, Germany.
   [Kullmann, Frank] Klinikum Weiden, Dept Med 1, Weiden, Germany.
   [Stauch, Martina] Onclg Practice, Kronach, Germany.
   [Scheithauer, Werner] Med Univ Vienna, Dept Internal Med 1, Vienna, Austria.
   [Scheithauer, Werner] Med Univ Vienna, Ctr Comprehens Canc, Vienna, Austria.
   [Uhlig, Jens] Onclg Practice, Naunhof, Germany.
   [Peuser, Bettina] Onklg Praxis Diakonissenhaus, Leipzig, Germany.
   [Denzlinger, Claudio] Marien Hosp, Stuttgart, Germany.
   [Held, Swantje] linAssess GmbH, Leverkusen, Germany.
   [Jung, Andreas; Kirchner, Thomas] Ludwig Maximilians Univ Munchen, Inst Pathol, Munich, Germany.
   [Heinemann, Volker] LMU Univ Hosp Munich, Comprehens Canc Ctr, CCC Munich LMU, Munich, Germany.
C3 University of Munich; Berlin Institute of Health; Free University of
   Berlin; Humboldt University of Berlin; Charite Universitatsmedizin
   Berlin; Free University of Berlin; Humboldt University of Berlin;
   Klinikum Bayreuth; Krankenhaus Nordwest; Medical University of Vienna;
   Medical University of Vienna; St. Marien Hospital; University of Munich;
   University of Munich
RP Fischer, LE (corresponding author), LMU Univ Hosp Munich, Dept Med 3, Munich, Germany.
EM laura.fischer@med.uni-muenchen.de
RI Modest, Dominik Paul/AAW-9756-2021; Stintzing, Sebastian/I-4538-2016
OI Stahler, Arndt/0000-0003-1041-0137; Stintzing,
   Sebastian/0000-0002-3297-5801; Decker, Thomas/0000-0003-3814-8775;
   Fischer, Laura/0000-0001-8752-5827
FU Pfizer GmbH, Germany; Merck KGaA, Darmstadt, Germany; Projekt DEAL
FX The legal funder (sponsor) of the trial is University Hospital, LMU
   Munich. This work was supported by grants from Pfizer GmbH, Germany, and
   Merck KGaA, Darmstadt, Germany. The funding sources had a role in the
   design and conduct of the study, and in the collection, management,
   analysis and interpretation of the data. Prior to 2009, cetuximab was
   supplied by Merck Serono GmbH, an affiliate of Merck KGaA, Darmstadt,
   Germany. Merck KGaA reviewed the paper for medical accuracy only and had
   no role in the decision to submit the paper for publication. The authors
   are fully responsible for the content of this paper, and the views and
   opinions described in the publication solely reflect those of the
   authors. Open Access funding enabled and organized by Projekt DEAL.
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NR 35
TC 6
Z9 6
U1 1
U2 3
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD SEP 1
PY 2022
VL 127
IS 5
BP 836
EP 843
DI 10.1038/s41416-022-01854-y
EA MAY 2022
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 4E3AZ
UT WOS:000802901300001
PM 35637412
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Germani, MM
   Vetere, G
   Santamaria, F
   Intini, R
   Ghelardi, F
   Bensi, M
   Boccaccino, A
   Minelli, A
   Carullo, M
   Ciraci, P
   Passardi, A
   Santucci, S
   Giampieri, R
   Persano, M
   Fenocchio, E
   Puccini, A
   Lonardi, S
   Pietrantonio, F
   Salvatere, L
   Cremolini, C
AF Germani, M. M.
   Vetere, G.
   Santamaria, F.
   Intini, R.
   Ghelardi, F.
   Bensi, M.
   Boccaccino, A.
   Minelli, A.
   Carullo, M.
   Ciraci, P.
   Passardi, A.
   Santucci, S.
   Giampieri, R.
   Persano, M.
   Fenocchio, E.
   Puccini, A.
   Lonardi, S.
   Pietrantonio, F.
   Salvatere, L.
   Cremolini, C.
TI Treatment of patients with BRAFV<SUP>600E</SUP>-mutated metastatic
   colorectal cancer after progression to encorafenib and cetuximab: data
   from a real-world nationwide dataset
SO ESMO OPEN
LA English
DT Article
DE BRAF (V600E) mutation; metastatic colorectal cancer; real-world analysis
ID PLUS CETUXIMAB; CLINICAL CHARACTERISTICS; BRAF(V600E) MUTATION; BRAF;
   CHEMOTHERAPY; BINIMETINIB; INHIBITION; RESISTANCE; SAFETY; TRIAL
AB Background: Targeted therapy (TT) with encorafenib and cetuximab is the current standard for patients with BRAF(V600E)-mutated metastatic colorectal cancer (mCRC) who received one or more prior systemic treatments. However, the median progression-free survival (mPFS) is similar to 4 months, and little is known about the possibility of administering subsequent therapies, their efficacy, and clinicopathological determinants of outcome. Methods: A real-world dataset including patients with BRAF(V600E)-mutated mCRC treated with TT at 21 Italian centers was retrospectively interrogated. We assessed treatments after progression, attrition rates, and outcomes. Results: Of the 179 patients included, 85 (47%), 32 (18%), and 7 (4%) received one, two, or three lines of treatment after TT, respectively. Those receiving TT in the second line were more likely to receive at least one subsequent therapy (53%), as compared with those treated with TT in the third line or beyond (30%; P < 0.0001), and achieved longer postprogression survival (PPS), also in a multivariate model (P = 0.0001). Among 62 patients with proficient mismatch repair/microsatellite stable (pMMR/MSS) tumors receiving one or more lines of treatment after second-line TT, combinatory chemotherapy +/- anti-vascular endothelial growth factor (anti-VEGF) was associated with longer PFS and PPS as compared with trifluridine-tipiracil or regorafenib (mPFS: 2.6 versus 2.0 months, P = 0.07; PPS: 6.5 versus 4.4 months, P = 0.04). Conclusions: Our real-world data suggest that TT should be initiated as soon as possible after the failure of first-line treatment in BRAF(V600E)-mutated mCRC. Among patients with pMMR/MSS tumors, combinatory chemotherapy +/- anti-VEGF appears the preferred treatment choice after TT failure.
C1 [Germani, M. M.; Carullo, M.; Ciraci, P.; Passardi, A.; Cremolini, C.] Univ Pisa, Dept Translat Res & New Technol Med, Pisa, Italy.
   [Germani, M. M.; Carullo, M.; Ciraci, P.; Cremolini, C.] Azienda Osped Univ Pisana, Unit Med Oncol 2, Via Roma 67, I-56126 Pisa, Italy.
   [Vetere, G.; Santamaria, F.] Sapienza Univ Rome, Dept Expt Med, Rome, Italy.
   [Intini, R.] Veneto Inst Oncol IOV IRCCS, Dept Oncol, Padua, Italy.
   [Ghelardi, F.; Pietrantonio, F.] Fdn IRCCS Ist Nazl Tumori, Dept Med Oncol, Milan, Italy.
   [Bensi, M.; Salvatere, L.] Fdn Policlin Univ Agostino Gemelli IRCCS, Comprehens Canc Ctr, Med Oncol Unit, Rome, Italy.
   [Bensi, M.; Salvatere, L.] Univ Cattolica Sacro Cuore, Med Oncol Unit, Rome, Italy.
   [Boccaccino, A.] Ravenna Hosp, AUSL Romagna, Oncol Unit, Ravenna, Italy.
   [Minelli, A.] Univ Campus Biomed, Dept Med Oncol, Rome, Italy.
   [Passardi, A.] IRCCS Ist Romagnolo Studio Tumori IRST Dino Amado, Dept Med Oncol, Meldola, Italy.
   [Santucci, S.; Giampieri, R.] Univ Politecn Marche, Dipartimento Sci Clin & Mol, Oncol Clin, Ancona, Italy.
   [Santucci, S.; Giampieri, R.] Azienda Osped Univ Marche, Oncol Clin, Ancona, Italy.
   [Persano, M.] Univ Hosp Cagliari, Med Oncol, Cagliari, Italy.
   [Persano, M.] Univ Cagliari, Med Oncol, Cagliari, Italy.
   [Fenocchio, E.] Univ Turin, Candiolo Canc Inst, Med Sch, Dept Med Oncol,FPO,IRCCS, Turin, Italy.
   [Puccini, A.] IRCCS Humanitas Res Hosp, Humanitas Canc Ctr, Med Oncol & Hematol Unit, Milan, Italy.
C3 University of Pisa; University of Pisa; Azienda Ospedaliero
   Universitaria Pisana; Sapienza University Rome; IRCCS Istituto
   Oncologico Veneto (IOV); Fondazione IRCCS Istituto Nazionale Tumori
   Milan; Catholic University of the Sacred Heart; IRCCS Policlinico
   Gemelli; Catholic University of the Sacred Heart; IRCCS Policlinico
   Gemelli; AUSL della Romagna; University Campus Bio-Medico - Rome Italy;
   Marche Polytechnic University; University of Cagliari; Azienda
   Ospedaliero-Universitaria di Cagliari; University of Cagliari;
   University of Turin; IRCCS Fondazione del Piemonte per l'Oncologia
RP Cremolini, C (corresponding author), Azienda Osped Univ Pisana, Unit Med Oncol 2, Via Roma 67, I-56126 Pisa, Italy.
EM chiaracremolini@gmail.com
RI Cremolini, Chiara/AAC-1889-2019; Puccini, Alberto/F-3255-2018;
   Pietrantonio, Filippo/C-2180-2017; Bensi, Maria/AAC-5711-2022
OI Pietrantonio, Filippo/0000-0002-8530-8420; Carullo,
   Martina/0000-0003-2846-2517; Vetere, Guglielmo/0000-0001-6943-2897;
   Santamaria, Fiorenza/0000-0002-1214-9342; Ciraci,
   Paolo/0000-0002-3791-6288; Bensi, Maria/0000-0002-5647-0525; Puccini,
   Alberto/0000-0002-2492-4043; GERMANI, MARCO MARIA/0000-0002-1036-5869;
   CREMOLINI, CHIARA/0000-0002-0520-4841
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NR 29
TC 3
Z9 3
U1 0
U2 0
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2059-7029
J9 ESMO OPEN
JI ESMO Open
PD APR
PY 2024
VL 9
IS 4
AR 102996
DI 10.1016/j.esmoop.2024.102996
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SQ6M9
UT WOS:001235957000001
PM 38613911
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Lee, SF
   Choi, HCW
   Chan, SK
   Lam, KO
   Lee, VHF
   Wong, IOL
   Chiang, CL
AF Lee, Shing Fung
   Choi, Horace C. W.
   Chan, Sik Kwan
   Lam, Ka On
   Lee, Victor H. F.
   Wong, Irene O. L.
   Chiang, Chi Leung
TI Cost-Effectiveness of Anti-Epidermal Growth Factor Receptor Therapy
   <i>Versus</i> Bevacizumab in KRAS Wild-Type (WT), Pan-RAS WT, and
   Pan-RAS WT Left-Sided Metastatic Colorectal Cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colorectal cancer; economic evaluation; decision-making; economic
   evidence; simulation models
ID PLUS CETUXIMAB TREATMENT; 1ST-LINE TREATMENT; TUMOR LOCATION;
   CHEMOTHERAPY; MUTATIONS; FLUOROURACIL; OXALIPLATIN; LEUCOVORIN;
   SURVIVAL; METAANALYSIS
AB Objectives
   We aimed to compare the economic value of chemotherapy plus anti-epidermal growth factor receptor (anti-EGFR) monoclonal antibody (mAb) against chemotherapy with bevacizumab (Bev, an anti-vascular endothelial growth factor mAb) as first-line treatment in KRAS wild-type (WT), pan-RAS WT and pan-RAS WT left-sided metastatic colorectal cancer (mCRC) patients from the Hong Kong societal perspective.
   Materials and Methods
   We developed Markov models and 10-year horizon to estimate costs, quality-adjusted life years (QALYs), and incremental cost-effectiveness ratio (ICER) of chemotherapy plus anti-EGFR therapy against chemotherapy plus Bev in KRAS WT, pan-RAS WT, and pan-RAS WT left-sided mCRC. We considered two times of the local gross domestic product per capita (GDPpc) as the willingness-to-pay (WTP) threshold (2x GDPpc; US$97,832).
   Results
   Adding anti-EGFR mAb to chemotherapy provides additional 0.24 (95% confidence interval [CI] 0.19-0.29), 0.32 (95% CI 0.27-0.37), and 0.57 (95% CI 0.49-0.63) QALY compared to adding Bev in KRAS WT, pan-RAS WT, and left-sided pan-RAS WT mCRC populations respectively. The corresponding ICER is US$106,847 (95% CI 87,806-134,523), US$88,565 (95% CI 75,678-105,871), US$76,537 (95% CI 67,794-87,917) per QALY gained, respectively.
   Conclusions
   Anti-EGFR therapy is more cost-effective than Bev as a first-line targeted therapy in left-sided pan-RAS WT and pan-RAS WT, with ICER <US$100,000/QALY, compared to KRAS WT mCRC population.
C1 [Lee, Shing Fung; Chiang, Chi Leung] Tuen Mun Hosp, Dept Clin Oncol, Hong Kong, Peoples R China.
   [Choi, Horace C. W.; Chan, Sik Kwan; Lam, Ka On; Lee, Victor H. F.; Chiang, Chi Leung] Univ Hong Kong, Dept Clin Oncol, Hong Kong, Peoples R China.
   [Lam, Ka On; Lee, Victor H. F.; Chiang, Chi Leung] Univ Hong Kong, Clin Oncol Ctr, Shenzhen Hosp, Shenzhen, Peoples R China.
   [Wong, Irene O. L.] Univ Hong Kong, Sch Publ Hlth, Shenzhen, Peoples R China.
C3 Tuen Mun Hospital; University of Hong Kong; University of Hong Kong;
   University of Hong Kong
RP Chiang, CL (corresponding author), Tuen Mun Hosp, Dept Clin Oncol, Hong Kong, Peoples R China.; Chiang, CL (corresponding author), Univ Hong Kong, Dept Clin Oncol, Hong Kong, Peoples R China.; Chiang, CL (corresponding author), Univ Hong Kong, Clin Oncol Ctr, Shenzhen Hosp, Shenzhen, Peoples R China.
EM chiangcl@hku.hk
RI Lee, Victor/I-3554-2015; Chan, Sik/AAQ-2918-2021; Lee,
   Shing/N-9653-2019; Lam, Ka/D-7948-2011
OI Lee, Victor/0000-0002-6283-978X; Choi, Horace/0000-0001-8387-8780;
   Chiang, Chi-Leung/0000-0002-9836-6478
FU Health and Medical Research Fund, FHB, Hong Kong SAR [HMRF/15161781]
FX This work is supported by the Health and Medical Research Fund, FHB,
   Hong Kong SAR (HMRF/15161781).
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   Venook AP, 2017, J CLIN ONCOL, V35, DOI 10.1200/JCO.2017.35.15_suppl..3503
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NR 47
TC 5
Z9 5
U1 1
U2 7
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD MAY 3
PY 2021
VL 11
AR 651299
DI 10.3389/fonc.2021.651299
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SD1PG
UT WOS:000651138600001
PM 34012917
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Boeckx, N
   Op de Beeck, K
   Beyens, M
   Deschoolmeester, V
   Hermans, C
   De Clercq, P
   Garrigou, S
   Normand, C
   Monsaert, E
   Papadimitriou, K
   Laurent-Puig, P
   Pauwels, P
   Van Camp, G
   Taly, V
   Peeters, M
AF Boeckx, Nele
   Op de Beeck, Ken
   Beyens, Matthias
   Deschoolmeester, Vanessa
   Hermans, Christophe
   De Clercq, Peggy
   Garrigou, Sonia
   Normand, Corinne
   Monsaert, Els
   Papadimitriou, Konstantinos
   Laurent-Puig, Pierre
   Pauwels, Patrick
   Van Camp, Guy
   Taly, Valerie
   Peeters, Marc
TI Mutation and Methylation Analysis of Circulating Tumor DNA Can Be Used
   for Follow-up of Metastatic Colorectal Cancer Patients
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE Biomarker; Digital droplet PCR; Liquid biopsies; mCRC; NPY
ID CELL-FREE DNA; PERSONALIZED MEDICINE; TARGETED THERAPY; KRAS MUTATIONS;
   LUNG-CANCER; MUTANT-DNA; MARKER; PLASMA; BIOMARKERS
AB Improvements in follow-up methods of metastatic colorectal cancer patients during treatment are warranted to ensure response to therapy. The potential of circulating tumor DNA ( ctDNA) for follow-up was investigated using methylation and mutation analyses in different blood samples collected during treatment. Our results corresponded to the results of radiographic evaluation, and therefore the analysis of ctDNA is valuable to complement current follow-up methods.
   Background: Targeted therapies, although contributing to survival improvement in metastatic colorectal cancer ( mCRC), are expensive and may cause adverse effects. Therefore, confirming that patients are responding to these therapies is extremely important. Currently, follow-up is performed using radiographic evaluation, which has its limitations. Liquid biopsies, reflecting real-time tumor characteristics, hold great potential in monitoring tumor disease.
   Patients and Methods: Blood samples were collected at different time points during treatment of 24 mCRC patients. Mutation and NPY methylation picoliter droplet-based digital PCR ( ddPCR) assays were performed on circulating DNA to investigate whether these assays can be used for disease monitoring. Results: The results of the mutation and methylation assays were correlated with each other and corresponded with the results of radiographic evaluation. There was a steep decrease in circulating tumor DNA levels immediately after treatment initiation. Furthermore, circulating tumor DNA levels were increased in progressive samples and were undetectable in patients undergoing curative surgery. Conclusion: This prospective study showed that tumor-specific mutation and NPY methylation ddPCR assays performed on circulating DNA can be used for the follow-up of mCRC patients during treatment and could complement current follow-up methods. The analysis of NPY methylation is promising, as it has the additional advantage that no prior knowledge of tumor mutations is needed. (C) 2018 Elsevier Inc. All rights reserved.
C1 [Boeckx, Nele; Op de Beeck, Ken; Beyens, Matthias; Deschoolmeester, Vanessa; Hermans, Christophe; Pauwels, Patrick; Van Camp, Guy; Peeters, Marc] Univ Antwerp, Ctr Oncol Res CORE, Antwerp, Belgium.
   [Boeckx, Nele; Op de Beeck, Ken; Beyens, Matthias; Van Camp, Guy] Univ Antwerp, Ctr Med Genet, Antwerp, Belgium.
   [Boeckx, Nele; Op de Beeck, Ken; Beyens, Matthias; Van Camp, Guy] Univ Antwerp Hosp, Antwerp, Belgium.
   [Hermans, Christophe; Pauwels, Patrick] Antwerp Univ Hosp, Dept Pathol, Antwerp, Belgium.
   [De Clercq, Peggy; Papadimitriou, Konstantinos; Peeters, Marc] Antwerp Univ Hosp, Dept Oncol, Wilrijkstr 10, B-2650 Antwerp, Belgium.
   [Garrigou, Sonia; Normand, Corinne; Laurent-Puig, Pierre; Taly, Valerie] Paris Descartes Univ, CNRS, INSERM, SNC5014,UMR S1147,Equipe labellisee Ligue Nationa, Paris, France.
   [Monsaert, Els] Dept Gastroenterol, Ghent, Belgium.
   [Monsaert, Els] Integrated Canc Ctr, Ghent, Belgium.
   [Laurent-Puig, Pierre] Hop Europeen Georges Pompidou, AP HP, Dept Biol, Paris, France.
C3 University of Antwerp; University of Antwerp; University of Antwerp;
   University of Antwerp; University of Antwerp; Institut National de la
   Sante et de la Recherche Medicale (Inserm); Universite Paris Cite;
   Centre National de la Recherche Scientifique (CNRS); Assistance Publique
   Hopitaux Paris (APHP); Universite Paris Cite; Hopital Universitaire
   Europeen Georges-Pompidou - APHP
RP Peeters, M (corresponding author), Antwerp Univ Hosp, Dept Oncol, Wilrijkstr 10, B-2650 Antwerp, Belgium.; Taly, V (corresponding author), Paris Descartes Univ, CNRS, INSERM, SNC5014,UMR S1147, Rue St Peres 45, F-75006 Paris, France.
EM valerie.taly@parisdescartes.fr; marc.peeters@uza.be
RI papadimitriou, konstantinos/IUP-5946-2023; Peeters, Marc/C-5525-2013; de
   Beeck, Ken/J-5248-2016; Laurent-Puig, Pierre/B-2226-2013; TALY,
   VALERIE/N-9766-2014; Van Camp, Guy/F-3386-2013
OI Laurent-Puig, Pierre/0000-0001-8475-5459; TALY,
   VALERIE/0000-0002-3116-8602; Van Camp, Guy/0000-0001-5105-9000; Peeters,
   Marc/0000-0003-4969-2303
FU National Cancer Plan [NKP 29_38]; FWO [G0B4414N]; research grant
   'Emmanuel van der Schueren' from Kom Op Tegen Kanker (Stand up to
   Cancer); Ministere de l'Enseignement Superieur et de la Recherche;
   Universite Parise-Descartes; Centre National de la Recherche
   Scientifique (CNRS); Institut National de la Sante et de la Recherche
   Medicale (INSERM); SIRIC CARPEM; Ligue nationale contre le cancer (LNCC)
   [EL2016.LNCC/VaT]
FX The authors thank the doctors and study nurses of the collaborating
   hospitals (UZA, Maria Middelares Ghent, O.L.V. Van Lourdes Hospital
   Waregem) for patient recruitment. The authors thank all patients for
   participating in the study. Supported in part by grants from the
   National Cancer Plan (NKP 29_38) and FWO (G0B4414N); a research grant
   'Emmanuel van der Schueren' from Kom Op Tegen Kanker (Stand up to
   Cancer); by the Ministere de l'Enseignement Superieur et de la
   Recherche; the Universite Parise-Descartes; the Centre National de la
   Recherche Scientifique (CNRS); the Institut National de la Sante et de
   la Recherche Medicale (INSERM) and the SIRIC CARPEM; and the Ligue
   nationale contre le cancer (LNCC, Program "Equipe labelisee LIGUE,"
   EL2016.LNCC/VaT).
CR Barault L, 2018, GUT, V67, P1995, DOI 10.1136/gutjnl-2016-313372
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NR 31
TC 37
Z9 40
U1 0
U2 19
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1533-0028
EI 1938-0674
J9 CLIN COLORECTAL CANC
JI Clin. Colorectal Canc.
PD JUN
PY 2018
VL 17
IS 2
BP E369
EP E379
DI 10.1016/j.clcc.2018.02.006
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GG8WF
UT WOS:000432978800022
PM 29605591
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Varma, K
   Chauhan, A
   Bhargava, M
   Misra, V
   Srivastava, S
AF Varma, Kachnar
   Chauhan, Aprajita
   Bhargava, Mudita
   Misra, Vatsala
   Srivastava, Sapan
TI Association of different patterns of expression of beta-catenin and
   cyclin D1 with pathogenesis of breast carcinoma
SO INDIAN JOURNAL OF PATHOLOGY AND MICROBIOLOGY
LA English
DT Article
DE Beta-catenin; breast carcinoma; cyclin D1; Wnt signaling pathway
ID WNT SIGNALING PATHWAY; TARGET GENES; CANCER; COMPONENTS; MARKER
AB Background: Beta-catenin and cyclin D1 have attracted considerable attention in recent studies as potential proto-oncogenes in many human cancers especially colonic cancer. Beta-catenin plays multiple roles within the cell such as canonical Wnt signaling where cyclin D1 has been identified as one of its target genes. The role of beta-catenin and cyclin D1 in breast cancer has been evaluated in many studies but not established yet. Materials and Methods: The expression of beta-catenin and cyclin D1 was evaluated in 82 cases of breast carcinoma (BCa) and 32 cases of ductal carcinoma in situ (DCIS) by immunohistochemistry (IHC). Their relationship with clinicopathological features was also investigated. Statistical analysis was done to establish an association. Results: Abnormal expression of beta-catenin (ABE) was seen in 80.2% cases of invasive ductal carcinoma (IDC) and 47% cases of DCIS, while the cyclin D1 positive expression rate was 60.9% and 50%, respectively. In the cases showing ABE, cyclin D1 positivity was 88.1%. ABE showed significant association with high-grade BCa. The most common pattern of ABE was loss of membrane with nuclear positivity which is associated with worst prognosis. In addition, ABE in cases of BCa and DCIS showed concordant patterns. Conclusion: Therefore, an association exists between ABE and cyclin D1 in BCa and its precursor lesions implying that Wnt/beta-catenin oncogenic pathway may have a definite role in breast carcinogenesis and can be used for targeted therapy. Also, different patterns of beta-catenin expression may have prognostic and predictive value.
C1 [Varma, Kachnar; Chauhan, Aprajita; Bhargava, Mudita; Misra, Vatsala] MLN Med Coll, Dept Pathol & Surg, Allahabad, Uttar Pradesh, India.
   [Srivastava, Sapan] Kamla Nehru Mem Hosp, Dept Oncosurg, Allahabad, Uttar Pradesh, India.
C3 Moti Lal Nehru Medical College
RP Varma, K (corresponding author), MLN Med Coll, Dept Pathol, Allahabad, Uttar Pradesh, India.
EM kachnar12@gmail.com
CR Bordonaro M, 2015, WORLD J GASTROENTERO, V21, P8238, DOI 10.3748/wjg.v21.i27.8238
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NR 21
TC 10
Z9 10
U1 0
U2 1
PU WOLTERS KLUWER MEDKNOW PUBLICATIONS
PI MUMBAI
PA WOLTERS KLUWER INDIA PVT LTD , A-202, 2ND FLR, QUBE, C T S  NO 1498A-2
   VILLAGE MAROL, ANDHERI EAST, MUMBAI, 400059, INDIA
SN 0377-4929
EI 0974-5130
J9 INDIAN J PATHOL MICR
JI Indian J. Pathol. Microbiol.
PD JAN-MAR
PY 2020
VL 63
IS 1
BP 13
EP 18
AR PMID 32031116
DI 10.4103/IJPM.IJPM_419_19
PG 6
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA KL8MY
UT WOS:000513673500005
PM 32031116
OA gold
DA 2025-01-04
ER

PT J
AU Yoon, W
   Yoo, Y
   Chae, YS
   Kee, SH
   Kim, BM
AF Yoon, W.
   Yoo, Y.
   Chae, Y. S.
   Kee, S. -H.
   Kim, B. M.
TI Therapeutic advantage of genetically engineered <i>Salmonella
   typhimurium </i>carrying short hairpin RNA against inhibin alpha subunit
   in cancer treatment
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE inhibin alpha subunit (INHA); genetically modified attenuated Salmonella
   typhimurium; RNA interference (RNAi); syngeneic mouse models utilizing
   immunocompetent mice bearing tumors; treatment option for cancer therapy
ID TUMOR-SUPPRESSOR; PROSTATE-CANCER; GENE-THERAPY; EXPRESSION; STRAINS;
   MICE
AB Background: In contrast to its well-known endocrine function, the role of inhibin in cancer development and therapeutic response is unclear. Salmonella, particularly less toxic attenuated Salmonella strains, are used to treat cancer in two ways. First, Salmonella accumulate around tumors, penetrate the cell barrier, and replicate inside the tumors. Second, Salmonella can act as a vehicle for delivering anticancer agents or proapoptotic genes to attack tumors. In this study, we aimed to develop a suitable cancer therapeutic strategy by genetically modifying attenuated Salmonella typhimurium to harbor short hairpin RNA (shRNA) expression plasmids targeting alpha subunit of inhibin (sh-INHA).
   Methods: We analyzed the expression of human INHA in normal and cancer cells and tissues. We developed genetically engineered attenuated S. typhimurium harboring sh-INHA (S. typhimurium/sh-INHA) and assessed its cancer therapeutic effects by using cell culture models and syngeneic mouse tumor models.
   Results: INHA expression levels were markedly higher in colon cancer and melanoma cells and tissues than in their normal counterparts. Suppression of INHA expression mildly reduced cancer cell survival and induced caspase activation and downregulation of anti-apoptotic Bcl-2 and Bcl-xL expressions. Although the genetically engineered S. typhimurium mildly interfered with the invasion of S. typhimurium into host colon cancer and melanoma cells, S. typhimurium/sh-INHA caused remarkable cytotoxicity in cancer compared with unmodified S. typhimurium or S. typhimurium expressing a control scrambled shRNA (S. typhimurium/sh-Cont). Salmonella typhimurium/sh-INHA-treated mice also showed a significantly inhibited growth of colon cancers and melanomas, with a survival advantage.
   Conclusion: Our results suggest that tumor-targeted therapy using S. typhimurium/sh-INHA may provide a novel cancer treatment option.
C1 [Yoon, W.; Yoo, Y.] Korea Univ, Coll Med, Allergy Immunol Ctr, Seoul, South Korea.
   [Yoon, W.; Yoo, Y.] Korea Univ, Coll Med, Environm Hlth Ctr, Seoul, South Korea.
   [Yoo, Y.] Korea Univ, Coll Med, Dept Pediat, Seoul, South Korea.
   [Chae, Y. S.] Korea Univ, Coll Med, Dept Pathol, Seoul, South Korea.
   [Kee, S. -H.] Korea Univ, Coll Med, Dept Microbiol, Seoul, South Korea.
   [Kim, B. M.] Yonsei Univ, Coll Med, Severance Integrat Res Inst Cerebral & Cardiovasc, 50 Yonsei Ro, Seoul 03722, South Korea.
C3 Korea University; Korea University Medicine (KU Medicine); Korea
   University; Korea University Medicine (KU Medicine); Korea University;
   Korea University Medicine (KU Medicine); Korea University; Korea
   University Medicine (KU Medicine); Korea University; Korea University
   Medicine (KU Medicine); Yonsei University; Yonsei University Health
   System
RP Kim, BM (corresponding author), Yonsei Univ, Coll Med, Severance Integrat Res Inst Cerebral & Cardiovasc, 50 Yonsei Ro, Seoul 03722, South Korea.
EM bkim2@yuhs.ac
OI Yoon, wonsuck/0000-0002-7665-7629; Kim, Byeong Mo/0000-0002-0582-3132
FU Korea Healthcare Technology R&D Project, Ministry for Health & Welfare
   Affairs, Republic of Korea [HI08C2149]; Yonsei University College of
   Medicine [2016-32-0061, 2017-32-0099]; Basic Science Research Program
   through the NRF - Ministry of Education [2016R1D1A1B03930899]
FX This study was also supported by a grant from the Korea Healthcare
   Technology R&D Project, Ministry for Health & Welfare Affairs, Republic
   of Korea (No. HI08C2149), by a faculty research grant from Yonsei
   University College of Medicine for 2016 (No. 2016-32-0061) and 2017 (No.
   2017-32-0099), and by Basic Science Research Program through the NRF
   funded by the Ministry of Education (No. 2016R1D1A1B03930899) to BMK.
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NR 12
TC 31
Z9 33
U1 2
U2 13
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
EI 1569-8041
J9 ANN ONCOL
JI Ann. Oncol.
PD SEP
PY 2018
VL 29
IS 9
BP 2010
EP 2017
DI 10.1093/annonc/mdy240
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GV4RL
UT WOS:000446087800020
PM 30016386
OA hybrid
DA 2025-01-04
ER

PT J
AU Mauri, G
   Bonazzina, E
   Amatu, A
   Tosi, F
   Bencardino, K
   Gori, V
   Massihnia, D
   Cipani, T
   Spina, F
   Ghezzi, S
   Siena, S
   Sartore-Bianchi, A
AF Mauri, Gianluca
   Bonazzina, Erica
   Amatu, Alessio
   Tosi, Federica
   Bencardino, Katia
   Gori, Viviana
   Massihnia, Daniela
   Cipani, Tiziana
   Spina, Francesco
   Ghezzi, Silvia
   Siena, Salvatore
   Sartore-Bianchi, Andrea
TI The Evolutionary Landscape of Treatment for <i>BRAF<SUP>V600E</SUP></i>
   Mutant Metastatic Colorectal Cancer
SO CANCERS
LA English
DT Review
DE BRAF; colon cancer; immune checkpoint inhibitors; targeted agents;
   FOLFOXIRI
ID FOLFOXIRI PLUS BEVACIZUMAB; CLINICAL-PRACTICE GUIDELINES; KRAS
   WILD-TYPE; BRAF MUTATION; MICROSATELLITE INSTABILITY;
   ACQUIRED-RESISTANCE; 1ST-LINE TREATMENT; RAS MUTATIONS; OPEN-LABEL;
   POOLED ANALYSIS
AB Simple Summary
   The BRAF(V600E) mutation accounts for 8-10% of metastatic colorectal cancer (mCRC) patients and it is an established prognostic factor. Median overall survival of this subset of patients is indeed so poor that it is similar to first line PFS of patients without this molecular alteration. An exception is represented by patients displaying concomitant MSI-H status who can benefit from immunotherapy with checkpoint inhibitors (CPIs). Recently, a targeted therapy with the combination of encorafenib and cetuximab provided for the first time a survival gain and thus translation in the clinic, even though acquired resistance limits the possibility of more than an incremental benefit. Many studies exploiting other different strategies are ongoing. In this review we present current therapies specifically headed to BRAF(V600E) mutant mCRC and systematically review ongoing clinical trials identifying different approaches under investigations: targeting MAPK pathway (monotherapy or combinations), targeting MAPK pathway combined with cytotoxic agents, intensive cytotoxic regimen combinations, targeted agents combined with CPIs, oxidative stress induction, and cytotoxic agents combined with antiangiogenic drugs and CPIs.
   The BRAF(V600E) mutation is found in 8-10% of metastatic colorectal cancer (mCRC) patients and it is recognized as a poor prognostic factor with a median overall survival inferior to 20 months. At present, besides immune checkpoint inhibitors (CPIs) for those tumors with concomitant MSI-H status, recommended treatment options include cytotoxic chemotherapy + anti-VEGF in the first line setting, and a combination of EGFR and a BRAF inhibitor (cetuximab plus encorafenib) in second line. However, even with the latter targeted approach, acquired resistance limits the possibility of more than an incremental benefit and survival is still dismal. In this review, we discuss current treatment options for this subset of patients and perform a systematic review of ongoing clinical trials. Overall, we identified six emerging strategies: targeting MAPK pathway (monotherapy or combinations), targeting MAPK pathway combined with cytotoxic agents, intensive cytotoxic regimen combinations, targeted agents combined with CPIs, oxidative stress induction, and cytotoxic agents combined with antiangiogenic drugs and CPIs. In the future, the integration of new therapeutic strategies targeting key players in the BRAF(V600E) oncogenic pathways with current treatment approach based on cytotoxic chemotherapy and surgery is likely to redefine the treatment landscape of these CRC patients.
C1 [Mauri, Gianluca; Bonazzina, Erica; Amatu, Alessio; Tosi, Federica; Bencardino, Katia; Gori, Viviana; Massihnia, Daniela; Cipani, Tiziana; Spina, Francesco; Ghezzi, Silvia; Siena, Salvatore; Sartore-Bianchi, Andrea] Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, I-20162 Milan, Italy.
   [Mauri, Gianluca; Gori, Viviana; Massihnia, Daniela; Siena, Salvatore; Sartore-Bianchi, Andrea] Univ Milan, Dipartimento Oncol EmatoOncol, I-20122 Milan, Italy.
C3 University of Milan
RP Sartore-Bianchi, A (corresponding author), Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, I-20162 Milan, Italy.; Sartore-Bianchi, A (corresponding author), Univ Milan, Dipartimento Oncol EmatoOncol, I-20122 Milan, Italy.
EM gianluca.mauri@ospedaleniguarda.it;
   ericafrancesca.bonazzina@ospedaleniguarda.it;
   alessio.amatu@ospedaleniguarda.it; federica.tosi@ospedaleniguarda.it;
   katiabruna.bencardino@ospedaleniguarda.it;
   yiyiana.gori@ospedaleniguarda.it; daniela.massihnia@ospedaleniguarda.it;
   tiziana.cipani@ospedaleniguarda.it; francesco.spina@ospedaleniguarda.it;
   silvia.ghezzi@ospedaleniguarda.it; salyatore.siena@unimi.it;
   andrea.sartorebianchi@unimi.it
RI TOSI, FEDERICA MARIA/AIA-1174-2022; Siena, Salvatore/ACK-2413-2022;
   Sartore-Bianchi, Andrea/AAB-9848-2019; Amatu, Alessio/K-2669-2018
OI Sartore-Bianchi, Andrea/0000-0003-0780-0409; Amatu,
   Alessio/0000-0001-5396-3378; Mauri, Gianluca/0000-0002-7646-0973; TOSI,
   FEDERICA MARIA/0000-0001-6146-7411
FU Fondazione Regionale Ricerca Biomedica Regione Lombardia [CP 12/2018
   IANG CRC]; H2020 [635342-2 MoTriColor]; AIRC IG [20685]; Fondazione
   Oncologia Niguarda Onlus; FONDAZIONE AIRC [21091]
FX The work of the authors is supported, in part, by Fondazione Regionale
   Ricerca Biomedica Regione Lombardia, Project CP 12/2018 IANG CRC (S.S.,
   A.S.-B.); H2020 grant agreement no. 635342-2 MoTriColor (S.S.); AIRC IG
   no. 20685 (S.S.); Terapia Molecolare Tumori by Fondazione Oncologia
   Niguarda Onlus (A.S.-B. and S.S.); FONDAZIONE AIRC under 5 per Mille
   2018-ID. 21091 program-G.L. Siena Salvatore.
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NR 75
TC 48
Z9 49
U1 0
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JAN
PY 2021
VL 13
IS 1
AR 137
DI 10.3390/cancers13010137
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PP4IT
UT WOS:000605828500001
PM 33406649
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Sadat, SMA
   Paiva, IM
   Shire, Z
   Sanaee, F
   Morgan, TDR
   Paladino, M
   Karimi-Busheri, F
   Mani, RS
   Martin, GR
   Jirik, FR
   Hall, DG
   Weinfeld, M
   Lavasanifar, A
AF Sadat, Sams M. A.
   Paiva, Igor M.
   Shire, Zahra
   Sanaee, Forughalsadat
   Morgan, Timothy D. R.
   Paladino, Marco
   Karimi-Busheri, Feridoun
   Mani, Rajam S.
   Martin, Gary R.
   Jirik, Frank R.
   Hall, Dennis G.
   Weinfeld, Michael
   Lavasanifar, Afsaneh
TI A synthetically lethal nanomedicine delivering novel inhibitors of
   polynucleotide kinase 3′-phosphatase (PNKP) for targeted therapy of
   PTEN-deficient colorectal cancer
SO JOURNAL OF CONTROLLED RELEASE
LA English
DT Article
DE PNKP; PTEN; Synthetic lethality; Colorectal cancer; CETSA; Nanoparticle
ID POLYMERIC MICELLES; CREMOPHOR-EL; IN-VITRO; PACLITAXEL;
   PHARMACOKINETICS; DOXORUBICIN; PIK3CA; KRAS; POLYMORPHISMS; METASTASES
AB Phosphatase and TENsin homolog deleted on chromosome 10 (PTEN) is a major tumor-suppressor protein that is lost in up to 75% of aggressive colorectal cancers (CRC). The co-depletion of PTEN and a DNA repair protein, polynucleotide kinase 3 '-phosphatase (PNKP), has been shown to lead to synthetic lethality in several cancer types including CRC. This finding inspired the development of novel PNKP inhibitors as potential new drugs against PTEN-deficient CRC. Here, we report on the in vitro and in vivo evaluation of a nano-encapsulated potent, but poorly water-soluble lead PNKP inhibitor, A83B4C63, as a new targeted therapeutic for PTEN-deficient CRC. Our data confirmed the binding of A83B4C63, as free or nanoparticle (NP) formulation, to intracellular PNKP using the cellular thermal shift assay (CETSA), in vitro and in vivo. Dose escalating toxicity studies in healthy CD-1 mice, based on measurement of animal weight changes and biochemical blood analysis, revealed the safety of both free and nano-encapsulated A83B4C63, at assessed doses of <= 50 mg/kg. Nano-carriers of A83B4C63 effectively inhibited the growth of HCT116/PTEN-/- xenografts in NIH-III nude mice following intravenous (IV) administration, but not that of wild-type HCT116/PTEN+/+ xenografts. This was in contrast to IV administration of A83B4C63 solubilized with the aid of Cremophor EL: Ethanol (CE), which led to similar tumor growth to that of formulation excipients (NP or CE without drug) or 5% dextrose. This observation was attributed to the higher levels of A83B4C63 delivered to tumor tissue by its NP formulation. Our data provide evidence for the success of NPs of A83B4C63, as novel synthetically lethal nano-therapeutics in the treatment of PTEN-deficient CRC. This research also highlights the potential of successful application of nanomedicine in the drug development process.
C1 [Sadat, Sams M. A.; Paiva, Igor M.; Sanaee, Forughalsadat; Lavasanifar, Afsaneh] Univ Alberta, Fac Pharm & Pharmaceut Sci, Edmonton, AB, Canada.
   [Shire, Zahra; Karimi-Busheri, Feridoun; Mani, Rajam S.; Weinfeld, Michael] Univ Alberta, Fac Med & Dent, Dept Oncol, Edmonton, AB T6G 1Z2, Canada.
   [Morgan, Timothy D. R.; Paladino, Marco; Hall, Dennis G.] Univ Alberta, Fac Sci, Dept Chem, Edmonton, AB, Canada.
   [Shire, Zahra; Weinfeld, Michael] Cross Canc Inst, Dept Expt Oncol, Calgary, AB, Canada.
   [Martin, Gary R.; Jirik, Frank R.] Univ Calgary, Dept Biochem & Mol Biol, Calgary, AB, Canada.
   [Martin, Gary R.; Jirik, Frank R.] Univ Calgary, Dept Med, Calgary, AB, Canada.
   [Lavasanifar, Afsaneh] Univ Alberta, Dept Chem & Mat Engn, Edmonton, AB, Canada.
C3 University of Alberta; University of Alberta; University of Alberta;
   University of Calgary; University of Alberta; University of Calgary;
   University of Calgary; University of Alberta
RP Weinfeld, M (corresponding author), Univ Alberta, Fac Med & Dent, Dept Oncol, Edmonton, AB T6G 1Z2, Canada.; Lavasanifar, A (corresponding author), Fac Pharm & Pharmaceut Sci, Edmonton, AB T6G 2E1, Canada.
EM mweinfeld@ualberta.ca; afsaneh@ualberta.ca
RI Karimi-Busheri, Feridoun/AAX-7541-2020; Paiva, Igor/AAB-3769-2022
FU Canadian Institutes of Health Research [MOP 15385, MOP 159757]; Alberta
   Cancer Foundation Transformative Program Project [26603]; Nanomedicine
   Innovation Network (NMIN) grant [2019-T1-06]; Alberta Innovates
   Fellowship; CIHR Fellowship
FX We thank Dr. Mary Hitt, Dr. Raymond Lai, Dr Quincy chu, Dr. Gregory
   Tyrrell, and Moinul Haque in Faculty of Medicine and Dentistry
   (University of Alberta) for their advice and technical assistance. We
   acknowledge Dr Jaber Emami's contribution and advice on the
   interpretation of pharmaokinetic data. We also thank Mesfin Fanta and
   Xiaoyan Yang (Cross Cancer Institute, Edmonton, Canada) for their
   support. We also thank Hao Fu and Dr. Burcin Akgun for support in the
   HPLC analysis and purification of compound A83B4C63. This work was
   supported by grants funded by the Canadian Institutes of Health Research
   (MOP 15385) to M.W. and (MOP 159757) to A.L., the Alberta Cancer
   Foundation Transformative Program Project (26603) and Nanomedicine
   Innovation Network (NMIN) grant (2019-T1-06) to D.H., F.J., A.L., and
   M.W., and both Alberta Innovates and CIHR Fellowships to Sams M. A.
   Sadat. The authors also acknowledge contributions from Alberta Cure
   Cancer Foudnation.
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   Zhou Yuan, 2015, Asian Pac J Cancer Prev, V16, P1605
NR 62
TC 12
Z9 13
U1 2
U2 18
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-3659
EI 1873-4995
J9 J CONTROL RELEASE
JI J. Control. Release
PD JUN 10
PY 2021
VL 334
BP 335
EP 352
DI 10.1016/j.jconrel.2021.04.034
EA MAY 2021
PG 18
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA SN5ZK
UT WOS:000658367200006
PM 33933518
OA hybrid
DA 2025-01-04
ER

PT J
AU Elsafadi, M
   Manikandan, M
   Almalki, S
   Mahmood, A
   Shinwari, T
   Vishnubalaji, R
   Mobarak, M
   Alfayez, M
   Aldahmash, A
   Kassem, M
   Alajez, NM
AF Elsafadi, Mona
   Manikandan, Muthurangan
   Almalki, Sami
   Mahmood, Amer
   Shinwari, Tasneem
   Vishnubalaji, Radhakrishnan
   Mobarak, Mohammad
   Alfayez, Musaad
   Aldahmash, Abdullah
   Kassem, Moustapha
   Alajez, Nehad M.
TI Transgelin is a poor prognostic factor associated with advanced
   colorectal cancer (CRC) stage promoting tumor growth and migration in a
   TGFβ-dependent manner
SO CELL DEATH & DISEASE
LA English
DT Article
ID ACTIN-BINDING PROTEIN; EXPRESSION; METASTASIS; TGF-BETA-1; CARCINOMA;
   INVASION; GENE; SM22
AB Colorectal cancer (CRC) is the fourth most common cancer type globally. Investigating the signaling pathways that maintain cancer cell phenotype can identify new biomarkers for targeted therapy. Aberrant transforming growth factor-beta (TGF beta) signaling has been implicated in CRC progression, however, the exact mechanism by which TGF beta exerts its function is still being unraveled. Herein, we investigated TAGLN expression, prognostic value, and its regulation by TGF beta in CRC. While TAGLN was generally found to be downregulated in CRC, elevated expression of TAGLN was associated with advanced CRC stage and predicted poor overall survival (hazard ratio (HR)=1.8, log-rank test P-value=0.014) and disease-free survival (HR=1.6, log-rank test P-value=0.046), hence implicating TAGLN as poor prognostic factor in CRC. Forced expression of TAGLN was associated with enhanced CRC cell proliferation, clonogenic growth, cell migration and in vivo tumor formation in immunocompromised mice, while targeted depletion of TAGLN exhibited opposing biological effects. Global gene expression profiling of TAGLN-overexpressing or TAGLN-deficient CRC cell lines revealed deregulation of multiple cancer-related genes and signaling pathways. Transmission electron microscopy (TEM) revealed ultrastructural changes due to loss of TAGLN, including disruption of actin cytoskeleton organization and aberrant actin filament distribution. Hierarchical clustering, principle component, and ingenuity pathway analyses revealed distinct molecular profile associated with TAGLN(high) CRC patients with remarkable activation of a number of mechanistic networks, including SMARCA4, TGF beta 1, and P38 MAPK. The P38 MAPK was the top predicted upstream regulator network promoting cell movement through regulation of several intermediate molecules, including TGF beta 1. Concordantly, functional categories associated with cellular movement and angiogenesis were also enriched in TAGLN(high) CRC, supporting a model for the molecular mechanisms linking TGF beta -induced upregulation of TAGLN and CRC tumor progression and suggesting TAGLN as potential prognostic marker associated with advanced CRC pathological stage.
C1 [Elsafadi, Mona; Manikandan, Muthurangan; Almalki, Sami; Mahmood, Amer; Shinwari, Tasneem; Alfayez, Musaad; Aldahmash, Abdullah] King Saud Univ, Dept Anat, Coll Med, Stem Cell Unit, Riyadh 11461, Saudi Arabia.
   [Vishnubalaji, Radhakrishnan; Alajez, Nehad M.] Hamad Bin Khalifa Univ HBKU, Qatar Biomed Res Inst QBRI, Qatar Fdn, Canc Res Ctr, Doha, Qatar.
   [Mobarak, Mohammad] King Saud Univ, Dept Histopathol, Coll Med, Riyadh 11461, Saudi Arabia.
   [Kassem, Moustapha] Univ Hosp Odense, Dept Endocrinol, Mol Endocrinol Unit KMEB, Odense, Denmark.
   [Kassem, Moustapha] Univ Southern Denmark, Odense, Denmark.
C3 King Saud University; Qatar Foundation (QF); Hamad Bin Khalifa
   University-Qatar; Qatar Biomedical Research Institute (QBRI); King Saud
   University; University of Southern Denmark; Odense University Hospital;
   University of Southern Denmark
RP Alajez, NM (corresponding author), Hamad Bin Khalifa Univ HBKU, Qatar Biomed Res Inst QBRI, Qatar Fdn, Canc Res Ctr, Doha, Qatar.
EM nalajez@hbku.edu.qa
RI muthurangan, manikandan/GVU-5356-2022; Kassem, Moustapha/J-7688-2013;
   Mahmood, Amer/HSG-7976-2023; Aldahmash, Abdullah/D-4693-2015
OI muthurangan, manikandan/0000-0003-3057-1851; Alajez,
   Nehad/0000-0002-1546-1091; Elsafadi, Mona/0000-0002-7096-998X
FU Deanship of Scientific Research at King Saud University [RG-1438-033]
FX We would like to thank the Deanship of Scientific Research at King Saud
   University (Research Group No. RG-1438-033) for funding this work.
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NR 47
TC 30
Z9 33
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD MAY 11
PY 2020
VL 11
IS 5
DI 10.1038/s41419-020-2529-6
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA LP5GE
UT WOS:000534345100002
PM 32393769
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ubink, I
   Bloemendal, HJ
   Elias, SG
   Brink, MA
   Schwartz, MP
   Holierhoek, YCW
   Verheijen, PM
   Boerman, AW
   Mathijssen, RHJ
   de Leng, WWJ
   de Weger, RA
   van Grevenstein, WMU
   Koopman, M
   Lolkema, MP
   Kranenburg, O
   Rinkes, IHMB
AF Ubink, I.
   Bloemendal, H. J.
   Elias, S. G.
   Brink, M. A.
   Schwartz, M. P.
   Holierhoek, Y. C. W.
   Verheijen, P. M.
   Boerman, A. W.
   Mathijssen, R. H. J.
   de Leng, W. W. J.
   de Weger, R. A.
   van Grevenstein, W. M. U.
   Koopman, M.
   Lolkema, M. P.
   Kranenburg, O.
   Rinkes, I. H. M. Borel
TI Imatinib treatment of poor prognosis mesenchymal-type primary colon
   cancer: a proof-of-concept study in the preoperative window period
   (ImPACCT)
SO BMC CANCER
LA English
DT Article
DE Colon carcinoma; Targeted therapy; Imatinib; Proof-of-concept;
   Pre-operative window; RNA sequencing
ID ADJUVANT TREATMENT; TRIAL; METASTASIS; SUBTYPES; FLUOROURACIL;
   OXALIPLATIN; EXPRESSION; THERAPY
AB Background: The identification of four Consensus Molecular Subtypes (CMS1-4) of colorectal cancer forms a new paradigm for the design and evaluation of subtype-directed therapeutic strategies. The most aggressive subtype CMS4 -has the highest chance of disease recurrence. Novel adjuvant therapies for patients with CMS4 tumours are therefore urgently needed. CMS4 tumours are characterized by expression of mesenchymal and stem-like genes. Previous pre-clinical work has shown that targeting Platelet-Derived Growth Factor Receptors (PDGFRs) and the related KIT receptor with imatinib is potentially effective against mesenchymal-type colon cancer. In the present study we aim to provide proof for the concept that imatinib can reduce the aggressive phenotype of primary CMS4 colon cancer.
   Methods: Tumour biopsies from patients with newly diagnosed stage I-III colon cancer will be analysed with a novel RT-qPCR test to pre-select patients with CMS4 tumours. Selected patients (n = 27) will receive treatment with imatinib (400 mg per day) starting two weeks prior to planned tumour resection. To assess treatment-induced changes in the aggressive CMS4 phenotype, RNA sequencing will be performed on pre-and post-treatment tissue samples.
   Discussion: The development of effective adjuvant therapy for primary colon cancer is hindered by multiple factors. First, new drugs that may have value in the prevention of (early) distant recurrence are almost always first tested in patients with heavily pre-treated metastatic disease. Second, measuring on-target drug effects and biological consequences in tumour tissue is not commonly a part of the study design. Third, due to the lack of patient selection tools, clinical trials in the adjuvant setting require large patient populations. Finally, the evaluation of recurrence-prevention requires a long-term follow-up. In the ImPACCT trial these issues are addressed by including newly diagnosed pre-selected patients with CMS4 tumours prior to primary tumour resection, rather than non-selected patients with late-stage disease. By making use of the pre-operative window period, the biological effect of imatinib treatment on CMS4 tumours can be rapidly assessed. Delivering proof-of-concept for drug action in early stage disease should form the basis for the design of future trials with subtype-targeted therapies in colon cancer patients.
C1 [Ubink, I.; van Grevenstein, W. M. U.; Kranenburg, O.; Rinkes, I. H. M. Borel] Univ Med Ctr Utrecht, Dept Surg Oncol, Canc Ctr, Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands.
   [Bloemendal, H. J.; Koopman, M.] Univ Med Ctr Utrecht, Dept Med Oncol, Canc Ctr, Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands.
   [Bloemendal, H. J.; Boerman, A. W.] Meander Med Ctr, Dept Med Oncol, Maatweg 3, NL-3813 TZ Amersfoort, Netherlands.
   [Elias, S. G.] Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Univ Weg 100, NL-3584 CG Utrecht, Netherlands.
   [Brink, M. A.; Schwartz, M. P.; Holierhoek, Y. C. W.] Meander Med Ctr, Dept Gastroenterol, Maatweg 3, NL-3813 TZ Amersfoort, Netherlands.
   [Verheijen, P. M.] Meander Med Ctr, Dept Surg, Maatweg 3, NL-3813 TZ Amersfoort, Netherlands.
   [Mathijssen, R. H. J.; Lolkema, M. P.] Erasmus MC Canc Inst, Dept Med Oncol, S Gravendijkwal 230, NL-3015 CE Rotterdam, Netherlands.
   [de Leng, W. W. J.; de Weger, R. A.] Univ Med Ctr Utrecht, Dept Pathol, Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands.
C3 Utrecht University; Utrecht University Medical Center; Utrecht
   University; Utrecht University Medical Center; Meander Medisch Centrum;
   Utrecht University; Utrecht University Medical Center; Meander Medisch
   Centrum; Meander Medisch Centrum; Erasmus University Rotterdam; Erasmus
   MC; Erasmus MC Cancer Institute; Utrecht University; Utrecht University
   Medical Center
RP Kranenburg, O; Rinkes, IHMB (corresponding author), Univ Med Ctr Utrecht, Dept Surg Oncol, Canc Ctr, Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands.
EM o.kranenburg@umcutrecht.nl; i.h.m.borelrinkes@umcutrecht.nl
RI Elias, Sjoerd/E-6057-2011; Lolkema, M.P./AAE-2906-2019
OI Mathijssen, Ron/0000-0001-5667-5697; Verheijen,
   Paul/0000-0003-2213-8310; Bloemendal, Haiko/0000-0002-8902-4337;
   Lolkema, Martijn/0000-0003-0466-2928
FU Dutch Cancer Society [UU2014-6617]; ZonMw [95104001]
FX This study is supported by grants from the Dutch Cancer Society
   (UU2014-6617) and ZonMw (95104001). The funders had no involvement in
   the study design, in writing of this manuscript or in the decision to
   submit the paper for publication.
CR Allegra CJ, 2011, J CLIN ONCOL, V29, P11, DOI 10.1200/JCO.2010.30.0855
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NR 26
TC 13
Z9 14
U1 0
U2 1
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD APR 19
PY 2017
VL 17
AR 282
DI 10.1186/s12885-017-3264-y
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ES6OW
UT WOS:000399669300002
PM 28424071
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Elsamany, S
   Elsisi, GH
   Hassanin, FAM
   Saleh, K
   Tashkandi, E
AF Elsamany, Shereef
   Elsisi, Gihan Hamdy
   Hassanin, Fayza Ahmed Mohamed
   Saleh, Khaldoon
   Tashkandi, Emad
TI Cost-Effectiveness of First-Line Cetuximab in Metastatic Colorectal
   Cancer in Saudi Arabia
SO VALUE IN HEALTH REGIONAL ISSUES
LA English
DT Article
DE bevacizumab; cetuximab; cost-effectiveness; metastatic colorectal
   cancer; target therapy
ID PRIMARY TUMOR LOCATION; LIVER METASTASES; CHEMOTHERAPY; BEVACIZUMAB;
   RAS; SURVIVAL; PROGRESSION; ANTIBODIES; THERAPY; LINES
AB Objectives: Our objective was to evaluate the cost-effectiveness of first-line cetuximab in relation to primary tumor location and after resection from the perspective of the Saudi healthcare system over a lifetime horizon.
   Methods: Two standard partitioned survival models were developed in this study comprising 3 health states in each model. The first model was to simulate outcomes and costs of folinic acid, fluorouracil, and irinotecan (FOLFIRI) plus cetuximab compared with FOLFIRI alone in 2 target groups-first, in RAS wild-type left-sided metastatic colorectal cancer (mCRC) and second, in patients administered with 4 cycles of FOLFIRI plus cetuximab, who underwent a resection of liver metastases. The second model compared FOLFIRI plus cetuximab with FOLFIRI plus bevacizumab in wild-type left-sided mCRC and after resection. All cost data and utilities were extracted from published data.
   Results: FOLFIRI plus cetuximab in RAS wild-type left-sided mCRC compared with FOLFIRI alone resulted in an incremental cost-effectiveness ratio of Saudi Riyal (SAR) 180 880 per quality-adjusted life-year (QALY) gained ($102 019; cost-effective). After resection of liver metastases, it resulted in SAR140 442 ($79 211) per QALY gained (cost-effective). When comparing FOLFIRI plus cetuximab with FOLFIRI plus bevacizumab, it resulted in SAR35 818 ($20 201) per QALY gained (highly cost-effective). After resection, it resulted in SAR109 612 ($61822) per QALY gained (highly cost-effective). Thus, FOLFIRI plus cetuximab improved QALYs compared with FOLFIRI plus bevacizumab at the minimized difference in costs in left-sided mCRC and patients with unresectable metastases.
   Conclusion: FOLFIRI plus cetuximab is cost-effective compared with FOLFIRI plus bevacizumab or FOLFIRI alone in RAS wildtype left-sided mCRC and patients who undergo resection.
C1 [Elsamany, Shereef; Tashkandi, Emad] King Abdullah Med City, Oncol Ctr, Mecca, Saudi Arabia.
   [Elsamany, Shereef] Mansoura Univ, Oncol Ctr, Mansoura, Egypt.
   [Elsisi, Gihan Hamdy] HTA Off LLC, Cairo, Egypt.
   [Elsisi, Gihan Hamdy] Cairo Univ, Fac Econ & Polit Sci, Giza, Egypt.
   [Hassanin, Fayza Ahmed Mohamed] King Abdullah Med City, Oncol Nursing, Mecca, Saudi Arabia.
   [Saleh, Khaldoon] King Abdullah Med City, Clin Pharm, Mecca, Saudi Arabia.
   [Tashkandi, Emad] Umm AlQura Univ, Coll Med, Mecca, Saudi Arabia.
C3 King Abdullah Medical City; Egyptian Knowledge Bank (EKB); Mansoura
   University; Egyptian Knowledge Bank (EKB); Cairo University; King
   Abdullah Medical City; King Abdullah Medical City; Umm Al Qura
   University
RP Elsisi, GH (corresponding author), Cairo Univ, Fac Econ & Polit Sci, 51 Helmy Hassan Aly St, Cairo, Egypt.
EM gihan.elsisi@htaoffice.com
RI Elsisi, Gihan/ABE-8471-2020; Tashkandi, Emad/GQP-2634-2022
OI Tashkandi, Emad/0000-0002-0260-8947
FU Merck Serono Middle East FZ-Ltd [4502836386]
FX This work was supported by grant 4502836386 from Merck Serono Middle
   East FZ-Ltd.
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NR 45
TC 2
Z9 2
U1 0
U2 3
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2212-1099
J9 VALUE HEALTH REG ISS
JI Value Health Reg. Iss.
PD MAR
PY 2022
VL 28
BP 67
EP 75
PG 9
WC Health Care Sciences & Services; Health Policy & Services
WE Emerging Sources Citation Index (ESCI)
SC Health Care Sciences & Services
GA 2P9RG
UT WOS:000820068100010
PM 34801961
DA 2025-01-04
ER

PT J
AU Zhang, P
   Li, RD
   Xiao, H
   Liu, WZ
   Zeng, XY
   Xie, GC
   Yang, WC
   Shi, L
   Yin, YP
   Tao, KX
AF Zhang, Peng
   Li, Ruidong
   Xiao, Hua
   Liu, Weizhen
   Zeng, Xiangyu
   Xie, Genchen
   Yang, Wenchang
   Shi, Liang
   Yin, Yuping
   Tao, Kaixiong
TI BRD4 Inhibitor AZD5153 Suppresses the Proliferation of Colorectal Cancer
   Cells and Sensitizes the Anticancer Effect of PARP Inhibitor
SO INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
LA English
DT Article
DE Colorectal cancer; BRD4; AZD5153; PARP inhibitor; targeted therapy
ID BET INHIBITOR; IN-VITRO; BROMODOMAIN; PROTEINS; EXPRESSION
AB Background: Bromodomain-containing protein 4(BRD4) is reported to play a vital role in the development of numerous malignant diseases, which is considered as a promising target for cancer therapy. AZD5153, a novel specific BRD4 inhibitor, showed potent anticancer effects in several cancer types, but its therapeutic potential has not been fully evaluated in colorectal cancer cells.
   Objective: We sought to evaluate the therapeutic potential of BRD4 inhibition of by AZD5153 and its combined anticancer cancer effect with PARP inhibitor BMN673 in vitro and in vivo in colorectal cancer.
   Methods: We analyzed The Cancer Genome Atlas (TCGA) database to investigate BRD4 expression in colorectal cancer patient. Clonogenic assays, MTT assays and PI/Annexin V staining were used to determine the effect of AZD5153 and BMN673 and combination therapy on cell viability and apoptosis induction. Western blotting was applied to detect relevant molecules changes. Propidium iodide staining was performed to examine cell cycle distributions after monotherapy or combination therapy. Nude mice xenograft model was generated to confirm the therapeutic effect of AZD5153 and BMN673 combination in vivo, and IHC staining was used to detect the expression level of BRD4 and related markers in colorectal patient and xenograft.
   Results: Analysis of TCGA database indicated that BRD4 was overexpressed in colorectal cancer patient. The clonogenic and MTT assays and PI/Annexin V staining demonstrated that AZD5153 significantly suppressed cell proliferation and induced apoptosis in colorectal cancer cells HCT116 and LoVo. Western blotting showed that AZD5153 inhibited the expression of c-Myc and increased expression of the apoptosis markers, cleaved caspase-3 and poly(ADP-ribose) polymerase (PARP), besides, we found that BRD4 knockdown could also inhibited cell proliferation and induced cell apoptosis. Moreover, AZD5153 inhibited the expression of Weel and impaired G2M cell cycle checkpoint, thus sensitized the anticancer effect of BMN673 in vitro and in vivo.
   Conclusion: Our data revealed that AZD5153suppressed the proliferation of colorectal cancer cells and sensitized them to the anticancer effect of the PARP inhibitor BMN673 via Weel inhibition in vitro and in vivo. This suggested that targeting BRD4 might be a valuable strategy for colorectal cancer treatment.
C1 [Zhang, Peng; Li, Ruidong; Liu, Weizhen; Zeng, Xiangyu; Xie, Genchen; Yang, Wenchang; Shi, Liang; Yin, Yuping; Tao, Kaixiong] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Gastrointestinal Surg, Wuhan 430022, Hubei, Peoples R China.
   [Xiao, Hua] Cent S Univ, Xiangya Sch Med, Hunan Canc Hosp, Dept Gastroduodenal & Pancreat Surg, 283 Tongzipo Rd, Changsha 410013, Hunan, Peoples R China.
   [Xiao, Hua] Cent S Univ, Xiangya Sch Med, Affiliated Canc Hosp, 283 Tongzipo Rd, Changsha 410013, Hunan, Peoples R China.
C3 Huazhong University of Science & Technology; Central South University;
   Central South University
RP Yin, YP; Tao, KX (corresponding author), 1277 Jiefang Ave, Wuhan 430022, Hubei, Peoples R China.
EM yinyuping2017@hust.edu.cn; kaixiongtao@hust.edu.cn
RI Zeng, Xiangyu/HTL-4612-2023; Yang, Wenchang/C-3245-2015; Zhang,
   Zhao/B-5136-2010
OI Yin, Yuping/0000-0003-4568-8315; xiangyu, zeng/0000-0003-4913-3704
FU national key basic research program of china [2015cb5540007]; national
   science and technology major project [2017yfc0113503]; national natural
   science foundation of china [81572413, 81701883, 81702386, 81874184];
   foundation of independent innovation fund of huazhong university of
   science and technology [2017kfyxjj230]; natural science foundation of
   hubei province [2016cfa100]
FX This study and all the authors were supported by the national key basic
   research program of china (2015cb5540007), the national science and
   technology major project (2017yfc0113503), the national natural science
   foundation of china (no. 81572413, 81701883, 81702386and 81874184), the
   foundation of independent innovation fund of huazhong university of
   science and technology (2017kfyxjj230) and the natural science
   foundation of hubei province (2016cfa100).
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NR 36
TC 40
Z9 53
U1 1
U2 14
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1449-2288
J9 INT J BIOL SCI
JI Int. J. Biol. Sci.
PY 2019
VL 15
IS 9
BP 1942
EP 1954
DI 10.7150/ijbs.34162
PG 13
WC Biochemistry & Molecular Biology; Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics
GA IR6VK
UT WOS:000481578100014
PM 31523195
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Hashemkhani, M
   Demirci, G
   Bayir, A
   Muti, A
   Sennaroglu, A
   Hadi, LM
   Yaghini, E
   Loizidou, M
   MacRobert, AJ
   Acar, HY
AF Hashemkhani, Mahshid
   Demirci, Gozde
   Bayir, Ali
   Muti, Abdullah
   Sennaroglu, Alphan
   Mohammad Hadi, Layla
   Yaghini, Elnaz
   Loizidou, Marilena
   MacRobert, Alexander J.
   Yagci Acar, Havva
TI Cetuximab-Ag<sub>2</sub>S quantum dots for fluorescence imaging and
   highly effective combination of ALA-based photodynamic/chemo-therapy of
   colorectal cancer cells
SO NANOSCALE
LA English
DT Article
ID CONTROLLED DRUG-DELIVERY; GROWTH-FACTOR RECEPTOR; 5-AMINOLEVULINIC ACID;
   NANOPARTICLES; ENHANCEMENT; DERIVATIVES; DESIGN; SW480; PDT
AB Colorectal cancer (CRC) has a poor prognosis and urgently needs better therapeutic approaches. 5-Aminolevulinic acid (ALA) induced protoporphyrin IX (PpIX) based photodynamic therapy (PDT) is already used in the clinic for several cancers but not yet well investigated for CRC. Currently, systemic administration of ALA offers a limited degree of tumour selectivity, except for intracranial tumours, limiting its wider use in the clinic. The combination of effective ALA-PDT and chemotherapy may provide a promising alternative approach for CRC treatment. Herein, theranostic Ag2S quantum dots (AS-2MPA) optically trackable in near-infrared (NIR), conjugated with endothelial growth factor receptor (EGFR) targeting Cetuximab (Cet) and loaded with ALA for PDT monotherapy or ALA/5-fluorouracil (5FU) for the combination therapy are proposed for enhanced treatment of EGFR(+) CRC. AS-2MPA-Cet exhibited excellent targeting of the high EGFR expressing cells and showed a strong intracellular signal for NIR optical detection in a comparative study performed on SW480, HCT116, and HT29 cells, which exhibit high, medium and low EGFR expression, respectively. Targeting provided enhanced uptake of the ALA loaded nanoparticles by strong EGFR expressing cells and formation of higher levels of PpIX. Cells also differ in their efficiency to convert ALA to PpIX, and SW480 was the best, followed by HT29, while HCT116 was determined as unsuitable for ALA-PDT. The therapeutic efficacy was evaluated in 2D cell cultures and 3D spheroids of SW480 and HT29 cells using AS-2MPA with either electrostatically loaded, hydrazone or amide linked ALA to achieve different levels of pH or enzyme sensitive release. Most effective phototoxicity was observed in SW480 cells using AS-2MPA-ALA-electrostatic-Cet due to enhanced uptake of the particles, fast ALA release and effective ALA-to-PpIX conversion. Targeted delivery reduced the effective ALA concentration significantly which was further reduced with codelivery of 5FU. Delivery of ALA via covalent linkages was also effective for PDT, but required a longer incubation time for the release of ALA in therapeutic doses. Phototoxicity was correlated with high levels of reactive oxygen species (ROS) and apoptotic/necrotic cell death. Hence, both AS-2MPA-ALA-Cet based PDT and AS-2MPA-ALA-Cet-5FU based chemo/PDT combination therapy coupled with strong NIR tracking of the nanoparticles demonstrate an exceptional therapeutic effect on CRC cells and excellent potential for synergistic multistage tumour targeting therapy.
C1 [Hashemkhani, Mahshid; Demirci, Gozde; Bayir, Ali; Sennaroglu, Alphan; Yagci Acar, Havva] Koc Univ, Grad Sch Mat Sci & Engn, TR-34450 Istanbul, Turkey.
   [Muti, Abdullah; Sennaroglu, Alphan] Koc Univ, Dept Phys & Elect Elect Engn, TR-34450 Istanbul, Turkey.
   [Sennaroglu, Alphan] Koc Univ, KUYTAM, TR-34450 Istanbul, Turkey.
   [Mohammad Hadi, Layla; Yaghini, Elnaz; Loizidou, Marilena; MacRobert, Alexander J.] UCL, Ctr Nanomed & Surg Theranost, Div Surg & Intervent Sci, Royal Free Campus,Rowland Hill St, London NW3 2PE, England.
   [Yagci Acar, Havva] Koc Univ, Dept Chem, TR-34450 Istanbul, Turkey.
C3 Koc University; Koc University; Koc University; University of London;
   University College London; Koc University
RP Acar, HY (corresponding author), Koc Univ, Grad Sch Mat Sci & Engn, TR-34450 Istanbul, Turkey.; MacRobert, AJ (corresponding author), UCL, Ctr Nanomed & Surg Theranost, Div Surg & Intervent Sci, Royal Free Campus,Rowland Hill St, London NW3 2PE, England.; Acar, HY (corresponding author), Koc Univ, Dept Chem, TR-34450 Istanbul, Turkey.
EM a.macrobert@ucl.ac.uk; fyagci@ku.edu.tr
RI MUTI, ABDULLAH/AAK-8105-2021; Hashemkhani, Mahshid/ABC-9640-2021;
   Sennaroglu, Alphan/Y-9604-2018
OI Demirci, Gozde/0000-0003-4952-7981; Sennaroglu,
   Alphan/0000-0003-4391-0189; Loizidou, Marilena/0000-0002-0900-9795;
   Yagci Acar, Havva/0000-0001-5601-8814; Hashemkhani,
   Mahshid/0000-0002-8436-2214
FU Newton-Katip Celebi Fund (British Council); TUBITAK [216Z131, 334995]
FX The authors would like to thank Dr Gulsu Simek for help on the
   preparation of ICP-MS, respectively. This work was supported partly
   through the Newton-Katip Celebi Fund (British Council and TUBITAK grant
   codes: GA 334995, TUBITAK grant code: 216Z131).
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NR 71
TC 28
Z9 28
U1 1
U2 41
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 2040-3364
EI 2040-3372
J9 NANOSCALE
JI Nanoscale
PD SEP 21
PY 2021
VL 13
IS 35
BP 14879
EP 14899
DI 10.1039/d1nr03507j
EA AUG 2021
PG 21
WC Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials
   Science, Multidisciplinary; Physics, Applied
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science;
   Physics
GA UR7CK
UT WOS:000691694200001
PM 34533177
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Hosseinpour-Soleimani, F
   Salmasi, Z
   Ghasemi, Y
   Tajbakhsh, A
   Savardashtaki, A
AF Hosseinpour-Soleimani, Fatemeh
   Salmasi, Zahra
   Ghasemi, Younes
   Tajbakhsh, Amir
   Savardashtaki, Amir
TI MicroRNAs and proteolytic cleavage of receptors in cancers: A
   comprehensive review of regulatory interactions and therapeutic
   implications
SO HELIYON
LA English
DT Review
DE MicroRNA; miRNA; Soluble receptors; Cancer; Shedding; Targeted therapy;
   Drug resistance
ID HEPATOCELLULAR-CARCINOMA CELLS; TUMOR-SUPPRESSOR MICRORNA; LUNG-CANCER;
   REPLACEMENT THERAPY; COLORECTAL-CANCER; IN-VIVO; PROLIFERATION;
   INVASION; ADAM17; MIGRATION
AB ancer remains a challenging disease worldwide, necessitating innovative approaches to better comprehend its underlying molecular mechanisms and devise effective therapeutic strategies. Over the past decade, microRNAs (miRNAs) have emerged as crucial players in cancer progression due to their regulatory roles in various cellular processes. Moreover, the involvement of unwanted soluble receptors has gained increasing attention because they contribute to tumorigenesis or drug resistance by disrupting normal signaling pathways and neutralizing ligands. This comprehensive review explores the intricate interplay between miRNAs and unwanted-soluble receptors in the context of cancer biology. This study provides an analysis of the regulatory interactions between miRNAs and these receptors, elucidating how miRNAs can either suppress or enhance their expression. MiRNAs can directly target receptor transcripts, thereby regulating soluble receptor levels. They also modulate the proteolytic cleavage of membrane-bound receptors into soluble forms by targeting sheddases, such as ADAMs and MMPs. Furthermore, the review delves into the therapeutic potential of manipulating miRNAs to modulate unwanted soluble receptors. Various strategies, including synthetic miRNA mimics or anti-miRNAs, hold promise for restoring or inhibiting miRNA function to counteract aberrant receptor activity. Moreover, exploring miRNA-based delivery systems may provide targeted and precise therapies that minimizing off-target effects. In conclusion, this review sheds light on the intricate regulatory networks involving miRNAs and unwanted soluble receptors in cancer biology thereby uncovering novel therapeutic targets, and paving the way for developing innovative anti -cancer therapies.
C1 [Hosseinpour-Soleimani, Fatemeh] Shiraz Univ Med Sci, Student Res Comm, Shiraz, Iran.
   [Hosseinpour-Soleimani, Fatemeh] Shiraz Univ Med Sci, Sch Adv Med Sci & Technol, Dept Appl Cell Sci & Tissue Engn, Shiraz, Iran.
   [Salmasi, Zahra] Mashhad Univ Med Sci, Pharmaceut Technol Inst, Nanotechnol Res Ctr, Mashhad, Iran.
   [Salmasi, Zahra] Mashhad Univ Med Sci, Sch Pharm, Dept Pharmaceut Nanotechnol, Mashhad, Iran.
   [Ghasemi, Younes] Shiraz Univ Med Sci, Sch Pharm, Dept Pharmaceut Biotechnol, Shiraz, Iran.
   [Ghasemi, Younes; Tajbakhsh, Amir] Shiraz Univ Med Sci, Pharmaceut Sci Res Ctr, POB 71345-1583, Shiraz, Iran.
   [Tajbakhsh, Amir] Shiraz Univ Med Sci, Sch Adv Med Sci & Technol, Dept Mol Med, Shiraz, Iran.
   [Tajbakhsh, Amir; Savardashtaki, Amir] Shiraz Univ Med Sci, Dept Med Biotechnol, Sch Adv Med Sci & Technol, Shiraz 7136281407, Iran.
   [Savardashtaki, Amir] Shiraz Univ Med Sci, Infertil Res Ctr, Shiraz, Iran.
C3 Shiraz University of Medical Science; Shiraz University of Medical
   Science; Mashhad University of Medical Sciences; Mashhad University of
   Medical Sciences; Shiraz University of Medical Science; Tehran
   University of Medical Sciences; Shiraz University of Medical Science;
   Shiraz University of Medical Science; Shiraz University of Medical
   Science; Shiraz University of Medical Science
RP Tajbakhsh, A (corresponding author), Shiraz Univ Med Sci, Pharmaceut Sci Res Ctr, POB 71345-1583, Shiraz, Iran.; Tajbakhsh, A; Savardashtaki, A (corresponding author), Shiraz Univ Med Sci, Dept Med Biotechnol, Sch Adv Med Sci & Technol, Shiraz 7136281407, Iran.
EM A_tajbakhsh@sums.ac.ir; Dashtaki63@gmail.com
RI Savardashtaki, Amir/M-6041-2018; Tajbakhsh, Amir/AAB-1925-2019; salmasi,
   zahra/C-6617-2018; Tajbakhsh, Amir/HMV-4969-2023
OI Tajbakhsh, Amir/0000-0002-2311-6554
FU Pharmaceutical Sciences Research Center, Shiraz University of Medical
   Sciences
FX Authors wish to thank Pharmaceutical Sciences Research Center, Shiraz
   University of Medical Sciences.
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NR 139
TC 1
Z9 1
U1 4
U2 4
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
EI 2405-8440
J9 HELIYON
JI Heliyon
PD APR 15
PY 2024
VL 10
IS 7
AR e28167
DI 10.1016/j.heliyon.2024.e28167
PG 15
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA RA3F2
UT WOS:001224905900001
PM 38560206
OA gold, Green Accepted
DA 2025-01-04
ER

PT J
AU Gu, JJ
   Wang, CY
   Xu, XX
   Zhao, L
   Zhou, JF
   Bai, CM
   Sun, Z
AF Gu, Junjie
   Wang, Chenyu
   Xu, Xiuxiu
   Zhao, Lin
   Zhou, Jianfeng
   Bai, Chunmei
   Sun, Zhao
TI Immunohistochemical detection of cancer-associated fibroblasts in
   gastrointestinal cancer as a potential prognostic biomarker of survival:
   meta-analysis
SO TRANSLATIONAL CANCER RESEARCH
LA English
DT Article
DE Meta-analysis; prognosis; cancer-associated fibroblasts (CAFs);
   gastrointestinal cancer
ID MESENCHYMAL STEM-CELLS; ACTIVATION PROTEIN; GASTRIC-CANCER; TUMOR
   MICROENVIRONMENT; COLORECTAL-CANCER; POOR-PROGNOSIS; LUNG-CANCER;
   EXPRESSION; CARCINOMA; FAP
AB Background: The association between cancer-associated fibroblasts (CAFs) and prognosis of gastrointestinal cancer patients remains controversial. The purpose of the present article is to assess the role of CAFs in gastrointestinal cancer patients by performing a meta-analysis of the clinical trials published in the literature.
   Methods: Several studies were conducted to compare survival between high proportion of CAFs and low proportion of CAFs in gastrointestinal cancer patients. Search strategies were performed in PubMed, EMBASE, Medline and the Cochrane Library database. Methodological quality was assessed with the Newcastle-Ottawa Quality Assessment Scale (NOS).
   Results: Among 3,763 patients enrolled in 18 studies, the pooled hazard ratio (HR) 1.64 (95% CI, 1.43 to 1.87; P<0.001) for overall survival (OS) indicated that a high proportion of CAFs was associated with shorter OS. Among 3,137 patients in 7 studies, the pooled HR 2.56 (95% CI, 1.55 to 4.22, P<0.001) for disease-free survival (DFS) exhibited that a high proportion of CAFs was associated with higher risk of recurrence. The subgroup analyses based on different tumor types showed consistent results. CAFs had no correlation with age, gender, tumor localization, TNM stage, tumor grade, and tumor type.
   Conclusions: The meta-analysis indicates that high proportion of CAFs is a valuable predictor of the prognosis in gastrointestinal cancer patients, and it may provide new ideas for targeted therapy in gastrointestinal cancer patients.
C1 [Gu, Junjie; Wang, Chenyu; Xu, Xiuxiu; Zhao, Lin; Zhou, Jianfeng; Bai, Chunmei; Sun, Zhao] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Oncol, Beijing, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Peking Union Medical College Hospital
RP Bai, CM; Sun, Z (corresponding author), Peking Union Med Coll Hosp, Dept Oncol, 41 Damucanghutong, Beijing 100032, Peoples R China.
EM baichunmei1964@163.com; jessiesz@126.com
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NR 49
TC 5
Z9 6
U1 0
U2 2
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2218-676X
EI 2219-6803
J9 TRANSL CANCER RES
JI Transl. Cancer Res.
PD NOV
PY 2020
VL 9
IS 11
BP 6629
EP 6638
DI 10.21037/tcr-20-2365
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OX4WB
UT WOS:000593565600002
PM 35117273
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Walter, RFH
   Werner, R
   Wessolly, M
   Mairinger, E
   Borchert, S
   Schmeller, J
   Kollmeier, J
   Mairinger, T
   Hager, T
   Bankfalvi, A
   Christoph, DC
   Eberhardt, WEE
   Plönes, T
   Aigner, C
   Schmid, KW
   Wohlschlaeger, J
   Mairinger, FD
AF Walter, Robert F. H.
   Werner, Robert
   Wessolly, Michael
   Mairinger, Elena
   Borchert, Sabrina
   Schmeller, Jan
   Kollmeier, Jens
   Mairinger, Thomas
   Hager, Thomas
   Bankfalvi, Agnes
   Christoph, Daniel C.
   Eberhardt, Wilfried E. E.
   Ploenes, Till
   Aigner, Clemens
   Schmid, Kurt W.
   Wohlschlaeger, Jeremias
   Mairinger, Fabian D.
TI Inhibition of MDM2 via Nutlin-3A: A Potential Therapeutic Approach for
   Pleural Mesotheliomas with MDM2-Induced Inactivation of Wild-Type P53
SO JOURNAL OF ONCOLOGY
LA English
DT Article
ID PEMETREXED-BASED CHEMOTHERAPY; MESSENGER-RNA LEVELS; DNA-DAMAGE REPAIR;
   THYMIDYLATE SYNTHASE; EMBRYONIC LETHALITY; MDM2-DEFICIENT MICE;
   MUTATIONAL ANALYSIS; COLORECTAL-CANCER; PLUS CARBOPLATIN; PROGNOSTIC
   VALUE
AB Previously, our group demonstrated that nuclear expression of E3 ubiquitin ligase (MDM2) in malignant pleural mesothelioma (MPM) is significantly associated with decreased overall survival. A possible explanation may be that overexpression of MDM2 leads to a proteasomal degradation of TP53 that eventually results in a loss of TP53-induced apoptosis and senescence. It is well known from other tumor entities that restoration of TP53 activity, e.g., by MDM2 inhibition, results in an instant TP53-induced stress and/or DNA damage response of cancer cells. Nutlin-3A (a cis-imidazoline analogue) has been described as a potent and selective MDM2 inhibitor preventing MDM2-TP53-interaction by specific binding to the hydrophobic TP53-binding pocket of MDM2. In the present study, the effects of MDM2 inhibition in MPM via Nutlin-3A and standard platinum based chemotherapeutic agents were comparatively tested in three MPM cell lines (NCI-H2052, MSTO-211H, and NCI-H2452) showing different expression profiles of TP53, MDM2, and its physiological inhibitor of MDM2-P14/ARF. Our in vitro experiments on MPM cell lines revealed that Nutlin-3A in combination with cisplatin resulted in up to 9.75 times higher induction of senescence (p=0.0050) and up to 5 times higher apoptosis rate (p=0.0067) compared to the commonly applied cisplatin and pemetrexed regimens. Thus Nutlin-3A, a potent inhibitor of MDM2, is associated with a significant induction of senescence and apoptosis in MPM cell lines, making Nutlin-3A a promising substance for a targeted therapy in the subgroup of MPM showing MDM2 overexpression.
C1 [Walter, Robert F. H.; Wessolly, Michael; Mairinger, Elena; Borchert, Sabrina; Schmeller, Jan; Hager, Thomas; Bankfalvi, Agnes; Schmid, Kurt W.; Wohlschlaeger, Jeremias; Mairinger, Fabian D.] Univ Duisburg Essen, Univ Hosp Essen, Inst Pathol, Essen, Germany.
   [Walter, Robert F. H.; Mairinger, Elena; Eberhardt, Wilfried E. E.] Univ Duisburg Essen, Univ Hosp Essen, West German Lung Ctr, Ruhrlandklin, Essen, Germany.
   [Werner, Robert; Mairinger, Thomas] Helios Klinikum Emil von Behring, Dept Pathol, Berlin, Germany.
   [Kollmeier, Jens] Helios Klinikum Emil von Behring, Dept Pneumol, Berlin, Germany.
   [Christoph, Daniel C.; Eberhardt, Wilfried E. E.] Univ Duisburg Essen, Univ Hosp Essen, Dept Med Oncol, West German Canc Ctr, Essen, Germany.
   [Christoph, Daniel C.] Kliniken Essen Mitte, Dept Internist Oncol, Essen, Germany.
   [Ploenes, Till; Aigner, Clemens] Univ Duisburg Essen, Univ Hosp Essen, Dept Thorac Surg & Thorac Endoscopy, Ruhrlandklin, Essen, Germany.
   [Wohlschlaeger, Jeremias] Diakonissenkrankenhaus Flensburg, Dept Pathol, Flensburg, Germany.
C3 University of Duisburg Essen; University of Duisburg Essen; Helios
   Kliniken; Helios Kliniken; University of Duisburg Essen; Kliniken
   Essen-Mitte; University of Duisburg Essen
RP Mairinger, FD (corresponding author), Univ Duisburg Essen, Univ Hosp Essen, Inst Pathol, Essen, Germany.
EM fabian.mairinger@uk-essen.de
RI Wessolly, Michael/ACS-2732-2022; Eberhardt, Wilfried/JNS-6276-2023;
   Plönes, Till/AAK-8208-2021; Borchert, Sabrina/Q-3052-2019; Mairinger,
   Thomas/IST-2128-2023; Aigner, Clemens/A-7284-2019; Mairinger, Fabian
   Dominik/IST-1621-2023
OI Kollmeier, Jens/0000-0002-8048-3895; Mairinger,
   Fabian/0000-0003-1067-0051; Aigner, Clemens/0000-0002-7787-991X;
   Borchert, Sabrina/0000-0002-0447-3206; Walter,
   Robert/0000-0003-3725-7064; Schmeller, Jan/0000-0002-2012-2350;
   Wessolly, Michael/0000-0002-4399-8646; Eberhardt, Wilfried Ernst
   Erich/0000-0003-4284-3586
FU Institute of Pathology, University Hospital Essen; Ruhrlandklinik Essen
FX The study was financed by the Institute of Pathology, University
   Hospital Essen, and Ruhrlandklinik Essen.
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NR 68
TC 12
Z9 15
U1 0
U2 6
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1687-8450
EI 1687-8469
J9 J ONCOL
JI J. Oncol.
PY 2018
VL 2018
AR 1986982
DI 10.1155/2018/1986982
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GP0KZ
UT WOS:000440499900001
PM 30112000
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Diao, CL
   Guo, P
   Yang, WJ
   Sun, Y
   Liao, YN
   Yan, Y
   Zhao, AS
   Cai, X
   Hao, JJ
   Hu, S
   Yu, WD
   Chen, MY
   Wang, RZ
   Li, WY
   Zuo, Y
   Pan, JJ
   Hua, CY
   Lu, XN
   Fan, WH
   Zheng, ZH
   Deng, WG
   Luo, GY
   Guo, W
AF Diao, Chaoliang
   Guo, Ping
   Yang, Wenjing
   Sun, Yao
   Liao, Yina
   Yan, Yue
   Zhao, Anshi
   Cai, Xin
   Hao, Jiaojiao
   Hu, Sheng
   Yu, Wendan
   Chen, Manyu
   Wang, Ruozhu
   Li, Wenyang
   Zuo, Yan
   Pan, Jinjin
   Hua, Chunyu
   Lu, Xiaona
   Fan, Wenhua
   Zheng, Zongheng
   Deng, Wuguo
   Luo, Guangyu
   Guo, Wei
TI SPT6 recruits SND1 to co-activate human telomerase reverse transcriptase
   to promote colon cancer progression
SO MOLECULAR ONCOLOGY
LA English
DT Article
DE colorectal cancer; hTERT; SND1; SPT6; transcription regulation
ID INFLAMMATORY-BOWEL-DISEASE; TUMOR ANGIOGENESIS; CATALYTIC SUBUNIT;
   HTERT; METASTASIS; EXPRESSION; SURVIVAL; BREAST; GROWTH; CELLS
AB Human telomerase reverse transcriptase (hTERT) plays an extremely important role in cancer initiation and development, including colorectal cancer (CRC). However, the precise upstream regulatory mechanisms of hTERT in different cancer types remain poorly understood. Here, we uncovered the candidate transcriptional factor of hTERT in CRC and explored its role and the corresponding molecular mechanisms in regulating hTERT expression and CRC survival with an aim of developing mechanism-based combinational targeting therapy. The possible binding proteins at the hTERT promoter were uncovered using pull-down/mass spectrometry analysis. The regulation of SPT6 on hTERT expression and CRC survival was evaluated in human CRC cell lines and mouse models. Mechanistic studies focusing on the synergy between SPT6 and staphylococcal nuclease and Tudor domain containing 1 (SND1) in controlling hTERT expression and CRC progression were conducted also in the above two levels. The expression correlation and clinical significance of SPT6, SND1, and hTERT were investigated in tumor tissues from murine models and patients with CRC in situ. SPT6 was identified as a possible transcriptional factor to bind to the hTERT promoter. SPT6 knockdown decreased the activity of hTERT promoter, downregulated the protein expression level of hTERT, suppressed proliferation, invasion, and stem-like properties, promoted apoptosis induction, and enhanced chemotherapeutic drug sensitivity in vitro. SPT6 silencing also led to the delay of tumor growth and metastasis in mice carrying xenografts of human-derived colon cancer cells. Mechanistically, SND1 interacted with SPT6 to co-control hTERT expression and CRC cell proliferation, stemness, and growth in vitro and in vivo. SPT6, SND1, and hTERT were highly expressed simultaneously in CRC tissues, both from the murine model and patients with CRC in situ, and pairwise expression among these three factors showed a significant positive correlation. In brief, our research demonstrated that SPT6 synergized with SND1 to promote CRC development by targeting hTERT and put forward that inhibiting the SPT6-SND1-hTERT axis may create a therapeutic vulnerability in CRC.
C1 [Diao, Chaoliang; Guo, Ping; Yang, Wenjing; Sun, Yao; Liao, Yina; Cai, Xin; Hao, Jiaojiao; Hu, Sheng; Yu, Wendan; Chen, Manyu; Wang, Ruozhu; Li, Wenyang; Zuo, Yan; Pan, Jinjin; Hua, Chunyu; Lu, Xiaona; Guo, Wei] Dalian Med Univ, Inst Canc Stem Cells, Dalian 116044, Peoples R China.
   [Diao, Chaoliang; Guo, Ping; Yang, Wenjing; Sun, Yao; Liao, Yina; Cai, Xin; Hao, Jiaojiao; Hu, Sheng; Yu, Wendan; Chen, Manyu; Wang, Ruozhu; Li, Wenyang; Zuo, Yan; Pan, Jinjin; Hua, Chunyu; Lu, Xiaona; Guo, Wei] Dalian Med Univ, Affiliated Hosp 1, Dalian, Peoples R China.
   [Yan, Yue; Zhao, Anshi; Fan, Wenhua; Deng, Wuguo; Luo, Guangyu] Sun Yat Sen Univ, State Key Lab Oncol South China, Collaborat Innovat Ctr Canc Med, Canc Ctr, Guangzhou, Peoples R China.
   [Zheng, Zongheng] Sun Yat Sen Univ, Affiliated Hosp 3, Guangzhou, Peoples R China.
C3 Dalian Medical University; Dalian Medical University; Sun Yat Sen
   University; State Key Lab Oncology South China; Sun Yat Sen University
RP Guo, W (corresponding author), Dalian Med Univ, Inst Canc Stem Cells, Dalian 116044, Peoples R China.; Luo, GY (corresponding author), Sun Yat Sen Univ Canc Ctr, Guangzhou, Peoples R China.
EM luogy@sysucc.org.cn; wei1015@dmu.edu.cn
RI ; Diao, Chaoliang/U-7111-2018
OI Pan, Jinjin/0000-0002-1506-7799; Diao, Chaoliang/0000-0002-1386-7258
FU National Natural Science Foundation of China [81772975, 81572706];
   Liaoning Bai-Qian-Wan Talents Program; Scientific Research Fund project
   of Education Department of Liaoning Province - Service local project
   [LZ2020005]
FX This study was supported by the funds from the National Natural Science
   Foundation of China (81772975, 81572706) and the Liaoning Bai-Qian-Wan
   Talents Program and the Scientific Research Fund project of Education
   Department of Liaoning Province - Service local project (LZ2020005). We
   thank Wei Cheng, Haibo Chen, and Hui Wang from the Public Technical
   Supporting Platforms of the Institute of CSCs in Dalian Medical
   University for the support at immunofluorescence microscopes and flow
   cytometry assay.
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NR 54
TC 8
Z9 9
U1 2
U2 21
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1574-7891
EI 1878-0261
J9 MOL ONCOL
JI Mol. Oncol.
PD APR
PY 2021
VL 15
IS 4
BP 1180
EP 1202
DI 10.1002/1878-0261.12878
EA JAN 2021
PG 23
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RJ0GN
UT WOS:000606853500001
PM 33305480
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Li, X
   Ye, JJ
   Wang, JY
   Quan, ZY
   Li, GY
   Ma, WH
   Zhang, MR
   Yang, WD
   Wang, JL
   Ma, TQ
   Kang, F
   Wang, J
AF Li, Xiang
   Ye, Jiajun
   Wang, Jingyi
   Quan, Zhiyong
   Li, Guiyu
   Ma, Wenhui
   Zhang, Mingru
   Yang, Weidong
   Wang, Junling
   Ma, Taoqi
   Kang, Fei
   Wang, Jing
TI First-in-Humans PET Imaging of<i> KRAS<SUP>G12C</SUP></i> Mutation
   Status in Non-Small Cell Lung and Colorectal Cancer Patients Using
   [<SUP>18</SUP>F]PFPMD
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE KRAS mutation; AMG510; PET; NSCLC; CRC
ID MESSENGER-RNA; AMG 510; KRAS; HETEROGENEITY; XENOGRAFTS; INHIBITOR
AB Kirsten rat sarcoma (KRAS) mutations are an important marker for tumor-targeted therapy. In this study, we sought to develop a KRAS(G12C) oncoprotein-targeted PET tracer and to evaluate its translational potential for noninvasive imaging of the KRAS(G12C) mutation in non-small cell lung cancer (NSCLC) and colorectal cancer (CRC) patients. Methods: [F-18]PFPMD was synthesized on the basis of AMG510 (sotorasib) by attaching a polyethylene glycol chain to the quinazolinone structure. The binding selectivity and imaging potential of [F-18]PFPMD were verified by cellular uptake, internalization, and blocking (H358: KRAS(G12C) mutation; A549: non-KRAS(G12C) mutation) studies, as well as by a small-animal PET/CT imaging study on tumor-bearing mice. Five healthy volunteers were enrolled to assess the safety, biodistribution, and dosimetry of [F-18]PFPMD. Subsequently, 14 NSCLC or CRC patients with or without the KRAS(G12C) mutation underwent [F-18]PFPMD and [F-18]FDG PET/CT imaging. The SUVmax of tumor uptake of [F-18]PFPMD was measured and compared between patients with and without the KRAS(G12C) mutation. Results: [F-18]PFPMD was obtained with a high radiochemical yield, radiochemical purity, and stability. The protein-binding assay showed that [F-18]PFPMD selectively binds to the KRAS(G12C) protein. [F-18]PFPMD uptake was significantly higher in H358 than in A549 and was decreased by pretreatment with AMG510 (H358 vs. A549: 3.22% +/- 0.28% vs. 2.50% +/- 0.25%, P < 0.05; block: 2.06% +/- 0.13%, P < 0.01). Similar results were observed in tumor-bearing mice on PET imaging (H358 vs. A549: 3.93% +/- 0.24% vs. 2.47% +/- 0.26% injected dose/g, P < 0.01; block: 2.89% +/- 0.29% injected dose/g; P < 0.05). [F-18]PFPMD was safe in humans and was excreted primarily by the gallbladder and intestines. The whole-body effective dose was comparable to that of [F-18]FDG. The accumulation of [F-18]PFPMD in KRAS(G12C) mutation tumors was significantly higher than that in non-KRAS(G12C) mutation tumors (SUVmax: 3.73 +/- 0.58 vs. 2.39 +/- 0.22, P < 0.01) in NSCLC and CRC patients. Conclusion: [F-18]PFPMD is a safe and promising PET tracer for noninvasive screening of the KRAS(G12C) mutation status in NSCLC and CRC patients.
C1 [Li, Xiang; Ye, Jiajun; Wang, Jingyi; Quan, Zhiyong; Li, Guiyu; Ma, Wenhui; Zhang, Mingru; Yang, Weidong; Wang, Junling; Ma, Taoqi; Kang, Fei; Wang, Jing] Fourth Mil Med Univ, Xijing Hosp, Dept Nucl Med, Xian, Peoples R China.
   Fourth Mil Med Univ, Xijing Hosp, State Key Lab Holist Integrat Management Gastroint, Xian, Peoples R China.
C3 Air Force Military Medical University; Air Force Military Medical
   University
RP Kang, F; Wang, J (corresponding author), Fourth Mil Med Univ, Xijing Hosp, Dept Nucl Med, Xian, Peoples R China.
EM fmmukf@qq.com; 13909245902@163.com
RI Ma, Wenhui/A-6287-2015; Kang, Fei/IAL-9937-2023; Yang,
   Weidong/ABA-5036-2021
FU National Natural Science Founda- tion of China [91959208, 92259304,
   82122033, 81971646, 82202208, 81871379]
FX This study was supported by National Natural Science Founda- tion of
   China grants 91959208, 92259304, 82122033, 81971646, 82202208, and
   81871379. No other potential con fl ict of interest relevant to this
   article was reported.
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NR 28
TC 4
Z9 4
U1 7
U2 25
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD DEC 1
PY 2023
VL 64
IS 12
BP 1880
EP 1888
DI 10.2967/jnumed.123.265715
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA CI9D3
UT WOS:001124731600029
PM 37827842
OA Bronze
DA 2025-01-04
ER

PT J
AU Einstien, D
   Thanigaimani, GD
   Mouleeswaran, KS
   Prathiba, A
   Sarumathy, G
   Vergilin, J
AF Einstien, Dinisha
   Thanigaimani, Gayathri Devi
   Mouleeswaran, K. S.
   Prathiba, A.
   Sarumathy, G.
   Vergilin, John
TI Expression of PD-L1 in Microsatellite Instability High Tumours: A
   Retrospective Study
SO JOURNAL OF CLINICAL AND DIAGNOSTIC RESEARCH
LA English
DT Article
DE Lynch syndrome; Mismatch repair deficiency; Mismatch repair proteins;
   Programmed cell death protein ligand 1
ID MISMATCH REPAIR-DEFICIENCY; IMMUNE CHECKPOINT BLOCKADE; CANCER; PROTEINS
AB Introduction: Microsatellite Instability (MSI) is the hallmark of Lynch syndrome/Constitutional Mismatch Repair Deficiency (CMMRD) and is also found in many sporadic cancers like colorectal cancer, endometrial, gastric, small intestine, urothelial, central nervous system and sebaceous gland neoplasms. MSI is a predictive biomarker for immunotherapy and Immunohistochemistry (IHC) antibodies against four Mismatch Repair (MMR) proteins: MutL Homolog 1 (MLH1), MutS Homolog 2 (MSH2), MutS Homolog 6 (MSH6) and Postmeiotic Segregation increased 2 (PMS2) can identify the MSI status of the tumour. In addition to MSI, immune checkpoint Programmed Cell Death Protein 1 (PD -1) expression and its ligand PD -L1 are biomarkers that can predict response to immunotherapy. Considering this increasing interest to identify deficient MMR (dMMR) status in different cancers, authors have assessed the expression of PD -L1 and status of MSI in various cancer types. Aim: To evaluate the expression of PD -L1 in MSI-high status tumours. Materials and Methods: This retrospective cross-sectional study was done in the Department of Pathology, Panimalar Medical College Hospital and Research Institute, Chennai, Tamil Nadu, India for a period of six months from July 2022 to December 2022. A total of 151 cases were identified for the period of three years from January 2020 to December 2022. The slides and blocks were retrieved from the archives. Tumour sections from the paraffin embedded tissues were deparaffinised and antigen retrieval was done. IHC using four antibodies (MLH1, MH2, MSH6 and PMS2) was performed on these slides to assess the MSI status. The slides were reviewed and were further subjected to PD -L1 IHC. PD -L1 expression on tumour cells was compared with the MSI status of different cancer types. The p -value was calculated using t -test and p<0.5 was considered statistically significant. Statistical analysis was done using International Business Machines (IBM) Statistical Package for the Social Sciences (SPSS) software version 21.0. Results: A total of 151 cases were included in the present study. A positive nuclear stain for the four MMR proteins denote expression of wild type MMR proteins, hence MSI low status. A loss of nuclear expression denotes mutation of MMR proteins and hence MSI high (MSI-H) status. The MSI was high in nine out of 48 cases (18.75%) of colon cancer, three out of 15 cases (20%) of endometrial cancers, three out of 20 cases (15%) of gastric cancers. Rest were one out of sixteen cases of ovarian cancer, one out of two malignant melanoma and one out of three glioblastoma. Out of these, PD -L1 was positive in seven of the 18 MSI-H cases (38.88% of MSI-H cases). The MSI was low/ stable in the remaining 133 cases. The p -value of significance was 0.03 (statistically significant). Conclusion: This study shows a significant association of MSI-H with PD -L1 expression in tumours. Further large scale studies can help in assessing the role of PD -L1 as an effective therapeutic biomarker in MSI-high status patients who can benefit from targeted therapy.
C1 [Einstien, Dinisha; Thanigaimani, Gayathri Devi; Prathiba, A.; Sarumathy, G.] Panimalar Med Coll Hosp & Res Inst, Dept Pathol, Outer Ring Rd, Chennai 600123, Tamil Nadu, India.
   [Mouleeswaran, K. S.] Tagore Med Coll & Hosp, Dept Pathol, Chennai, Tamil Nadu, India.
   [Vergilin, John] Gleneagles Global Hlth City, Dept Pathol, Chennai, Tamil Nadu, India.
RP Prathiba, A (corresponding author), Panimalar Med Coll Hosp & Res Inst, Dept Pathol, Outer Ring Rd, Chennai 600123, Tamil Nadu, India.
EM acs.path@gmail.com
RI Einstien, Dinisha/AGV-8900-2022
CR Ahn S, 2017, ENDOCR-RELAT CANCER, V24, P97, DOI 10.1530/ERC-16-0421
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NR 32
TC 0
Z9 0
U1 0
U2 0
PU PREMCHAND SHANTIDEVI RESEARCH FOUNDATION
PI DELHI
PA 71 JAIN COLONY, VEER NAGAR, DELHI, 110 007, INDIA
SN 2249-782X
EI 0973-709X
J9 J CLIN DIAGN RES
JI J. Clin. Diagn. Res.
PD JUN
PY 2023
VL 17
IS 6
BP EC6
EP EC9
DI 10.7860/JCDR/2023/63627.18029
PG 4
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA KH2Q7
UT WOS:001179006700002
OA gold
DA 2025-01-04
ER

PT J
AU Fanget, F
   Kefleyesus, A
   Peron, J
   Bonnefoy, I
   Villeneuve, L
   Passot, G
   Rousset, P
   You, BN
   Benzerdjeb, N
   Glehen, O
   Kepenekian, V
AF Fanget, Florian
   Kefleyesus, Amaniel
   Peron, Julien
   Bonnefoy, Isabelle
   Villeneuve, Laurent
   Passot, Guillaume
   Rousset, Pascal
   You, Benoit
   Benzerdjeb, Nazim
   Glehen, Olivier
   Kepenekian, Vahan
TI Comparison of Neoadjuvant Systemic Chemotherapy Protocols for the
   Curative-Intent Management of Peritoneal Metastases from Colorectal
   Cancer, Regarding Morphological Response, Pathological Response, and
   Long-Term Outcomes: A Retrospective Study
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Article
ID HYPERTHERMIC INTRAPERITONEAL CHEMOTHERAPY; CYTOREDUCTIVE SURGERY; LIVER
   METASTASES; DRUG PENETRATION; BEVACIZUMAB; CARCINOMATOSIS; THERAPY;
   FOLFOXIRI; SURVIVAL; HIPEC
AB BackgroundSelected patients with colorectal cancer peritoneal metastases (CRPM) could be offered a curative-intent strategy based on complete cytoreductive surgery (CRS), potentially combined with hyperthermic intraperitoneal chemotherapy (HIPEC) and perioperative systemic chemotherapy. The impact of different neoadjuvant systemic chemotherapy (NACT) regimens remains unclear due to a lack of comparative data.MethodsConsecutive CRPM patients from a monocentric database who were treated with complete CRS after single-line NACT were included in this study. Chemotherapy regimens were tailored as a doublet drug (FOLFOX/FOLFIRI) with/without targeted therapy (anti-epidermal growth factor receptor/bevacizumab) and triplet-drug combination (FOLFIRINOX). Morphological response (MR) was assessed using the Response Evaluation Criteria in Solid Tumors criteria, and pathological response (PR) was assessed using the Peritoneal Regression Grading Score (PRGS). Long-term oncologic outcomes were compared.ResultsThe cohort comprised 388 patients, including 127, 202, and 59 patients in the doublet, doublet + targeted, and triplet groups, respectively. MR rates were higher in the triplet (68.0%) and doublet + targeted groups (64.2%) when compared with the doublet group (42.4%, p = 0.003). Complete and major PRs were observed in 13.6% and 32.0% of patients, respectively. Higher MR rates were observed after doublet + targeted or triplet regimens, while no difference was observed for PR rates. In multivariate analysis, FOLFIRINOX was independently associated with better overall survival (hazard ratio 0.49, 95% confidence interval 0.25-0.96; p = 0.037). FOLFIRINOX also resulted in a higher rate of severe postoperative complications.ConclusionsIn this retrospective study, a FOLFIRINOX regimen as NACT seemed to result in better long-term outcomes for CRPM patients after complete CRS/HIPEC, although with higher morbidity. Prospective studies are needed, including groups without NACT and those with FOLFIRINOX + bevacizumab.
C1 [Fanget, Florian; Kefleyesus, Amaniel; Passot, Guillaume; Glehen, Olivier; Kepenekian, Vahan] Hosp Civils Lyon, Hop Lyon Sud, Surg Oncol Dept, Serv Chirurg Digest & Oncol, Pierre Benite, France.
   [Fanget, Florian; Bonnefoy, Isabelle; Villeneuve, Laurent; Passot, Guillaume; Rousset, Pascal; You, Benoit; Benzerdjeb, Nazim; Glehen, Olivier; Kepenekian, Vahan] Univ Claude Bernard Lyon 1 UCBL1, EA3738 CICLY, Villeurbanne, France.
   [Kefleyesus, Amaniel] Lausanne Univ Hosp, CHUV, Dept Visceral Surg, Lausanne, Switzerland.
   [Peron, Julien; You, Benoit] Univ Claude Bernard Lyon I UCBL1, Hop Lyon Sud, Med Oncol Dept,Lab Biomet & Biol Evolut, Hosp Civils Lyon,Equipe Biostat Sante, Lyon, France.
   [Rousset, Pascal] Hop Lyon Sud, Dept Radiol, Hosp Civils Lyon, Pierre Benite, France.
   [Benzerdjeb, Nazim] Hop Lyon Sud, Dept Pathol, Hosp Civils Lyon, Pierre Benite, France.
C3 CHU Lyon; Universite Claude Bernard Lyon 1; University of Lausanne;
   Centre Hospitalier Universitaire Vaudois (CHUV); VetAgro Sup; Universite
   Claude Bernard Lyon 1; CHU Lyon; CHU Lyon; CHU Lyon
RP Kepenekian, V (corresponding author), Hosp Civils Lyon, Hop Lyon Sud, Surg Oncol Dept, Serv Chirurg Digest & Oncol, Pierre Benite, France.; Kepenekian, V (corresponding author), Univ Claude Bernard Lyon 1 UCBL1, EA3738 CICLY, Villeurbanne, France.
EM vahan.kepenekian@chu-lyon.fr
RI Passot, Guillaume/K-6271-2012; Benzerdjeb, Nazim/AAR-9309-2020;
   Kepenekian, Vahan/AFF-8361-2022; Kefleyesus, Amaniel/AAT-9227-2020;
   peron, julien/AAC-6200-2021; VILLENEUVE, LAURENT/V-4513-2019
OI VILLENEUVE, LAURENT/0000-0002-8713-7821; Kefleyesus,
   Amaniel/0000-0002-7951-4041
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NR 52
TC 5
Z9 5
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1068-9265
EI 1534-4681
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD JUN
PY 2023
VL 30
IS 6
BP 3304
EP 3315
DI 10.1245/s10434-023-13150-x
EA FEB 2023
PG 12
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA AS6C9
UT WOS:000925883000001
PM 36729351
DA 2025-01-04
ER

PT J
AU Fang, XY
   Huang, EM
   Xie, XP
   Yang, K
   Wang, SQ
   Huang, XQ
   Song, M
AF Fang, Xueying
   Huang, Enmin
   Xie, Xiaopeng
   Yang, Kai
   Wang, Shuqian
   Huang, Xiaoqing
   Song, Mei
TI A novel senescence-related lncRNA signature that predicts prognosis and
   the tumor microenvironment in patients with lung adenocarcinoma
SO FRONTIERS IN GENETICS
LA English
DT Article
DE cellular senescence; lncRNA; prognosis; tumor microenvironment;
   immunotherapy; lung adenocarcinoma
ID LONG NONCODING RNA; COLORECTAL-CANCER; NIVOLUMAB; PROLIFERATION;
   CONSTRUCTION; ASSOCIATION; VALIDATION; EXPRESSION; DOCETAXEL; HALLMARKS
AB Background: Cellular senescence has recently been considered a new cancer hallmark. However, the factors regulating cellular senescence have not been well characterized. The aim of this study is to identify long non-coding RNAs (lncRNAs) associated with senescence and prognosis in patients with lung adenocarcinoma (LUAD). Methods: Using RNA sequence data from the Cancer Genome Atlas Lung Adenocarcinoma (TCGA-LUAD) and senescence genes from the CellAge database, a subset of senescence-related lncRNAs was first identified. Then, using univariate and multivariate Cox regression analyses, a senescence lncRNA signature (LUADSenLncSig) associated with LUAD prognosis was developed. Based on the median LUADSenLncSig risk score, LUAD patients were divided into high-risk and low-risk groups. Kaplan-Meier analysis was used to compare the overall survival (OS) in the high- and low-risk score subgroups. Differences in Gene Set Enrichment Analysis (GSEA), immune infiltration, tumor mutation burden (TMB), tumor immune dysfunction and exclusion (TIDE) module score, chemotherapy, and targeted therapy selection were also compared between the high-risk and low-risk groups. Results: A prognostic risk model was obtained consisting of the following nine senescence-related lncRNAs: LINC01116, AC005838.2, SH3PXD2A-AS1, VIMS-AS1, SH3BP5-AS1, AC092279.1, AC026355.1, AC027020.2, and LINC00996. The LUADSenLncSig high-risk group was associated with poor OS (hazard ratio = 1.17, 95% confidence interval = 1.102-1.242; p < 0.001). The accuracy of the model was further supported based on receiver operating characteristic (ROC), principal component analysis (PCA), and internal validation cohorts. In addition, a nomogram was developed consisting of LUADSenLncSig for LUAD prognosis, which is consistent with the actual probability of OS. Furthermore, immune infiltration analysis showed the low-risk group had a stronger anti-tumor immune response in the tumor microenvironment. Notably, the levels of immune checkpoint genes such as CTLA-4, PDCD-1, and CD274, and the TIDE scores were significantly higher in the low-risk subgroups than in high-risk subgroups (p < 0.001). This finding indicates the LUADSenLncSig can potentially predict immunotherapy efficacy. Conclusion: In this study, a lncRNA signature, LUADSenLncSig, that has dual functions of senescence phenotype identification and prognostic prediction as well as the potential to predict the LUAD response to immunotherapy was developed.
C1 [Fang, Xueying; Xie, Xiaopeng; Yang, Kai; Wang, Shuqian; Huang, Xiaoqing; Song, Mei] Shantou Univ Med Coll, Affiliated Hosp 2, Dept Resp & Crit Care Med, Shantou, Peoples R China.
   [Huang, Enmin] Sun Yat Sen Univ, Natl Key Clin Discipline, Guangdong Prov Key Lab Colorectal & Pelv Floor Dis, Dept Gastroenterol Surg, Guangzhou, Peoples R China.
   [Huang, Enmin] Sun Yat Sen Univ, Affiliated Hosp 6, Hernia Ctr, Guangzhou, Peoples R China.
C3 Shantou University; Sun Yat Sen University; Sun Yat Sen University
RP Song, M (corresponding author), Shantou Univ Med Coll, Affiliated Hosp 2, Dept Resp & Crit Care Med, Shantou, Peoples R China.
EM smeisong@126.com
OI Huang, Xiaoqing/0000-0002-0358-4684
FU Medical Research Fund Project of Guangdong Province; Medical and Health
   Science and Technology Project of Shantou City [B2021388]; 
   [2021[68]-51]
FX This work was supported by grants from the Medical Research Fund Project
   of Guangdong Province (No. B2021388) and Medical and Health Science and
   Technology Project of Shantou City (No. 2021[68]-51).
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NR 70
TC 5
Z9 5
U1 1
U2 12
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1664-8021
J9 FRONT GENET
JI Front. Genet.
PD NOV 3
PY 2022
VL 13
AR 951311
DI 10.3389/fgene.2022.951311
PG 21
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA 6J0AB
UT WOS:000886489700001
PM 36406130
OA Green Published
DA 2025-01-04
ER

PT J
AU Kurosaki, A
   Hasegawa, K
   Kato, T
   Abe, K
   Hanaoka, T
   Miyara, A
   O'Shannessy, DJ
   Somers, EB
   Yasuda, M
   Sekino, T
   Fujiwara, K
AF Kurosaki, Akira
   Hasegawa, Kosei
   Kato, Tomomi
   Abe, Kenji
   Hanaoka, Tatsuya
   Miyara, Akiko
   O'Shannessy, Daniel J.
   Somers, Elizabeth B.
   Yasuda, Masanori
   Sekino, Tetsuo
   Fujiwara, Keiichi
TI Serum folate receptor alpha as a biomarker for ovarian cancer:
   Implications for diagnosis, prognosis and predicting its local tumor
   expression
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE ovarian cancer; folate receptor alpha; serum biomarker; FRA; diagnostic
ID PRECLINICAL EVALUATION; MONOCLONAL-ANTIBODY; BINDING-PROTEIN; PHASE-II;
   CA125; ENDOMETRIOSIS; FARLETUZUMAB; VINTAFOLIDE; ASSOCIATION; SURVIVAL
AB Folate receptor alpha (FRA) is a GPI-anchored glycoprotein and encoded by the FOLR1 gene. High expression of FRA is observed in specific malignant tumors of epithelial origin, including ovarian cancer, but exhibits very limited normal tissue expression, making it as an attractive target for the ovarian cancer therapy. FRA is known to shed from the cell surface into the circulation which allows for its measurement in the serum of patients. Recently, methods to detect the soluble form of FRA have been developed and serum FRA (sFRA) is considered a highly promising biomarker for ovarian cancer. We prospectively investigated the levels of sFRA in patients clinically suspected of having malignant ovarian tumors. A total of 231 patients were enrolled in this study and analyzed for sFRA as well as tumor expression of FRA by immunohistochemistry. High sFRA was predominantly observed in epithelial ovarian cancer patients, but not in patients with benign or borderline gynecological disease or metastatic ovarian tumors from advanced colorectal cancers. Levels of sFRA were highly correlated to clinical stage, tumor grade and histological type and demonstrated superior accuracy for the detection of ovarian cancer than did serum CA125. High sFRA was significantly associated with shorter progression-free survival in both early and advanced ovarian cancer patients. Finally, tumor FRA expression status was strongly correlated with sFRA levels. Taken together, these data suggest that sFRA might be a useful noninvasive serum biomarkers for future clinical trials assessing FRA-targeted therapy.
   What's new? Folate receptor alpha can be found on malignant ovarian cancer cells, but not normal cells. Better yet, it sheds into the bloodstream, making it a tempting candidate for diagnostic testing. These authors sampled the blood of patients suspected of having ovarian cancer, looking for FRA. They found that people with ovarian cancer had high levels of FRA in the bloodstream, while those with other gynecological disease, or metastatic ovarian tumors from colorectal cancer, did not. The amount of FRA strongly correlated with tumor grade, histological type, and clinical stage, making it potentially very effective as a diagnostic tool.
C1 [Kurosaki, Akira; Hasegawa, Kosei; Hanaoka, Tatsuya; Fujiwara, Keiichi] Saitama Med Univ, Int Med Ctr, Dept Gynecol Oncol, 1397-1 Yamane, Hidaka, Saitama 3501298, Japan.
   [Kurosaki, Akira; Hasegawa, Kosei; Hanaoka, Tatsuya; Miyara, Akiko; Fujiwara, Keiichi] Saitama Med Univ, Res Ctr Genom Med, Project Res Div, Gynecol Oncol Translat Res Unit, Saitama, Japan.
   [Kato, Tomomi; Yasuda, Masanori] Saitama Med Univ, Int Med Ctr, Dept Pathol, Saitama, Japan.
   [Abe, Kenji; Sekino, Tetsuo] EIDIA Co Ltd, Dept Res & Dev, Inashiki, Ibaraki, Japan.
   [O'Shannessy, Daniel J.; Somers, Elizabeth B.] Morphotek Inc, Dept Translat Med & Diagnost, Exton, PA USA.
C3 Saitama Medical University; Saitama Medical University; Saitama Medical
   University; Eisai Co Ltd
RP Hasegawa, K (corresponding author), Saitama Med Univ, Int Med Ctr, Dept Gynecol Oncol, 1397-1 Yamane, Hidaka, Saitama 3501298, Japan.
EM koseih@saitama-med.ac.jp
RI Miyara, Akiko/G-5726-2019
OI Miyara, Akiko/0000-0003-2915-9472
FU Ministry of Education, Culture, Sports, Science and Technology, Japan;
   Hidaka Research Projects in Saitama Medical University
FX Grant sponsors: Ministry of Education, Culture, Sports, Science and
   Technology, Japan and Hidaka Research Projects in Saitama Medical
   University
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NR 40
TC 86
Z9 96
U1 0
U2 40
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD APR 15
PY 2016
VL 138
IS 8
BP 1994
EP 2002
DI 10.1002/ijc.29937
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DD7CU
UT WOS:000370082100019
PM 26595060
OA Bronze
DA 2025-01-04
ER

PT J
AU Liu, X
   Ma, XT
   Ou, K
   Wang, Q
   Gao, LZ
   Yang, L
AF Liu, Xiu
   Ma, Xiaoting
   Ou, Kai
   Wang, Qi
   Gao, Lizhen
   Yang, Lin
TI Real-World Results of Raltitrexed Combined with S-1 and Bevacizumab in
   Heavily Pretreated Metastatic Colorectal Cancer
SO CANCER MANAGEMENT AND RESEARCH
LA English
DT Article
DE refractory metastatic colorectal cancer; chemotherapy; target therapy;
   angiogenesis
ID PHASE-II; ASIAN PATIENTS; DOUBLE-BLIND; OPEN-LABEL; TAS-102; SURVIVAL;
   PLACEBO; REGORAFENIB; MULTICENTER; MONOTHERAPY
AB Purpose: Treatment options for refractory metastatic colorectal cancer (CRC) are scarce. This retrospective study aimed to evaluate the efficacy and safety of raltitrexed combined with S-1 and bevacizumab in patients with heavily pretreated metastatic CRC in a clinical real-world setting.Patients and Methods: Records of patients with metastatic CRC refractory to standard therapies who initiated raltitrexed plus S-1 and bevacizumab from October 2017 to December 2021 were retrospectively reviewed at our institution. The study endpoints included median overall survival (OS), overall response rate (ORR), progression-free survival (PFS), disease control rate (DCR), and adverse events (AEs).Results: Forty-four patients with metastatic CRC, who had previously undergone standard chemotherapy received the regimen comprising raltitrexed plus S-1 and bevacizumab. As of March 2022, the median follow-up was 23.2 months (95% confidence interval 15.8-30.6). The median OS and median PFS were 13.5 (95% CI 9.9-17.1) and 4.7 months (95% CI 3.6-5.8), respectively, with a 16-week PFS rate of 60.9%. Among 43 patients with measurable lesions, the ORR and DCR were 7.0% (3/43) and 65.1% (28/43), respectively. Patients without peritoneal metastases (P = 0.003, hazard ratio 0.160, 95% CI 0.048-0.531), lower carcinoembryonic antigen level (<= 42.8 ng/mL) (P = 0.039, HR 0.382, 95% CI 0.153-0.952), and no previous treatment with both vascular endothelial growth factor inhibitors (VEGF) and S-1 (P = 0.020, HR 0.215, 95% CI 0.059-0.785) had better OS. The incidence of any grade of treatment-related AEs was 88.6%, most of which were mild to moderate, and no treatment-related deaths occurred.Conclusion: Raltitrexed combined with S-1 and bevacizumab shows promising antitumor activity and safety and could be an alternative for patients with metastatic CRC who are refractory or intolerant to standard therapy.
C1 [Liu, Xiu; Ma, Xiaoting; Ou, Kai; Wang, Qi; Gao, Lizhen; Yang, Lin] Chinese Acad Med Sci & Peking Union Med Coll, Canc Hosp, Natl Canc Ctr, Natl Clin Res Ctr Canc,Dept Med Oncol, Beijing, Peoples R China.
   [Wang, Qi] Beijing Chaoyang Dist Sanhuan Canc Hosp, Dept Med Oncol, Beijing, Peoples R China.
   [Gao, Lizhen] Beijing Chaoyang Huanxing Canc Hosp, Dept Med Oncol, Beijing, Peoples R China.
   [Yang, Lin] Chinese Acad Med Sci & Peking Union Med Coll, Canc Hosp, Natl Canc Ctr, Natl Clin Res Ctr Canc,Dept Med Oncol, 17 Panjiyuanninli, Beijing 10021, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Peking Union Medical College; Cancer Institute & Hospital - CAMS;
   Chinese Academy of Medical Sciences - Peking Union Medical College;
   Peking Union Medical College; Cancer Institute & Hospital - CAMS
RP Yang, L (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Canc Hosp, Natl Canc Ctr, Natl Clin Res Ctr Canc,Dept Med Oncol, 17 Panjiyuanninli, Beijing 10021, Peoples R China.
EM linyangcicams@126.com
FU Development Project of Medical Oncology Key Foundation of Cancer
   Hospital Chinese Academy of Medical Sciences [CICAMS-MODP2022002]
FX Funding This work was supported by the Development Project of Medical
   Oncology Key Foundation of Cancer Hospital Chinese Academy of Medical
   Sciences (CICAMS-MODP2022002) .
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NR 46
TC 2
Z9 2
U1 0
U2 2
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1179-1322
J9 CANCER MANAG RES
JI Cancer Manag. Res.
PY 2023
VL 15
BP 277
EP 289
DI 10.2147/CMAR.S398539
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA A0BC7
UT WOS:000951855200001
PM 36969545
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yang, H
   Xiao, X
   Zeng, LL
   Zeng, HT
   Zheng, YY
   Wang, JS
   Li, GH
   Dai, WG
   He, YL
   Wang, SH
   Peng, JJ
   Chen, W
AF Yang, Huan
   Xiao, Xing
   Zeng, Leli
   Zeng, Haiteng
   Zheng, Yueyuan
   Wang, Jingshu
   Li, Guanghua
   Dai, Weigang
   He, Yulong
   Wang, Suihai
   Peng, Jianjun
   Chen, Wei
TI Integrating cfDNA liquid biopsy and organoid-based drug screening
   reveals PI3K signaling as a promising therapeutic target in colorectal
   cancer
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
DE Liquid biopsy; cfDNA; Colorectal cancer; Organoid; PIK3CA; Alpelisib
ID CIRCULATING TUMOR DNA; RESISTANCE; MUTATIONS
AB BackgroundThe current precision medicine relies on biomarkers, which are mainly obtained through next-generation sequencing (NGS). However, this model failed to find effective drugs for most cancer patients. This study tried to combine liquid biopsy with functional drug tests using organoid models to find potential drugs for cancer patients.MethodsColorectal cancer (CRC) patients were prospectively enrolled and blood samples were collected from patients before the start of treatment. Targeted deep sequencing of cfDNA samples was performed using a 14-gene panel. Gastrointestinal (GI) cancer organoids were established and PI3K and mTOR inhibitors were evaluated on organoid models.ResultsA total of 195 mutations were detected across 58 cfDNA samples. The most frequently mutated genes were KRAS, TP53, PIK3CA, and BRAF, all of which exhibited higher mutation rates than tissue biopsy. Although 81% of variants had an allele frequency of less than 1%, certain mutations in KRAS, TP53, and SMAD4 had high allele frequencies exceeding 10%. Notably, among the seven patients with high allele frequency mutations, six had metastatic tumors, indicating that a high allele frequency of ctDNA could potentially serve as a biomarker of later-stage cancer. A high rate of PIK3CA mutation (31 out of 67, or 46.3%) was discovered in CRC patients, suggesting possible tumor progression mechanisms and targeted therapy opportunities. To evaluate the value of anti PI3K strategy in GI cancer, different lines of GI cancer organoids were established. The organoids recapitulated the morphologies of the original tumors. Organoids were generally insensitive to PI3K inhibitors. However, CRC-3 and GC-4 showed response to mTOR inhibitor Everolimus, and GC-3 was sensitive to PI3K delta inhibitor Idelalisib. The CRC organoid with a PIK3CA mutation showed greater sensitivity to the PI3K inhibitor Alpelisib than wildtype organoids, suggesting potential treatment options for the corresponding patients.ConclusionLiquid biopsy holds significant promise for improving precision treatment and tumor prognosis in colorectal cancer patients. The combination of biomarker-based drug prediction with organoid-based functional drug sensitivity assay may lead to more effective cancer treatment.
C1 [Yang, Huan; Li, Guanghua; Dai, Weigang; Peng, Jianjun] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Guangzhou, Guangdong, Peoples R China.
   [Yang, Huan; Xiao, Xing; Zeng, Haiteng; He, Yulong; Chen, Wei] Guangdong Prov Key Lab Digest Canc Res, Shenzhen, Guangdong, Peoples R China.
   [Zeng, Leli] Sun Yat Sen Univ, Affiliated Hosp 7, Dept Biobank, Shenzhen, Guangdong, Peoples R China.
   [Zheng, Yueyuan] Sun Yat Sen Univ, Affiliated Hosp 7, Clin Big Data Res Ctr, Sci Res Ctr, Shenzhen, Peoples R China.
   [Wang, Jingshu] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Oncol, Guangzhou, Guangdong, Peoples R China.
   [He, Yulong; Chen, Wei] Sun Yat Sen Univ, Affiliated Hosp 7, Dept Gastrointestinal Surg, Shenzhen, Guangdong, Peoples R China.
   [Wang, Suihai] Southern Med Univ, Sch Lab Med & Biotechnol, Guangzhou, Guangdong, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen University;
   Sun Yat Sen University; Sun Yat Sen University; Southern Medical
   University - China
RP Peng, JJ (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Guangzhou, Guangdong, Peoples R China.; Chen, W (corresponding author), Guangdong Prov Key Lab Digest Canc Res, Shenzhen, Guangdong, Peoples R China.; Chen, W (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 7, Dept Gastrointestinal Surg, Shenzhen, Guangdong, Peoples R China.; Wang, SH (corresponding author), Southern Med Univ, Sch Lab Med & Biotechnol, Guangzhou, Guangdong, Peoples R China.
EM suihaiw65@163.com; pjianj@mail.sysu.edu.cn; chenw296@mail.sysu.edu.cn
FU Natural Science Foundation of Guangdong Province
FX No applicable.
CR Adalsteinsson VA, 2017, NAT COMMUN, V8, DOI 10.1038/s41467-017-00965-y
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NR 33
TC 1
Z9 1
U1 2
U2 8
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD FEB 3
PY 2024
VL 22
IS 1
AR 132
DI 10.1186/s12967-023-04675-6
PG 13
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA HA1X8
UT WOS:001156685400004
PM 38310289
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Yao, YC
   Jin, Y
   Lei, XF
   Wang, ZX
   Zhang, DS
   Wang, FH
   Li, YH
   Xu, RH
   Wang, F
AF Yao, Yi-Chen
   Jin, Ying
   Lei, Xue-Fen
   Wang, Zi-Xian
   Zhang, Dong-Sheng
   Wang, Feng-Hua
   Li, Yu-Hong
   Xu, Rui-Hua
   Wang, Feng
TI Impact of mismatch repair or microsatellite status on the prognosis and
   efficacy to chemotherapy in metastatic colorectal cancer patients: A
   bi-institutional, propensity score-matched study
SO JOURNAL OF CANCER
LA English
DT Article
DE Colorectal cancer; Deficient mismatch repair; Microsatellite
   instability; Chemotherapy; Prognosis
ID INSTABILITY STATUS; 1ST-LINE CHEMOTHERAPY; BRAF MUTATION; PRIMARY TUMOR;
   IRINOTECAN; SURVIVAL; BENEFIT; OXALIPLATIN; ASSOCIATION; BEVACIZUMAB
AB Background: Deficient mismatch repair (dMMR) or the microsatellite instability (MSI) phenotype occupied approximately 15-18% of CRC patients. Previous studies showed that dMMR/MSI status is a favorable prognostic factor for stage II/III CRC patients. For metastatic colorectal cancer (mCRC) patients, only 5% of patients have the dMMR/MSI-H phenotype. The relationship between dMMR/MSI, chemosensitivity and survival in mCRC patients of real-world is still not clear.
   Materials and methods: In this study, we enrolled 77 dMMR/MSI-H mCRC patients and compared their clinicopathological characteristics with those of 510 proficient MMR (pMMR) or microsatellite stable (MSS) mCRC patients. With propensity score matching (PSM) analysis, we further compared the chemosensitivity and survival of dMMR/MSI-H mCRC patients with pMMR/MSS patients. We also analyzed the efficacy of different chemotherapy and target therapy in the dMMR/MSI-H population.
   Results: In PSM cohort, the objective response rate (ORR) of mCRC patients with dMMR/MSI-H undergoing first-line palliative chemotherapy was 35.2%, which was similar with patients with pMMR/MSS (35.4%, p = 1.00). The median progression-free survival (PFS) of first-line chemotherapy was significantly different (dMMR/MSI-H vs pMMR/MSS = 7.4 months vs 10.2 months; HR = 0.74; 95%Cl, 0.57-0.98; p = 0.03). Overall survival (OS) of patients did not significantly differ by status (dMMR/MSI-H vs pMMR/MSS = 40.0 months vs 41.3 months; HR = 1.09; 95%Cl, 0.74-1.59; p = 0.68). For second-line palliative chemotherapy, there was no difference in ORR (p = 0.53) or in PFS (HR = 0.88; 95%Cl, 0.59-1.33; p = 0.56) between dMMR/MSI-H and pMMR/MSS tumors. We also found that in the overall cohort, the ORR of patients who received oxaliplatin-based and irinotecan-based chemotherapy were 28.8% and 54.5%, respectively, which were not significantly different (p = 0.16). Our results also showed that the use of bevacizumab could lead to a significantly higher ORR in dMMR/MSI-H mCRC patients compared to chemotherapy alone (55.0% vs 22.2%; p = 0.02), whereas cetuximab could not.
   Conclusion: The dMMR/MSI-H is not a prognostic factor for mCRC patients but is correlated with shorter PFS to first-line palliative chemotherapy.
C1 [Yao, Yi-Chen; Jin, Ying; Wang, Zi-Xian; Zhang, Dong-Sheng; Wang, Feng-Hua; Li, Yu-Hong; Xu, Rui-Hua; Wang, Feng] Sun Yat Sen Univ Canc Ctr, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Guangzhou 510060, Peoples R China.
   [Yao, Yi-Chen; Jin, Ying; Wang, Zi-Xian; Zhang, Dong-Sheng; Wang, Feng-Hua; Li, Yu-Hong; Xu, Rui-Hua; Wang, Feng] Chinese Acad Med Sci, Res Unit Precis Diag & Treatment Gastrointestinal, Guangzhou 510060, Peoples R China.
   [Lei, Xue-Fen] Kunming Med Univ, Affiliated Hosp 2, Dept Med Oncol, 374 Dianmian Ave, Kunming 650101, Yunnan, Peoples R China.
C3 State Key Lab Oncology South China; Sun Yat Sen University; Chinese
   Academy of Medical Sciences - Peking Union Medical College; Kunming
   Medical University
RP Wang, F (corresponding author), Sun Yat Sen Univ Canc Ctr, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Guangzhou 510060, Peoples R China.; Wang, F (corresponding author), Chinese Acad Med Sci, Res Unit Precis Diag & Treatment Gastrointestinal, Guangzhou 510060, Peoples R China.
EM wangfeng@sysucc.org.cn
RI Dongsheng, ZHANG/AAL-6913-2020
FU Foundation for Medical Science and Technique Research Program of
   Guangdong Province [A2022054]; Fundamental Research Funds of Sun Yat-sen
   University Cancer Center [20ykzd166]; Precision Oncology Research
   Program of Guangdong
FX This work was supported by the Foundation for Medical Science and
   Technique Research Program of Guangdong Province (A2022054); the
   Fundamental Research Funds of Sun Yat-sen University Cancer Center
   (20ykzd166); the Precision Oncology Research Program of Guangdong.
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NR 41
TC 1
Z9 1
U1 0
U2 4
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1837-9664
J9 J CANCER
JI J. Cancer
PY 2022
VL 13
IS 9
BP 2912
EP 2921
DI 10.7150/jca.50285
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3A4ZX
UT WOS:000827270900009
PM 35912009
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Kuang, ZX
   Li, X
   Liu, RQ
   Chen, SX
   Tu, JN
AF Kuang, Zhixing
   Li, Xun
   Liu, Rongqiang
   Chen, Shaoxing
   Tu, Jiannan
TI Comprehensive Characterization of Cachexia-Inducing Factors in Diffuse
   Large B-Cell Lymphoma Reveals a Molecular Subtype and a
   Prognosis-Related Signature
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Article
DE cachexia-inducing factors; molecular subtype; prognosis-related;
   signature; diffuse large B-cell lymphoma
ID UNITED-STATES VETERANS; HODGKIN-LYMPHOMA; IMMUNE LANDSCAPE; WEIGHT
   CHANGE; EXPRESSION; CANCER; METASTASIS; VALIDATION; BLOCKADE; SURVIVAL
AB Background Cachexia is defined as an involuntary decrease in body weight, which can increase the risk of death in cancer patients and reduce the quality of life. Cachexia-inducing factors (CIFs) have been reported in colorectal cancer and pancreatic adenocarcinoma, but their value in diffuse large B-cell lymphoma (DLBCL) requires further genetic research. Methods We used gene expression data from Gene Expression Omnibus to evaluate the expression landscape of 25 known CIFs in DLBCL patients and compared them with normal lymphoma tissues from two cohorts [GSE56315 (n = 88) and GSE12195 (n = 136)]. The mutational status of CIFs were also evaluated in The Cancer Genome Atlas database. Based on the expression profiles of 25 CIFs, a single exploratory dataset which was merged by the datasets of GSE10846 (n = 420) and GSE31312 (n = 498) were divided into two molecular subtypes by using the method of consensus clustering. Immune microenvironment between different subtypes were assessed via single-sample gene set enrichment analysis and the CIBERSORT algorithm. The treatment response of commonly used chemotherapeutic drugs was predicted and gene set variation analysis was utilized to reveal the divergence in activated pathways for distinct subtypes. A risk signature was derived by univariate Cox regression and LASSO regression in the merged dataset (n = 882), and two independent cohorts [GSE87371 (n = 221) and GSE32918 (n = 244)] were used for validation, respectively. Results Clustering analysis with CIFs further divided the cases into two molecular subtypes (cluster A and cluster B) associated with distinct prognosis, immunological landscape, chemosensitivity, and biological process. A risk-prognostic signature based on CCL2, CSF2, IL15, IL17A, IL4, TGFA, and TNFSF10 for DLBCL was developed, and significant differences in overall survival analysis were found between the low- and high-risk groups in the training dataset and another two independent validation datasets. Multivariate regression showed that the risk signature was an independently prognostic factor in contrast to other clinical characteristics. Conclusion This study demonstrated that CIFs further contribute to the observed heterogeneity of DLBCL, and molecular classification and a risk signature based on CIFs are both promising tools for prognostic stratification, which may provide important clues for precision medicine and tumor-targeted therapy.
C1 [Kuang, Zhixing; Liu, Rongqiang] Fujian Med Univ, Nanping Hosp 1, Dept Radiat Oncol, Nanping, Peoples R China.
   [Li, Xun] Cent South Univ, Xiangya Med Coll, Haikou Hosp, Dept Oncol, Haikou, Hainan, Peoples R China.
   [Chen, Shaoxing] Fujian Med Univ, Zhangzhou Hosp, Dept Radiat Oncol, Zhangzhou, Peoples R China.
   [Tu, Jiannan] Fujian Med Univ, Nanping Hosp 1, Dept Oncol, Nanping, Peoples R China.
C3 Fujian Medical University; Fujian Medical University; Fujian Medical
   University
RP Li, X (corresponding author), Cent South Univ, Xiangya Med Coll, Haikou Hosp, Dept Oncol, Haikou, Hainan, Peoples R China.; Tu, JN (corresponding author), Fujian Med Univ, Nanping Hosp 1, Dept Oncol, Nanping, Peoples R China.
EM smxlixun@sina.com; jiannantu@gmail.com
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NR 57
TC 7
Z9 7
U1 0
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-634X
J9 FRONT CELL DEV BIOL
JI Front. Cell. Dev. Biol.
PD MAY 17
PY 2021
VL 9
AR 648856
DI 10.3389/fcell.2021.648856
PG 14
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA SK5MY
UT WOS:000656260500001
PM 34079795
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ryu, WJ
   Lee, JD
   Park, JC
   Cha, PH
   Cho, YH
   Kim, JY
   Sohn, JH
   Paik, S
   Choi, KY
AF Ryu, Won-Ji
   Lee, Jeong Dong
   Park, Jong-Chan
   Cha, Pu-Hyeon
   Cho, Yong-Hee
   Kim, Jee Ye
   Sohn, Joo Hyuk
   Paik, Soonmyung
   Choi, Kang-Yell
TI Destabilization of β-catenin and RAS by targeting the Wnt/β-catenin
   pathway as a potential treatment for triple-negative breast cancer
SO EXPERIMENTAL AND MOLECULAR MEDICINE
LA English
DT Article
ID RECEPTOR; CELLS; CHEMOTHERAPY; RESISTANCE; CARCINOMA; PHENOTYPE
AB Breast cancer: Dual pathway blockade shrinks aggressive tumors The triple-negative breast cancer (TNBC), a highly aggressive form of breast cancer may be susceptible to drug therapy that targets two critical signaling pathways, one that governs cell fate and the other that controls the cell cycle. Researchers from Yonsei University in Seoul, South Korea, had previously synthesized a small-molecule called KYA1797K and found that could lower levels of the proteins, beta-catenin (a master regulator of cell fate decisions) and RAS (which controls cell division), in colorectal cancer cells. Now, Kang-Yell Choi, Soonmyung Paik, and colleagues have shown that KYA1797K has the same effects on beta-catenin and RAS levels in cells taken from patients with TNBC. In cell lines and mouse models, KY1797K suppressed the proliferation and metastatic capability of TNBC, highlighting the therapeutic potential of this strategy degrading both beta-catenin and RAS.
   Triple-negative breast cancer (TNBC) is a severe and heterogeneous disease that lacks an approved targeted therapy and has a poor clinical outcome to chemotherapy. Although the RAS-ERK signaling axis is rarely mutated in TNBC, ~50% of TNBCs show an increased copy number and overexpression of epidermal growth factor receptor (EGFR). However, EGFR-targeted therapies have offered no improvement in patient survival, underscoring the need to explore downstream targets, including RAS. We found that both beta-catenin and RAS, as well as epidermal growth factor receptor (EGFR), are overexpressed and correlated with one another in tumor tissues of TNBC patients. KYA1797K, an Axin-binding small molecule reducing beta-catenin and RAS expression via degradation and suppressing EGFR expression via transcriptional repression, inhibited the proliferation and the metastatic capability of stable cell lines as well as patient-derived cells (PDCs) established from TNBC patient tissues. KYA1797K also suppressed the stemness of 3D-cultured PDCs and xenografted tumors established by using residual tumors from TNBC patients and those established by the TNBC cell line. Targeting both the Wnt/beta-catenin and RAS-ERK pathways via small molecules simultaneously reducing the levels of beta-catenin, RAS, and EGFR could be a potential therapeutic approach for TNBC.
C1 [Ryu, Won-Ji; Park, Jong-Chan; Cha, Pu-Hyeon; Cho, Yong-Hee; Choi, Kang-Yell] Yonsei Univ, Coll Life Sci & Biotechnol, Dept Biotechnol, Seoul 03722, South Korea.
   [Lee, Jeong Dong] Yonsei Univ, Dept Human Biol & Genom, Brain Korea 21 PLUS Project Med Sci, Coll Med, Seoul 03722, South Korea.
   [Kim, Jee Ye] Yonsei Univ, Dept Surg, Coll Med, Seoul 03722, South Korea.
   [Sohn, Joo Hyuk] Yonsei Univ, Div Med Oncol, Coll Med, Dept Internal Med, Seoul 03722, South Korea.
   [Paik, Soonmyung] Yonsei Univ, Coll Med, Severance Biomed Res Inst, Seoul 03722, South Korea.
   [Paik, Soonmyung] Yonsei Univ, Coll Med, Dept Med Oncol, Seoul 03722, South Korea.
   [Choi, Kang-Yell] CK Biotechnol Inc, Seoul 03722, South Korea.
C3 Yonsei University; Yonsei University; Yonsei University Health System;
   Yonsei University; Yonsei University Health System; Yonsei University;
   Yonsei University Health System; Yonsei University; Yonsei University
   Health System; Yonsei University; Yonsei University Health System
RP Choi, KY (corresponding author), Yonsei Univ, Coll Life Sci & Biotechnol, Dept Biotechnol, Seoul 03722, South Korea.; Paik, S (corresponding author), Yonsei Univ, Coll Med, Severance Biomed Res Inst, Seoul 03722, South Korea.; Paik, S (corresponding author), Yonsei Univ, Coll Med, Dept Med Oncol, Seoul 03722, South Korea.; Choi, KY (corresponding author), CK Biotechnol Inc, Seoul 03722, South Korea.
EM SOONMYUNGPAIK@yuhs.ac; kychoi@yonsei.ac.kr
RI Kim, Hye Jin/HHZ-7128-2022; Lee, jeongdong/AAI-3771-2021; cha,
   puhyeon/ABA-7719-2020
OI Paik, Soonmyung/0000-0001-9688-6480; Sohn, Joohyuk/0000-0002-2303-2764
FU National Research Foundation of Korea (NRF) [2015H1A2A1034548,
   2019R1A2C3002751, 2015R1A2A1A05001873] Funding Source: Medline
CR Bauer KR, 2007, CANCER, V109, P1721, DOI 10.1002/cncr.22618
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NR 31
TC 24
Z9 25
U1 0
U2 12
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1226-3613
EI 2092-6413
J9 EXP MOL MED
JI Exp. Mol. Med.
PD MAY
PY 2020
VL 52
IS 5
BP 832
EP 842
DI 10.1038/s12276-020-0440-y
PG 11
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine
GA LU9CH
UT WOS:000538044200012
PM 32457491
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Stintzing, S
   Wirapati, P
   Lenz, HJ
   Neureiter, D
   von Weikersthal, LF
   Decker, T
   Kiani, A
   Kaiser, F
   Al-Batran, S
   Heintges, T
   Lerchenmüller, C
   Kahl, C
   Seipelt, G
   Kullmann, F
   Moehler, M
   Scheithauer, W
   Held, S
   Modest, DP
   Jung, A
   Kirchner, T
   Aderka, D
   Tejpar, S
   Heinemann, V
AF Stintzing, S.
   Wirapati, P.
   Lenz, H. J.
   Neureiter, D.
   von Weikersthal, L. Fischer
   Decker, T.
   Kiani, A.
   Kaiser, F.
   Al-Batran, S.
   Heintges, T.
   Lerchenmueller, C.
   Kahl, C.
   Seipelt, G.
   Kullmann, F.
   Moehler, M.
   Scheithauer, W.
   Held, S.
   Modest, D. P.
   Jung, A.
   Kirchner, T.
   Aderka, D.
   Tejpar, S.
   Heinemann, V
TI Consensus molecular subgroups (CMS) of colorectal cancer (CRC) and
   first-line efficacy of FOLFIRI plus cetuximab or bevacizumab in the
   FIRE3 (AIO KRK-0306) trial
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE colorectal cancer; CMS; cetuximab; bevacizumab
ID OPEN-LABEL; SUBTYPES
AB Background: FIRE-3 compared first-line therapy with FOLFIRI plus either cetuximab or bevacizumab in 592 KRAS exon 2 wild-type metastatic colorectal cancer (mCRC) patients. The consensus molecular subgroups (CMS) are grouping CRC samples according to their gene-signature in four different subtypes. Relevance of CMS for the treatment of mCRC has yet to be defined.
   Patients and Methods: In this exploratory analysis, patients were grouped according to the previously published tumor CRC-CMSs. Objective response rates (ORR) were compared using chi-square test. Overall survival (OS) and progression-free survival (PFS) times were compared using Kaplan-Meier estimation, log-rank tests. Hazard ratios (HR) were estimated according to the Cox proportional hazard method.
   Results: CMS classification could be determined in 438 out of 514 specimens available from the intent-to-treat (ITT) population (n = 592). Frequencies for the remaining 438 samples were as follows: CMS1 (14%), CMS2 (37%), CMS3 (15%), CMS4 (34%). For the 315 RAS wild-type tumors, frequencies were as follows: CMS1 (12%), CMS2 (41%), CMS3 (11%), CMS4 (34%). CMS distribution in right- versus (vs) left-sided primary tumors was as follows: CMS1 (27% versus 11%), CMS2 (28% versus 45%), CMS3 (10% versus 12%), CMS4 (35% versus 32%). Independent of the treatment, CMS was a strong prognostic factor for ORR (P = 0.051), PFS (P < 0.001), and OS (P < 0.001). Within the RAS wild-type population, OS observed in CMS4 significantly favored FOLFIRI cetuximab over FOLFIRI bevacizumab. In CMS3, OS showed a trend in favor of the cetuximab arm, while OS was comparable in CMS1 and CMS2, independent of targeted therapy.
   Conclusions: CMS classification is prognostic for mCRC. Prolonged OS induced by FOLFIRI plus cetuximab versus FOLFIRI plus bevacizumab in the FIRE-3 study appears to be driven by CMS3 and CMS4. CMS classification provides deeper insights into the biology to CRC, but at present time has no direct impact on clinical decision-making.
C1 [Stintzing, S.] Charite Univ Med Berlin, Dept Med, Div Hematol Oncol & Tumor Immunol CCM, Berlin, Germany.
   [Wirapati, P.] Swiss Inst Bioinformat, Bioinformat Core Facil, Lausanne, Switzerland.
   [Lenz, H. J.] USC Norris Comprehens Canc Ctr, Los Angeles, CA USA.
   [Neureiter, D.] Paracelsus Med Univ, Inst Pathol, Salzburger Landeskliniken SALK, Salzburg, Austria.
   [von Weikersthal, L. Fischer] Gesundheitszentrum St Marien, Amberg, Germany.
   [Kiani, A.] Klinikum Bayreuth, Med Klin 4, Bayreuth, Germany.
   [Kaiser, F.] VK&K Studien GbR, Landshut, Germany.
   [Al-Batran, S.] Krankenhaus NW Frankfurt, Dept Hematol & Oncol, Frankfurt, Germany.
   [Heintges, T.] Stadt Klinikum Neuss, Dept Med 2, Neuss, Germany.
   [Kahl, C.] Staedt Klinikum Magdeburg, Haematol & Oncol, Magdeburg, Germany.
   [Kullmann, F.] Klinikum Weiden, Dept Med 1, Weiden, Germany.
   [Moehler, M.] Univ Hosp Mainz, Mainz, Germany.
   [Scheithauer, W.] Med Univ Vienna, Dept Internal Med 1, Vienna, Austria.
   [Scheithauer, W.] Med Univ Vienna, Comprehens Canc Ctr, Vienna, Austria.
   [Held, S.] ClinAssess GmbH, Leverkusen, Germany.
   [Modest, D. P.; Heinemann, V] Ludwig Maximilians Univ Munchen, Dept Med 3, Univ Hosp, Munich, Germany.
   [Jung, A.; Kirchner, T.] Univ Munich, Inst Pathol, Munich, Germany.
   [Aderka, D.] Chaim Sheba Med Ctr, Dept Gastrointestinal Oncol, Ramat Gan, Israel.
   [Tejpar, S.] UZ Leuven, Mol Digest Oncol, Leuven, Belgium.
C3 Berlin Institute of Health; Free University of Berlin; Humboldt
   University of Berlin; Charite Universitatsmedizin Berlin; Swiss
   Institute of Bioinformatics; University of Southern California;
   Paracelsus Private Medical University; Klinikum Bayreuth; Krankenhaus
   Nordwest; University Hospital Mainz; Medical University of Vienna;
   Medical University of Vienna; University of Munich; University of
   Munich; Chaim Sheba Medical Center; KU Leuven; University Hospital
   Leuven
RP Stintzing, S (corresponding author), Charite Univ Med Berlin, Div Hematol Oncol & Tumor Immunol CCM, Charitepl 1, D-10117 Berlin, Germany.
EM sebastian.stintzing@charite.de
RI Modest, Dominik Paul/AAW-9756-2021; Stintzing, Sebastian/I-4538-2016
OI Decker, Thomas/0000-0003-3814-8775; Stintzing,
   Sebastian/0000-0002-3297-5801
FU Merck KGaA, Darmstadt, Germany; Pfizer GmbH, Germany; ALMAC Ltd,
   Belfast, UK; Roche Pharma AG, Grenzach, Germany
FX Funding for the clinical study came from Merck KGaA, Darmstadt, Germany,
   and Pfizer GmbH, Germany. Funding for the transcriptome based microarray
   for gene-expression using XcelV (R) Array came from ALMAC Ltd, Belfast,
   UK. Funding for FoundationOneV (R)-based sequencing analysis (MSI) was
   obtained from Roche Pharma AG, Grenzach, Germany (no grant numbers
   apply).
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NR 17
TC 133
Z9 142
U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
EI 1569-8041
J9 ANN ONCOL
JI Ann. Oncol.
PD NOV
PY 2019
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IS 11
BP 1796
EP 1803
DI 10.1093/annonc/mdz387
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KD0XE
UT WOS:000507594800015
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU DiPeri, TP
   Evans, KW
   Raso, MG
   Zhao, M
   Rizvi, YQ
   Zheng, XF
   Wang, BL
   Kirby, BP
   Kong, KT
   Kahle, M
   Yap, TA
   Dumbrava, EE
   Ajani, JA
   Fu, SQ
   Keyomarsi, K
   Meric-Bernstam, F
AF DiPeri, Timothy P.
   Evans, Kurt W.
   Raso, Maria Gabriela
   Zhao, Ming
   Rizvi, Yasmeen Q.
   Zheng, Xiaofeng
   Wang, Bailiang
   Kirby, Bryce P.
   Kong, Kathleen
   Kahle, Michael
   Yap, Timothy A.
   Dumbrava, Ecaterina E.
   Ajani, Jaffer A.
   Fu, Siqing
   Keyomarsi, Khandan
   Meric-Bernstam, Funda
TI Adavosertib Enhances Antitumor Activity of Trastuzumab Deruxtecan in
   HER2-Expressing Cancers
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID CYCLIN-E AMPLIFICATION/OVEREXPRESSION; TOPOISOMERASE-I INHIBITOR;
   BREAST-CANCER; SOLID TUMORS; OPEN-LABEL; RESISTANCE; ANTIBODY; HER2;
   CARCINOSARCOMA; MULTICENTER
AB Purpose: Cyclin E (CCNE1) has been proposed as a biomarker of sensitivity to adavosertib, a Wee1 kinase inhibitor, and a mechanism of resistance to HER2-targeted therapy.Experimental Design: Copy number and genomic sequencing data from The Cancer Genome Atlas and MD Anderson Cancer Center databases were analyzed to assess ERBB2 and CCNE1 expression. Molecular characteristics of tumors and patient-derived xenografts (PDX) were assessed by next-generation sequencing, whole-exome sequencing, fluorescent in situ hybridization, and IHC. In vitro, CCNE1 was overexpressed or knocked down in HER2+ cell lines to evaluate drug combination efficacy. In vivo, NSG mice bearing PDXs were subjected to combinatorial therapy with various treatment regimens, followed by tumor growth assessment. Pharmacodynamic markers in PDXs were characterized by IHC and reverse-phase protein array.Results: Among several ERBB2-amplified cancers, CCNE1 co-amplification was identified (gastric 37%, endometroid 43%, and ovarian serous adenocarcinoma 41%). We hypothesized that adavosertib may enhance activity of HER2 antibody-drug conjugate trastuzumab deruxtecan (T-DXd). In vitro, sensitivity to T-DXd was decreased by cyclin E overexpression and increased by knockdown, and adavosertib was synergistic with topoisomerase I inhibitor DXd. In vivo, the T-DXd + adavosertib combination significantly increased gamma H2AX and antitumor activity in HER2 low, cyclin E amplified gastroesophageal cancer PDX models and prolonged event-free survival (EFS) in a HER2-overexpressing gastroesophageal cancer model. T-DXd + adavosertib treatment also increased EFS in other HER2-expressing tumor types, including a T-DXd-treated colon cancer model.Conclusions: We provide rationale for combining T-DXd with adavosertib in HER2-expressing cancers, especially with co-occuring CCNE1 amplifications. See related commentary by Rolfo et al., p. 4317Conclusions: We provide rationale for combining T-DXd with adavosertib in HER2-expressing cancers, especially with co-occuring CCNE1 amplifications. See related commentary by Rolfo et al., p. 4317
C1 [DiPeri, Timothy P.; Meric-Bernstam, Funda] Univ Texas MD Anderson Canc Ctr, Dept Surg Oncol, Houston, TX 77030 USA.
   [Evans, Kurt W.; Zhao, Ming; Rizvi, Yasmeen Q.; Zheng, Xiaofeng; Wang, Bailiang; Kirby, Bryce P.; Kong, Kathleen; Yap, Timothy A.; Dumbrava, Ecaterina E.; Fu, Siqing; Meric-Bernstam, Funda] Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapeut, 1400 Holcombe Blvd, Houston, TX 77030 USA.
   [Raso, Maria Gabriela] Univ Texas MD Anderson Canc Ctr, Dept Translat Mol Pathol, Houston, TX 77030 USA.
   [Kahle, Michael] Univ Texas MD Anderson Canc Ctr, Inst Personalized Canc Therapy, Houston, TX 77030 USA.
   [Ajani, Jaffer A.] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
   [Keyomarsi, Khandan] Univ Texas MD Anderson Canc Ctr, Dept Expt Radiat Oncol, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; University of
   Texas System; UTMD Anderson Cancer Center; University of Texas System;
   UTMD Anderson Cancer Center; University of Texas System; UTMD Anderson
   Cancer Center; University of Texas System; UTMD Anderson Cancer Center;
   University of Texas System; UTMD Anderson Cancer Center
RP Meric-Bernstam, F (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapeut, 1400 Holcombe Blvd, Houston, TX 77030 USA.
EM fmeric@mdanderson.org
RI Raso, Maria/J-9898-2019; Meric-Bernstam, Funda/JRZ-1866-2023; Kahle,
   Michael/GMX-2228-2022; Wang, Bailiang/T-3483-2018; Yap,
   Timothy/AAV-3573-2020; Keyomarsi, Khandan/H-2716-2016
OI DiPeri, Timothy/0000-0003-1190-1640; Kahle, Michael/0000-0002-5982-3832;
   Raso, Maria Gabriela/0000-0003-2105-5556; Rizvi,
   Yasmeen/0009-0000-2719-4093; Zheng, Xiaofeng/0009-0007-2171-7210
FU National Institutes of Health (NIH) [5T32CA009599-32, 5U54CA224065-04];
   NIH Training of Academic Surgical Oncologists [5UL1TR003167-03]; Center
   for Clinical and Translational Science [P30 CA016672]; MD Anderson
   Cancer Center
FX This work was supported by the following: NIH Training of Academic
   Surgical Oncologists (Award No. 5T32CA009599-32), University of Texas
   PDX Development and Trial Center (Award No. 5U54CA224065-04), Center for
   Clinical and Translational Science (Award No. 5UL1TR003167-03), and the
   MD Anderson Cancer Center support grant (Award No. P30 CA016672). We
   thank Ms. Susanna Brisendine for preparing submission documents and
   submission.
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NR 51
TC 8
Z9 8
U1 3
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 1
PY 2023
VL 29
IS 21
BP 4385
EP 4398
DI 10.1158/1078-0432.CCR-23-0103
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DV7Z2
UT WOS:001134935100013
PM 37279095
OA hybrid, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Zhou, X
   Ling, KJ
   Liu, MY
   Zhang, XJ
   Ding, J
   Dong, Y
   Liang, ZQ
   Li, JJ
   Zhang, JX
AF Zhou, Xing
   Ling, Kaijian
   Liu, Mengyu
   Zhang, Xiangjun
   Ding, Jun
   Dong, Yan
   Liang, Zhiqing
   Li, Jianjun
   Zhang, Jianxiang
TI Targeted Delivery of Cisplatin-Derived Nanoprecursors via a Biomimetic
   Yeast Microcapsule for Tumor Therapy by the Oral Route
SO THERANOSTICS
LA English
DT Article
DE cisplatin; nanoprecursor; yeast microcapsule; oral delivery; targeted
   tumor therapy
ID POLYMERIC MICELLES; CANCER-THERAPY; MULTIDRUG-RESISTANCE;
   HYALURONIC-ACID; PLATINUM DRUGS; COLON-CANCER; NANOPARTICLES; PRODRUG;
   TOXICITY; BACTERIA
AB Targeted therapy via the patient-friendly oral route remains the holy grail of chemotherapy for cancer. Herein we report a yeast-derived platform for targeted oral delivery of cisplatin (CDDP) that is one of the most effective drugs for chemotherapy of various types of cancers.
   Methods: The optimal conditions were first established to fabricate yeast microcapsules (YCs) with desirable loading capability. Then, CDDP-derived precursor nanoparticles (PreCDDP) were prepared and packaged into YC to produce orally deliverable PreCDDP/YC. The physiochemical properties, in vitro drug release profiles, in vitro antitumor activity, oral targeting capability, in vivo pharmacokinetics, and in vivo efficacy of the YC-based biomimetic delivery system were examined.
   Results: YCs obtained under the optimized condition showed desirable loading efficiency for quantum dots that were used as a model nanocargo. In vitro experiments demonstrated rapid endocytosis and prolonged retention of YC in macrophages. By electrostatic force-mediated self-deposition, PreCDDP was efficiently loaded into YC. PreCDDP/YC showed potent cytotoxicity in different tumor cells, indicating that PreCDDP loaded in YC maintained its antitumor activity after intracellular release. As compared to CDDP and PreCDDP, orally administered PreCDDP/YC displayed significantly higher bioavailability. Post oral delivery, YC could accumulate in A549 human lung carcinoma xenografts in mice, achieving by monocyte/macrophage-mediated translocation via the lymphatic system. Through this targeting effect, orally administered PreCDDP/YC showed desirable efficacy in A549 xenograft-bearing mice, which was comparable to that of free CDDP administered by intravenous injection. Orally administered free CDDP, however, did not afford antitumor effects. Furthermore, oral treatment with PreCDDP/YC displayed better safety than free CDDP administered via the oral or intravenous route.
   Conclusions: This biomimetic approach can serve as an effective strategy to develop targeted oral chemotherapies based on CDDP or its derivatives.
C1 [Zhou, Xing; Liu, Mengyu; Zhang, Xiangjun; Zhang, Jianxiang] Third Mil Med Univ, Coll Pharm, Dept Pharmaceut, 30 Gaotanyan Main St, Chongqing 400038, Peoples R China.
   [Ling, Kaijian; Liang, Zhiqing] Third Mil Med Univ, Southwest Hosp, Dept Obstet & Gynaecol, 30 Gaotanyan Main St, Chongqing 400038, Peoples R China.
   [Ding, Jun] Third Mil Med Univ, Southwest Hosp, Dept Ultrasound, Chongqing 400038, Peoples R China.
   [Dong, Yan; Li, Jianjun] Third Mil Med Univ, Southwest Hosp, Dept Oncol, 30 Gaotanyan Main St, Chongqing 400038, Peoples R China.
   [Dong, Yan; Li, Jianjun] Third Mil Med Univ, Southwest Hosp, Southwest Canc Ctr, 30 Gaotanyan Main St, Chongqing 400038, Peoples R China.
C3 Army Medical University; Army Medical University; Army Medical
   University; Army Medical University; Army Medical University
RP Zhang, JX (corresponding author), Third Mil Med Univ, Coll Pharm, Dept Pharmaceut, 30 Gaotanyan Main St, Chongqing 400038, Peoples R China.; Liang, ZQ (corresponding author), Third Mil Med Univ, Southwest Hosp, Dept Obstet & Gynaecol, 30 Gaotanyan Main St, Chongqing 400038, Peoples R China.; Li, JJ (corresponding author), Third Mil Med Univ, Southwest Hosp, Dept Oncol, 30 Gaotanyan Main St, Chongqing 400038, Peoples R China.; Li, JJ (corresponding author), Third Mil Med Univ, Southwest Hosp, Southwest Canc Ctr, 30 Gaotanyan Main St, Chongqing 400038, Peoples R China.
EM zhi.lzliang@gmail.com; jianjunli@tmmu.edu.cn; jxzhang1980@gmail.com
RI Zhang, Xiangjun/N-2143-2018; Deng, Jun/X-6902-2019; yan,
   dong/HJH-5409-2023; Zhang, Jianxiang/A-6626-2009; Zhou, Xing/X-3497-2019
OI Zhou, Xing/0000-0003-0852-0687
FU National Natural Science Foundation of China [81601592]; Program for
   Distinguished Young Scholars of TMMU
FX This study was supported by the National Natural Science Foundation of
   China (No. 81601592) and the Program for Distinguished Young Scholars of
   TMMU.
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NR 85
TC 41
Z9 42
U1 3
U2 62
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1838-7640
J9 THERANOSTICS
JI Theranostics
PY 2019
VL 9
IS 22
BP 6568
EP 6586
DI 10.7150/thno.35353
PG 19
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA IY7LL
UT WOS:000486577100015
PM 31588236
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Gao, S
   Wang, JJ
   Tian, R
   Wang, GH
   Zhang, LW
   Li, YS
   Li, L
   Ma, QJ
   Zhu, L
AF Gao, Shi
   Wang, Jingjing
   Tian, Rui
   Wang, Guohao
   Zhang, Liwen
   Li, Yesen
   Li, Lu
   Ma, Qingjie
   Zhu, Lei
TI Construction and Evaluation of a Targeted Hyaluronic Acid
   Nanoparticle/Photosensitizer Complex for Cancer Photodynamic Therapy
SO ACS APPLIED MATERIALS & INTERFACES
LA English
DT Article
DE photodynamic therapy; nanomedicine; hyaluronic acid nanoparticle;
   positron emission tomography; targeted therapy; [F-18] FDG
ID THERANOSTIC AGENT; FDG PET/CT; NANOPARTICLES; DELIVERY; SYSTEM; TUMORS;
   CELLS; CD44
AB Photodynamic therapy (PDT) is a novel treatment modality that is under intensive preclinical investigations for a variety of diseases, including cancer. Despite extensive studies in this area, selective and effective photodynamic agents that can specifically accumulate in tumors to reach a therapeutic concentration are limited. Although recent attempts have produced photosensitizers (PSs) complexed with various nanomaterials, the tedious preparation steps and poor tumor efficiency of therapy hamper their utilization. Here, we developed a CD44-targeted nanophotodynamic agent by physically encapsulating a photosensitizer, Ce6, into a hyaluronic acid nanoparticle (HANP), which was hereby denoted HANP/Ce6. Its physical features and capability for photodynamic therapy were characterized in vitro and in vivo. Systemic delivery of HANP/Ce6 resulted in its accumulation in a human colon cancer xenograft model. The tumor/muscle ratio reached 3.47 +/- 0.46 at 4 h post injection, as confirmed by fluorescence imaging. Tumor growth after HANP/Ce6 treatment with laser irradiation (0.15 W/cm(2), 630 nm) was significantly inhibited by 9.61 +/- 1.09-fold compared to that in tumor control groups, which showed no change in tumor growth. No apparent systemic and local toxic effects on the mice were observed. HANP/Ce6-mediated tumor growth inhibition was accessed and observed for the first time by F-18-fluoro-2-deoxy-D-glucose positron emission tomography as early as 1 day after treatment and persisted for 14 days within our treatment time window. In sum, our results highlight the imaging properties and therapeutic effects of the novel HANP/Ce6 theranostic nanoparticle for CD44-targeted PDT cancer therapy that may be potentially utilized in the clinic. This HANP system may also be applied for the delivery of other hydrophobic PSs, particularly those that could not be chemically modified.
C1 [Gao, Shi; Li, Lu; Ma, Qingjie] Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China.
   [Wang, Jingjing; Wang, Guohao; Zhang, Liwen; Li, Yesen] Xiamen Univ, Sch Publ Hlth, State Key Lab Mol Vaccinol & Mol Diagnost, Xiamen 361005, Peoples R China.
   [Wang, Jingjing; Wang, Guohao; Zhang, Liwen; Li, Yesen] Xiamen Univ, Sch Publ Hlth, Ctr Mol Imaging & Translat Med, Xiamen 361005, Peoples R China.
   [Tian, Rui] Jilin Univ, Hosp 2, Dept Ophthalmol, Changchun 130033, Jilin, Peoples R China.
   [Zhu, Lei] Emory Univ, Sch Med, Dept Surg, Atlanta, GA 30322 USA.
C3 Jilin University; Xiamen University; Xiamen University; Jilin
   University; Emory University
RP Ma, QJ (corresponding author), Jilin Univ, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China.; Zhu, L (corresponding author), Emory Univ, Sch Med, Dept Surg, Atlanta, GA 30322 USA.
EM maqingjiejlu@163.com; lei.zhu@emory.edu
RI Zhang, Liwen/JAC-8446-2023; Wang, Jingjing/KRP-8843-2024
OI Wang, Jingjing/0000-0002-6105-995X; Zhang, Liwen/0000-0003-2594-3227
FU National Science Foundation of China [81571708, 81771869, 81501506,
   51373144, 81201129]; National High Technology Research and Development
   Program of China (863 Program) [2014AA020708]; Fundamental Research
   Funds for the Central Universities [20720150064]; Research Fund of
   Science and Technology Department of Jilin Province [20160101001JC];
   Department of Education of Jilin Province for Thirteen-Five Scientific
   Technique Research [[2016]460]; Norman Bethune Program of Jilin
   University [2015219]
FX The National Science Foundation of China (Grant Nos. 81571708, 81771869,
   81501506, 51373144, and 81201129), National High Technology Research and
   Development Program of China (863 Program) (Grant No. 2014AA020708), the
   Fundamental Research Funds for the Central Universities (Grant No.
   20720150064), the Research Fund of Science and Technology Department of
   Jilin Province (Grant No. 20160101001JC), the Department of Education of
   Jilin Province for Thirteen-Five Scientific Technique Research (Grant
   No. [2016]460), and the Norman Bethune Program of Jilin University
   (Grant No. 2015219) supported this study.
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NR 34
TC 45
Z9 50
U1 2
U2 79
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1944-8244
EI 1944-8252
J9 ACS APPL MATER INTER
JI ACS Appl. Mater. Interfaces
PD SEP 27
PY 2017
VL 9
IS 38
BP 32509
EP 32519
DI 10.1021/acsami.7b09331
PG 11
WC Nanoscience & Nanotechnology; Materials Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Materials Science
GA FI7BB
UT WOS:000412149800014
PM 28875691
DA 2025-01-04
ER

PT J
AU Yu, ST
   Feng, WJ
   Zeng, JZ
   Zhou, ST
   Peng, YH
   Zhang, PH
AF Yu, Site
   Feng, Wenjie
   Zeng, Jizhang
   Zhou, Situo
   Peng, Yinghua
   Zhang, Pihong
TI GALNT12 promotes fibrosarcoma growth by accelerating YAP1 nuclear
   localization
SO ONCOLOGY LETTERS
LA English
DT Article
DE fibrosarcoma; polypeptide N-acetylgalactosaminyl-transferase 12; yes1
   associated transcriptional regulator; tumor growth
ID CANCER; EXPRESSION; SURVIVAL; GENE
AB Fibrosarcoma is a highly malignant type of soft tissue sarcoma that currently lacks effective treatment options. Polypeptide N-acetylgalactosaminyltransferase 12 (GALNT12) belongs to the uridine diphosphate N-acetylgalactosamine gene family, which is involved in numerous biological processes of diseases, such as tumor progression. Its upregulated expression is closely associated with the development of colorectal cancer. However, research on the role of GALNT12 in fibrosarcoma is currently limited. The present study aimed to assess the expression and biological function of GALNT12 in fibrosarcoma. Patient data and tissue samples were collected and public datasets were obtained from the Gene Expression Omnibus (GSE24369 and GSE21124). Immunofluorescence assays were performed to observe the cellular localization of GALNT12. GALNT12 expression was measured using reverse transcription-quantitative PCR, western blotting and immunohistochemistry. Small interfering RNAs were constructed to knock down GALNT12 expression in HT-1080 cells. Cell Counting Kit-8 and EdU assays were used to assess fibrosarcoma cell proliferation. Wound healing and Transwell assays were used to detect migration. Gene set enrichment analysis was performed to identify key pathways. Paired and unpaired Student's t-test, Fisher's exact test and one-way ANOVA (followed by Tukey's Honest Significant Difference test) were used to analyze the data. It was demonstrated that GALNT12 expression was upregulated in both fibrosarcoma cell lines and tissue samples and predicted poor patient prognosis. In vitro experiments demonstrated that high GALNT12 expression levels significantly increased HT-1080 cell proliferation and migration. Furthermore, it was demonstrated that high GALNT12 expression levels were closely associated with the yes1 associated transcriptional regulator (YAP1) signaling pathway. Knockdown of GALNT12 inhibited YAP1 nuclear translocation, which affected activation of key downstream genes including AMOTL2, BIRC5 and CYR61. Therefore, the present study demonstrated that GALNT12 promoted fibrosarcoma progression. GALNT12 could be a potential biomarker for this disease and may potentially provide new ideas for targeted therapy of fibrosarcoma in the future.
C1 [Yu, Site; Feng, Wenjie; Zeng, Jizhang; Zhou, Situo; Peng, Yinghua; Zhang, Pihong] Cent South Univ, Xiangya Hosp, Dept Burns & Plast Surg, 87 Xiangya Rd, Changsha 410008, Hunan, Peoples R China.
C3 Central South University
RP Zhang, PH (corresponding author), Cent South Univ, Xiangya Hosp, Dept Burns & Plast Surg, 87 Xiangya Rd, Changsha 410008, Hunan, Peoples R China.
EM zphong2022@126.com
RI zhang, xuyang/GQH-3712-2022; Peng, Yinghua/D-3327-2011
FU Academic Construction Funding of Xiangya Hospital, Central South
   University
FX Not applicable.
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NR 43
TC 1
Z9 1
U1 0
U2 5
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD DEC
PY 2023
VL 26
IS 6
AR 543
DI 10.3892/ol.2023.14131
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA Y8LO9
UT WOS:001107722400001
PM 38020290
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ivanov, M
   Laktionov, K
   Breder, V
   Chernenko, P
   Novikova, E
   Telysheva, E
   Musienko, S
   Baranova, A
   Mileyko, V
AF Ivanov, Maxim
   Laktionov, Konstantin
   Breder, Valery
   Chernenko, Polina
   Novikova, Ekaterina
   Telysheva, Ekaterina
   Musienko, Sergey
   Baranova, Ancha
   Mileyko, Vladislav
TI Towards standardization of next-generation sequencing of FFPE samples
   for clinical oncology: intrinsic obstacles and possible solutions
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
DE NGS; Non-small cell lung cancer; Cancer; Oncology; Precision oncology;
   Targeted therapy
ID CELL LUNG-CANCER; DE-NOVO; AGGRESSIVE FIBROMATOSIS; TARGETED THERAPIES;
   COLORECTAL-CANCER; IMATINIB MESYLATE; TUMOR-SUPPRESSOR; READ ALIGNMENT;
   MUTANT P53; IN-VITRO
AB Background: Next generation sequencing has a potential to revolutionize the management of cancer patients within the framework of precision oncology. Nevertheless, lack of standardization decelerated entering of the technology into the clinical testing space. Here we dissected a number of common problems of NGS diagnostics in oncology and introduced ways they can be resolved.
   Methods: DNA was extracted from 26 formalin fixed paraffin embedded (FFPE) specimens and processed with the TrueSeq Amplicon Cancer Panel (Illumina Inc, San Diego, California) targeting 48 cancer-related genes and sequenced in single run. Sequencing data were comparatively analyzed by several bioinformatics pipelines.
   Results: Libraries yielded sufficient coverage to detect even low prevalent mutations. We found that the number of FFPE sequence artifacts significantly correlates with pre-normalization concentration of libraries (rank correlation -0.81; p < 1e-10), thus, contributing to sample-specific variant detection cut-offs. Surprisingly, extensive validation of EGFR mutation calls by a combination of aligners and variant callers resulted in identification of two false negatives and one false positive that were due to complexity of underlying genomic change, confirmed by Sanger sequencing. Additionally, the study of the non-EGFR amplicons revealed 33 confirmed unique mutations in 17 genes, with TP53 being the most frequently mutated. Clinical relevance of these finding is discussed.
   Conclusions: Reporting of entire mutational spectrum revealed by targeted sequencing is questionable, at least until the clinically-driven guidelines on reporting of somatic mutations are established. The standardization of sequencing protocols, especially their data analysis components, requires assay-, disease-, and, in many cases, even sample-specific customization that could be performed only in cooperation with clinicians.
C1 [Ivanov, Maxim; Baranova, Ancha] State Univ, Moscow Inst Phys & Technol, Dolgoprudnyi 141700, Moscow Region, Russia.
   [Ivanov, Maxim; Musienko, Sergey; Baranova, Ancha; Mileyko, Vladislav] Atlas Biomed Grp, Moscow 121069, Russia.
   [Ivanov, Maxim; Mileyko, Vladislav] Inst Chem Biol & Fundamental Med SB RAS, Novosibirsk 630090, Russia.
   [Laktionov, Konstantin; Breder, Valery; Chernenko, Polina] Minist Hlth Russian Federat, NN Blokhin Russian Canc Res Ctr, Kashirskoe Sh 24, Moscow 115478, Russia.
   [Novikova, Ekaterina; Telysheva, Ekaterina] Minist Healthcare Russian Federat, Russian Sci Ctr Roentgenoradiol, Fed State Budgetary Inst, Russian Sci Ctr Roentgenoradiol RSCRR, Moscow 117485, Russia.
   [Baranova, Ancha] Med Genet Res Ctr, Moscow 115478, Russia.
   [Baranova, Ancha] George Mason Univ, Sch Syst Biol, Ctr Study Chron Metab & Rare Dis, Fairfax, VA 22030 USA.
C3 Moscow Institute of Physics & Technology; Russian Academy of Sciences;
   Institute of Chemical Biology & Fundamental Medicine, Siberian Branch of
   the RAS; Ministry of Health of the Russian Federation; N.N. Blokhin
   Russian Cancer Research Center; Research Centre for Medical Genetics;
   George Mason University
RP Baranova, A (corresponding author), State Univ, Moscow Inst Phys & Technol, Dolgoprudnyi 141700, Moscow Region, Russia.; Baranova, A (corresponding author), Atlas Biomed Grp, Moscow 121069, Russia.; Baranova, A (corresponding author), Med Genet Res Ctr, Moscow 115478, Russia.; Baranova, A (corresponding author), George Mason Univ, Sch Syst Biol, Ctr Study Chron Metab & Rare Dis, Fairfax, VA 22030 USA.
EM abaranov@gmu.edu
RI Laktionov, Konstantin/G-1431-2019; Ivanov, Maxim/ABG-1625-2022;
   Novikova, Ekaterina/D-2824-2019; Baranova, Ancha/B-4608-2012
OI Laktionov, Konstantin/0000-0003-4469-502X; Novikova,
   Ekaterina/0000-0003-4437-3661; Breder, Valeriy/0000-0002-6244-4294;
   Baranova, Ancha/0000-0001-6810-5982
FU Ministry of Science and Education, Russia [RFMEFI60714X0098]
FX This study was supported by Ministry of Science and Education, Russia
   (Project No. RFMEFI60714X0098).
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NR 87
TC 22
Z9 25
U1 0
U2 6
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD JAN 31
PY 2017
VL 15
AR 22
DI 10.1186/s12967-017-1125-8
PG 13
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA EM8LE
UT WOS:000395562000002
PM 28137276
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Li, L
   Tan, HW
   Zhou, JX
   Hu, FM
AF Li, Lei
   Tan, Hongwei
   Zhou, Jiexue
   Hu, Fengming
TI Predicting response of immunotherapy and targeted therapy and prognosis
   characteristics for renal clear cell carcinoma based on m1A methylation
   regulators
SO SCIENTIFIC REPORTS
LA English
DT Article
ID T-CELLS; MESSENGER-RNA; INFILTRATION; RECURRENCE; INHIBITORS; LANDSCAPE;
   SUNITINIB; METHYLOME; SIGNATURE
AB In recent years, RNA methylation modification has been found to be related to a variety of tumor mechanisms, such as rectal cancer. Clear cell renal cell carcinoma (ccRCC) is most common in renal cell carcinoma. In this study, we get the RNA profiles of ccRCC patients from ArrayExpress and TCGA databases. The prognosis model of ccRCC was developed by the least absolute shrinkage and selection operator (LASSO) regression analysis, and the samples were stratified into low-high risk groups. In addition, our prognostic model was validated through the receiver operating characteristic curve (ROC). "pRRophetic" package screened five potential small molecule drugs. Protein interaction networks explore tumor driving factors and drug targeting factors. Finally, polymerase chain reaction (PCR) was used to verify the expression of the model in the ccRCC cell line. The mRNA matrix in ArrayExpress and TCGA databases was used to establish a prognostic model for ccRCC through LASSO regression analysis. Kaplan Meier analysis showed that the overall survival rate (OS) of the high-risk group was poor. ROC verifies the reliability of our model. Functional enrichment analysis showed that there was a obviously difference in immune status between the high-low risk groups. "pRRophetic" package screened five potential small molecule drugs (A.443654, A.770041, ABT.888, AG.014699, AMG.706). Protein interaction network shows that epidermal growth factor receptor [EGRF] and estrogen receptor 1 [ESR1] are tumor drivers and drug targeting factors. To further analyze the differential expression and pathway correlation of the prognosis risk model species. Finally, polymerase chain reaction (PCR) showed the expression of YTHN6-Methyladenosine RNA Binding Protein 1[YTHDF1], TRNA Methyltransferase 61B [TRMT61B], TRNA Methyltransferase 10C [TRMT10C] and AlkB Homolog 1[ALKBH1] in ccRCC cell lines. To sum up, the prognosis risk model we created not only has good predictive value, but also can provide guidance for accurately predicting the prognosis of ccRCC.
C1 [Li, Lei] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Urol, Wuhan, Hubei, Peoples R China.
   [Tan, Hongwei; Zhou, Jiexue; Hu, Fengming] Guangdong Second Prov Gen Hosp, Dept Organ Transplantat, Guangzhou, Guangdong, Peoples R China.
C3 Huazhong University of Science & Technology
RP Zhou, JX; Hu, FM (corresponding author), Guangdong Second Prov Gen Hosp, Dept Organ Transplantat, Guangzhou, Guangdong, Peoples R China.
EM zhoujiexuezs@tom.com; hfm1473057445@163.com
RI hu, fengming/R-4077-2019; Li, Lei/HSA-7146-2023
OI Zhou, Jiexue/0009-0002-7576-2491
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NR 70
TC 7
Z9 8
U1 0
U2 4
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD AUG 4
PY 2023
VL 13
IS 1
AR 12645
DI 10.1038/s41598-023-39935-4
PG 18
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA O3YS3
UT WOS:001043211800029
PM 37542141
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Bilen, MA
   Patel, A
   Hess, KR
   Munoz, J
   Busaidy, NL
   Wheler, JJ
   Janku, F
   Falchook, GS
   Hong, DS
   Meric-Bernstam, F
   Habra, MA
   Naing, A
AF Bilen, Mehmet Asim
   Patel, Amy
   Hess, Kenneth R.
   Munoz, Javier
   Busaidy, Naifa L.
   Wheler, Jennifer J.
   Janku, Filip
   Falchook, Gerald S.
   Hong, David S.
   Meric-Bernstam, Funda
   Habra, Mouhammed Amir
   Naing, Aung
TI Association between new-onset hypothyroidism and clinical response in
   patients treated with tyrosine kinase inhibitor therapy in phase I
   clinical trials
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE Tyrosine kinase inhibitor; Phase I; Toxicity; Hypothyroidism; Clinical
   response
ID RENAL-CELL CARCINOMA; CANCER-PATIENTS; ANTITUMOR-ACTIVITY; SUNITINIB;
   BEVACIZUMAB; TEMSIROLIMUS; HYPERTENSION; BIOMARKER; TARGET; TUMORS
AB Tyrosine kinase inhibitor (TKI)-induced thyroid dysfunction has been identified as an important but manageable adverse effect of targeted therapy. Several studies have suggested that patients who develop hypothyroidism respond better to TKIs, but this relationship is not well elucidated. We evaluated the relationship between new-onset hypothyroidism and clinical response in patients with advanced cancers treated with TKIs at our institution.
   We retrospectively reviewed records for patients from four clinical trials that included at least one TKI therapy between January 2006 and December 2011. Patients with preexisting thyroid disease, including thyroid cancer, hypothyroidism, or hyperthyroidism, were excluded. Analysis of 197 patients was performed. Response was determined using RECIST 1.0. Clinical benefit was described as complete response, partial response, or stable disease greater than 4 months. Multivariable logistic regression analysis was performed to correlate patient characteristics with clinical response.
   The median age for the 197 patients was 58 years (range, 13-85 years), and 56 % were female. Of the 197 patients, 52 (26 %) developed hypothyroidism after therapy. Clinical benefit rates were 50 % in patients with new-onset hypothyroidism versus 34 % in patients without hypothyroidism. In the univariate model, the odds ratio (OR) for new-onset hypothyroidism was 1.9 [95 % confidence interval (CI) (1.0, 3.6) and p = 0.05]. We grouped tumor types into six categories (breast, colorectal carcinoma, melanoma, non-small cell lung cancer, pancreas, and other). When adjusted for tumor type, age (> 50 years) and sex, the OR was 2.9 [95 % CI (1.3, 6.5) and p = 0.012] for new-onset hypothyroidism.
   New-onset hypothyroidism was associated with favorable clinical response in patients who received TKI treatment.
C1 [Bilen, Mehmet Asim] Univ Texas MD Anderson Canc Ctr, Div Canc Med, Houston, TX 77030 USA.
   [Patel, Amy; Wheler, Jennifer J.; Janku, Filip; Falchook, Gerald S.; Hong, David S.; Meric-Bernstam, Funda; Naing, Aung] Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapeut, 1515 Holcombe Blvd,Box 455, Houston, TX 77030 USA.
   [Hess, Kenneth R.] Univ Texas MD Anderson Canc Ctr, Dept Biostat, Houston, TX 77030 USA.
   [Munoz, Javier] Banner MD Anderson Canc Ctr, Dept Hematol Oncol, Gilbert, AR USA.
   [Busaidy, Naifa L.; Habra, Mouhammed Amir] Univ Texas MD Anderson Canc Ctr, Dept Endocrine Neoplasia & Hormonal Disorders, Houston, TX 77030 USA.
   [Meric-Bernstam, Funda] Univ Texas MD Anderson Canc Ctr, Dept Surg Oncol, Houston, TX 77030 USA.
   [Meric-Bernstam, Funda] Univ Texas MD Anderson Canc Ctr, Sheikh Khalifa Bin Zayed Nahyan Inst Personalized, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; University of
   Texas System; UTMD Anderson Cancer Center; University of Texas System;
   UTMD Anderson Cancer Center; University of Texas System; UTMD Anderson
   Cancer Center; Banner Research; Banner Health; University of Texas
   System; UTMD Anderson Cancer Center; University of Texas System; UTMD
   Anderson Cancer Center; University of Texas System; UTMD Anderson Cancer
   Center
RP Naing, A (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapeut, 1515 Holcombe Blvd,Box 455, Houston, TX 77030 USA.
EM anaing@mdanderson.org
RI Hess, Kenneth/K-6546-2019; Janku, Filip/ABB-9136-2020; Hong,
   David/HKW-1105-2023; Meric-Bernstam, Funda/JRZ-1866-2023
OI Naing, Aung/0000-0002-4803-8513; Habra, Mouhammed
   Amir/0000-0002-4148-9637; S. Hong, David/0000-0001-8721-1609
FU NIH/NCI [P30CA016672]
FX This study was supported by the NIH/NCI under Award Number P30CA016672
   and used the Clinical Trials Support Resource. The results of this study
   were presented in a poster at the American Association for Cancer
   Research annual meeting in San Diego, CA, on April 7, 2014.
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NR 22
TC 16
Z9 17
U1 0
U2 9
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
EI 1432-0843
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD JUL
PY 2016
VL 78
IS 1
BP 167
EP 171
DI 10.1007/s00280-016-3073-z
PG 5
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA DQ2IY
UT WOS:000379027200017
PM 27286994
DA 2025-01-04
ER

PT J
AU Song, HC
   Zhou, HC
   Gu, P
   Bao, B
   Sun, Q
   Mei, TM
   Cui, W
   Yao, K
   Yao, HZ
   Zhang, SY
   Wang, YS
   Song, RP
   Wang, JZ
AF Song, Hua-Chuan
   Zhou, Hang-Cheng
   Gu, Ping
   Bao, Bing
   Sun, Quan
   Mei, Tian-Ming
   Cui, Wei
   Yao, Kang
   Yao, Huan-Zhang
   Zhang, Shen-Yu
   Wang, Yong-Shuai
   Song, Rui-Peng
   Wang, Ji-Zhou
TI Tumour response following preoperative chemotherapy is affected by body
   mass index in patients with colorectal liver metastases
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Colorectal liver metastases; Body mass index; Tumour regression grade;
   Preoperative chemotherapy; Hepatectomy
ID PHYSICAL-ACTIVITY; INSULIN-RESISTANCE; CANCER RECURRENCE; OBESITY;
   SURVIVAL; EXERCISE; ASSOCIATION; IMPACT; REDUCTION; CHEMORADIOTHERAPY
AB BACKGROUND Colorectal cancer is the third most prevalent malignancy globally and ranks second in cancer-related mortality, with the liver being the primary organ of metastasis. Preoperative chemotherapy is widely recommended for initially or potentially resectable colorectal liver metastases (CRLMs). Tumour pathological response serves as the most important and intuitive indicator for assessing the efficacy of chemotherapy. However, the postoperative pathological results reveal that a considerable number of patients exhibit a poor response to preoperative chemotherapy. Body mass index (BMI) is one of the factors affecting the tumorigenesis and progression of colorectal cancer as well as prognosis after various antitumour therapies. Several studies have indicated that overweight and obese patients with metastatic colorectal cancer experience worse prognoses than those with normal weight, particularly when receiving first-line chemotherapy regimens in combination with bevacizumab. AIM To explore the predictive value of BMI regarding the pathologic response following preoperative chemotherapy for CRLMs. METHODS A retrospective analysis was performed in 126 consecutive patients with CRLM who underwent hepatectomy following preoperative chemotherapy at four different hospitals from October 2019 to July 2023. Univariate and multivariate logistic regression models were applied to analyse potential predictors of tumour pathological response. The Kaplan-Meier method with log rank test was used to compare progression-free survival (PFS) between patients with high and low BMI. BMI < 24.0 kg/m2 was defined as low BMI, and tumour regression grade 1-2 was defined as complete tumour response. RESULTS Low BMI was observed in 74 (58.7%) patients and complete tumour response was found in 27 (21.4%) patients. The rate of complete tumour response was significantly higher in patients with low BMI (29.7% vs 9.6%, P = 0.007). Multivariate analysis revealed that low BMI [odds ratio (OR) = 4.56, 95% confidence interval (CI): 1.42-14.63, P = 0.011], targeted therapy with bevacizumab (OR = 3.02, 95%CI: 1.10-8.33, P = 0.033), preoperative carcinoembryonic antigen level < 10 ng/mL (OR = 3.84, 95%CI: 1.19-12.44, P = 0.025) and severe sinusoidal dilatation (OR = 0.17, 95%CI: 0.03-0.90, P = 0.037) were independent predictive factors for complete tumour response. The low BMI group exhibited a significantly longer median PFS than the high BMI group (10.7 mo vs 4.7 mo, P = 0.011). CONCLUSION In CRLM patients receiving preoperative chemotherapy, a low BMI may be associated with better tumour response and longer PFS.
C1 [Song, Hua-Chuan; Yao, Huan-Zhang; Wang, Ji-Zhou] Anhui Med Univ, Prov Hosp, Dept Gen Surg, 218 Jixi Rd, Hefei 230001, Anhui, Peoples R China.
   [Song, Hua-Chuan; Zhang, Shen-Yu; Wang, Yong-Shuai; Song, Rui-Peng; Wang, Ji-Zhou] Univ Sci & Technol China, Affiliated Hosp 1, Dept Hepatobiliary Surg, Div Life Sci & Med, Hefei 230001, Anhui, Peoples R China.
   [Zhou, Hang-Cheng; Gu, Ping] Univ Sci & Technol China, Affiliated Hosp 1, Dept Pathol, Div Life Sci & Med, Hefei 230001, Anhui, Peoples R China.
   [Bao, Bing] Tongcheng Peoples Hosp, Dept Gastrointestinal Surg, Tongcheng 231400, Anhui, Peoples R China.
   [Sun, Quan; Mei, Tian-Ming] Anhui Med Univ, Suzhou Hosp, Dept Gastrointestinal Surg, Suzhou 234000, Anhui, Peoples R China.
   [Cui, Wei; Yao, Kang] Xuancheng Peoples Hosp, Dept Gen Surg, Xuancheng 242000, Anhui, Peoples R China.
C3 Anhui Medical University; Chinese Academy of Sciences; University of
   Science & Technology of China, CAS; Chinese Academy of Sciences;
   University of Science & Technology of China, CAS; Anhui Medical
   University
RP Wang, JZ (corresponding author), Anhui Med Univ, Prov Hosp, Dept Gen Surg, 218 Jixi Rd, Hefei 230001, Anhui, Peoples R China.
EM wangjoe@ustc.edu.cn
RI Cui, Wei/LMO-5038-2024; Ping, Gu/JXM-1659-2024
FU National Natural Science Foundation of China [82170618]
FX Supported by National Natural Science Foundation of China, No. 82170618
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NR 50
TC 1
Z9 1
U1 1
U2 2
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD FEB 15
PY 2024
VL 16
IS 2
DI 10.4251/wjgo.v16.i2.331
PG 13
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA KQ6B8
UT WOS:001181461700008
PM 38425385
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zhou, SZ
   Sun, DZ
   Mao, WJ
   Liu, Y
   Cen, W
   Ye, LC
   Liang, F
   Xu, JM
   Shi, HC
   Ji, Y
   Wang, LS
   Chang, WJ
AF Zhou, Shizhao
   Sun, Dazhen
   Mao, Wujian
   Liu, Yu
   Cen, Wei
   Ye, Lechi
   Liang, Fei
   Xu, Jianmin
   Shi, Hongcheng
   Ji, Yuan
   Wang, Lisheng
   Chang, Wenju
TI Deep radiomics-based fusion model for prediction of bevacizumab
   treatment response and outcome in patients with colorectal cancer liver
   metastases: a multicentre cohort study
SO ECLINICALMEDICINE
LA English
DT Article
DE Colorectal cancer; Liver metastases; Multi-modal; Deep learning;
   Treatment efficacy
ID LYMPH-NODE METASTASIS; PREOPERATIVE PREDICTION; HEPATIC RESECTION;
   RECURRENCE; NOMOGRAM; THERAPY; RECIST; CEA
AB Background Accurate tumour response prediction to targeted therapy allows for personalised conversion therapy for patients with unresectable colorectal cancer liver metastases (CRLM). In this study, we aimed to develop and validate a multi-modal deep learning model to predict the efficacy of bevacizumab in patients with initially unresectable CRLM using baseline PET/CT, clinical data, and colonoscopy biopsy specimens. Methods In this multicentre cohort study, we retrospectively collected data of 307 patients with CRLM from the BECOME study (NCT01972490) (Zhongshan Hospital of Fudan University, Shanghai) and two independent Chinese cohorts (internal validation cohort from January 1, 2018 to December 31, 2018 at Zhongshan Hospital of Fudan University; external validation cohort from January 1, 2020 to December 31, 2020 at Zhongshan Hospital-Xiamen, Shanghai, and the First Hospital of Wenzhou Medical University, Wenzhou). The main inclusion criteria were that patients with CRLM had pre-treatment PET/CT images as well as colonoscopy specimens. After extracting PET/CT features with deep neural networks (DNN) and selecting related clinical factors using LASSO analysis, a random forest classifier was built as the Deep Radiomics Bevacizumab efficacy predicting model (DERBY). Furthermore, by combining histopathological biomarkers into DERBY, we established DERBY+. The performance of model was evaluated using area under the curve (AUC), sensitivity, specificity, positive predictive value, and negative predictive value. Findings DERBY achieved promising performance in predicting bevacizumab sensitivity with an AUC of 0.77 and 95% confidence interval (CI) [0.67-0.87]. After combining histopathological features, we developed DERBY+, which had more robust accuracy for predicting tumour response in external validation cohort (AUC 0.83 and 95% CI [0.75-0.92], sensitivity 80.4%, specificity 76.8%). DERBY+ also had prognostic value: the responders had longer progression-free survival (median progression-free survival: 9.6 vs 6.3 months, p = 0.002) and overall survival (median overall survival: 27.6 vs 18.5 months, p = 0.010) than non-responders. Interpretation This multi-modal deep radiomics model, using PET/CT, clinical data and histopathological data, was able to identify patients with bevacizumab-sensitive CRLM, providing a favourable approach for precise patient treatment. To further validate and explore the clinical impact of this work, future prospective studies with larger patient cohorts are warranted. Funding The National Natural Science Foundation of China; Fujian Provincial Health Commission Project; Xiamen Science and Technology Agency Program; Clinical Research Plan of SHDC; Shanghai Science and Technology Committee Project; Clinical Research Plan of SHDC; Zhejiang Provincial Natural Science Foundation of China; and National Science Foundation of Xiamen.
C1 [Zhou, Shizhao; Liu, Yu; Xu, Jianmin; Chang, Wenju] Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Dept Colorectal Surg, Shanghai 200032, Peoples R China.
   [Zhou, Shizhao; Liu, Yu; Xu, Jianmin; Chang, Wenju] Fudan Univ, Zhongshan Hosp, Canc Ctr, Shanghai 200032, Peoples R China.
   [Sun, Dazhen; Wang, Lisheng] Shanghai Jiao Tong Univ, Dept Automat, Shanghai 200240, Peoples R China.
   [Mao, Wujian; Shi, Hongcheng] Fudan Univ, Zhongshan Hosp, Dept Nucl Med, Shanghai 200032, Peoples R China.
   [Cen, Wei] Wenzhou Med Univ, Affiliated Hosp 1, Dept Surg, Wenzhou 325000, Zhejiang, Peoples R China.
   [Liang, Fei] Fudan Univ, Zhongshan Hosp, Dept Biostat, Shanghai, Peoples R China.
   [Ji, Yuan] Fudan Univ, Zhongshan Hosp, Dept Pathol, Shanghai 200032, Peoples R China.
   [Chang, Wenju] Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Xiamen Branch, Xiamen 361015, Fujian, Peoples R China.
   [Chang, Wenju] Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Dept Colorectal Surg, 180 Fenglin Rd, Shanghai 200032, Peoples R China.
   [Ji, Yuan] Fudan Univ, Zhongshan Hosp, Dept Nucl Med, 180 Fenglin Rd, Shanghai 200032, Peoples R China.
   [Xu, Jianmin] Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Dept Colorectal Surg, 180 Fenglin Rd, Shanghai 200032, Peoples R China.
C3 Fudan University; Fudan University; Shanghai Jiao Tong University; Fudan
   University; Wenzhou Medical University; Fudan University; Fudan
   University; Fudan University; Fudan University; Fudan University; Fudan
   University
RP Wang, LS (corresponding author), Shanghai Jiao Tong Univ, Dept Automat, Shanghai 200240, Peoples R China.; Shi, HC (corresponding author), Fudan Univ, Zhongshan Hosp, Dept Nucl Med, Shanghai 200032, Peoples R China.; Chang, WJ (corresponding author), Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Dept Colorectal Surg, 180 Fenglin Rd, Shanghai 200032, Peoples R China.; Ji, Y (corresponding author), Fudan Univ, Zhongshan Hosp, Dept Nucl Med, 180 Fenglin Rd, Shanghai 200032, Peoples R China.; Xu, JM (corresponding author), Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Dept Colorectal Surg, 180 Fenglin Rd, Shanghai 200032, Peoples R China.
EM xujmin@aliyun.com; shi.hongcheng@zs-hospital.sh.cn;
   ji.yuan@zs-hospital.sh.cn; lswang@sjtu.edu.cn;
   chang.wenju@zs-hospital.sh.cn
OI Liang, Fei/0000-0002-4184-7844
FU National Natural Science Foundation of China [82072653, 81602035,
   82172816]; Fujian Provincial Health Commission Project [2021GGB032];
   Xiamen Science and Technology Agency Program [3502Z20224ZD1067];
   Clinical Research Plan of SHDC [SHDC2020CR3037B, SHDC2020CR5006];
   Shanghai Science and Technology Committee Project [19511121300];
   Zhejiang Provincial Natural Science Foundation of China [LY22H160021];
   National Science Foundation of Xiamen [2023J06057]; Zhong-shan Hospital
   Xiamen of Fudan University
FX This trial was funded by the National Natural Science Foundation of
   China (82072653, 81602035, 82172816) ; Fujian Provincial Health
   Commission Project (2021GGB032) ; Xiamen Science and Technology Agency
   Program (3502Z20224ZD1067) ; Clinical Research Plan of SHDC (No.
   SHDC2020CR5006) ; Shanghai Science and Technology Committee Project
   (19511121300) ; Clinical Research Plan of SHDC (No. SHDC2020CR3037B) ;
   Zhejiang Provincial Natural Science Foundation of China (LY22H160021) ;
   National Science Foundation of Xiamen (2023J06057) . We thank
   collaborators at Zhongshan Hospital and Zhong-shan Hospital Xiamen of
   Fudan University, the First Affiliated Hospital of Wenzhou Medical
   University for assistance with histopathology.
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NR 54
TC 7
Z9 8
U1 12
U2 26
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2589-5370
J9 ECLINICALMEDICINE
JI EClinicalMedicine
PD NOV
PY 2023
VL 65
AR 102271
DI 10.1016/j.eclinm.2023.102271
EA OCT 2023
PG 15
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA Z6BT1
UT WOS:001112912400001
PM 37869523
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Grsic, K
   Opacic, IL
   Sitic, S
   Perisa, MM
   Suton, P
   Sarcevic, B
AF Grsic, Kresimir
   Opacic, Iva Ledinsky
   Sitic, Sanda
   Perisa, Marija Milkovic
   Suton, Petar
   Sarcevic, Bozena
TI The prognostic significance of estrogen receptor in head and neck
   squamous cell carcinoma
SO ONCOLOGY LETTERS
LA English
DT Article
DE head and neck squamous cell carcinoma; estrogen receptor; recurrence;
   survival; prognosis
ID LARYNGEAL CARCINOMA; PROGESTERONE-RECEPTORS; CANCER; BETA; EXPRESSION;
   ALPHA; INVASION
AB Head and neck squamous cell carcinoma (HNSCC) is the fifth most common cancer in the world. Although multimodal and targeted therapy is now used in therapeutic procedures, the survival of patients with HNSCC has remained unchanged over the last 30 years. A number of studies have demonstrated that the increased expression of intranuclear ER in breast, lung and colon cancer is a favorable prognostic marker associated with higher survival rates. However, the clinical significance of sex hormone receptors in HNSCC remains unclear. The current study aimed to assess the expression of ER in HNSCC immunohistochemically and investigate any possible association between ER expression, and clinical and histopathological factors, disease recurrence and patient survival. The present study included 174 patients (165 males and 9 females) with a median age of 60.8 years (range, 39-79) with HNSCC who were primary surgically treated between January 2000 and December 2006. Immunohistochemical reactions for ER demonstrated that 73 patients (42%) exhibited positive ER expression. Distribution of ER status among different head and neck subsites indicated that >40% of all negative cases were located in laryngeal primaries, while incidence of other sublocalization within positive cases was similar and comparable (P=0.04). Furthermore, a correlation was observed between ER immunopositivity and the survival of patients, with respect to the primary tumor site. Patients with ER positive oropharyngeal cancer had a survival rate of 35.3% at 5-years compared with 25% for patients with negative expression. However, ER status was not significantly correlated with any other clinical or histopathological parameter. After an average follow-up time of 38.5 months (range, 3-60 months), 54 patients (31.1%) had succumbed to disease recurrence while 50 (28.7%) succumbed to other causes. In conclusion, ER positivity indicates improved survival of patients with oropharyngeal cancer. Further research is required in order to implement novel therapeutic strategies.
C1 [Grsic, Kresimir; Opacic, Iva Ledinsky] Univ Hosp Tumors, Div Head & Neck Surg, Dept Surg Oncol, Clin Hosp Ctr Sisters Char, Ilica 197, Zagreb 10000, Croatia.
   [Sitic, Sanda; Perisa, Marija Milkovic; Sarcevic, Bozena] Univ Hosp Tumors, Dept Clin Pathol, Clin Hosp Ctr Sisters Char, Zagreb 10000, Croatia.
   [Suton, Petar] Univ Hosp Tumors, Div Radiat Oncol, Dept Radiotherapy & Med Oncol, Clin Hosp Ctr Sisters Char, Zagreb 10000, Croatia.
RP Grsic, K (corresponding author), Univ Hosp Tumors, Div Head & Neck Surg, Dept Surg Oncol, Clin Hosp Ctr Sisters Char, Ilica 197, Zagreb 10000, Croatia.
EM kresimir.grsic@yahoo.com
RI Suton, Petar/GRJ-5548-2022
OI Grsic, Kresimir/0000-0002-2907-8640; Milkovic Perisa,
   Marija/0000-0002-9530-9208
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NR 31
TC 12
Z9 13
U1 0
U2 7
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD NOV
PY 2016
VL 12
IS 5
BP 3861
EP 3865
DI 10.3892/ol.2016.5142
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ED4RR
UT WOS:000388838900120
PM 27895741
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Liu, XD
   Feng, DQ
   Wang, WH
   Liang, J
   Yu, H
   Ling, B
AF Liu, Xiaodie
   Feng, Dingqing
   Wang, Wenhui
   Liang, Jing
   Yu, Huan
   Ling, Bin
TI Tumor Microenvironment CD8 T and Treg Cells-related Genes Signature
   Distinguishes Distinct Prognosis and Targeted Therapies Response in
   Endometrial Cancer
SO JOURNAL OF IMMUNOTHERAPY
LA English
DT Article
DE endometrial cancer; tumor immune microenvironment; prognosis signature;
   targeted therapy; drugs prediction
ID HOMOLOGOUS RECOMBINATION; IMMUNE MICROENVIRONMENT; COLORECTAL-CANCER;
   EXPRESSION; OVARIAN; REPAIR; INSTABILITY; DEFICIENCY; IPILIMUMAB;
   CARCINOMA
AB Although most endometrial cancer (EC) patients have a favorable prognosis, the overall survival (OS) of metastatic and recurrent EC could hardly be improved by the current chemoradiotherapy. We aimed to reveal the tumor microenvironment immune infiltration characteristics to elucidate the underlying mechanism of EC progression and guide clinical decisions. In the Cancer Genome Atlas (TCGA) cohort, Kaplan-Meier survival curves confirmed Tregs and CD8 T cells were prognosis-protective factors in OS of EC (P<0.05). Weighted gene coexpression network analysis identified 2 gene modules closely correlated with Tregs and CD8 T-cell infiltration. We randomly split the TCGA EC cohort into the training and testing cohorts at a ratio of 7:3. An immune-related prognosis risk index (IRPRI), including NR3C1, E2F1, OTOG, TTK, PPP1R16B, and FOXP3, was established by univariate, Least Absolute Shrinkage and Selection Operator, and multivariate Cox regression with area under the curve >0.67. Distinct clinical, immune, and mutation characteristics existed between IRPRI groups by multiomics analysis. Cell proliferation and DNA damage repair-related pathways were activated, and immune-related pathways were inactivated in the IRPRI-high group. Furthermore, patients in the IRPRI-high group had lower tumor mutation burden, programmed death-ligand 1 expression, and Tumor Immune Dysfunction and Exclusion scores, indicating a poor response to immune checkpoint inhibitors therapy (P<0.05), which was also validated in the TCGA testing cohort and independent cohorts, GSE78200, GSE115821, and GSE168204. Also, the higher mutation frequencies of BRCA1, BRCA2, and genes enrolled in homologous recombination repair in the IRPRI-low group predicted a good response to PARP inhibitors. Finally, a nomogram integrating the IRPRI group and prognosis significant clinicopathological factors for EC OS prediction was developed and validated with good discrimination and calibration.
C1 [Liu, Xiaodie; Ling, Bin] Chinese Acad Med Sci & Peking Union Med Coll, China Japan Friendship Hosp, Inst Clin Med Sci, Dept Obstet & Gynecol, Beijing, Peoples R China.
   [Feng, Dingqing; Wang, Wenhui; Liang, Jing; Yu, Huan; Ling, Bin] China Japan Friendship Hosp, Dept Obstet & Gynecol, Beijing, Peoples R China.
   [Ling, Bin] China Japan Friendship Hosp, Dept Obstet & Gynecol, 2 Dong St, Beijing 100029, Peoples R China.
C3 China-Japan Friendship Hospital; Chinese Academy of Medical Sciences -
   Peking Union Medical College; Peking Union Medical College; China-Japan
   Friendship Hospital; China-Japan Friendship Hospital
RP Ling, B (corresponding author), China Japan Friendship Hosp, Dept Obstet & Gynecol, 2 Dong St, Beijing 100029, Peoples R China.
EM 15153129355@163.com; dingqing_feng@yahoo.com; wwh5016@126.com;
   jacyliang@sina.com; yuhuan2000@sina.com; lingbin.ling@vip.sina.com
OI Ling, Bin/0000-0001-5048-0311; Wang, Wenhui/0000-0003-3258-1885
FU National Key R&D Program of China [2018YFC1003900]
FX CONFLICTS OF INTEREST/FINANCIAL DISCLOSURES The study was funded by the
   National Key R&D Program of China (2018YFC1003900). All the authors
   declared that there are no financial conflicts of interest with regard
   to this work.
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NR 69
TC 3
Z9 3
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1524-9557
EI 1537-4513
J9 J IMMUNOTHER
JI J. Immunother.
PD JUN
PY 2023
VL 46
IS 5
BP 178
EP 191
DI 10.1097/CJI.0000000000000463
PG 14
WC Oncology; Immunology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology; Research & Experimental Medicine
GA F8RH3
UT WOS:000984959600003
PM 37098928
DA 2025-01-04
ER

PT J
AU Oukkal, M
   Bouzid, K
   Bounedjar, A
   Alnajar, A
   Abou Taleb, F
   Alsharm, A
   Mahfouf, H
   Larbaoui, B
   Abdelaziz, A
   Ouamer, A
   Bashir, L
AF Oukkal, Mohammed
   Bouzid, Kamel
   Bounedjar, Adda
   Alnajar, Abdulsalam
   Abou Taleb, Fouad
   Alsharm, Abdullah
   Mahfouf, Hassen
   Larbaoui, Blaha
   Abdelaziz, Amr
   Ouamer, Assia
   Bashir, Linah
TI Middle East and North Africa Registry to Characterize Rate of RAS
   Testing Status in Newly Diagnosed Patients with Metastatic Colorectal
   Cancer
SO TURKISH JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Colorectal cancer; metastatic disease; observational trial; RAS testing
ID ANTI-EGFR THERAPY; 1ST-LINE TREATMENT; PHASE-III; FLUOROURACIL;
   PANITUMUMAB; LEUCOVORIN; CETUXIMAB; MULTICENTER; MUTATIONS; TOXICITY
AB Background: Rat sarcoma virus mutational status guides first-line treatment in metastatic colorectal cancer. This study was a multicenter, multi-country ambispective, observational study in the Middle East and North Africa assessing regional rat sarcoma virus testing practices in newly diagnosed patients.
   Methods: The retrospective arm (2011-2014) included adults with metastatic colorectal cancer who had initiated first-line therapy with >= 1 post-baseline visit and survival data. The prospective arm (2014-2019) enrolled newly diagnosed patients with histologically proven metastatic colorectal cancer with >= 1 measurable lesion per Response Evaluation Criteria in Solid Tumors, and tissue availability for biomarker analysis. Data look-back and follow-up were 2 years; the rate of RAS mutation was evaluated.
   Results: RAS testing was ordered for patients in retrospective (326/417) and prospective (407/500) studies. In the former, testing was typically prescribed after first-line treatment initiation, significantly more in patients with stage IV disease (P <.005), resulting in the addition of targeted therapy (41.8% anti-epidermal growth factor receptor, 30.2% anti-vascular endothelial growth factor) in wild-type metastatic colorectal cancer, and significantly impacted the treatment of left-sided tumors (P =.037). In the latter, 58.4% were RAS wild-type; 41.6% were RAS mutant. Non-prescription of RAS testing was attributed to test unavailability, financial, or medical reasons; predictors of testing prescription were older age, primary tumor in ascending colon, and high tumor grade. RAS status knowledge resulted in the addition of anti-vascular endothelial growth factor (20.4%) or anti-epidermal growth factor receptor therapy (21.2%).
   Conclusion: Before 2014, RAS testing in patients with colorectal cancer in the Middle East and North Africa was often performed after first-line treatment. Testing is more routine in newly diagnosed patients, potentially shifting early treatment patterns.
C1 [Oukkal, Mohammed] Univ Ctr Beni Messous, Dept Med Oncol, Algiers, Algeria.
   [Bouzid, Kamel] Ctr Pierre & Marie Curie, Dept Med Oncol, Algiers, Algeria.
   [Bounedjar, Adda] Univ Ctr Blida, Dept Med Oncol, Blida, Algeria.
   [Alnajar, Abdulsalam] Kuwait Canc Control Ctr, GI Oncol Dept, Sabah Hlth Region, Kuwait.
   [Abou Taleb, Fouad] Zagazig Univ, Dept Med Oncol, Fac Med, Zagazih, Al Sharkeyya, Egypt.
   [Alsharm, Abdullah] King Fahad Med City Hosp, Comprehens Canc Ctr, Dept Med Oncol, Riyadh, Saudi Arabia.
   [Mahfouf, Hassen] Publ Hosp Rouiba, Dept Med Oncol, Algiers, Algeria.
   [Larbaoui, Blaha] Canc Ctr Oran, Dept Med Oncol, Messerghine, Algeria.
   [Abdelaziz, Amr] Alexandria Univ, Dept Med Oncol, Fac Med, Alexandria, Egypt.
   [Ouamer, Assia] AMGEN Maghreb, Dept Oncol, Algiers, Algeria.
   [Bashir, Linah] AMGEN Middle East, Dept Oncol Hematol & Nephrol, Dubai, U Arab Emirates.
C3 Egyptian Knowledge Bank (EKB); Zagazig University; King Fahad Medical
   City; Egyptian Knowledge Bank (EKB); Alexandria University
RP Oukkal, M (corresponding author), Univ Ctr Beni Messous, Dept Med Oncol, Algiers, Algeria.
EM mohammedoukkal@gmail.com
FU Amgen (Middle East) FZ-LLC
FX This study was supported by Amgen (Middle East) FZ-LLC.
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NR 31
TC 2
Z9 2
U1 0
U2 0
PU AVES
PI SISLI
PA BUYUKDERE CAD 105-9, MECIDIYEKOY, SISLI, ISTANBUL 34394, Turkiye
EI 2148-5607
J9 TURK J GASTROENTEROL
JI Turk. J. Gastroenterol.
PD FEB
PY 2023
VL 34
IS 2
BP 118
EP 127
DI 10.5152/tjg.2022.22106
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA A5OH6
UT WOS:000955608100004
PM 36445057
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Cavalloni, G
   Peraldo-Neia, C
   Varamo, C
   Chiorino, G
   Sassi, F
   Aglietta, M
   Leone, F
AF Cavalloni, Giuliana
   Peraldo-Neia, Caterina
   Varamo, Chiara
   Chiorino, Giovanna
   Sassi, Francesco
   Aglietta, Massimo
   Leone, Francesco
TI Preclinical activity of EGFR and MEK1/2 inhibitors in the treatment of
   biliary tract carcinoma
SO ONCOTARGET
LA English
DT Article
DE biliary tract carcinoma; K-RAS mutation; target therapy; MEK inhibitor;
   preclinical models
ID K-RAS MUTATION; PHASE-II; INTRAHEPATIC CHOLANGIOCARCINOMAS; P53
   OVEREXPRESSION; COLORECTAL-CANCER; OPEN-LABEL; GEMCITABINE; RESISTANCE;
   KRAS; OXALIPLATIN
AB Biliary tract carcinomas (BTC) are malignant tumors with limited therapeutic options. Clinical experiences with anti-EGFR therapies have produced unsatisfactory results. The strategies of combined inhibition of EGFR and MEK1/2 could be a promising therapeutic option in BTC treatment. Preclinical activity of Panitumumab and Trametinib was tested in in vitro (EGI-1, MT-CHC01 and WITT cells) and in in vivo (xenograft) BTC models with different K-RAS mutational status. Trametinib reduced MAPK phosphorylation in wild type (WT) WITT cells and in both K-RAS mutated cells; in EGI-1 was also able to switch off EGFR activation. Panitumumab reduced the activation of its target only in EGI-1 cells, and of MAPK only in WITT cells. While Trametinib inhibited cell growth in K-RAS mutated cell lines, Panitumumab had no effect on proliferation independently by K-RAS status. The addition of Panitumumab to Trametinib did not significantly potentiate its anti-proliferative effect also in mutated cells. In vivo, Trametinib was able to significantly slow the tumor growth in K-RAS mutated xenograft models, but did not have effect on K-RAS WT cells; the addition of Panitumumab potentiated the Trametinib efficacy in MT-CHC01 and overcame the resistance to the anti-EGFR in WITT cells, in which the monotherapy was ineffective. Only in K-RAS mutated xenografts Trametinib alone or in combination with Panitumumab significantly decreased Ki67 positive cell fraction and CD31 angiogenesis markers. In conclusion, this preclinical study provides a rational to plan clinical trials assessing the efficacy of Trametinib in K-RAS mutated BTC patients and the combination with anti-EGFR in WT BTC patients.
C1 [Cavalloni, Giuliana; Aglietta, Massimo; Leone, Francesco] Candiolo Canc Inst IRCCS, FPO, Div Med Oncol, Candiolo, Italy.
   [Peraldo-Neia, Caterina; Varamo, Chiara; Aglietta, Massimo; Leone, Francesco] Univ Turin, Candiolo Canc Inst IRCCS, Dept Oncol, Candiolo, Italy.
   [Chiorino, Giovanna] Fdn Edo & Elvo Tempia Valenta, Canc Genom Lab, Biella, Italy.
   [Sassi, Francesco] Univ Turin, Sch Med, Candiolo Canc Inst IRCCS, Unit Mol Pharmacol, Candiolo, Italy.
C3 IRCCS Fondazione del Piemonte per l'Oncologia; University of Turin;
   IRCCS Fondazione del Piemonte per l'Oncologia; University of Turin;
   IRCCS Fondazione del Piemonte per l'Oncologia
RP Cavalloni, G (corresponding author), Candiolo Canc Inst IRCCS, FPO, Div Med Oncol, Candiolo, Italy.
EM giuliana.cavalloni@ircc.it
RI Leone, Francesco/AAB-2355-2022; Peraldo-Neia, Caterina/AAB-5226-2022;
   sassi, francesco/AAB-6844-2020; LEONE, Francesco/R-3248-2016; Chiorino,
   Giovanna/K-5037-2016
OI AGLIETTA, Massimo/0000-0002-2255-7972; LEONE,
   Francesco/0000-0001-5422-9706; Cavalloni, Giuliana/0000-0002-9965-3436;
   Peraldo-Neia, Caterina/0000-0002-5484-2030; Chiorino,
   Giovanna/0000-0002-9502-6400; Varamo, Chiara/0000-0002-6115-3276; Sassi,
   Francesco/0000-0002-4741-0408
FU Associazione Italiana Ricerca sul Cancro-AIRC 5X1000 Ministry of Health,
   FPO [16:30]; Fondazione Piemontese per la Ricerca sul Cancro - Onlus -
   "Identification of new druggable pathways in intrahepatic
   cholangiocarcinoma" 5 per Mille Ministero della Salute; Universita di
   Torino anno - Fondo per la ricerca locale (Linea B)
   [LEOF_RIC_LOC_14_01]; FPO; University of Turin; Compagnia di San Paolo
FX This work was supported by grant from "Associazione Italiana Ricerca sul
   Cancro-AIRC 5X1000 2010-Ministry of Health, FPO. Project no16:30
   "Identificazione di nuove vie di trasduzione del segnale intracellulare
   sensibili ai farmaci nel colangiocarcinoma intraepatico (ICC)".
   Fondazione Piemontese per la Ricerca sul Cancro - Onlus -
   "Identification of new druggable pathways in intrahepatic
   cholangiocarcinoma" 5 per Mille 2010 Ministero della Salute; Universita
   di Torino anno 2014 - Fondo per la ricerca locale (Linea B),
   LEOF_RIC_LOC_14_01 project title: "Transcriptomic and genetic analysis
   of paired primary and recurrent intrahepatic cholangiocarcinoma"; GC and
   FS are supported by FPO; CPN is supported by University of Turin; GC is
   supported by a grant of Compagnia di San Paolo; MA and FL are supported
   by University of Turin and FPO.
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NR 30
TC 13
Z9 13
U1 0
U2 6
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD AUG 9
PY 2016
VL 7
IS 32
BP 52354
EP 52363
DI 10.18632/oncotarget.10587
PG 10
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DY9CC
UT WOS:000385429100124
PM 27429047
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Kwan, J
   Pua, U
AF Kwan, Justin
   Pua, Uei
TI Review of Intra-Arterial Therapies for Colorectal Cancer Liver
   Metastasis
SO CANCERS
LA English
DT Review
DE colorectal liver metastasis; liver-directed intra-arterial therapy;
   hepatic arterial infusion therapy; trans-arterial chemoembolization;
   radioembolization
ID HEPATIC-ARTERIAL-INFUSION; INTERNAL RADIATION-THERAPY; DRUG-ELUTING
   BEADS; Y-90 RESIN MICROSPHERES; RANDOMIZED CONTROLLED-TRIAL; MULTICENTER
   PHASE-II; TRANSARTERIAL CHEMOEMBOLIZATION; HEPATOCELLULAR-CARCINOMA;
   SYSTEMIC CHEMOTHERAPY; PRETREATED PATIENTS
AB Simple Summary
   Colorectal cancer liver metastasis occurs in more than 50% of patients with colorectal cancer and is thought to be the most common cause of death from this cancer. The mainstay of treatment for inoperable liver metastasis has been combination systemic chemotherapy with or without the addition of biological targeted therapy with a goal for disease downstaging, for potential curative resection, or more frequently, for disease control. For patients with dominant liver metastatic disease or limited extrahepatic disease, liver-directed intra-arterial therapies including hepatic arterial chemotherapy infusion, chemoembolization and radioembolization are alternative treatment strategies that have shown promising results, most commonly in the salvage setting in patients with chemo-refractory disease. In recent years, their role in the first-line setting in conjunction with concurrent systemic chemotherapy has also been explored. This review aims to provide an update on the current evidence regarding liver-directed intra-arterial treatment strategies and to discuss potential trends for the future.
   The liver is frequently the most common site of metastasis in patients with colorectal cancer, occurring in more than 50% of patients. While surgical resection remains the only potential curative option, it is only eligible in 15-20% of patients at presentation. In the past two decades, major advances in modern chemotherapy and personalized biological agents have improved overall survival in patients with unresectable liver metastasis. For patients with dominant liver metastatic disease or limited extrahepatic disease, liver-directed intra-arterial therapies such as hepatic arterial chemotherapy infusion, chemoembolization and radioembolization are treatment strategies which are increasingly being considered to improve local tumor response and to reduce systemic side effects. Currently, these therapies are mostly used in the salvage setting in patients with chemo-refractory disease. However, their use in the first-line setting in conjunction with systemic chemotherapy as well as to a lesser degree, in a neoadjuvant setting, for downstaging to resection have also been investigated. Furthermore, some clinicians have considered these therapies as a temporizing tool for local disease control in patients undergoing a chemotherapy 'holiday' or acting as a bridge in patients between different lines of systemic treatment. This review aims to provide an update on the current evidence regarding liver-directed intra-arterial treatment strategies and to discuss potential trends for the future.
C1 [Kwan, Justin; Pua, Uei] Tan Tock Seng Hosp, Dept Vasc & Intervent Radiol, Singapore 388403, Singapore.
C3 Tan Tock Seng Hospital
RP Kwan, J (corresponding author), Tan Tock Seng Hosp, Dept Vasc & Intervent Radiol, Singapore 388403, Singapore.
EM Justin_kwan@ttsh.com.sg; pua_uei@ttsh.com.sg
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NR 134
TC 11
Z9 11
U1 1
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD MAR
PY 2021
VL 13
IS 6
AR 1371
DI 10.3390/cancers13061371
PG 27
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RE7MF
UT WOS:000634332600001
PM 33803606
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Thota, R
   Yang, ML
   Pflieger, L
   Schell, MJ
   Rajan, M
   Davis, TB
   Wang, HM
   Presson, A
   Pledger, WJ
   Yeatman, TJ
AF Thota, Ramya
   Yang, Mingli
   Pflieger, Lance
   Schell, Michael J.
   Rajan, Malini
   Davis, Thomas B.
   Wang, Heiman
   Presson, Angela
   Pledger, Warren Jack
   Yeatman, Timothy J.
TI APC and TP53 Mutations Predict Cetuximab Sensitivity across Consensus
   Molecular Subtypes
SO CANCERS
LA English
DT Article
DE colorectal cancer; APC; TP53; mutations; CMS classification; EGFR
   inhibitors; cetuximab
ID METASTATIC COLORECTAL-CANCER; DEPENDENT CELLULAR CYTOTOXICITY; 1ST-LINE
   TREATMENT; TUMOR LOCATION; KRAS MUTATION; COLON-CANCER; CHEMOTHERAPY;
   RECEPTOR; GROWTH; EGFR
AB Simple Summary: Colorectal cancer (CRC) is a major cause of cancer deaths. Cetuximab is an FDA-approved, underutilized therapeutic targeting the epidermal growth factor receptor (EGFR) in metastatic CRC. To date, despite selection of patients with wild-type RAS, it is still difficult to identify patients who may benefit from EGFR inhibitor (e.g., cetuximab) therapy. Our aim is to molecularly classify CRC patients to better identify subpopulations sensitive to EGFR targeted therapy. APC and TP53 are two major tumor suppressor genes in CRC whose mutations contribute to tumor initiation and progression and may identify cetuximab-sensitive tumors. Recently, it has been suggested that the consensus molecular subtype (CMS) classification may be used to help identify cetuximab-sensitive patients. Here, we report an analysis of multiple CRC tumor/PDX/cell line datasets using combined APC and TP53 mutations to refine the CMS classification to better predict responses to cetuximab to improve patient outcomes.</p>
   Recently, it was suggested that consensus molecular subtyping (CMS) may aide in predicting response to EGFR inhibitor (cetuximab) therapies. We recently identified that APC and TP53 as two tumor suppressor genes, when mutated, may enhance cetuximab sensitivity and may represent easily measured biomarkers in tumors or blood. Our study aimed to use APC and TP53 mutations (AP) to refine the CMS classification to better predict responses to cetuximab. In total, 433 CRC tumors were classified into CMS1-4 subtypes. The cetuximab sensitivity (CTX-S) signature scores of AP vs. non-AP tumors were determined across each of the CMS classes. Tumors harboring combined AP mutations were predominantly enriched in the CMS2 class, and to a lesser degree, in the CMS4 class. On the other hand, AP mutated CRCs had significantly higher CTX-S scores compared to non-AP CRCs across all CMS classes. Similar results were also obtained in independent TCGA tumor collections (n = 531) and in PDMR PDX/PDO/PDC models (n = 477). In addition, the in vitro cetuximab growth inhibition was preferentially associated with the CMS2 cell lines harboring A/P genotypes. In conclusion, the AP mutation signature represents a convenient biomarker that refines the CMS classification to identify CRC subpopulations predicted to be sensitive to EGFR targeted therapies.</p>
C1 [Thota, Ramya] Intermt Healthcare, Clin Oncol Program, Murray, UT 84107 USA.
   [Yang, Mingli; Rajan, Malini; Davis, Thomas B.; Wang, Heiman; Pledger, Warren Jack; Yeatman, Timothy J.] Univ Utah, Dept Surg, Salt Lake City, UT 84132 USA.
   [Pflieger, Lance] Intermt Healthcare, Precis Genom Translat Sci Ctr, Murray, UT 84107 USA.
   [Schell, Michael J.] H Lee Moffitt Canc Ctr & Res Inst, Dept Biostat & Bioinformat, Tampa, FL 33612 USA.
   [Presson, Angela] Univ Utah, Div Epidemiol, Dept Internal Med, Salt Lake City, UT 84132 USA.
   [Pledger, Warren Jack; Yeatman, Timothy J.] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
C3 Intermountain Healthcare; Intermountain Medical Center; Utah System of
   Higher Education; University of Utah; Intermountain Healthcare;
   Intermountain Medical Center; H Lee Moffitt Cancer Center & Research
   Institute; Utah System of Higher Education; University of Utah; Utah
   System of Higher Education; University of Utah; Huntsman Cancer
   Institute
RP Thota, R (corresponding author), Intermt Healthcare, Clin Oncol Program, Murray, UT 84107 USA.; Yeatman, TJ (corresponding author), Univ Utah, Dept Surg, Salt Lake City, UT 84132 USA.; Yeatman, TJ (corresponding author), Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
EM ramya.thota@imail.org; mingli.yang@utah.edu; Lance.Pflieger@imail.org;
   Michael.Schell@moffitt.org; heiman.wang@utah.edu;
   angela.presson@hsc.utah.edu
RI Yang, Mingli/LKN-2926-2024; Rajan, Malini/AAV-5433-2021; Yeatman,
   Timothy/LJK-6730-2024
OI Yang, Mingli/0000-0002-4781-690X
FU National Institutes of Health [UH3CA227955]; Intermountain Healthcare
FX FundingThis research was funded by the National Institutes of Health,
   grant number UH3CA227955 (to T.J.Y.). This research was also funded by
   generous support from Intermountain Healthcare.
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NR 70
TC 10
Z9 10
U1 0
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD NOV
PY 2021
VL 13
IS 21
AR 5394
DI 10.3390/cancers13215394
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA WX3SQ
UT WOS:000718520200001
PM 34771559
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Cohen, R
   Raeisi, M
   Chibaudel, B
   Yoshino, T
   Shi, Q
   Zalcberg, JR
   Adams, R
   Cremolini, C
   Grothey, A
   Mayer, RJ
   Van Cutsem, E
   Tabernero, J
   Bando, H
   Misumi, T
   Overman, MJ
   Andre, T
   de Gramont, A
AF Cohen, Romain
   Raeisi, Morteza
   Chibaudel, Benoist
   Yoshino, Takayuki
   Shi, Qian
   Zalcberg, John R.
   Adams, Richard
   Cremolini, Chiara
   Grothey, Axel
   Mayer, Robert J.
   Van Cutsem, Eric
   Tabernero, Josep
   Bando, Hideaki
   Misumi, Toshihiro
   Overman, Michael J.
   Andre, Thierry
   de Gramont, Aimery
TI Efficacy of immune checkpoint inhibitors for metastatic colorectal
   cancer with microsatellite instability in second or latter line using
   synthetic control arms: A non-randomised evaluation
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE Immune checkpoint inhibitors; Microsatellite instability metastatic
   colorectal; cancer; Placebo; Synthetic control arms; Matching
ID RANDOMIZED-TRIAL; POOLED ANALYSIS; DOUBLE-BLIND; PLACEBO; PLUS;
   MULTICENTER; OXALIPLATIN; IPILIMUMAB
AB Purpose Immune checkpoint inhibitors (ICIs) appeared active in single-arm trials for patients with chemoresistant metastatic colorectal cancer (mCRC) harboring microsatellite instability (MSI). Given the paucity of randomised controlled trials (RCTs) in this setting, we evaluated the effect size of ICIs using intra-patients comparison and ARCAD database as historical controls. Patients and methods Individual-patient data from NIPICOL and CheckMate 142 phase II trials that evaluated a combination of ICIs for MSI mCRC patients (N = 176) and from five non-ICI mCRC historical RCTs in second-line or latter (N = 4026) were analyzed. Firstly, promising of ICIs was identified using intra-patient comparison based on growth modulation index (GMI) defined the ratio of progression-free survivals (PFS) on ICIs and previous line of therapy. Survival outcomes of ICIs-treated patients were then compared with those matched non-ICIs treated from ARCAD database historical RCTs. Results Among ICIs-treated patients, median PFS on ICIs was 32.66 (range 0.10-74.25) versus 4.07 months (range 0.7-49.87) on prior therapy, resulting on median GMI of 4.97 (range 0.07-59.51; hazard-ratio (HR)= 0.16 (95 %CI=0.11-0.22, P < 0.001)). Compared to matched non-ICI patients, in third-line, median overall survival (OS) was not reached with ICIs versus 3.52 months with placebo (HR=0.20, 95 %CI=0.10-0.41, P < 0.001), and 6.51 months with active drugs (HR=0.30, 95 %CI=0.15-0.60, P = 0.001). In second-line, median OS was not reached with ICIs versus 11.7 months with chemotherapy+placebo (HR=0.12, 95 %CI=0.07-0.22, P < 0.001), and 16.3 months with chemotherapy+targeted therapy (HR=0.10, 95 %CI=0.05-0.19, P < 0.001). Conclusion ICIs demonstrates high effect size for MSI mCRC patients in second-line and later. This work might be useful as an example of methodology to avoid RCTs when benefit from experimental therapy is likely to be high.
C1 [Cohen, Romain] Sorbonne Univ, Hop St Antoine, AP HP, Paris, France.
   [Cohen, Romain] INSERM, UMRS 938, SIRIC CURAMUS, Ctr Rech St Antoine,Dept Med Oncol,Equipe Instabil, Paris, France.
   [Raeisi, Morteza] ARCAD Fdn, Stat Unit, Paris, France.
   [Chibaudel, Benoist] Franco British Hosp, Fdn Cognacq Jay, Dept Med Oncol, Levallois Perret, France.
   [Yoshino, Takayuki; Bando, Hideaki] Natl Canc Ctr Hosp East, Dept Gastroenterol & Gastrointestinal Oncol, Kashiwa, Japan.
   [Shi, Qian] Mayo Clin, Dept Quantitat Hlth Sci, Rochester, MN USA.
   [Zalcberg, John R.] Monash Univ, Alfred Hlth, Sch Publ Hlth & Prevent Med, Dept Med Oncol, Melbourne, Vic, Australia.
   [Adams, Richard] Cardiff Univ, Velindre Canc Ctr, Cardiff, Wales.
   [Cremolini, Chiara] Univ Pisa, Dept Translat Res & New Technol Med & Surg, Pisa, Italy.
   [Grothey, Axel] West Canc Ctr, Germantown, TN USA.
   [Mayer, Robert J.] Dana Farber Canc Inst, Boston, MA USA.
   [Van Cutsem, Eric] Univ Hosp Leuven, Digest Oncol Unit, Dept Gastrointestinal & Liver Dis, Leuven, Belgium.
   [Van Cutsem, Eric] Katholieke Univ Leuven, Leuven, Belgium.
   [Tabernero, Josep] Vall dhebron Hosp Campus, Vall dhebron Inst Oncol VHIO, Barcelona, Spain.
   [Misumi, Toshihiro] Natl Canc Ctr Hosp East, Dept Data Sci, Kashiwa, Japan.
   [Overman, Michael J.] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Div Canc Med, Houston, TX USA.
   [Andre, Thierry; de Gramont, Aimery] ARCAD Fdn, Paris, France.
   [de Gramont, Aimery] Franco British Hosp, Dept Med Oncol, Levallois Perret, France.
   [Raeisi, Morteza] ARCAD Fdn, Stat Unit, 45 Rue Croulebarbe, F-75013 Paris, France.
C3 Assistance Publique Hopitaux Paris (APHP); Sorbonne Universite; Hopital
   Universitaire Saint-Antoine - APHP; Sorbonne Universite; Institut
   National de la Sante et de la Recherche Medicale (Inserm); National
   Cancer Center - Japan; Mayo Clinic; Monash University; Cardiff
   University; Velindre Cancer Centre; University of Pisa; Harvard
   University; Dana-Farber Cancer Institute; KU Leuven; University Hospital
   Leuven; KU Leuven; Vall d'Hebron Institut d'Oncologia (VHIO); National
   Cancer Center - Japan; University of Texas System; UTMD Anderson Cancer
   Center
RP Raeisi, M (corresponding author), ARCAD Fdn, Stat Unit, 45 Rue Croulebarbe, F-75013 Paris, France.
EM morteza.raeisi@fondationarcad.org
RI Shi, Qian/AAW-8907-2020; Cremolini, Chiara/AAC-1889-2019; Raeisi,
   Morteza/KOC-0922-2024; André, Thierry/N-8830-2017; Cohen,
   Romain/AAC-9089-2019
OI Raeisi, Morteza/0000-0002-9999-4097; CREMOLINI,
   CHIARA/0000-0002-0520-4841; Shi, Qian/0000-0002-4640-8832; Cohen,
   Romain/0000-0001-9602-5162; Adams, Richard/0000-0003-3915-7243
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NR 26
TC 3
Z9 3
U1 1
U2 2
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 0959-8049
EI 1879-0852
J9 EUR J CANCER
JI Eur. J. Cancer
PD MAR
PY 2024
VL 199
AR 113537
DI 10.1016/j.ejca.2024.113537
EA JAN 2024
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JD4G3
UT WOS:001171202300001
PM 38241818
DA 2025-01-04
ER

PT J
AU Schally, AV
   Perez, R
   Block, NL
   Rick, FG
AF Schally, Andrew V.
   Perez, Roberto
   Block, Norman L.
   Rick, Ferenc G.
TI Potentiating effects of GHRH analogs on the response to chemotherapy
SO CELL CYCLE
LA English
DT Article
DE antagonist; breast cancer; chemotherapy; combination therapy; drug
   resistance; growth-hormone-releasing hormone; growth factor;
   neuropeptide; prostate cancer; targeted therapy
ID HORMONE-RELEASING-HORMONE; CYTOTOXIC SOMATOSTATIN ANALOG;
   EPITHELIAL-MESENCHYMAL TRANSITION; BENIGN PROSTATIC HYPERPLASIA;
   NEGATIVE BREAST CANCERS; U-87 MG GLIOBLASTOMA; HUMAN COLON-CANCER;
   IN-VIVO; GROWTH-INHIBITION; SYNERGISTIC INHIBITION
AB Growth hormone releasing hormone (GHRH) from hypothalamus nominatively stimulates growth hormone release from adenohypophysis. GHRH is also produced by cancers, acting as an autocrine/paracrine growth factor. This growth factor function is seen in lymphoma, melanoma, colorectal, liver, lung, breast, prostate, kidney, bladder cancers. Pituitary type GHRH receptors and their splice variants are also expressed in these malignancies. Synthetic antagonists of the GHRH receptor inhibit proliferation of cancers. Besides direct inhibitory effects on tumors, GHRH antagonists also enhance cytotoxic chemotherapy. GHRH antagonists potentiate docetaxel effects on growth of H460 non-small cell lung cancer (NSCLC) and MX-1 breast cancer plus suppressive action of doxorubicin on MX-1 and HCC1806 breast cancer. We investigated mechanisms of antagonists on tumor growth, inflammatory signaling, doxorubicin response, expression of drug resistance genes, and efflux pump function. Triple negative breast cancer cell xenografted into nude mice were treated with GHRH antagonist, doxorubicin, or their combination. The combination reduced tumor growth, inflammatory gene expression, drug-resistance gene expression, cancer stemcell marker expression, and efflux-pump function. Thus, antagonists increased the efficacy of doxorubicin in HCC1806 and MX-1 tumors. Growth inhibition of H460 NSCLC by GHRH antagonists induced marked downregulation in expression of prosurvival proteins K-Ras, COX-2, and pAKT. In HT-29, HCT116 and HCT-15 colorectal cancer lines, GHRH antagonist treatment caused cellular arrest in S-phase of cell cycle, potentiated inhibition of in vitro proliferation and in vivo growth produced by S-phase specific cytotoxic agents, 5-FU, irinotecan and cisplatin. This enhancement of cytotoxic therapy by GHRH antagonists should have clinical applications.
C1 [Schally, Andrew V.; Perez, Roberto; Block, Norman L.; Rick, Ferenc G.] Vet Affairs Med Ctr, Miami, FL 33125 USA.
   [Schally, Andrew V.; Perez, Roberto; Block, Norman L.; Rick, Ferenc G.] South Florida VA Fdn Res & Educ, Miami, FL 33125 USA.
   [Schally, Andrew V.; Block, Norman L.] Univ Miami, Miller Sch Med, Dept Pathol, Miami, FL 33136 USA.
   [Schally, Andrew V.; Block, Norman L.] Univ Miami, Miller Sch Med, Div Hematol Oncol, Miami, FL 33136 USA.
   [Schally, Andrew V.] Univ Miami, Miller Sch Med, Dept Med, Div Endocrinol, Miami, FL 33136 USA.
   [Schally, Andrew V.; Block, Norman L.] Univ Miami, Miller Sch Med, Sylvester Comprehens Canc Ctr, Miami, FL 33136 USA.
   [Rick, Ferenc G.] Florida Int Univ, Herbert Wertheim Coll Med, Dept Urol, Miami, FL 33199 USA.
C3 US Department of Veterans Affairs; Veterans Health Administration (VHA);
   University of Miami; University of Miami; University of Miami;
   University of Miami; State University System of Florida; Florida
   International University
RP Rick, FG (corresponding author), Vet Affairs Med Ctr, Miami, FL 33125 USA.
EM ferencrick@gmail.com
RI Rick, Ferenc/F-2237-2010
FU Research Service of Department of Veterans Affairs; Sylvester
   Comprehensive Cancer Center (SCCC); Department of Medicine, Division of
   Hematology/Oncology, of the University of Miami Miller School of
   Medicine; L. Austin Weeks Family Endowment for Research
FX Experimental studies cited in this article were supported by the
   Research Service of Department of Veterans Affairs, the Sylvester
   Comprehensive Cancer Center (SCCC), the Department of Medicine, Division
   of Hematology/Oncology, of the University of Miami Miller School of
   Medicine, and the L. Austin Weeks Family Endowment for Research.
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NR 57
TC 16
Z9 18
U1 0
U2 7
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1538-4101
EI 1551-4005
J9 CELL CYCLE
JI Cell Cycle
PD MAR 1
PY 2015
VL 14
IS 5
BP 699
EP 704
DI 10.1080/15384101.2015.1010893
PG 6
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA CD3JE
UT WOS:000350973600006
PM 25648497
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Pawar, S
   Kumar, K
   Gupta, MK
   Rawal, RK
AF Pawar, Swati
   Kumar, Kapil
   Gupta, Manish K.
   Rawal, Ravindra K.
TI Synthetic and Medicinal Perspective of Fused-Thiazoles as Anticancer
   Agents
SO ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
LA English
DT Review
DE Fused thiazole; cancer; inhibitors; cancer cell lines; heterocycles;
   chemotherapy
ID BIOLOGICAL EVALUATION; BREAST-CANCER; TARGETED THERAPY; ONE-POT;
   ANTIPROLIFERATIVE ACTIVITY; CYTOTOXICITY EVALUATION; DERIVATIVES
   SYNTHESIS; ANTITUMOR-ACTIVITY; IN-SILICO; DESIGN
AB Cancer is the second most leading cause for human mortality after cardiovascular disease. According to the recent report of WHO, new cases have risen to 18.1 million in 2018. Cancer is an uncontrolled growth of malignant cells that arise in any part of the body caused by abnormal growth in normal cells. The symptoms of cancer are not general or specific and mainly characterized by the type of cancer such as liver, lung, stomach, breast and colon cancer are most common. Cancer is the most formidable affliction characterized by a change in the mechanism that affects cell proliferation and differentiation resulted in solid tumors including sarcomas, lymphomas and carcinomas [1]. One of the most fatal forms is Leukaemia, which generally occurs through blood [2]. The main therapeutic treatment includes chemotherapy, radiotherapy and
   Background: Cancer is second leading disease after cardiovascular disease. Presently, Chemotherapy, Radiotherapy and use of chemicals are some treatments available these days. Thiazole and its hybrid compounds extensively used scaffolds in drug designing and development of novel anticancer agents due to their wide pharmacological profiles. Fused thiazole scaffold containing drugs are available in market as a promising group of anticancer agents.
   Methods: The detailed study has been done using different database that focused on potent thiazole hybrid compounds with anticancer activity. The literature included in this review is focused on novel fused thiazole derivatives exhibiting anticancer potency in last decade.
   Results: Literature suggested that thiazoles and its fused and linked congener serve excellent pharmacological profile as an anticancer agent. Various synthetic strategies for fused thiazole are also summarized in this article. Novel thiazole and its fused congener showed anticancer activity against various cancer cell lines.
   Interpretation: Thiazole is a promising scaffold reported in literature with broad range of biological activities. This article covers the thiazole compounds fused with other carbocyclic/heterocycle including benzene, imidazole, pyridine, pyrimidine, quinoline, phenothiazine, thiopyrano, steroids, pyrrole etc. with anticancer activity from last decades. Several inhibitors for breast cancer, colon cancer, melanoma cancer, ovarian cancer, tubulin cancer etc. were reported in this review. Thus, this review will definitely aid to develop a lead for the new selective anticancer agents in future.
C1 [Pawar, Swati; Rawal, Ravindra K.] Maharishi Markandeshwar Deemed Univ, Dept Chem, Ambala 33207, Haryana, India.
   [Kumar, Kapil] SVKMs NMIMS, Sch Pharm & Technol Management, Hyderabad 509301, Telangana, India.
   [Gupta, Manish K.] SGT Univ, SGT Coll Pharm, Gurugram Badli Rd, Gurugram 122505, Haryana, India.
   [Rawal, Ravindra K.] CSIR North East Inst Sci & Technol, Jorhat 785006, Assam, India.
C3 SVKM's NMIMS (Deemed to be University); Council of Scientific &
   Industrial Research (CSIR) - India; CSIR - North East Institute of
   Science & Technology (NEIST)
RP Rawal, RK (corresponding author), Maharishi Markandeshwar Deemed Univ, Dept Chem, Mullana 133207, Haryana, India.
EM rawal.ravindra@gmail.com
RI Kumar, Dr. Kapil/ABC-3733-2020; Rawal, Ravindra/F-9486-2010
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NR 110
TC 31
Z9 31
U1 0
U2 24
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1871-5206
EI 1875-5992
J9 ANTI-CANCER AGENT ME
JI Anti-Cancer Agents Med. Chem.
PY 2021
VL 21
IS 11
BP 1379
EP 1402
DI 10.2174/1871520620666200728133017
PG 24
WC Oncology; Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA RE7JF
UT WOS:000634324800005
PM 32723259
DA 2025-01-04
ER

PT J
AU Helisch, A
   Kratochwil, C
   Kleist, C
   Kräuromer, S
   Castillo, JJR
   Dendl, K
   Rathke, H
   von Goetze, I
   Schreckenberger, M
   Jäger, D
   Lindner, T
   Mier, W
   Giesel, F
   Haberkorn, U
   Röhrich, M
AF Helisch, Andreas
   Kratochwil, Clemens
   Kleist, Christian
   Kraeuromer, Susanne
   Castillo, Juan Jose Rosales
   Dendl, Katharina
   Rathke, Hendrik
   von Goetze, Isabelle
   Schreckenberger, Mathias
   Jaeger, Dirk
   Lindner, Thomas
   Mier, Walter
   Giesel, Frederik
   Haberkorn, Uwe
   Roehrich, Manuel
TI Feasibility, Tolerability, and Preliminary Clinical Response of
   Fractionated Radiopharmaceutical Therapy with 213 Bi-FAPI-46: Pilot
   Experience in Patients with End-Stage, Progressive Metastatic Tumors
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE FAPI; radiopharmaceutical therapy; bismuth; a-therapy; targeted therapy
ID PET
AB Radiopharmaceutical therapies (RPTs) based on fibroblast activation protein (FAP) and FAP inhibitors (FAPIs) are a new option for progressive metastatic cancer in patients pretreated multiple times. To date, published in-human data refer to initial experiences with b-emitting 90 Y- and 177 Lu-based RPT. However, the short tumor retention time of FAPI ligands is considered a major limitation of FAPI RPT. Therefore, fractionated FAPI RPT with 213 Bi, an a-emitter with a half-life of 46 min, appears to be a promising FAPI RPT regimen. Here, we report on our initial experiences with regard to the feasibility, tolerability, and response of fractionated 213 Bi-FAPI-46 RPT. Methods: Six patients (4 women and 2 men) with progressive metastatic solid tumors (3 colon cancer, 1 anal cancer, 1 breast cancer, and 1 prostate cancer) aged 16-77 y were treated with a mean of 1,609 MBq of 213 Bi-FAPI-46, fractionated into 53 single applications (range, 5-12 RPT applications per patient; mean, 8.8 applications) over a period of up to 107 h per patient. Of the 6 patients, 4 patients received adjuvant treatment with pembrolizumab. 18 F-FDG (4 patients) and 68 Ga-FAPI-46 (5 patients) PET/CT scans were performed before and after RPT. PET images were assessed visually and by calculating total lesion glycolysis and total lesion FAPI. Results: RPT with 213 Bi-FAPI-46 was well tolerated without adverse side effects. In terms of visual response assessment, there was 1 partial response (16.7%), 1 patient with stable disease (16.7%), and 4 patients with progressive disease (66.7%). Concordantly, total lesion glycolysis and total lesion FAPI were decreased in the responding patient (not applicable and 2 24.3%, respectively), slightly decreased in the patient with stable disease (210.6% and 2 5.9%, respectively), and increased in the 4 patients with progression (mean, + 104.4% and + 321.3%, respectively). Conclusion: Fractionated FAPI RPT with the short-half-life a-emitter 213 Bi-FAPI-46 is a promising approach that matches the pharmacokinetics of FAPI-46 better than the 177 Lu- or 90 Y-labeled compounds. In this pilot project, fractionated RPT with 213 Bi-FAPI-46 showed good clinical tolerability and even led to regressive or stable disease in the short term in 2 of 6 patients. Further studies with larger patient cohorts are required to evaluate the actual efficacy and long-term effects of this variant of FAPI RPT.
C1 [Helisch, Andreas; Rathke, Hendrik; Schreckenberger, Mathias; Roehrich, Manuel] Univ Med Ctr, Dept Nucl Med, Mainz, Germany.
   [Kratochwil, Clemens; Kleist, Christian; Kraeuromer, Susanne; Dendl, Katharina; Lindner, Thomas; Mier, Walter; Giesel, Frederik; Haberkorn, Uwe; Roehrich, Manuel] Heidelberg Univ Hosp, Dept Nucl Med, Heidelberg, Germany.
   [Kratochwil, Clemens; Roehrich, Manuel] German Ctr Lung Res, Heidelberg, Germany.
   [Castillo, Juan Jose Rosales] Univ Clin Navarra, Dept Nucl Med, Pamplona, Spain.
   [Giesel, Frederik] Cantonal Hosp Graubunden, Dept Radiol, Chur, Switzerland.
   [Jaeger, Dirk] Heidelberg Univ Hosp, Natl Ctr Tumor Dis, Dept Med Oncol, Heidelberg, Germany.
   [Lindner, Thomas] Evergreen Theragnost, Springfield, NJ USA.
   [Giesel, Frederik] Univ Hosp, Dept Nucl Med, Dusseldorf, Germany.
   [Haberkorn, Uwe] German Canc Res Ctr, Clin Cooperat Unit Nucl Med, Heidelberg, Germany.
RP Röhrich, M (corresponding author), Univ Med Ctr, Dept Nucl Med, Mainz, Germany.; Röhrich, M (corresponding author), Heidelberg Univ Hosp, Dept Nucl Med, Heidelberg, Germany.; Röhrich, M (corresponding author), German Ctr Lung Res, Heidelberg, Germany.
EM manuel.roehrich@unimedizin-mainz.de
FU Federal Ministry of Education and Research [13N 13341]
FX This work was funded by the Federal Ministry of Education and Research,
   grant number 13N 13341. Uwe Haberkorn, Clemens Kratochwil, and Frederik
   Giesel have filed a patent application for quinoline-based FAP-targeting
   agents for imaging and therapy in nuclear medicine. Uwe Haberkorn has
   shares of a consultancy group for iTheranostics. No other potential
   conflict of interest relevant to this article was reported.
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NR 19
TC 0
Z9 0
U1 2
U2 2
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD DEC 1
PY 2024
VL 65
IS 12
BP 1917
EP 1922
DI 10.2967/jnumed.124.268386
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA P9U5G
UT WOS:001381266600019
PM 39477492
DA 2025-01-04
ER

PT J
AU Holch, JW
   Held, S
   Stintzing, S
   von Weikersthal, LF
   Decker, T
   Kiani, A
   Kaiser, F
   Heintges, T
   Kahl, C
   Kullmann, F
   Scheithauer, W
   Moehler, M
   von Einem, JC
   Michl, M
   Heinemann, V
AF Holch, J. W.
   Held, S.
   Stintzing, S.
   von Weikersthal, L. Fischer
   Decker, T.
   Kiani, A.
   Kaiser, F.
   Heintges, T.
   Kahl, C.
   Kullmann, F.
   Scheithauer, W.
   Moehler, M.
   von Einem, J. C.
   Michl, M.
   Heinemann, V
TI Relation of cetuximab-induced skin toxicity and early tumor shrinkage in
   metastatic colorectal cancer patients: results of the randomized phase 3
   trial FIRE-3 (AIO KRK0306)
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE bevacizumab; biomarker; cetuximab; early tumor shrinkage; metastatic
   colorectal cancer; skin toxicity
ID FOLFIRI PLUS BEVACIZUMAB; OPEN-LABEL; 1ST-LINE TREATMENT; METAANALYSIS;
   PANITUMUMAB
AB Background: Cetuximab-induced skin toxicity (Cet-ST) is positively associated with outcome in metastatic colorectal cancer (mCRC). Besides its predictive relevance for targeted therapy, we investigated its prognostic impact with early tumor shrinkage (ETS) >= 20%, another on-treatment surrogate for clinical outcome in FIRE-3.
   Patients and methods: FIRE-3 evaluated first-line FOLFIRI (folinic acid, fluorouracil and irinotecan) plus cetuximab (FOLFIRI/Cet) versus FOLFIRI plus bevacizumab (FOLFIRI/Bev) in mCRC patients with RAS-WT tumors (i.e. wild-type in KRAS and NRAS exons 2-4). Retrospective data on Cet-ST that occurred during cycles 1-3 of treatment were correlated with efficacy endpoints, including ETS. To control for guarantee-time bias, only patients who had completed three or more treatment cycles were considered.
   Results: Of 199 patients treated with FOLFIRI/Cet, 181 (91.0%) completed three or more treatment cycles. A significant survival benefit of FOLFIRI/Cet over FOLFIRI/Bev was only evident in patients developing Cet-ST grade 2-3 [41.0 versus 26.6 months; hazard ratio (HR) = 0.73; 95% confidence interval (CI): 0.61-0.87; P < 0.001] compared with Cet-ST grade 0-1 (HR = 0.90; 95% CI: 0.67-1.20; P = 0.48). Regarding prognosis, Cet-ST grade 2-3 (n = 75; 41.4%), compared with Cet-ST grade 0-1 (n = 106; 58.6%), was associated with prolonged overall survival (OS; HR = 0.62; 95% CI: 0.42-0.91; P = 0.01). In multivariate analysis, both Cet-ST (HR = 0.66; 95% CI: 0.50-0.87; P = 0.003) and ETS (HR = 0.55; 95% CI: 0.41-0.74; P < 0.0001) were independently prognostic for OS. Absence of both Cet-ST grade >= 2 and ETS identified a subgroup of patients with very poor prognosis (median OS 15.1 months).
   Conclusions: In FIRE-3, the addition of cetuximab to FOLFIRI was associated with superior OS compared with FOLFIRI/Bev only in patients developing Cet-ST grade >= 2. Regarding prognostic relevance, both Cet-ST and ETS were independent and early predictors of survival. The present analysis supports that a combined evaluation of on-treatment parameters such as Cet-ST and ETS may help to guide treatment of mCRC.
C1 [Holch, J. W.; Michl, M.; Heinemann, V] Ludwig Maximilians Univ Munchen, Dept Med 3, Univ Hosp, Munich, Germany.
   [Holch, J. W.; Michl, M.; Heinemann, V] Comprehens Canc Ctr Munich, Munich, Germany.
   [Holch, J. W.; Michl, M.; Heinemann, V] German Canc Consortium DKTK, Partner Site Munich, Heidelberg, Germany.
   [Holch, J. W.; Michl, M.; Heinemann, V] German Canc Res Ctr, Heidelberg, Germany.
   [Held, S.] ClinAssess GmbH, Leverkusen, Germany.
   [Stintzing, S.; von Einem, J. C.] Charite Univ Med Berlin, Med Dept, Div Hematol Oncol & Tumor Immunol CCM, Berlin, Germany.
   [von Weikersthal, L. Fischer] Gesundheitszentrum St Marien GmbH, Praxis Onkol Haematol, Amberg, Germany.
   [Decker, T.] Onkol Ravensburg, Ravensburg, Germany.
   [Kiani, A.] Klinikum Bayreuth GmbH, Dept Med 4, Bayreuth, Germany.
   [Kaiser, F.] Hamato Onkol Tagesklin, Landshut, Germany.
   [Heintges, T.] Lukaskrankenhaus, Dept Med 2, Neuss, Germany.
   [Kahl, C.] Klinikum Magdeburg gGmbH, Dept Hematol Oncol & Palliat Care, Magdeburg, Germany.
   [Kullmann, F.] Klinikum Weiden, Dept Internal Med 1, Weiden, Germany.
   [Scheithauer, W.] Med Univ Vienna, Dept Internal Med I&CCC, Vienna, Austria.
   [Moehler, M.] Univ Med Ctr Mainz, Dept Internal Med 1, Mainz, Germany.
C3 University of Munich; Helmholtz Association; German Cancer Research
   Center (DKFZ); Helmholtz Association; German Cancer Research Center
   (DKFZ); Berlin Institute of Health; Free University of Berlin; Humboldt
   University of Berlin; Charite Universitatsmedizin Berlin; Klinikum
   Bayreuth; Medical University of Vienna; Johannes Gutenberg University of
   Mainz
RP Holch, JW (corresponding author), Ludwig Maximilians Univ Munchen, Comprehens Canc Ctr Munich, Dept Med 3, Univ Hosp, Marchioninistr 15, D-81377 Munich, Germany.
EM julian.holch@med.uni-muenchen.de
RI ; Stintzing, Sebastian/I-4538-2016
OI Decker, Thomas/0000-0003-3814-8775; Stintzing,
   Sebastian/0000-0002-3297-5801
FU Merck KGaA; Pfizer
FX The FIRE-3 trial was funded by Merck KGaA and Pfizer. However, for the
   present analysis no funding was received and thus no grant number is
   applicable. The funding sources had no role in the design,
   interpretation, or conduct of this evaluation, writing the manuscript,
   or decision to submit or publish the data. Merck KGaA and Pfizer
   reviewed the manuscript before journal submission. However, the authors
   are fully responsible for the content of this manuscript, and the views
   and opinions described in the publication reflect solely those of the
   authors.
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NR 16
TC 17
Z9 17
U1 1
U2 4
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29a, 1043 NX AMSTERDAM, NETHERLANDS
SN 0923-7534
EI 1569-8041
J9 ANN ONCOL
JI Ann. Oncol.
PD JAN
PY 2020
VL 31
IS 1
BP 72
EP 78
DI 10.1016/j.annonc.2019.10.001
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KQ1TG
UT WOS:000516712000012
PM 31912799
OA Bronze
DA 2025-01-04
ER

PT J
AU Mandelker, D
   Zhang, LY
   Kemel, Y
   Stadler, ZK
   Joseph, V
   Zehir, A
   Pradhan, N
   Arnold, A
   Walsh, MF
   Li, YR
   Balakrishnan, AR
   Syed, A
   Prasad, M
   Nafa, K
   Carlo, MI
   Cadoo, KA
   Sheehan, M
   Fleischut, MH
   Salo-Mullen, E
   Trottier, M
   Lipkin, SM
   Lincoln, A
   Mukherjee, S
   Ravichandran, V
   Cambria, R
   Galle, J
   Abida, W
   Arcila, ME
   Benayed, R
   Shah, R
   Yu, K
   Bajorin, DF
   Coleman, JA
   Leach, SD
   Lowery, MA
   Garcia-Aguilar, J
   Kantoff, PW
   Sawyers, CL
   Dickler, MN
   Saltz, L
   Motzer, RJ
   O'Reilly, EM
   Scher, HI
   Baselga, J
   Klimstra, DS
   Solit, DB
   Hyman, DM
   Berger, MF
   Ladanyi, M
   Robson, ME
   Offit, K
AF Mandelker, Diana
   Zhang, Liying
   Kemel, Yelena
   Stadler, Zsofia K.
   Joseph, Vijai
   Zehir, Ahmet
   Pradhan, Nisha
   Arnold, Angela
   Walsh, Michael F.
   Li, Yirong
   Balakrishnan, Anoop R.
   Syed, Aijazuddin
   Prasad, Meera
   Nafa, Khedoudja
   Carlo, Maria I.
   Cadoo, Karen A.
   Sheehan, Meg
   Fleischut, Megan H.
   Salo-Mullen, Erin
   Trottier, Magan
   Lipkin, Steven M.
   Lincoln, Anne
   Mukherjee, Semanti
   Ravichandran, Vignesh
   Cambria, Roy
   Galle, Jesse
   Abida, Wassim
   Arcila, Marcia E.
   Benayed, Ryma
   Shah, Ronak
   Yu, Kenneth
   Bajorin, Dean F.
   Coleman, Jonathan A.
   Leach, Steven D.
   Lowery, Maeve A.
   Garcia-Aguilar, Julio
   Kantoff, Philip W.
   Sawyers, Charles L.
   Dickler, Maura N.
   Saltz, Leonard
   Motzer, Robert J.
   O'Reilly, Eileen M.
   Scher, Howard I.
   Baselga, Jose
   Klimstra, David S.
   Solit, David B.
   Hyman, David M.
   Berger, Michael F.
   Ladanyi, Marc
   Robson, Mark E.
   Offit, Kenneth
TI Mutation Detection in Patients With Advanced Cancer by Universal
   Sequencing of Cancer-Related Genes in Tumor and Normal DNA vs
   Guideline-Based Germline Testing
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID MEDICAL GENETICS; AMERICAN-COLLEGE; ASSOCIATION; VARIANTS; GENOMICS
AB IMPORTANCE Guidelines for cancer genetic testing based on family history may miss clinically actionable genetic changes with established implications for cancer screening or prevention.
   OBJECTIVE To determine the proportion and potential clinical implications of inherited variants detected using simultaneous sequencing of the tumor and normal tissue ("tumor-normal sequencing") compared with genetic test results based on current guidelines.
   DESIGN, SETTING, AND PARTICIPANTS From January 2014 until May 2016 at Memorial Sloan Kettering Cancer Center, 10 336 patients consented to tumor DNA sequencing. Since May 2015, 1040 of these patients with advanced cancer were referred by their oncologists for germline analysis of 76 cancer predisposition genes. Patients with clinically actionable inherited mutations whose genetic test results would not have been predicted by published decision rules were identified. Follow-up for potential clinical implications of mutation detection was through May 2017.
   EXPOSURE Tumor and germline sequencing compared with the predicted yield of targeted germline sequencing based on clinical guidelines.
   MAIN OUTCOMES AND MEASURES Proportion of clinically actionable germline mutations detected by universal tumor-normal sequencing that would not have been detected by guideline-directed testing.
   RESULTS Of 1040 patients, the median age was 58 years (interquartile range, 50.5-66 years), 65.3% were male, and 81.3% had stage IV disease at the time of genomic analysis, with prostate, renal, pancreatic, breast, and colon cancer as the most common diagnoses. Of the 1040 patients, 182 (17.5%; 95% CI, 15.3%-19.9%) had clinically actionable mutations conferring cancer susceptibility, including 149 with moderate-to high-penetrance mutations; 101 patients tested (9.7%; 95% CI, 8.1%-11.7%) would not have had these mutations detected using clinical guidelines, including 65 with moderate-to high-penetrance mutations. Frequency of inherited mutations was related to case mix, stage, and founder mutations. Germline findings led to discussion or initiation of change to targeted therapy in 38 patients tested (3.7%) and predictive testing in the families of 13 individuals (1.3%), including 6 for whom genetic evaluation would not have been initiated by guideline-based testing.
   CONCLUSIONS AND RELEVANCE In this referral population with selected advanced cancers, universal sequencing of a broad panel of cancer-related genes in paired germline and tumor DNA samples was associated with increased detection of individuals with potentially clinically significant heritable mutations over the predicted yield of targeted germline testing based on current clinical guidelines. Knowledge of these additional mutations can help guide therapeutic and preventive interventions, but whether all of these interventions would improve outcomes for patients with cancer or their family members requires further study.
C1 [Mandelker, Diana; Zhang, Liying; Kemel, Yelena; Stadler, Zsofia K.; Joseph, Vijai; Zehir, Ahmet; Pradhan, Nisha; Arnold, Angela; Walsh, Michael F.; Li, Yirong; Balakrishnan, Anoop R.; Syed, Aijazuddin; Prasad, Meera; Nafa, Khedoudja; Carlo, Maria I.; Cadoo, Karen A.; Sheehan, Meg; Fleischut, Megan H.; Salo-Mullen, Erin; Trottier, Magan; Lincoln, Anne; Mukherjee, Semanti; Ravichandran, Vignesh; Cambria, Roy; Galle, Jesse; Abida, Wassim; Arcila, Marcia E.; Benayed, Ryma; Shah, Ronak; Yu, Kenneth; Bajorin, Dean F.; Coleman, Jonathan A.; Leach, Steven D.; Lowery, Maeve A.; Garcia-Aguilar, Julio; Kantoff, Philip W.; Sawyers, Charles L.; Dickler, Maura N.; Saltz, Leonard; Motzer, Robert J.; O'Reilly, Eileen M.; Scher, Howard I.; Baselga, Jose; Klimstra, David S.; Solit, David B.; Hyman, David M.; Berger, Michael F.; Ladanyi, Marc; Robson, Mark E.; Offit, Kenneth] Mem Sloan Kettering Canc Ctr, New York, NY USA.
   [Kemel, Yelena; Joseph, Vijai; Mukherjee, Semanti; Shah, Ronak; Garcia-Aguilar, Julio; Sawyers, Charles L.; Scher, Howard I.; Baselga, Jose; Solit, David B.; Berger, Michael F.; Ladanyi, Marc; Offit, Kenneth] Sloan Kettering Inst, New York, NY USA.
   [Stadler, Zsofia K.; Joseph, Vijai; Walsh, Michael F.; Carlo, Maria I.; Cadoo, Karen A.; Lipkin, Steven M.; Abida, Wassim; Yu, Kenneth; Bajorin, Dean F.; Coleman, Jonathan A.; Leach, Steven D.; Lowery, Maeve A.; Garcia-Aguilar, Julio; Kantoff, Philip W.; Sawyers, Charles L.; Dickler, Maura N.; Saltz, Leonard; Motzer, Robert J.; O'Reilly, Eileen M.; Scher, Howard I.; Baselga, Jose; Klimstra, David S.; Solit, David B.; Hyman, David M.; Berger, Michael F.; Robson, Mark E.; Offit, Kenneth] Weill Cornell Med Coll, New York, NY USA.
C3 Memorial Sloan Kettering Cancer Center; Memorial Sloan Kettering Cancer
   Center; Cornell University; Weill Cornell Medicine
RP Offit, K (corresponding author), Mem Sloan Kettering Canc Ctr, Clin Genet Serv, 1275 York Ave, New York, NY 10065 USA.
EM offitk@mskcc.org
RI Balakrishnan Rema, Anoop/AAE-1889-2022; Ladanyi, Marc/AAG-8585-2019;
   Solit, David/AAC-5309-2019; Joseph, Vijai/C-9792-2010; Baselga,
   Jose/L-1629-2016; lowery, maeve/AAG-2575-2019; Zehir,
   Ahmet/ABE-7155-2020; Lincoln, Anne/ABE-7459-2021; Arcila,
   Maria/ABE-2235-2021; Shah, Ronak/H-9726-2017; Joseph, Vijai/J-9158-2013
OI Coleman, Jonathan/0000-0002-6428-7835; Ravichandran,
   Vignesh/0000-0002-1532-2593; Lincoln, Anne/0000-0002-6441-1445; Shah,
   Ronak/0000-0001-9042-6213; O'Reilly, Eileen M./0000-0002-8076-9199;
   Carlo, Maria/0000-0002-4786-7408; Kemel, Yelena/0000-0002-5042-5651;
   Joseph, Vijai/0000-0002-7933-151X; Lowery, Maeve/0000-0003-1354-7606;
   Solit, David/0000-0002-6614-802X; Kantoff, Philip/0000-0001-7275-0597
FU Robert and Kate Niehaus Center for Inherited Cancer Genomics at Memorial
   Sloan Kettering Cancer Center; Andrew Sabin Family Foundation; Sharon
   Levine Corzine Research Fund from Memorial Sloan Kettering Cancer
   Center; Breast Cancer Research Foundation; J. Randall and Kathleen L.
   MacDonald Renal Cancer Research Fund; David M. Rubenstein Center for
   Pancreatic Cancer Research; Cancer Center Support Grant from the
   National Cancer Institute [P30 CA008748-50]
FX This study was supported by the Robert and Kate Niehaus Center for
   Inherited Cancer Genomics at Memorial Sloan Kettering Cancer Center, the
   Andrew Sabin Family Foundation, the Sharon Levine Corzine Research Fund
   from Memorial Sloan Kettering Cancer Center, the Breast Cancer Research
   Foundation, Marie-Josee and Henry R. Kravis, the J. Randall and Kathleen
   L. MacDonald Renal Cancer Research Fund, the David M. Rubenstein Center
   for Pancreatic Cancer Research, and Cancer Center Support Grant P30
   CA008748-50 from the National Cancer Institute.
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NR 29
TC 357
Z9 368
U1 4
U2 40
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD SEP 5
PY 2017
VL 318
IS 9
BP 825
EP 835
DI 10.1001/jama.2017.11137
PG 11
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA FF7GE
UT WOS:000409183700014
PM 28873162
OA Green Accepted
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Palanca-Ballester, C
   Rodriguez-Casanova, A
   Torres, S
   Calabuig-Fariñas, S
   Exposito, F
   Serrano, D
   Redin, E
   Valencia, K
   Jantus-Lewintre, E
   Diaz-Lagares, A
   Montuenga, L
   Sandoval, J
   Calvo, A
AF Palanca-Ballester, Cora
   Rodriguez-Casanova, Aitor
   Torres, Susana
   Calabuig-Farinas, Silvia
   Exposito, Francisco
   Serrano, Diego
   Redin, Esther
   Valencia, Karmele
   Jantus-Lewintre, Eloisa
   Diaz-Lagares, Angel
   Montuenga, Luis
   Sandoval, Juan
   Calvo, Alfonso
TI Cancer Epigenetic Biomarkers in Liquid Biopsy for High Incidence
   Malignancies
SO CANCERS
LA English
DT Review
DE epigenetic biomarkers; cancer; DNA methylation; micro-RNAs
ID CELL LUNG-CANCER; CIRCULATING TUMOR-CELLS; DNA METHYLATION BIOMARKERS;
   PROVIDES PROGNOSTIC INFORMATION; GENE PROMOTER HYPERMETHYLATION; LONG
   NONCODING RNA; BREAST-CANCER; PROSTATE-CANCER; BLADDER-CANCER; SERUM DNA
AB Simple Summary Apart from genetic changes, cancer is characterized by epigenetic alterations, which indicate modifications in the DNA (such as DNA methylation) and histones (such as methylation and acetylation), as well as gene expression regulation by non-coding (nc)RNAs. These changes can be used in biological fluids (liquid biopsies) for diagnosis, prognosis and prediction of cancer drug response. Although these alterations are not widely used as biomarkers in the clinical practice yet, increasing number of commercial kits and clinical trials are expected to prove that epigenetic changes are able to offer valuable information for cancer patients. Early alterations in cancer include the deregulation of epigenetic events such as changes in DNA methylation and abnormal levels of non-coding (nc)RNAs. Although these changes can be identified in tumors, alternative sources of samples may offer advantages over tissue biopsies. Because tumors shed DNA, RNA, and proteins, biological fluids containing these molecules can accurately reflect alterations found in cancer cells, not only coming from the primary tumor, but also from metastasis and from the tumor microenvironment (TME). Depending on the type of cancer, biological fluids encompass blood, urine, cerebrospinal fluid, and saliva, among others. Such samples are named with the general term "liquid biopsy" (LB). With the advent of ultrasensitive technologies during the last decade, the identification of actionable genetic alterations (i.e., mutations) in LB is a common practice to decide whether or not targeted therapy should be applied. Likewise, the analysis of global or specific epigenetic alterations may also be important as biomarkers for diagnosis, prognosis, and even for cancer drug response. Several commercial kits that assess the DNA promoter methylation of single genes or gene sets are available, with some of them being tested as biomarkers for diagnosis in clinical trials. From the tumors with highest incidence, we can stress the relevance of DNA methylation changes in the following genes found in LB: SHOX2 (for lung cancer); RASSF1A, RARB2, and GSTP1 (for lung, breast, genitourinary and colon cancers); and SEPT9 (for colon cancer). Moreover, multi-cancer high-throughput methylation-based tests are now commercially available. Increased levels of the microRNA miR21 and several miRNA- and long ncRNA-signatures can also be indicative biomarkers in LB. Therefore, epigenetic biomarkers are attractive and may have a clinical value in cancer. Nonetheless, validation, standardization, and demonstration of an added value over the common clinical practice are issues needed to be addressed in the transfer of this knowledge from "bench to bedside".
C1 [Palanca-Ballester, Cora; Sandoval, Juan] IIS, Biomarkers & Precis Med UBMP, Valencia 46026, Spain.
   [Palanca-Ballester, Cora; Sandoval, Juan] IIS, Epigen Unit, Valencia 46026, Spain.
   [Rodriguez-Casanova, Aitor; Diaz-Lagares, Angel] Univ Clin Hosp Santiago CHUS SERGAS, Hlth Res Inst Santiago IDIS, Canc Epigen, Translat Med Oncol Oncomet, Santiago De Compostela 15706, Spain.
   [Rodriguez-Casanova, Aitor] Hlth Res Inst Santiago IDIS, Translat Med Oncol Grp Oncomet, Roche CHUS Joint Unit, Santiago De Compostela 15706, Spain.
   [Torres, Susana; Calabuig-Farinas, Silvia; Exposito, Francisco; Redin, Esther; Valencia, Karmele; Jantus-Lewintre, Eloisa; Diaz-Lagares, Angel; Montuenga, Luis; Calvo, Alfonso] ISCIII, CIBERONC, Madrid 28029, Spain.
   [Torres, Susana; Calabuig-Farinas, Silvia; Jantus-Lewintre, Eloisa] Univ Valencia, Fdn Hosp Gen, Mol Oncol Lab, Valencia 46014, Spain.
   [Torres, Susana; Calabuig-Farinas, Silvia; Jantus-Lewintre, Eloisa] Univ Valencia, Ctr Invest Principe Felipe Fdn Invest Hosp Gen, Trial Mixed Unit, Valencia 46014, Spain.
   [Calabuig-Farinas, Silvia] Univ Valencia, Dept Pathol, Valencia 46010, Spain.
   [Exposito, Francisco; Serrano, Diego; Redin, Esther; Valencia, Karmele; Montuenga, Luis; Calvo, Alfonso] Ctr Appl Med Res CIMA, DISNA & Program Solid Tumors, Pamplona 31008, Spain.
   [Exposito, Francisco; Serrano, Diego; Redin, Esther; Montuenga, Luis; Calvo, Alfonso] Univ Navarra, Sch Med, Dept Pathol Anat & Physiol, Pamplona 31008, Spain.
   [Valencia, Karmele] Univ Navarra, Sch Sci, Dept Biochem & Genet, Pamplona 31008, Spain.
   [Jantus-Lewintre, Eloisa] Univ Politecn Valencia, Dept Biotechnol, Valencia 46022, Spain.
C3 CIBER - Centro de Investigacion Biomedica en Red; CIBERONC; Instituto de
   Salud Carlos III; University of Valencia; University of Valencia;
   University of Valencia; University of Navarra; University of Navarra;
   University of Navarra; Universitat Politecnica de Valencia
RP Sandoval, J (corresponding author), IIS, Biomarkers & Precis Med UBMP, Valencia 46026, Spain.; Sandoval, J (corresponding author), IIS, Epigen Unit, Valencia 46026, Spain.; Calvo, A (corresponding author), ISCIII, CIBERONC, Madrid 28029, Spain.; Calvo, A (corresponding author), Ctr Appl Med Res CIMA, DISNA & Program Solid Tumors, Pamplona 31008, Spain.; Calvo, A (corresponding author), Univ Navarra, Sch Med, Dept Pathol Anat & Physiol, Pamplona 31008, Spain.
EM cora_palanca@iislafe.es; aitorrodriguez@me.com;
   susana.torres@alu.umh.es; calabuix_sil@gva.es; fexposito@unay.es;
   dserrano@unay.es; eredin@alumni.unay.es; kvalencia@external.unav.es;
   jantus_elo@gva.es; angel.diaz.lagares@sergas.es; lmontuenga@unay.es;
   epigenomica@iislafe.es; acalvo@unav.es
RI Redin Resano, Esther/JHS-5038-2023; Valencia, Karmele/JAC-4673-2023;
   torres, susana/AEF-2708-2022; Expósito, Francisco/ADH-7394-2022;
   sandoval, juan/M-4593-2015; Fariñas, Silvia/D-8196-2018;
   Rodriguez-Casanova, Aitor/JPX-6133-2023; Valencia, Karmele/I-8729-2017;
   Jantus Lewintre, Eloisa/B-4630-2009; Calvo, Alfonso/V-7945-2017;
   Montuenga, Luis M/AAF-7783-2020
OI Valencia, Karmele/0000-0002-2882-7427; Jantus Lewintre,
   Eloisa/0000-0001-7395-4380; TORRES MARTINEZ, SUSANA/0000-0001-8366-8337;
   Calvo, Alfonso/0000-0003-4074-4242; Calabuig,
   Silvia/0000-0001-7749-174X; Redin Resano, Esther/0000-0001-9539-7298;
   Palanca Ballester, Cora/0000-0002-4520-1514; Rodriguez-Casanova,
   Aitor/0000-0002-9828-3613; Montuenga, Luis M/0000-0002-8739-1387;
   Exposito Rincon, Francisco/0000-0002-5406-0768; Serrano,
   Diego/0000-0002-3729-9195; sandoval, juan/0000-0002-5100-973X
FU FIMA (Foundation for Applied Medical Research); ISCIIIFondo de
   Investigacion Sanitaria-Fondo Europeo de Desarrollo Regional "Una manera
   de hacer Europa" [PI19/00230, PI19/00098]; CIBERONC [CB16/12/00443];
   AECC; Ramon Areces Foundations; FIS grant from the FEDER [PI19/00572];
   FSE; Carlos III Health Institute (ISCIII); Spanish Health Institute
   Carlos III (ISCII, Fondo de Investigacion Sanitaria) [CB16/12/00350,
   PI18/00266]; Generalitat Valenciana; Fondo Social Europeo
   [ACIF/2018/275]; Spanish Health Institute Carlos III (ISCIII)
   [JR17/00016]; ISCIII [PI18/00307]; European Regional Development Fund
   (FEDER); Roche-CHUS Joint Unit - GAIN, Conselleria de Economia, Emprego
   e Industria [IN853B2018/03]; FPU, Spanish Ministry of Education; Juan de
   la Cierva-Incorporacion, Spanish Ministry of Science and Innovation; 
   [INNVA1/2020/71]
FX A.C. and L.M. were funded by FIMA (Foundation for Applied Medical
   Research), ISCIIIFondo de Investigacion Sanitaria-Fondo Europeo de
   Desarrollo Regional "Una manera de hacer Europa" (PI19/00230, to AC;
   PI19/00098 to LMM), CIBERONC CB16/12/00443, AECC, and Ramon Areces
   Foundations (all to L.M.). J.S. was funded by FIS grant (PI19/00572)
   from the FEDER, FSE, Carlos III Health Institute (ISCIII) and
   INNVA1/2020/71 de la Linea 1 de Valorizacion y Transferencia a las
   empresas, de la Agencia Valenciana de la Innovacion. E.J-L. was
   supported by the Spanish Health Institute Carlos III (ISCII, Fondo de
   Investigacion Sanitaria: CB16/12/00350 and PI18/00266). S.T. was
   supported by the Generalitat Valenciana and Fondo Social Europeo,
   fellowship ACIF/2018/275. A.D-L. was funded by a contract Juan Rodes
   from Spanish Health Institute Carlos III (ISCIII) (JR17/00016) and by a
   research grant (PI18/00307) co-funded by ISCIII and the European
   Regional Development Fund (FEDER). A.R-C. was supported by the
   Roche-CHUS Joint Unit (IN853B2018/03) funded by GAIN, Conselleria de
   Economia, Emprego e Industria". Fellowship support: E.R. "FPU, Spanish
   Ministry of Education"; D.S., "Juan de la Cierva-Incorporacion, Spanish
   Ministry of Science and Innovation".
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NR 194
TC 47
Z9 52
U1 1
U2 33
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUN
PY 2021
VL 13
IS 12
AR 3016
DI 10.3390/cancers13123016
PG 24
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SZ0UF
UT WOS:000666290900001
PM 34208598
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Moosavi, F
   Giovannetti, E
   Saso, L
   Firuzi, O
AF Moosavi, Fatemeh
   Giovannetti, Elisa
   Saso, Luciano
   Firuzi, Omidreza
TI HGF/MET pathway aberrations as diagnostic, prognostic, and predictive
   biomarkers in human cancers
SO CRITICAL REVIEWS IN CLINICAL LABORATORY SCIENCES
LA English
DT Review
DE Receptor tyrosine kinases; c-MET; neoplasms; biomarker discovery;
   targeted therapy
ID HEPATOCYTE GROWTH-FACTOR; CELL LUNG-CANCER; SOLUBLE C-MET; RECEPTOR
   TYROSINE KINASE; RANDOMIZED PHASE-II; GENE COPY NUMBER; BREAST-CANCER;
   GASTRIC-CANCER; CLINICAL-SIGNIFICANCE; HUMAN-PAPILLOMAVIRUS
AB Cancer is a major cause of death worldwide. MET tyrosine kinase receptor [MET, c-MET, hepatocyte growth factor (HGF) receptor] pathway activation is associated with the appearance of several hallmarks of cancer. The HGF/MET pathway has emerged as an important actionable target across many solid tumors; therefore, biomarker discovery becomes essential in order to guide clinical intervention and patient stratification with the aim of moving towards personalized medicine. The focus of this review is on how the aberrant activation of the HGF/MET pathway in tumor tissue or the circulation can provide diagnostic and prognostic biomarkers and predictive biomarkers of drug response. Many meta-analyses have shown that aberrant activation of the MET pathway in tumor tissue, including MET gene overexpression, gene amplification, exon 14 skipping and other activating mutations, is almost invariably associated with shorter survival and poor prognosis. Most meta-analyses have been performed in non-small cell lung cancer (NSCLC), breast, head and neck cancers as well as colorectal, gastric, pancreatic and other gastrointestinal cancers. Furthermore, several studies have shown the predictive value of MET biomarkers in the identification of patients who gain the most benefit from HGF/MET targeted therapies administered as single or combination therapies. The highest predictive values have been observed for response to foretinib and savolitinib in renal cancer, as well as tivantinib in NSCLC and colorectal cancer. However, some studies, especially those based on MET expression, have failed to show much value in these stratifications. This may be rooted in lack of standardization of methodologies, in particular in scoring systems applied in immunohistochemistry determinations or absence of oncogenic addiction of cancer cells to the MET pathway, despite detection of overexpression. Measurements of amplification and mutation aberrations are less likely to suffer from these pitfalls. Increased levels of MET soluble ectodomain (sMET) in circulation have also been associated with poor prognosis; however, the evidence is not as strong as it is with tissue-based biomarkers. As a diagnostic biomarker, sMET has shown its value in distinguishing cancer patients from healthy individuals in prostate and bladder cancers and in melanoma. On the other hand, increased circulating HGF has also been presented as a valuable prognostic and diagnostic biomarker in many cancers; however, there is controversy on the predictive value of HGF as a biomarker. Other biomarkers such as circulating tumor DNA (ctDNA) and tumor HGF levels have also been briefly covered. In conclusion, HGF/MET aberrations can provide valuable diagnostic, prognostic and predictive biomarkers and represent vital assets for personalized cancer therapy.
C1 [Moosavi, Fatemeh; Firuzi, Omidreza] Shiraz Univ Med Sci, Med & Nat Prod Chem Res Ctr, 1 Neshat St, Shiraz 7144816645, Iran.
   [Giovannetti, Elisa] Vrije Univ Amsterdam, Med Ctr VUmc, Amsterdam UMC, Dept Med Oncol,Canc Ctr Amsterdam, Amsterdam, Netherlands.
   [Giovannetti, Elisa] Fdn Pisana Sci Onlus, AIRC Start Unit, Canc Pharmacol Lab, Pisa, Italy.
   [Saso, Luciano] Sapienza Univ, Dept Physiol & Pharmacol, Rome, Italy.
C3 Shiraz University of Medical Science; Vrije Universiteit Amsterdam;
   University of Amsterdam; Sapienza University Rome
RP Firuzi, O (corresponding author), Shiraz Univ Med Sci, Med & Nat Prod Chem Res Ctr, 1 Neshat St, Shiraz 7144816645, Iran.
EM firuzio@sums.ac.ir
RI Moosavi, Fatemeh/D-5466-2018; giovannetti, elisa/F-4261-2011; Firuzi,
   Omidreza/A-1025-2012; saso, luciano/F-6306-2012
OI Moosavi, Fatemeh/0000-0001-8078-1297; saso, luciano/0000-0003-4530-8706;
   Giovannetti, Elisa/0000-0002-7565-7504
FU National Institute for Medical Research Development (NIMAD) [957652]
FX This work was supported by the National Institute for Medical Research
   Development (NIMAD, Grant number: 957652) and Vice-Chancellor for
   Research, Shiraz University of Medical Sciences.
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NR 246
TC 119
Z9 131
U1 1
U2 36
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1040-8363
EI 1549-781X
J9 CRIT REV CL LAB SCI
JI Crit. Rev. Clin. Lab. Sci.
PD NOV 17
PY 2019
VL 56
IS 8
BP 533
EP 566
DI 10.1080/10408363.2019.1653821
EA SEP 2019
PG 34
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA JA6GH
UT WOS:000486514800001
PM 31512514
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Wang, W
   Wang, J
   Ren, XX
   Yue, HL
   Li, Z
AF Wang, Wei
   Wang, Jing
   Ren, Xiu-Xiu
   Yue, Hai-Long
   Li, Zheng
TI Effects of invigorating-spleen and anticancer prescription on
   extracellular signal-regulated kinase/mitogen-activated protein kinase
   signaling pathway in colon cancer mice model
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Colon cancer; Invigorating-spleen and anticancer formula; Extracellular
   signal-regulated kinase/mitogen-activated protein kinase signaling
   pathway; Mice model; C-MYC
ID COLORECTAL-CANCER; METASTASIS
AB BACKGROUND Colon cancer (CC) is one of the most common malignant tumors in the gastrointestinal system. Overall, CC had the third highest incidence but the second highest mortality rate globally in 2020. Nowadays, CC is mainly treated with capecitabine chemotherapy regimen, supplemented by radiotherapy, immunotherapy and targeted therapy, but there are still limitations, so Chinese medicine plays an important role. AIM To investigate the effects of invigorating-spleen and anticancer prescription (ISAP) on body weight, tumor inhibition rate and expression levels of proteins in extracellular-signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) signaling pathway in CC mice model. METHODS The CC mice model were established and the mice were randomly divided into 5 groups, including the control group, capecitabine group, the low-dose, medium-dose and high-dose groups of ISAP, with 8 mice in each group, respectively. After 2 weeks of intervention, the body weight and tumor inhibition rate of mice were observed, and the expression of RAS, ERK, phosphorylated ERK (p-ERK), C-MYC and matrix metalloproteinase 2 (MMP2) proteins in the tissues of tumors were detected. RESULTS Compared with the control group, the differences of body weight before and after treatment was much smaller in the groups of ISAP, with the smallest difference in the high-dose group of ISAP, while the capecitabine group had the greatest difference, indicating ISAP had a significant inhibiting effect on the growth of transplanted tumor in mice. The expression of RAS protein was decreased in the low- and medium-dose groups of ISAP, and the change of p-ERK was significant in the medium- and high- dose groups of ISAP. MMP2 protein expression was significantly decreased in both the low-dose and medium-dose groups of ISAP. There were no significant changes in ERK in the ISAP group compared to the capecitabine group, while RAS, MMP2, and C-MYC protein expression were reduced in the ISAP group. The expression level of C-MYC protein decreased after treated with ISAP, and the decrease was the most significant in the medium-dose group of ISAP. CONCLUSION ISAP has a potential inhibiting effect on transplanted tumor in mice, and could maintain the general conditions, physical strength and body weight of mice. The expression levels of RAS, p-ERK, MMP2 and c-myc were also decreased to a certain extent. By inhibiting the expression of upstream proteins, the expression levels of downstream proteins in ERK/MAPK signaling pathway were significantly decreased. Therefore, it can be concluded that ISAP may exert an anti-tumor effect by blocking the ERK/MAPK signaling pathway and inhibiting the expression of MMP2 and c-myc proteins.
C1 [Wang, Wei; Li, Zheng] China Med Univ, Liaoning Canc Hosp & Inst, Canc Hosp, Dept Integrated Tradit Chinese & Western Med Med O, 44 Xiaoheyan Rd, Shenyang 110042, Liaoning, Peoples R China.
   [Wang, Jing; Ren, Xiu-Xiu; Yue, Hai-Long] Liaoning Univ Chinese Med, Clin Sch 1, Shenyang 110847, Liaoning, Peoples R China.
C3 China Medical University
RP Li, Z (corresponding author), China Med Univ, Liaoning Canc Hosp & Inst, Canc Hosp, Dept Integrated Tradit Chinese & Western Med Med O, 44 Xiaoheyan Rd, Shenyang 110042, Liaoning, Peoples R China.
EM fox_dl1984@163.com
RI xiuxiu, ren/JWO-0977-2024
FU Liaoning Provincial Science and Technology Department Project
   [2023JH2/101700149]; Open Fund Project of Liaoning University of
   Traditional Chinese Medicine [zyzx2205]
FX Supported by Liaoning Provincial Science and Technology Department
   Project, No. 2023JH2/101700149; and Open Fund Project of Liaoning
   University of Traditional Chinese Medicine, No. zyzx2205.
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   Wang M, 2024, PHYTOMEDICINE, V127, DOI 10.1016/j.phymed.2024.155391
   Wang QS, 2022, MSc Thesis dissertations
   Xu BW, 2022, FRONT CELL INFECT MI, V12, DOI 10.3389/fcimb.2022.875225
   Yang R, 2024, CANCER GENE THER, V31, P562, DOI 10.1038/s41417-024-00731-5
   Yeoh A, 2023, CLIN GASTROENTEROL H, V21, P507, DOI 10.1016/j.cgh.2022.07.028
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NR 29
TC 0
Z9 0
U1 1
U2 1
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD NOV 15
PY 2024
VL 16
IS 11
DI 10.4251/wjgo.v16.i11.4468
PG 10
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA M5L8I
UT WOS:001357958700005
PM 39554742
DA 2025-01-04
ER

PT J
AU Mattiello, L
   Rehim, SSA
   Musella, M
   Sistigu, A
   Guarracino, A
   Vitale, S
   Corradi, F
   Galassi, C
   Sperati, F
   Manic, G
   De Maria, R
   Vitale, I
AF Mattiello, Luca
   Soliman Abdel Rehim, Sara
   Musella, Martina
   Sistigu, Antonella
   Guarracino, Andrea
   Vitale, Sara
   Corradi, Francesca
   Galassi, Claudia
   Sperati, Francesca
   Manic, Gwenola
   De Maria, Ruggero
   Vitale, Ilio
TI The Targeting of MRE11 or RAD51 Sensitizes Colorectal Cancer Stem Cells
   to CHK1 Inhibition
SO CANCERS
LA English
DT Article
DE colorectal cancer; chromosomal instability; DNA damage; targeted
   therapy; tumor-initiating cells
AB Simple Summary
   The ATR-CHK1 axis of the DNA damage response is crucial for the survival of most colorectal cancer stem cells (CRC-SCs), but a significant fraction of primary CRC-SCs either is resistant to ATR or CHK1 inhibitors or survives the abrogation of the ATR-CHK1 cascade despite an initial response. Here, we demonstrate that the targeting of RAD51 or MRE11 improves the sensitivity of primary CRC-SCs to the CHK1/2 inhibitor prexasertib by sequentially inducing replication stress, the abrogation of cell cycle checkpoints, and the emergence of mitotic defects. This results in the induction of mitotic catastrophe and CRC-SC killing via a caspase-dependent apoptosis.
   Cancer stem cells (CSCs) drive not only tumor initiation and expansion, but also therapeutic resistance and tumor relapse. Therefore, CSC eradication is required for effective cancer therapy. In preclinical models, CSCs demonstrated high capability to tolerate even extensive genotoxic stress, including replication stress, because they are endowed with a very robust DNA damage response (DDR). This favors the survival of DNA-damaged CSCs instead of their inhibition via apoptosis or senescence. The DDR represents a unique CSC vulnerability, but the abrogation of the DDR through the inhibition of the ATR-CHK1 axis is effective only against some subtypes of CSCs, and resistance often emerges. Here, we analyzed the impact of druggable DDR players in the response of patient-derived colorectal CSCs (CRC-SCs) to CHK1/2 inhibitor prexasertib, identifying RAD51 and MRE11 as sensitizing targets enhancing prexasertib efficacy. We showed that combined inhibition of RAD51 and CHK1 (via B02+prexasertib) or MRE11 and CHK1 (via mirin+prexasertib) kills CSCs by affecting multiple genoprotective processes. In more detail, these two prexasertib-based regimens promote CSC eradication through a sequential mechanism involving the induction of elevated replication stress in a context in which cell cycle checkpoints usually activated during the replication stress response are abrogated. This leads to uncontrolled proliferation and premature entry into mitosis of replication-stressed cells, followed by the induction of mitotic catastrophe. CRC-SCs subjected to RAD51+CHK1 inhibitors or MRE11+CHK1 inhibitors are eventually eliminated, and CRC-SC tumorspheres inhibited or disaggregated, via a caspase-dependent apoptosis. These results support further clinical development of these prexasertib-based regimens in colorectal cancer patients.
C1 [Mattiello, Luca; Soliman Abdel Rehim, Sara; Guarracino, Andrea; Manic, Gwenola; Vitale, Ilio] IRCSS, Italian Inst Genom Med IIGM, I-10060 Candiolo, Italy.
   [Mattiello, Luca; Manic, Gwenola; Vitale, Ilio] FPO IRCCS, Candiolo Canc Inst, I-10060 Candiolo, Italy.
   [Soliman Abdel Rehim, Sara; Guarracino, Andrea; Corradi, Francesca] Univ Roma Tor Vergata, Dept Biol, I-00133 Rome, Italy.
   [Musella, Martina; Sistigu, Antonella; Vitale, Sara; Galassi, Claudia; De Maria, Ruggero] Univ Cattolica Sacro Cuore, Dipartimento Med & Chirurg Traslaz, I-00168 Rome, Italy.
   [Sistigu, Antonella] IRCCS Regina Elena Natl Canc Inst, UOSD Tumor Immunol & Immunotherapy Unit, I-00144 Rome, Italy.
   [Sperati, Francesca] San Gallicano Dermatol Inst IRCCS, UOSD Biostat Bioinformat & Clin Trial Ctr, I-00144 Rome, Italy.
   [De Maria, Ruggero] Fdn Policlin Univ A Gemelli IRCCS, I-00168 Rome, Italy.
C3 IRCCS Fondazione del Piemonte per l'Oncologia; University of Rome Tor
   Vergata; Catholic University of the Sacred Heart; IRCCS Policlinico
   Gemelli; IRCCS Istituti Fisioterapici Ospitalieri (IFO); IRCCS San
   Gallicano Dermatological Institute (ISG); Catholic University of the
   Sacred Heart; IRCCS Policlinico Gemelli
RP Manic, G; Vitale, I (corresponding author), IRCSS, Italian Inst Genom Med IIGM, I-10060 Candiolo, Italy.; Manic, G; Vitale, I (corresponding author), FPO IRCCS, Candiolo Canc Inst, I-10060 Candiolo, Italy.; De Maria, R (corresponding author), Univ Cattolica Sacro Cuore, Dipartimento Med & Chirurg Traslaz, I-00168 Rome, Italy.; De Maria, R (corresponding author), Fdn Policlin Univ A Gemelli IRCCS, I-00168 Rome, Italy.
EM mattiello.borsisti@iigm.it; soliman.borsisti@iigm.it;
   martina.musella@unicatt.it; antonella.sistigu@unicatt.it;
   andrea.guarracino@uniroma2.it; sara.vitale@unicatt.it;
   francesca.corradi89@gmail.com; claudia.galassi@unicatt.it;
   francesca.sperati@ifo.gov.it; gwenola.manic@gmail.com;
   manic.esterni@iigm.it; iliovit@gmail.com
RI Vitale, Sara/AAB-9588-2019; Mattiello, Luca/AAB-8384-2022; Guarracino,
   Andrea/ABI-5879-2022; Manic, Gwenola/J-8496-2018; Sistigu,
   Antonella/J-8934-2018; De Maria, Ruggero/S-6385-2019; sperati,
   francesca/K-5843-2016; VITALE, ILIO/M-3960-2017; Musella,
   Martina/JMA-9073-2023
OI sperati, francesca/0000-0002-6038-2798; Soliman Abdel Rehim,
   Sara/0000-0002-6744-6010; Sistigu, Antonella/0000-0002-2528-1238;
   VITALE, ILIO/0000-0002-5918-1841; Musella, Martina/0000-0002-8021-9488;
   Mattiello, Luca/0000-0003-3543-977X; Guarracino,
   Andrea/0000-0001-9744-131X; Manic, Gwenola/0000-0003-3759-8029; vitale,
   sara/0000-0002-9011-9042
FU Associazione Italiana per la Ricerca sul Cancro (AIRC) [20417, 9979,
   18418]; Ministero Italiano della Salute [RF_RF-2018-12367044,
   RF_GR-2013-02357273]; Italian Institute for Genomic Medicine (Candiolo,
   Turin, Italy); Compagnia di San Paolo (Turin, Italy)
FX This work was supported by the Associazione Italiana per la Ricerca sul
   Cancro (AIRC, IG 2017 grant number 20417 to IV; AIRC 5 ~ 1000 grant
   number 9979 to RDM; Start-Up 2016 #18418 to AS), Ministero Italiano
   della Salute (RF_RF-2018-12367044 to RDM; YRF_GR-2013-02357273 to AS).
   IV is also supported by a startup grant from the Italian Institute for
   Genomic Medicine (Candiolo, Turin, Italy) and Compagnia di San Paolo
   (Turin, Italy).
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NR 50
TC 10
Z9 11
U1 1
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD APR
PY 2021
VL 13
IS 8
AR 1957
DI 10.3390/cancers13081957
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RS8BX
UT WOS:000643999500001
PM 33921638
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ho, AS
   Cheng, CC
   Peng, CL
   Sie, ZL
   Yeh, C
   Lee, SD
AF Ho, Ai-Sheng
   Cheng, Chun-Chia
   Peng, Cheng-Liang
   Sie, Zong-Lin
   Yeh, Chun
   Lee, Shou-Dong
TI STAT3 mediates cancer stem-like tumorsphere formation and PD-L1
   expression to contribute radioresistance in HBV-positive hepatocellular
   carcinoma
SO ADVANCES IN DIGESTIVE MEDICINE
LA English
DT Article
DE BBI608; EGF; hepatocellular carcinoma (HCC); IL-6; STAT3
ID HEPATITIS-B-VIRUS; COLORECTAL-CANCER; TUMOR PROGRESSION; LIVER-CANCER;
   X-PROTEIN; INFLAMMATION; ACTIVATION; APOPTOSIS; KINASES; PATHWAY
AB We proposed that cancer stem cells (CSCs) survived and presented resistance to radiotherapy (RT) in hepatocellular carcinoma (HCC) cells. Interleukin 6 (IL-6) has been reported to be particularly involved in HCC tumorigenesis. Therefore, we intended to validate that IL-6 downstream STAT3-mediated CSCs formation and immune checkpoint PD-L1 expression in HCC, thus contributing to radioresistance. HBV-positive HCC tumorspheres were formed and exposed with X-ray irradiation, cell viability of which was measured consequently. Specific inhibitors targeting EGFR (by gefitinib), STAT3 (by BBI608), and HCC-targeted therapy sorafenib were investigated to suppress tumorsphere formation. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used for detecting STAT3-downstream PD-L1 and anti-apoptosis MCL1 and BCL2 gene expression in the PLC5-derived tumorspheres and STAT3-knockdown PLC5. We found that RT significantly inhibited HBV-positive Hep3B and PLC5 cell viability but not for HCC-derived stem-like tumorspheres cultured by EGF, IL-6, bFGF, and HGF. It revealed that tumorspheres presented radioresistance compared with the parental cells. Specifically, RT induces IFNs, EGF, and IL-6 expression, resulting in STAT3 phosphorylation. Kaplan-Meier plotter indicated that highly EGF (p = .0024), IL-6 (p = .12), and FGF2 (p = .0041) were associated with poor survival probability in patients with HBV-positive HCC. We further demonstrated that BBI608 and sorafenib significantly suppressed PLC5 cell viability and PLC5-derived tumorsphere formation. To investigate the mechanism of CSC-presented radioresistance, STAT3 and STAT3-downstream genes, including PD-L1 and anti-apoptosis MCL1 and BCL2, were detected using qPCR. We demonstrated higher STAT3, PD-L1, MCL1, and BCL2 in Hep3B- and PLC5-derived CSCs compared to PLC5. In addition, knockdown of STAT3 reduced cell proliferation in PLC5 cells, resulting in down-regulation of IL-6-mediated PD-L1 and BCL-2. Meanwhile, we found that knockdown of STAT3 significantly improved RT-mediated suppression of tumorsphere formation. In conclusion, we found that CSCs presented radioresistance and figured out which may be mediated by STAT3 in HBV-positive HCC.
C1 [Ho, Ai-Sheng; Yeh, Chun; Lee, Shou-Dong] Cheng Hsin Gen Hosp, Div Gastroenterol, Taipei 112, Taiwan.
   [Cheng, Chun-Chia; Sie, Zong-Lin] Chang Gung Univ, Res Ctr Radiat Med, Taoyuan 333, Taiwan.
   [Peng, Cheng-Liang] Natl Atom Res Inst, Dept Isotope Applicat Res, Taoyuan, Taiwan.
C3 Cheng Hsin General Hospital; Chang Gung University
RP Lee, SD (corresponding author), Cheng Hsin Gen Hosp, Div Gastroenterol, Taipei 112, Taiwan.; Cheng, CC (corresponding author), Chang Gung Univ, Res Ctr Radiat Med, Taoyuan 333, Taiwan.
EM cccheng.biocompare@mail.com; ch9318@chgh.org.tw
RI Sie, Zong-Lin/LOS-6407-2024
OI Ho, Ai-Sheng/0000-0002-7207-774X
FU Ministry of Science and Technology, Taiwan; NSTC [112-2314-B-182-048];
   Cheng Hsin General Hospital, Taipei, Taiwan [CHGH111-(N)06]; Atomic
   Energy Council of Executive Yuan, Taiwan [111-2623-E-182-003-NU];  [MOST
   109-2314-B-182-011];  [MOST 110-2314-B-182-031]
FX The authors thank the Radiation Biology Core Laboratory of the Institute
   for Radiological Research, Chang Gung Memorial Hospital, for their
   technical support. This study was supported by grants from the Ministry
   of Science and Technology, Taiwan (MOST 109-2314-B-182-011, MOST
   110-2314-B-182-031, and NSTC 112-2314-B-182-048), Cheng Hsin General
   Hospital, Taipei, Taiwan (CHGH111-(N)06), and Atomic Energy Council of
   Executive Yuan, Taiwan (111-2623-E-182-003-NU).
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NR 40
TC 0
Z9 0
U1 0
U2 0
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2351-9797
EI 2351-9800
J9 ADV DIG MED
JI Adv. Dig. Med.
PD SEP
PY 2024
VL 11
IS 3
BP 140
EP 150
DI 10.1002/aid2.13393
EA APR 2024
PG 11
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA H3P8Z
UT WOS:001207447200001
OA Bronze
DA 2025-01-04
ER

PT J
AU Angus, JA
   Hughes, RJA
   Wright, CE
AF Angus, James A.
   Hughes, Richard J. A.
   Wright, Christine E.
TI Distortion of K<sub>B</sub> estimates of endothelin-1 ET<sub>A</sub> and
   ET<sub>B</sub> receptor antagonists in pulmonary arteries: Possible role
   of an endothelin-1 clearance mechanism
SO PHARMACOLOGY RESEARCH & PERSPECTIVES
LA English
DT Article
DE ambrisentan; bosentan; BQ788; endothelin-1; ETA receptors; ETB
   receptor-mediated clearance mechanism; ETB receptors; macitentan;
   sarafotoxin S6c
ID ET(B) RECEPTORS; NITRIC-OXIDE; PHARMACOLOGY; PUBLICATION; MACITENTAN;
   BLOCKADE; BOSENTAN; KIDNEY; VALUES; VIVO
AB Dual endothelin ETA and ETB receptor antagonists are approved therapy for pulmonary artery hypertension (PAH). We hypothesized that ETB receptor-mediated clearance of endothelin-1 at specific vascular sites may compromise this targeted therapy. Concentration-response curves (CRC) to endothelin-1 or the ETB agonist sarafotoxin S6c were constructed, with endothelin receptor antagonists, in various rat and mouse isolated arteries using wire myography or in rat isolated trachea. In rat small mesenteric arteries, bosentan displaced endothelin-1 CRC competitively indicative of ETA receptor antagonism. In rat small pulmonary arteries, bosentan 10molL(-1) left-shifted the endothelin-1 CRC, demonstrating potentiation consistent with antagonism of an ETB receptor-mediated endothelin-1 clearance mechanism. Removal of endothelium or L-NAME did not alter the EC50 or Emax of endothelin-1 nor increase the antagonism by BQ788. In the presence of BQ788 and L-NAME, bosentan displayed ETA receptor antagonism. In rat trachea (ETB), bosentan was a competitive ETB antagonist against endothelin-1 or sarafotoxin S6c. Modeling showed the importance of dual receptor antagonism where the potency ratio of ETA to ETB antagonism is close to unity. In conclusion, the rat pulmonary artery is an example of a special vascular bed where the resistance to antagonism of endothelin-1 constriction by ET dual antagonists, such as bosentan or the ETB antagonist BQ788, is possibly due to the competition of potentiation of endothelin-1 by blockade of ETB-mediated endothelin-1 clearance located on smooth muscle and antagonism of ETA- and ETB-mediated contraction. This conclusion may have direct application for the efficacy of endothelin-1 antagonists for treating PAH.
C1 [Angus, James A.; Hughes, Richard J. A.; Wright, Christine E.] Univ Melbourne, Dept Pharmacol & Therapeut, Cardiovasc Therapeut Unit, Melbourne, Vic, Australia.
C3 University of Melbourne
RP Angus, JA (corresponding author), Univ Melbourne, Dept Pharmacol & Therapeut, Cardiovasc Therapeut Unit, Melbourne, Vic, Australia.
EM jamesaa@unimelb.edu.au
RI ; Wright, Christine/B-2509-2012; Angus, James/F-6666-2014
OI Hughes, Richard/0009-0003-9222-8976; Wright,
   Christine/0000-0002-3339-040X; Angus, James/0000-0002-0605-9682
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NR 36
TC 8
Z9 8
U1 0
U2 1
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
SN 2052-1707
J9 PHARMACOL RES PERSPE
JI Pharmacol. Res. Perspect.
PD DEC
PY 2017
VL 5
IS 6
AR e00374
DI 10.1002/prp2.374
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA FP4SG
UT WOS:000417606100008
PM 29226623
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Karabulut, S
   Afsar, CU
   Karabulut, M
   Kilic, L
   Alis, H
   Kones, O
   Bilgin, E
   Aykan, NF
AF Karabulut, Senem
   Afsar, Cigdem Usul
   Karabulut, Mehmet
   Kilic, Leyla
   Alis, Halil
   Kones, Osman
   Bilgin, Elif
   Aykan, Nuri Faruk
TI Clinical significance of serum interleukin-17 levels in colorectal
   cancer patients
SO JOURNAL OF BUON
LA English
DT Article
DE colorectal cancer; diagnostic; IL-17; serum; survival
ID PROMOTES ANGIOGENESIS; PROGNOSTIC MARKER; GASTRIC-CANCER; EXPRESSION;
   IL-17; PROGRESSION; PREDICTOR; CELLS
AB Purpose: The proinflammatory cytokine, interleukin-17 (IL-17) plays a potent role in T-cell mediated angiogenesis and promotes tumorigenicity. The objective of this study was to determine the clinical outcomes of colorectal cancer (CRC) patients in relation to serum IL-17 levels.
   Methods: Ninety-six CRC patients were enrolled in this study. Pre-treatment serum IL-17 levels were determined by enzyme-linked immunosorbent assay (ELISA). Thirty age - and sex-matched healthy controls were included in the analysis.
   Results: The median patient age was 60 years (range: 24-84) and the most frequent localization was colon (N=59;61%). Median follow-up time was 14 months, 27 patients (28%) experienced disease progression, and 20 of the remaining patients (20%) died. The estimated and 1-year progression free survival (PFS) and 2-year overall survival (OS) rates for the whole patient group were 26.9% (95% confidence interval [CI]=9.9-44.0) and 71% (95% CI=56.0-85.0), respectively. The number of patients who received neoadjuvant treatment was 25. Of the patients who received palliative treatment, 11 had oxaliplatin whereas 18 and 7 had irinotecan and FU/capecitabine, chemotherapy (CTx). Twenty-four and nine of the patients who received targeted therapy had bevacizumab and cetuximab, respectively. Thirty-three percent of 36 metastatic patients who received palliative CTx were CTx-responsive. The baseline median serum IL-17 levels were significantly lower in patients with CRC than in the healthy control group (p=0.01). Moreover, known clinical variables including older age, poor grade and low albumin levels were found to be correlated with high serum IL-17 concentrations (p=0.02, p=0.02, and p=0.04, respectively). No statistically significant serum IL 17 concentrations were noted regarding PFS and OS.
   Conclusion: Serum levels of IL-17 may be diagnostic marker in CRC patients. However, no predictive and prognostic values were determined.
C1 [Karabulut, Senem; Kilic, Leyla; Aykan, Nuri Faruk] Istanbul Univ, Inst Oncol, Dept Med Oncol, Istanbul, Turkey.
   [Afsar, Cigdem Usul] Istanbul Educ & Res Hosp, Dept Med Oncol, Kasap Ilyas Mah Org Abdurrahman Nafiz Gurman Cad, TR-34098 Istanbul, Turkey.
   [Karabulut, Mehmet; Alis, Halil; Kones, Osman] Istanbul Bakirkoy Dr Sadi Konuk Educ & Res Hosp, Clin Gen Surg, Istanbul, Turkey.
   [Bilgin, Elif] Istanbul Univ, Inst Oncol, Dept Basic Oncol, Istanbul, Turkey.
C3 Istanbul University; Istanbul Training & Research Hospital; Bakirkoy Dr.
   Sadi Konuk Research & Training Hospital; Istanbul University
RP Afsar, CU (corresponding author), Istanbul Educ & Res Hosp, Dept Med Oncol, Kasap Ilyas Mah Org Abdurrahman Nafiz Gurman Cad, TR-34098 Istanbul, Turkey.
EM cigdemusul@yahoo.com
RI Karabulut, Mehmet/AAY-4248-2021; Doğru, Elif/A-6543-2018; Afsar,
   Cigdem/C-3436-2015; Alis, Halil/AAJ-6721-2020; Ozer, Leyla/D-1578-2015;
   karabulut, senem/AAT-3594-2020; Aykan, Nuri Faruk/I-6425-2019
OI Aykan, Nuri Faruk/0000-0002-5472-3218
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NR 23
TC 8
Z9 8
U1 0
U2 5
PU IMPRIMATUR PUBLICATIONS
PI ATHENS
PA 30 DEM POLIORKETES ST, ATHENS, 136 76, GREECE
SN 1107-0625
EI 2241-6293
J9 J BUON
JI J. BUON
PD SEP-OCT
PY 2016
VL 21
IS 5
BP 1137
EP 1145
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ED3XQ
UT WOS:000388782200013
PM 27837615
DA 2025-01-04
ER

PT J
AU Reguera-Nuñez, E
   Xu, P
   Chow, A
   Man, S
   Hilberg, F
   Kerbel, RS
AF Reguera-Nunez, Elaine
   Xu, Ping
   Chow, Annabelle
   Man, Shan
   Hilberg, Frank
   Kerbel, Robert S.
TI Therapeutic impact of Nintedanib with paclitaxel and/or a PD-L1 antibody
   in preclinical models of orthotopic primary or metastatic triple
   negative breast cancer
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Article
DE VEGF; Antiangiogenic drugs; Chemotherapy; Immune checkpoint therapy;
   PD-L1; Metastasis; Preclinical models
ID TUMOR-INFILTRATING LYMPHOCYTES; CELL LUNG-CANCER; ENDOTHELIAL
   GROWTH-FACTOR; LABEL DOSE-ESCALATION; PHASE-III TRIAL; 1ST-LINE
   TREATMENT; DOUBLE-BLIND; ANTIANGIOGENIC THERAPY; 2ND-LINE TREATMENT;
   COLORECTAL-CANCER
AB BackgroundTriple negative breast cancer (TNBC) is an aggressive malignancy with poor prognosis, in part because of the current lack of any approved molecularly targeted therapy. We evaluated various combinations of three different drugs: nintedanib, an antiangiogenic TKI targeting VEGF receptors, paclitaxel (PTX), or a PD-L1 antibody, using models of orthotopic primary or advanced metastatic TNBC involving a metastatic variant of the MDA-MB-231 human cell line (called LM2-4) in SCID mice and two mouse lines (EMT-6 and a drug-resistant variant, EMT-6/CDDP) in immunocompetent mice. These drugs were selected based on the following: PTX is approved for TNBC; nintedanib combined with docetaxel has shown phase III clinical trial success, albeit in NSCLC; VEGF can act as local immunosuppressive factor; and PD-L1 antibody plus taxane therapy was recently reported to have encouraging phase III trial benefit in TNBC.MethodsStatistical analyses were performed with ANOVA followed by Tukey's Multiple Comparison Test or with Kruskal-Wallis test followed by Dunn's Multiple Comparison Test. Survival curves were analyzed using a Log-rank (Mantel Cox) test. Differences were considered statistically significant when p values were<0.05.ResultsToxicity analyses showed that nintedanib is well tolerated when administered 5-days ON 2-days OFF; PTX toxicity differed in mice, varied with cell lines used and may have influenced median survival in the metastatic EMT6/CDDP model; while toxicity of PD-L1 therapy depended on the cell lines and treatment settings tested. In the LM2-4 system, combining nintedanib with PTX enhanced overall antitumor efficacy in both primary and metastatic treatment settings. In immunocompetent mice, combining nintedanib or PTX with the PD-L1 antibody improved overall antitumor efficacy. Using the advanced metastatic EMT-6/CDDP model, optimal efficacy results were obtained using the triple combination.ConclusionsThese results suggest circumstances where nintedanib plus PTX may be potentially effective in treating TNBC, and nintedanib with PTX may improve PD-L1 therapy of metastatic TNBC.
C1 [Reguera-Nunez, Elaine; Kerbel, Robert S.] Univ Toronto, Dept Med Biophys, Toronto, ON, Canada.
   [Reguera-Nunez, Elaine; Xu, Ping; Chow, Annabelle; Man, Shan; Kerbel, Robert S.] Sunnybrook Res Inst, Biol Sci Platform, 2075 Bayview Ave,Room S-217, Toronto, ON M4N 3M5, Canada.
   [Hilberg, Frank] Boehringer Ingelheim RCV, Vienna, Austria.
C3 University of Toronto; University of Toronto; Sunnybrook Health Science
   Center; Sunnybrook Research Institute; Boehringer Ingelheim
RP Kerbel, RS (corresponding author), Univ Toronto, Dept Med Biophys, Toronto, ON, Canada.; Kerbel, RS (corresponding author), Sunnybrook Res Inst, Biol Sci Platform, 2075 Bayview Ave,Room S-217, Toronto, ON M4N 3M5, Canada.
EM robert.kerbel@sri.utoronto.ca
FU Boehringer Ingelheim RCV, Vienna, Austria; Canadian Institutes of Health
   Research (CIHR)
FX This work was supported by a Sponsored Research Agreement from
   Boehringer Ingelheim RCV, Vienna, Austria and by a grant to RSK from the
   Canadian Institutes of Health Research (CIHR).
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NR 91
TC 29
Z9 31
U1 3
U2 35
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1756-9966
J9 J EXP CLIN CANC RES
JI J. Exp. Clin. Cancer Res.
PD JAN 11
PY 2019
VL 38
AR 16
DI 10.1186/s13046-018-0999-5
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HH1DC
UT WOS:000455458300001
PM 30635009
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Millis, SZ
   Ikeda, S
   Reddy, S
   Gatalica, Z
   Kurzrock, R
AF Millis, Sherri Z.
   Ikeda, Sadakatsu
   Reddy, Sandeep
   Gatalica, Zoran
   Kurzrock, Razelle
TI Landscape of Phosphatidylinositol-3-Kinase Pathway Alterations Across 19
   784 Diverse Solid Tumors
SO JAMA ONCOLOGY
LA English
DT Article
ID CELL LUNG-CANCER; PHASE-II TRIAL; RESISTANT PROSTATE-CANCER; PIK3CA
   MUTATION; BREAST-CANCER; PI3K/AKT/MTOR PATHWAY; HETEROGENEOUS TUMORS;
   COLORECTAL-CANCER; CATALYTIC SUBUNIT; SUPPRESSOR GENE
AB IMPORTANCE Molecular aberrations in the phosphatidylinositol-3-kinase (PI3K) pathway drive tumorigenesis. Frequently co-occurring alterations in hormone receptors and/or human epidermal growth factor receptor 2 (HER2) may be relevant to mechanisms of response and resistance.
   OBJECTIVE To identify patterns of aberration in the PI3K and interactive pathways that might lead to targeted therapy opportunities in clinical practice.
   DESIGN, SETTING, AND PARTICIPANTS From January 2013 through December 2014, 19 784 consecutive tumor samples (>40 cancer types) were sent from thousands of clinicians in 60 countries to a single commercial laboratory for molecular profiling, including next generation sequencing, protein expression (immunohistochemical analysis [IHC]), and gene amplification (fluorescent in situ hybridization or chromogenic in situ hybridization).
   MAIN OUTCOMES AND MEASURES Patterns in targetable genomic and proteomic alterations in the PI3K pathway and coincidence with hormone receptor and HER2 alterations.
   EXPOSURES Molecular profiling across solid tumors.
   RESULTS Overall, 38% of patients had an alteration in 1 or more PI3K pathway components, most commonly phosphatase and tensin homologue (PTEN) loss (by IHC) (30% of all patients), followed by mutations in PIK3CA (13%), PTEN (6%), or AKT1 (1%). Seventy percent of patients with endometrial cancer and more than 50% of patients with breast, prostate, anal, hepatocellular, colorectal, and cervical cancer exhibited alterations in at least 1 PI3K pathway gene and/or gene product. Examples of frequent aberrations included PTEN loss in hepatocellular (57% of patients), colorectal (48%), gastric (36%), prostate (52%), and endometrial cancer (49%); PIK3CA mutations in endometrial (37%), breast (31%), cervical (29%), and anal cancer (27%). PIK3CA, PTEN, and AKT1 mutations occurred more frequently in the presence of hormone receptor overexpression (androgen, progesterone, or estrogen receptor). PIK3CA mutations were also more common in the HER2-positive than in the HER2-negative group; the opposite pattern was seen for PTEN mutation or PTEN loss.
   CONCLUSIONS AND RELEVANCE PI3K pathway aberrations are among the most common in cancer. They do not segregate by classic cancer histologic characteristics. Patterns of biomarker coalterations involving HER2 and hormone receptors may be important for optimizing combination treatments across cancer types.
C1 [Millis, Sherri Z.; Reddy, Sandeep; Gatalica, Zoran] Caris Life Sci, Phoenix, AZ USA.
   [Ikeda, Sadakatsu] Tokyo Med & Dent Univ, Ctr Canc, Tokyo, Japan.
   [Ikeda, Sadakatsu; Kurzrock, Razelle] Univ Calif San Diego, Dept Med, Div Hematol Oncol, La Jolla, CA 92093 USA.
   [Ikeda, Sadakatsu; Kurzrock, Razelle] Univ Calif San Diego, Ctr Personalized Canc Therapy, La Jolla, CA 92093 USA.
   [Ikeda, Sadakatsu; Kurzrock, Razelle] Univ Calif San Diego, Moores Canc Ctr, 3855 Hlth Sci Dr,Rm 2306, La Jolla, CA 92093 USA.
C3 Institute of Science Tokyo; Tokyo Medical & Dental University (TMDU);
   University of California System; University of California San Diego;
   University of California System; University of California San Diego;
   University of California System; University of California San Diego
RP Ikeda, S (corresponding author), Univ Calif San Diego, Moores Canc Ctr, 3855 Hlth Sci Dr,Rm 2306, La Jolla, CA 92093 USA.
EM saikeda@ucsd.edu
RI Kurzrock, Razelle/AAU-9782-2020; reddy, sandeep/HTT-0221-2023
FU Joan and Irwin Jacobs Fund
FX This study was funded in part by the Joan and Irwin Jacobs Fund.
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NR 68
TC 196
Z9 213
U1 0
U2 16
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2374-2437
EI 2374-2445
J9 JAMA ONCOL
JI JAMA Oncol.
PD DEC 1
PY 2016
VL 2
IS 12
BP 1565
EP 1573
DI 10.1001/jamaoncol.2016.0891
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EF8TG
UT WOS:000390601900009
PM 27388585
OA Bronze
DA 2025-01-04
ER

PT J
AU Claassen, YHM
   van der Valk, MJM
   Breugom, AJ
   Frouws, MA
   Bastiaannet, E
   Liefers, GJ
   van de Velde, CJH
   Kapiteijn, E
AF Claassen, Yvette H. M.
   van der Valk, Maxime J. M.
   Breugom, Anne J.
   Frouws, Martine A.
   Bastiaannet, Esther
   Liefers, Gerrit-Jan
   de Velde, Cornelis J. H. van
   Kapiteijn, Ellen
TI Survival differences with immediate versus delayed chemotherapy for
   asymptomatic incurable metastatic colorectal cancer
SO COCHRANE DATABASE OF SYSTEMATIC REVIEWS
LA English
DT Review
ID 1ST-LINE TREATMENT; PLUS IRINOTECAN; BEVACIZUMAB; RESECTION;
   FLUOROURACIL; OXALIPLATIN; LEUCOVORIN; COMBINATION; STATISTICS; EFFICACY
AB Background
   For patients with asymptomatic, incurable, metastatic colorectal cancer, palliative, systemic treatment can be started immediately, or can be delayed until disease-related symptoms occur. How the potential survival benefit of starting palliative, systemic treatment immediately after diagnosis weighs up against the potential side effects is currently under debate, and was investigated in this review.
   Objectives
   To assess the effects of immediate versus delayed chemotherapy, with or without targeted therapy, on overall survival, toxicity, quality of life, progression-free survival, and compliance with chemotherapy for individuals with asymptomatic, metastatic, incurable colorectal cancer.
   Search methods
   We searched CENTRAL; 2018, Issue 8, MEDLINE Ovid, Embase Ovid, PsycINFO, the World Health Organization International Clinical Trials Registry Platform, and Clinicaltrials.gov, from inception to 23 August 2018. We did not apply limitations based on language or date of publication. We searched the reference lists of all included studies to identify trials that may not have been identified from the electronic searches.
   Selection criteria
   Randomised controlled trials evaluating immediate versus delayed chemotherapy in persons with asymptomatic, metastatic, incurable colorectal cancer.
   Data collection and analysis
   We applied standard methodological procedures, according to the recommendations of Cochrane and Cochrane Colorectal Cancer. Two review authors independently reviewed the studies identified by literature searches, selected relevant trials, extracted data, and assessed risk of bias of the included studies. We used the Cochrane tool to assess risk of bias, Review Manager 5 software for meta-analysis, GRADE methods to evaluate the quality of the evidence, and GRADEpro GDT software to develop a 'Summary of findings' table.
   Main results
   We included three randomised controlled trials (351 participants) investigating immediate versus delayed chemotherapy in people diagnosed with asymptomatic, metastatic, incurable colorectal cancer. Giving immediate versus delayed chemotherapy may make little or no difference to overall survival (hazard ratio (HR) 1.17, 95% confidence interval (CI) 0.93 to 1.46; 3 studies, 351 persons; low-quality evidence). For toxicity, giving immediate versus delayed chemotherapy may make little or no difference to the risk of grade 3 or 4 nausea and vomiting (risk ratio (RR) 0.84, 95% CI 0.31 to 2.25; 2 studies, 140 persons; very low-quality evidence), stomatitis (RR 1.10, 95% CI 0.47 to 2.55; 2 studies, 140 persons; very low-quality evidence), or diarrhoea (RR 0.69, 95% CI 0.34 to 1.40; 2 studies, 140 persons, very low-quality evidence). We are uncertain whether delayed chemotherapy made a difference to quality of life (very low-quality evidence), progression-free survival (low-quality evidence), or compliance with chemotherapy (low-quality evidence), as we had insufficient data to pool for these outcomes.
   Authors 'conclusions
   Based on a limited number of trials, very sparse data, and uncertainty of the evidence, this review was unable to establish whether there was a difference in overall survival or other clinically relevant outcomes, between immediate or delayed chemotherapy in persons with metastatic, incurable, colorectal cancer. The results should be interpreted with caution.
C1 [Claassen, Yvette H. M.; van der Valk, Maxime J. M.; Breugom, Anne J.; Frouws, Martine A.; Bastiaannet, Esther; Liefers, Gerrit-Jan; de Velde, Cornelis J. H. van] Leiden Univ, Med Ctr, Dept Surg, Leiden, Netherlands.
   [Kapiteijn, Ellen] Leiden Univ, Med Ctr, Dept Med Oncol, Leiden, Netherlands.
C3 Leiden University - Excl LUMC; Leiden University; Leiden University
   Medical Center (LUMC); Leiden University - Excl LUMC; Leiden University;
   Leiden University Medical Center (LUMC)
RP Bastiaannet, E (corresponding author), Leiden Univ, Med Ctr, Dept Surg, Leiden, Netherlands.
EM e.bastiaannet@lumc.nl
RI van de Velde, Cornelis/AAY-8360-2020; Kapiteijn, Ellen/AAK-6065-2020
OI Kapiteijn, Ellen/0000-0002-4814-6426; Liefers, Gerrit
   Jan/0000-0001-7326-8313
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NR 46
TC 5
Z9 5
U1 0
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1469-493X
EI 1361-6137
J9 COCHRANE DB SYST REV
JI Cochrane Database Syst Rev.
PY 2018
IS 11
AR CD012326
DI 10.1002/14651858.CD012326.pub2
PG 40
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA HG7GW
UT WOS:000455159600025
PM 30480771
OA Green Published
DA 2025-01-04
ER

PT J
AU Yi, JM
   Peng, F
   Zhao, JL
   Gong, XS
AF Yi, Jianmei
   Peng, Feng
   Zhao, Jingli
   Gong, Xiaosong
TI METTL3/IGF2BP2 axis affects the progression of colorectal cancer by
   regulating m6A modification of STAG3
SO SCIENTIFIC REPORTS
LA English
DT Article
ID MESSENGER-RNA TRANSLATION; M(6)A MODIFICATION; METTL3; IGF2BP2
AB Colorectal cancer (CRC) is among the commonest malignant tumors of humans. Existing evidence has linked the poor prognosis of CRC with high expression of stromal antigen 3 (STAG3), but, the exact biological effect of STAG3 in CRC is still unclear. The aim of this research is to reveal the biological function and molecular mechanism of STAG3 in CRC. To investigate the differential expression of STAG3 in CRC tissues and cell lines compared to normal colon tissues and cell lines, Western blot (WB) and quantitative real-time PCR (qRT-PCR) techniques were utilized. STAG3 N6-methyladenosine (m6A) modification level were identified using m6A RNA immunoprecipitation (MeRIP). Additionally, the functional roles of methyltransferase-like protein 3 (METTL3) and insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) in CRC were explored by manipulating their levels via knockdown or overexpression. Cell proliferation was evaluated through Cell Counting Kit 8 (CCK-8) and clone formation experiments, while cell migration was assessed through wound healing experiments. Furthermore, cell apoptosis was detected using flow cytometry, and the protein expressions associated with proliferation and apoptosis were detected using WB. To identify the specific binding of target genes, RIP and pull-down assays were employed. Finally, the biological function of STAG3 in vivo was investigated through a xenotransplantation mouse tumor model. In CRC tissues and cell lines, STAG3 was up-regulated and accompanied by m6A methylation. Additionally, the expression of METTL3 was found to be upregulated in CRC tissues. Knocking down METTL3 resulted in a decrease in both the m6A level and protein expression of STAG3, inhibited cell proliferation and migration while promoting apoptosis, which were restored through STAG3 overexpression. Furthermore, online prediction indicated the interaction between STAG3 mRNA and IGF2BP2 protein, which was further verified by RIP experiments. IGF2BP2 downregulation led to decreased STAG3 protein expression, cell proliferation, and migration, but increased apoptosis. However, these impacts were reversed by STAG3 overexpression. Finally, subcutaneous tumor experiments conducted in nude mice also confirmed that METTL3 regulated CRC progression through STAG3 in vivo. The METTL3/IGF2BP2/STAG3 axis affects CRC progression in an m6A modification-dependent manner. This may guide targeted therapy in CRC patients.
C1 [Yi, Jianmei; Peng, Feng; Gong, Xiaosong] Cent South Univ, Zhuzhou Cent Hosp, Zhuzhou Hosp, Xiangya Sch Med,Dept Gen Surg 2, 116 Changjiang South Rd, Zhuzhu 412007, Hunan, Peoples R China.
   [Zhao, Jingli] Cent South Univ, Zhuzhou Cent Hosp, Zhuzhou Hosp, Xiangya Sch Med,Dept Operating Room, Zhuzhou 412007, Peoples R China.
C3 Central South University; Central South University
RP Gong, XS (corresponding author), Cent South Univ, Zhuzhou Cent Hosp, Zhuzhou Hosp, Xiangya Sch Med,Dept Gen Surg 2, 116 Changjiang South Rd, Zhuzhu 412007, Hunan, Peoples R China.
EM gongxiaosong0418@163.com
RI Peng, Feng/ABE-3834-2021
FU Zhuzhou Science and Technology Bureau Social Development Achievement
   Transformation Special Project [2021-005]
FX This work was supported by Zhuzhou Science and Technology Bureau 2021
   Social Development Achievement Transformation Special Project [No.
   2021-005].
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NR 40
TC 2
Z9 2
U1 1
U2 3
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD OCT 12
PY 2023
VL 13
IS 1
AR 17292
DI 10.1038/s41598-023-44379-x
PG 13
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA W1GS2
UT WOS:001089186400043
PM 37828232
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yang, Y
   Wen, W
   Chen, FL
   Zhang, YJ
   Liu, XC
   Yang, XY
   Hu, SS
   Jiang, Y
   Yuan, J
AF Yang, Ye
   Wen, Wu
   Chen, Feng-Lin
   Zhang, Ying-Jie
   Liu, Xiao-Cong
   Yang, Xiao-Yan
   Hu, Shan-Shan
   Jiang, Ye
   Yuan, Jing
TI Expression and significance of pigment epithelium-derived factor and
   vascular endothelial growth factor in colorectal adenoma and cancer
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Pigment epithelium-derived factors; Vascular endothelial growth factor;
   Microvessel density; Colorectal adenoma; Colorectal cancer; Targeted
   therapy
ID FACTOR PEDF; TUMOR ANGIOGENESIS; SCORING SYSTEM; GENE; DIFFERENTIATION;
   INHIBITOR; TEM7
AB BACKGROUND The incidence and mortality of colorectal cancer (CRC) are among the highest in the world, and its occurrence and development are closely related to tumor neovascularization. When the balance between pigment epithelium-derived factors (PEDF) that inhibit angiogenesis and vascular endothelial growth factors (VEGF) that stimulate angiogenesis is broken, angiogenesis is out of control, resulting in tumor development. Therefore, it is very necessary to find more therapeutic targets for CRC for early intervention and later treatment.
   AIM To investigate the expression and significance of PEDF, VEGF, and CD31-stained microvessel density values (CD31-MVD) in normal colorectal mucosa, adenoma, and CRC.
   METHODS In this case-control study, we collected archived wax blocks of specimens from the Digestive Endoscopy Center and the General Surgery Department of Chengdu Second People's Hospital from April 2022 to October 2022. Fifty cases of specimen wax blocks were selected as normal intestinal mucosa confirmed by electronic colonoscopy and concurrent biopsy (normal control group), 50 cases of specimen wax blocks were selected as colorectal adenoma confirmed by electronic colonoscopy and pathological biopsy (adenoma group), and 50 cases of specimen wax blocks were selected as CRC confirmed by postoperative pathological biopsy after inpatient operation of general surgery (CRC group). An immunohistochemical staining experiment was carried out to detect PEDF and VEGF expression in three groups of specimens, analyze their differences, study the relationship between the two and clinicopathological factors in CRC group, record CD31-MVD in the three groups, and analyze the correlation of PEDF, VEGF, and CD31-MVD in the colorectal adenoma group and the CRC group. The F test or adjusted F test is used to analyze measurement data statistically. Kruskal-Wallis rank sum test was used between groups for ranked data. The chi-square test, adjusted chi-square test, or Fisher's exact test were used to compare the rates between groups. All differences between groups were compared using the Bonferroni method for multiple comparisons. Spearman correlation analysis was used to test the correlation of the data. The test level (alpha) was 0.05, and a two-sided P< 0.05 was considered statistically significant.
   RESULTS The positive expression rate and expression intensity of PEDF were gradually decreased in the normal control group, adenoma group, and CRC group (100% vs 78% vs 50%, chi(2) = 34.430, P < 0.001; ++similar to++ vs +similar to++ vs -similar to+, H = 94.059, P < 0.001), while VEGF increased gradually (0% vs 68% vs 96%, chi(2) = 98.35, P < 0.001; - vs -similar to+ vs ++similar to+++, H = 107.734, P < 0.001). In the CRC group, the positive expression rate of PEDF decreased with the increase of differentiation degree, invasion depth, lymph node metastasis, distant metastasis, and TNM stage (chi(2) = 20.513, 4.160, 5.128, 6.349, 5.128, P < 0.05); the high expression rate of VEGF was the opposite (chi(2) = 10.317, 13.134, 17.643, 21.844, 17.643, P < 0.05). In the colorectal adenoma group, the expression intensity of PEDF correlated negatively with CD31-MVD (r = -0.601, P < 0.001), whereas VEGF was not significantly different (r = 0.258, P = 0.07). In the CRC group, the expression intensity of PEDF correlated negatively with the expression intensity of CD31-MVD and VEGF (r = -0.297, P < 0.05; r = -0.548, P < 0.05), while VEGF expression intensity was positively related to CD31-MVD (r = 0.421, P = 0.002).
   CONCLUSION It is possible that PEDF can be used as a new treatment and prevention target for CRC by upregulating the expression of PEDF while inhibiting the expression of VEGF.
C1 [Yang, Ye] Chengdu Qingbaijiang Dist Peoples Hosp, Digest Dis, Chengdu 610300, Sichuan, Peoples R China.
   [Wen, Wu; Zhang, Ying-Jie; Liu, Xiao-Cong; Yang, Xiao-Yan; Hu, Shan-Shan; Jiang, Ye; Yuan, Jing] Chengdu Second Peoples Hosp, Digest Dis, 10 Qingyunan St, Chengdu 610000, Sichuan, Peoples R China.
   [Chen, Feng-Lin] Chengdu Med Coll, Grad Sch, Chengdu 610000, Sichuan, Peoples R China.
C3 Chengdu Medical College
RP Wen, W (corresponding author), Chengdu Second Peoples Hosp, Digest Dis, 10 Qingyunan St, Chengdu 610000, Sichuan, Peoples R China.
EM wenwu2@qq.com
RI Chen, Fenglin/IUP-7513-2023; wen, wu/LDF-3495-2024; Yang,
   Xiaoyan/P-9080-2014; Hu, Shanshan/ABH-7729-2020
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NR 70
TC 0
Z9 0
U1 2
U2 2
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD MAR 15
PY 2024
VL 16
IS 3
DI 10.4251/wjgo.v16.i3.670
PG 18
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA NC4L5
UT WOS:001198236100010
PM 38577437
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Chang, S
   Choi, YL
   Shim, HS
   Lee, GK
   Ha, SY
AF Chang, Sunhee
   Choi, Yoon-La
   Shim, Hyo Sup
   Lee, Geon Kook
   Ha, Seung Yeon
CA Korean Cardiopulm Pathology Study
TI Usefulness of BRAF VE1 immunohistochemistry in non-small cell lung
   cancers: a multi-institutional study by 15 pathologists in Korea
SO JOURNAL OF PATHOLOGY AND TRANSLATIONAL MEDICINE
LA English
DT Article
DE BRAFV600E; Observer variation; Predictive value of tests;
   Immunohistochemistry; Adenocarcinoma of lung
ID V600E MUTATION; BRAF(V600E) MUTATION; COLORECTAL-CARCINOMA;
   MONOCLONAL-ANTIBODY; P.V600E MUTATIONS; MELANOMA; CONCORDANT
AB Background: Next-generation sequencing (NGS) is an approved test to select patients for BRAF V600E targeted therapy in Korea. How-ever, the high cost, long turnaround times, and the need for sophisticated equipment and skilled personnel limit the use of NGS in daily practice. Immunohistochemistry (IHC) is a rapid and relatively inexpensive assay available in most laboratories. Therefore, in this study, we evaluate the usefulness of BRAF VE1 IHC in terms of predictive value and interobserver agreement in non-small cell lung cancers (NSCLCs). Methods: A total of 30 cases with known BRAF mutation status were selected, including 20 cases of lung adenocarcinomas, six cases of colorectal adenocarcinomas, and four cases of papillary thyroid carcinomas. IHC for BRAF V600E was carried out using the VE1 antibody. Fifteen pathologists independently scored both the staining intensity and the percentage of tumor cell staining on whole slide images. Results: In the lung adenocarcinoma subset, interobserver agreement for the percentage of tumor cell staining and staining intensity was good (percentage of tumor cell staining, intraclass correlation coefficient = 0.869; staining intensity, kappa = 0.849). The interobserver agreement for the interpretation using the cutoff of 40% was almost perfect in the entire study group and the lung ad-enocarcinoma subset (kappa = 0.815). Sensitivity, specificity, positive predictive value, and negative predictive value of BRAF VE1 IHC were 80.0%, 90.0%, 88.9%, and 81.8%, respectively. Conclusions: BRAF VE1 IHC could be a screening test for the detection of BRAF V600E mutation in NSCLC. However, further studies are needed to optimize the protocol and to establish and validate interpretation cri -teria for BRAF VE1 IHC.
C1 [Chang, Sunhee] Inje Univ, Dept Pathol, Ilsan Paik Hosp, Goyang, South Korea.
   [Choi, Yoon-La] Sungkyunkwan Univ, Samsung Med Ctr, Dept Pathol & Translat Genom, Sch Med, Seoul, South Korea.
   [Shim, Hyo Sup] Yonsei Univ, Dept Pathol, Coll Med, Seoul, South Korea.
   [Lee, Geon Kook] Natl Canc Ctr, Dept Pathol, 323 Ilsan Ro, Goyang 10408, South Korea.
   [Ha, Seung Yeon] Gachon Univ, Gil Med Ctr, Dept Pathol, Coll Med, 21 Namdong Daero 774beon Gil, Incheon 21565, South Korea.
C3 Inje University; Sungkyunkwan University (SKKU); Samsung Medical Center;
   Yonsei University; Yonsei University Health System; National Cancer
   Center - Korea (NCC); Gachon University
RP Lee, GK (corresponding author), Natl Canc Ctr, Dept Pathol, 323 Ilsan Ro, Goyang 10408, South Korea.; Ha, SY (corresponding author), Gachon Univ, Gil Med Ctr, Dept Pathol, Coll Med, 21 Namdong Daero 774beon Gil, Incheon 21565, South Korea.
EM gklee@ncc.rek; syha@gilhospital.com
RI Shim, Hyo/ABI-6190-2020
OI Shim, Hyo Sup/0000-0002-5718-3624; Ha, Seung Yeon/0000-0001-7071-1623;
   Lee, Geon Kook/0000-0003-3138-3908; Choi, Yoon-La/0000-0002-5788-5140;
   Chang, Sunhee/0000-0002-7775-4711
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NR 28
TC 9
Z9 9
U1 0
U2 2
PU KOREAN SOC PATHOLOGISTS
PI SEOUL
PA 1209 GWANGHWAMUN OFFICIA, 92 SAEMUNAN-RO, JONGNO-GU, SEOUL, 03186, SOUTH
   KOREA
SN 2383-7837
EI 2383-7845
J9 J PATHOL TRANSL MED
JI J. Pathol. Transl. Med.
PD NOV
PY 2022
VL 56
IS 6
BP 334
EP 341
DI 10.4132/jptm.2022.08.22
EA OCT 2022
PG 8
WC Pathology
WE Emerging Sources Citation Index (ESCI)
SC Pathology
GA 7T9MG
UT WOS:000877567100001
PM 36288742
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Esfahani, SA
   Heidari, P
   Kim, SA
   Ogino, S
   Mahmood, U
AF Esfahani, Shadi A.
   Heidari, Pedram
   Kim, Sun A.
   Ogino, Shuji
   Mahmood, Umar
TI Optical Imaging of Mesenchymal Epithelial Transition Factor (MET) for
   Enhanced Detection and Characterization of Primary and Metastatic
   Hepatic Tumors
SO THERANOSTICS
LA English
DT Article
DE MET; Liver cancer; Tumor detection; Optical Imaging; Intra-operative
   interventions; molecularly-targeted therapy
ID HEPATOCYTE GROWTH-FACTOR; C-MET; HEPATOCELLULAR-CARCINOMA; INDOCYANINE
   GREEN; EXPRESSION; CANCER; RECEPTOR; PATHWAY; FUTURE; PET
AB Purpose: To assess optical imaging of Mesenchymal-Epithelial Transition factor (MET) for delineation and characterization of intrahepatic models of human hepatocellular carcinoma (HCC) and metastatic colorectal cancer (CRC), and thereby demonstrate its potential use in precision oncology.
   Materials and Methods: MET expression in human CRC and HCC was assessed in tissue microarrays. We used GE-137, a modified cyanine 5-tagged peptide for MET targeting. HepG2 and Huh-7 (HCC) and HT-29 (CRC) cells with MET overexpression, and LNCaP cells (negative control) with minimal MET expression were incubated with the probe. Correlation between the relative fluorescence signal intensity and cellular MET expression level was assessed. Flow cytometry was used to assess probe specific binding and dissociation constant (K-d). Orthotopic xenograft models of human HCC and metastatic CRC were generated in nu/nu mice by subcapsular implantation of cells. Epifluorescence imaging was performed to capture the changes in deferential probe accumulation at different time points after injection. Target-to-liver background ratio (TBR) was calculated and the probe biodistribution within different organs was assessed. Histopathologic analysis of extracted xenografts was performed to correlate the tumors MET expression with probe uptake by cancer cells.
   Results: Approximately 91.5% of HCC and 81% of CRC microarray cores showed MET expression. HCC and CRC cells incubated with the probe showed substantial fluorescence compared to control LNCaP, with strong correlation between fluorescence signal and MET expression (R-2 = 0.99, p < 0.001). Probe binding affinity to MET (K-d) was measured to be 2.9 +/- 0.36 nM. Epifluorescence imaging showed intense uptake in subcapsular tumors with peak TBR of 5.46 +/- 0.46 in Huh-7, 3.55 +/- 0.38 in HepG2, and 15.93 +/- 0.61 in HT-29 orthotopic xenografts at 4 hours post-injection (mean +/- standard deviation). We demonstrated that in vivo probe uptake in xenografts is specific and can be blocked when co-injected with unlabeled peptide; for instance the epifluorescence TBR is reduced from 13.5 +/- 1.2 to 1.7 +/- 0.3 (p < 0.05) in HT-29 and from 5.3 +/- 0.8 to 1.4 +/- 0.2 (p < 0.05) in Huh-7 xenografts after co-injection with unlabeled peptides. Biodistribution studies showed predominantly renal clearance of the probe.
   Conclusion: Optical imaging of MET resulted in high TBR in animal models of primary and metastatic hepatic tumors suggesting its utility for procedural guidance.
C1 [Esfahani, Shadi A.; Heidari, Pedram; Mahmood, Umar] Harvard Med Sch, Massachusetts Gen Hosp, Dept Radiol, Athinoula A Martinos Ctr Biomed Imaging, Boston, MA 02115 USA.
   [Kim, Sun A.; Ogino, Shuji] Harvard Med Sch, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA USA.
   [Ogino, Shuji] Harvard Med Sch, Brigham & Womens Hosp, Dept Pathol, Boston, MA USA.
   [Ogino, Shuji] Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
C3 Harvard University; Harvard Medical School; Massachusetts General
   Hospital; Harvard University; Dana-Farber Cancer Institute; Harvard
   Medical School; Harvard University; Brigham & Women's Hospital; Harvard
   Medical School; Harvard University; Harvard T.H. Chan School of Public
   Health
RP Mahmood, U (corresponding author), Massachusetts Gen Hosp, Dept Radiol, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
EM umahmood@mgh.harvard.edu
OI Ogino, Shuji/0000-0002-3909-2323; Abdar Esfahani,
   Shadi/0000-0002-6077-4580; Mahmood, Umar/0000-0001-7414-6123
FU NIH [U01CA084301, P50CA127003, R35 CA197735]
FX The authors would like to thank GE Healthcare for their generous gift of
   GE-137, and Mr. Igor Bagayev for his help with acquiring images using
   Zeiss Confocal Microscopy. This study was supported by NIH grants
   U01CA084301 and P50CA127003. S.O. was in part supported by NIH grant R35
   CA197735.
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NR 39
TC 15
Z9 15
U1 0
U2 12
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1838-7640
J9 THERANOSTICS
JI Theranostics
PY 2016
VL 6
IS 12
BP 2028
EP 2038
DI 10.7150/thno.15718
PG 11
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA ED0AR
UT WOS:000388505900002
PM 27698938
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Plöthner, M
   Ribbentrop, D
   Hartman, JP
   Frank, M
AF Ploethner, Marika
   Ribbentrop, Dana
   Hartman, Jan-Phillipp
   Frank, Martin
TI Cost-Effectiveness of Pharmacogenomic and Pharmacogenetic Test-Guided
   Personalized Therapies: A Systematic Review of the Approved Active
   Substances for Personalized Medicine in Germany
SO ADVANCES IN THERAPY
LA English
DT Review
DE Abacavir; Azathioprine; Carbamazepine; Cetuximab; Cost-effectiveness;
   Personalized medicine; Pharmacogenetic test; Targeted therapy
ID ADVERSE DRUG-REACTIONS; METASTATIC COLORECTAL-CANCER; CLINICAL-PRACTICE;
   BREAST-CANCER; ECONOMIC-EVALUATION; KRAS; AZATHIOPRINE; MUTATIONS;
   ABACAVIR; CHEMOTHERAPY
AB The use of targeted therapies has recently increased. Pharmacogenetic tests are a useful tool to guide patient treatment and to test a response before administering medicines. Pharmacogenetic tests can predict potential drug resistance and may be used for determining genotype-based drug dosage. However, their cost-effectiveness as a diagnostic tool is often debatable. In Germany, 47 active ingredients are currently approved. A prior predictive test is required for 39 of these and is recommended for eight. The objective of this study was to review the cost-effectiveness (CE) of pharmacogenetic test-guided drug therapy and compare the application of drugs with and without prior genetic testing.
   A systematic literature review was conducted to identify the CE and cost-utility of genetic tests. Studies from January 2000 until November 2015 were searched in 16 databases including Medline, Embase, and Cochrane. A quality assessment of the full-text publications was performed using the validated Quality of Health Economic Studies (QHES) instrument.
   In the majority of the included studies, the pharmacogenetic test-guided therapy represents a cost-effective/cost-saving treatment option. Only seven studies lacked a clear statement of CE or cost-savings, because of uncertainty, restriction to specific patient populations, or assumptions for comparative therapy. Moreover, the high quality of the available evidence was evaluated.
   Pharmacogenetic testing constitutes an opportunity to improve the CE of pharmacotherapy. The CE of targeted therapies depends on various factors including costs, prevalence of biomarkers, and test sensitivity and specificity. To guarantee the CE comparability of stratified drug therapies, national and international standards for evaluation studies should be defined.
C1 [Ploethner, Marika; Ribbentrop, Dana; Hartman, Jan-Phillipp; Frank, Martin] Leibniz Univ Hannover, CHERH, Hannover, Germany.
C3 Leibniz University Hannover
RP Plöthner, M (corresponding author), Leibniz Univ Hannover, CHERH, Hannover, Germany.
EM mp@cherh.de
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NR 85
TC 23
Z9 26
U1 1
U2 7
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0741-238X
EI 1865-8652
J9 ADV THER
JI Adv. Ther.
PD SEP
PY 2016
VL 33
IS 9
BP 1461
EP 1480
DI 10.1007/s12325-016-0376-8
PG 20
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA DX6XX
UT WOS:000384530500001
PM 27406232
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Riechelmann, RP
   Leite, LS
   Bariani, GM
   Glasberg, J
   Rivelli, TG
   da Fonseca, LG
   Nebuloni, DR
   Braghiroli, MI
   Queiroz, MA
   Isejima, AM
   Kappeler, C
   Kikuchi, L
   Hoff, PM
AF Riechelmann, Rachel P.
   Leite, Luiz S.
   Bariani, Giovanni M.
   Glasberg, Joao
   Rivelli, Thomas G.
   da Fonseca, Leonardo Gomes
   Nebuloni, Daniela R.
   Braghiroli, Maria, I
   Queiroz, Marcelo A.
   Isejima, Alice M.
   Kappeler, Christian
   Kikuchi, Luciana
   Hoff, Paulo M.
TI Regorafenib in Patients with Antiangiogenic-Naive and
   Chemotherapy-Refractory Advanced Colorectal Cancer: Results from a Phase
   IIb Trial
SO ONCOLOGIST
LA English
DT Article
DE Regorafenib; Colorectal neoplasms; Angiogenesis inhibitors; Computed
   tomography; Positron emission tomography
ID POSITRON-EMISSION-TOMOGRAPHY; SOLID TUMORS; DOUBLE-BLIND; PLACEBO;
   CRITERIA; MULTICENTER; IMATINIB; PERCIST; RECIST
AB Background Regorafenib is a multikinase inhibitor with antiangiogenic effects that improves overall survival (OS) in metastatic colorectal cancer (mCRC) after failure of standard therapies. We investigated the efficacy and safety of regorafenib in antiangiogenic therapy-naive chemotherapy-refractory advanced colorectal cancer. Patients and Methods This single-center, single-arm, phase IIb study (NCT02465502) enrolled adults with mCRC whose disease had progressed on, or who were intolerant to, standard therapy, but who were antiangiogenic therapy-naive. Patients received regorafenib 160 mg once daily for 3 weeks per 4-week cycle. The primary endpoint was progression-free survival (PFS) rate at week 8. Results Of 59 treated patients, almost half had received at least four prior lines of therapy. Patients received a median of 86% of the planned dose. The week 8 PFS rate was 53% (95% confidence interval [CI], 39.1-64.3); median PFS was 3.5 months (95% CI, 1.8-3.6). Median OS was 7.4 months (95% CI, 5.3-8.9). Tumor response (RECIST version 1.1) was 2%, and metabolic response rate (criteria from the European Organisation for Research and Treatment of Cancer) was 41%. The most frequently reported regorafenib-related grade >= 3 adverse events were hypertension (36%), hand-foot skin reaction (HFSR, 25%), and hypophosphatemia (24%). There were no regorafenib-related deaths. An exploratory analysis showed that patients with grade >= 2 HFSR had longer OS (10.2 months) with regorafenib treatment versus those with grades 0-1 (5.4 months). Conclusion These findings support the antitumor activity of regorafenib in antiangiogenic-naive patients with chemotherapy-refractory mCRC. Implications for Practice The multikinase inhibitor regorafenib improved overall survival in the phase III CORRECT and CONCUR trials in heavily pretreated patients with treatment-refractory metastatic colorectal cancer (mCRC). Exploratory subgroup analysis from CONCUR suggested that regorafenib treatment prior to targeted therapy (including bevacizumab) may improve outcomes. In this single-center, single-arm phase IIb study, regorafenib demonstrated antitumor activity in 59 antiangiogenic-naive patients with chemotherapy-refractory mCRC. Further studies should assess the efficacy of regorafenib in this patient population, as well as explore the reasons behind improved outcomes among patients who had a metabolic response and those who developed hand-foot skin reaction.
C1 [Riechelmann, Rachel P.; Leite, Luiz S.; Bariani, Giovanni M.; Glasberg, Joao; Rivelli, Thomas G.; da Fonseca, Leonardo Gomes; Nebuloni, Daniela R.; Braghiroli, Maria, I; Queiroz, Marcelo A.; Hoff, Paulo M.] Inst Canc Estado Sao Paulo, Dept Radiol & Oncol, Sao Paulo, Brazil.
   [Riechelmann, Rachel P.] AC Camargo Canc Ctr, Dept Clin Oncol, Rua Antonio Prudente 211, BR-01509010 Sao Paulo, Brazil.
   [Queiroz, Marcelo A.] Univ Sao Paulo, Div Nucl Med & Mol Imaging, Sao Paulo, Brazil.
   [Isejima, Alice M.] Med Affairs Study Support, Sao Paulo, Brazil.
   [Kikuchi, Luciana] Bayer SA, SBU Oncol, Med & Data Management, Sao Paulo, Brazil.
   [Kappeler, Christian] Bayer AG, Global Clin Oncol, Clin Stat, Berlin, Germany.
C3 A.C.Camargo Cancer Center; Universidade de Sao Paulo; Bayer AG; Bayer AG
RP Riechelmann, RP (corresponding author), AC Camargo Canc Ctr, Dept Clin Oncol, Rua Antonio Prudente 211, BR-01509010 Sao Paulo, Brazil.
EM rachel.riechelmann@accamargo.org.br
RI Fonseca, Leonardo/JCD-5745-2023; Hoff, Paulo Marcelo/AEF-9576-2022;
   Riechelmann, Rachel/C-3984-2012; /C-3640-2012; Gehm Hoff, Paulo
   Marcelo/M-7662-2017
OI Gehm Hoff, Paulo Marcelo/0000-0002-0065-2194; Riechelmann,
   Rachel/0000-0002-0107-9617; Queiroz, Marcelo/0000-0003-0052-0682;
   Bariani, Giovanni/0000-0002-6153-6816
FU Bayer
FX This study was sponsored by Bayer. Medical writing and editorial support
   for the development of this manuscript was provided by Yvonne E. Yarker,
   Ph.D., C.M.P.P., and Katrin Gudmundsdottir, Ph.D., at Open Health
   Medical Communications (London, UK), with financial support from Bayer.
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NR 24
TC 13
Z9 13
U1 1
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PD SEP
PY 2019
VL 24
IS 9
BP 1180
EP 1187
DI 10.1634/theoncologist.2019-0067
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IX8XT
UT WOS:000485972100025
PM 31175167
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Wang, XX
   Zhou, YW
   Wang, B
   Cao, P
   Luo, DY
   Li, CH
   Wang, K
   Qiu, M
AF Wang, Xiao-Xuan
   Zhou, Yu-Wen
   Wang, Bo
   Cao, Peng
   Luo, De-Yun
   Li, Chun-Hong
   Wang, Kai
   Qiu, Meng
TI A nomogram construction and multicenter validation for predicting
   overall survival after fruquintinib application in patients with
   metastatic colorectal cancer: a multicenter retrospective study
SO THERAPEUTIC ADVANCES IN GASTROENTEROLOGY
LA English
DT Article
DE fruquintinib; metastatic colorectal cancer; nomogram; overall survival
ID REGORAFENIB; DIAGNOSIS; TAS-102; PLACEBO
AB Background: Fruquintinib is a third-line and subsequent targeted therapy for patients with metastatic colorectal cancer (mCRC). Identifying survival predictors after fruquintinib is crucial for optimizing the clinical use of this medication. Objectives: We aimed to identify factors influencing the prognosis of patients with mCRC treated with fruquintinib and to leverage these insights to develop a nomogram model for estimating survival rates in this patient population. Design: Multicenter retrospective observational study. Methods: We collected patient data from January 2019 to October 2023, with one healthcare institution's data serving as the training cohort and the other three hospitals' data serving as the multicenter validation cohort. The nomogram for overall survival was calculated from Cox regression models, and variable selection was screened using the univariate Cox regression analysis with additional variables based on clinical experience. Model performance was measured by the concordance index (C-index), calibration curves, decision curve analyses (DCA), and utility (patient stratification into low-risk vs high-risk groups). Results: Data were ultimately collected on 240 patients, with 144 patients included in the training cohort and 96 included in the multicenter validation cohort. Predictors included in the nomogram were CA199, body mass index, T stage, the primary site of the tumor, and other metastatic and pathological differentiation. The C-index of the nomogram in the training set and multicenter validation was 0.714 and 0.729, respectively. The models were fully calibrated and their predictions aligned closely with the observed data. DCA curves indicated the promising clinical benefits of the predictive model. Finally, the reliability of the model was also verified through the risk classification using the nomogram. Conclusions: We constructed a nomogram for mCRC treated with fruquintinib based on six variables that may be used to assist in personalizing the use of the drug. A nomogram for predicting OS after application of fruquintinib in patients with mCRC The prognostic predictors of fruquintinib as a third-line and subsequent treatment agent for patients with mCRC have not been established. In this study, we explored possible factors influencing its prognosis and developed a nomogram model for estimating survival rates in this patient population. The nomogram, based on six key variables including CA199, BMI, T stage, primary tumor site, other metastatic sites, and pathological differentiation, was validated through a rigorous multicenter validation process. The nomogram has the potential to help clinicians personalize the use of fruquintinib for mCRC patients.
C1 [Wang, Xiao-Xuan; Zhou, Yu-Wen; Wang, Bo; Cao, Peng; Qiu, Meng] Sichuan Univ, West China Hosp, Colorectal Canc Ctr, Guoxue Rd 37, Chengdu 610041, Sichuan, Peoples R China.
   [Luo, De-Yun] Sichuan Univ, Shang Jin Hosp West China Hosp, Canc Ctr, Dept Abdominal Canc, Chengdu, Sichuan, Peoples R China.
   [Li, Chun-Hong] Suining Cent Hosp, Dept Oncol, Suining, Peoples R China.
   [Wang, Kai] Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Inst Emergency & Disaster Med, Chengdu, Sichuan, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan Provincial People's
   Hospital; University of Electronic Science & Technology of China
RP Qiu, M (corresponding author), Sichuan Univ, West China Hosp, Colorectal Canc Ctr, Guoxue Rd 37, Chengdu 610041, Sichuan, Peoples R China.
EM qiumeng33@hotmail.com
RI Zhou, Yuwen/IQR-6924-2023; li, chunhong/ABD-9811-2020
FU Department of Science and Technology of Sichuan Province [2024NSFSC1902,
   2024NSFSC0402]; Postdoctor Research Fund of West China Hospital, Sichuan
   University [2024HXBH029]; Nation-Sponsored Postdoctor Researcher Program
   [GZC20231836]; The 1.3.5 Project for Disciplines of Excellence, West
   China Hospital, Sichuan University [ZYJC21017]
FX The authors disclosed receipt of the following financial support for the
   research, authorship, and/or publication of this article: This study was
   supported by the Department of Science and Technology of Sichuan
   Province (2024NSFSC1902), the Department of Science and Technology of
   Sichuan Province (2024NSFSC0402), the Postdoctor Research Fund of West
   China Hospital, Sichuan University (2024HXBH029), the Nation-Sponsored
   Postdoctor Researcher Program (GZC20231836), the 1.3.5 Project for
   Disciplines of Excellence, West China Hospital, Sichuan University
   (ZYJC21017).
CR Biller LH, 2021, JAMA-J AM MED ASSOC, V325, P669, DOI 10.1001/jama.2021.0106
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   Deng YY, 2023, FRONT ONCOL, V13, DOI 10.3389/fonc.2023.1097911
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NR 23
TC 0
Z9 0
U1 2
U2 2
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1756-283X
EI 1756-2848
J9 THER ADV GASTROENTER
JI Ther. Adv. Gastroenterol.
PY 2024
VL 17
AR 17562848241284229
DI 10.1177/17562848241284229
PG 17
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA I6Q8K
UT WOS:001331493800001
PM 39386273
OA gold
DA 2025-01-04
ER

PT J
AU Kim, JE
   Chae, SY
   Kim, JH
   Kim, HJ
   Kim, TW
   Kim, KP
   Kim, SY
   Lee, JL
   Oh, SJ
   Kim, JS
   Ryu, JS
   Moon, DH
   Hong, YS
AF Kim, Jeong Eun
   Chae, Sun Young
   Kim, Jwa Hoon
   Kim, Hwa Jung
   Kim, Tae Won
   Kim, Kyu-pyo
   Kim, Sun Young
   Lee, Jae-Lyun
   Oh, Seung Jun
   Kim, Jae Seung
   Ryu, Jin-Sook
   Moon, Dae Hyuk
   Hong, Yong Sang
TI 3-Deoxy-3'-<SUP>18</SUP>F-Fluorothymidine and
   <SUP>18</SUP>F-Fluorodeoxyglucose positron emission tomography for the
   early prediction of response to Regorafenib in patients with metastatic
   colorectal cancer refractory to all standard therapies
SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
LA English
DT Article
DE F-18-fluorothymidine; F-18-fluorodeoxyglucose; Positron emission
   tomography; Regorafenib; Metastatic colorectal cancer
ID IMAGING PROLIFERATION; TARGETED-THERAPY; PHASE-III; IN-VIVO;
   CHEMOTHERAPY; BEVACIZUMAB; LEUCOVORIN; PET;
   3'-DEOXY-3'-F-18-FLUOROTHYMIDINE; FLUOROURACIL
AB PurposeThe purpose of this study was to evaluate the value of 3-deoxy-3-F-18-fluorothymidine (F-18-FLT) and F-18-fluorodeoxyglucose (F-18-FDG) positron emission tomography/computed tomography (PET/CT) for early prediction of standard anatomic response and survival outcomes in patients with metastatic colorectal cancer (mCRC) receiving Regorafenib.MethodsSixty-eight patients with mCRC refractory to standard cytotoxic chemotherapy were enrolled and received Regorafenib (160mg/day on days 1-21, following a 7-day break). Standard anatomical response was evaluated every 8weeks. Both scans were performed before and on day 21 of Regorafenib.ResultsOf the 61 patients included in per-protocol analysis, complete response was not observed, but partial response was observed in 8.2% (n=5), stable disease in 67.2% (n=41), and progressive disease in 24.6% (n=15). The objective response rate was 8.2% and disease control rate 75.4%. Five responders (8.2%) and 13 non-responders (21.3%) met the CT and F-18-FLT PET/CT criteria (maximum standardized uptake value decrease 10.6% for responders). Forty-three (70.5%) exhibited discordant responses on CT and F-18-FLT PET/CT (McNemar test, P<0.001). At a median follow-up of 8.9months, median progression-free survival (PFS) and median overall survival (OS) were 3.6months (95% confidence interval [CI], 3.34-3.80months) and 8.5months (95% CI, 6.95-10.10months), respectively. Comparison of PFS and OS according to F-18-FLT PET/CT response revealed slightly longer PFS (P=0.015) in responders, but the correlation with OS was not significant. The PET Response Criteria in Solid Tumours (PERCIST) of F-18-FDG PET/CT revealed differences in PFS and OS between partial metabolic response (PMR) and non-PMR (P=0.048 and P=0.014, respectively), and between progressive metabolic disease (PMD) and non-PMD (P=0.189 and P=0.007, respectively).ConclusionsSurvival outcome was significantly associated with PERCIST using F-18-FDG PET/CT but the change of F-18-FLT uptake was only slightly associated with PFS. F-18-FDG PET/CT can be used as imaging biomarker to predict clinical outcomes early in patients with mCRC receiving Regorafenib.
C1 [Kim, Jeong Eun; Kim, Jwa Hoon; Kim, Tae Won; Kim, Kyu-pyo; Kim, Sun Young; Lee, Jae-Lyun; Hong, Yong Sang] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Oncol, 88 Olymp Ro 43 Gil, Seoul 05505, South Korea.
   [Chae, Sun Young; Oh, Seung Jun; Kim, Jae Seung; Ryu, Jin-Sook; Moon, Dae Hyuk] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Nucl Med, Seoul, South Korea.
   [Kim, Hwa Jung] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Prevent Med, Seoul, South Korea.
C3 University of Ulsan; University of Ulsan; Asan Medical Center;
   University of Ulsan; Asan Medical Center
RP Hong, YS (corresponding author), Univ Ulsan, Coll Med, Asan Med Ctr, Dept Oncol, 88 Olymp Ro 43 Gil, Seoul 05505, South Korea.
EM yshong@amc.seoul.kr
RI Moon, Dae/ACK-5262-2022; Lee, Jae Lyun/AGI-4843-2022; Kim, Tae
   Won/GRX-7323-2022; Kim, Pyeong Hwa/KGM-1468-2024; Kim,
   Jwa/AAH-9915-2021; Kim, Ho Cheol/LIJ-9487-2024
OI Kim, Hwa Jung/0000-0003-1916-7014
FU Asan Institute for Life Sciences, Asan Medical Center, Seoul, Korea
   [2014-9079]; Korea Health Technology R&D Project through the Korea
   Health Industry Development Institute (KHIDI); Ministry of Health &
   Welfare, Republic of Korea [HI18C2383]
FX This study was supported by a grant (2014-9079) from the Asan Institute
   for Life Sciences, Asan Medical Center, Seoul, Korea, and a grant of the
   Korea Health Technology R&D Project through the Korea Health Industry
   Development Institute (KHIDI), funded by the Ministry of Health &
   Welfare, Republic of Korea (grant number: HI18C2383). Regorafenib was
   kindly provided by Bayer.
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NR 39
TC 9
Z9 10
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1619-7070
EI 1619-7089
J9 EUR J NUCL MED MOL I
JI Eur. J. Nucl. Med. Mol. Imaging
PD JUL
PY 2019
VL 46
IS 8
BP 1713
EP 1722
DI 10.1007/s00259-019-04330-7
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA IE1WR
UT WOS:000472177000018
PM 31041456
DA 2025-01-04
ER

PT J
AU Pastorino, A
   Di Bartolomeo, M
   Maiello, E
   Iaffaioli, V
   Ciuffreda, L
   Fasola, G
   Di Costanzo, F
   Frassineti, GL
   Marchetti, P
   Antoniotti, C
   Leone, F
   Zaniboni, A
   Aprile, G
   Zilocchi, C
   Sobrero, A
   Bordonaro, R
AF Pastorino, Alessandro
   Di Bartolomeo, Maria
   Maiello, Evaristo
   Iaffaioli, Vincenzo
   Ciuffreda, Libero
   Fasola, Gianpiero
   Di Costanzo, Francesco
   Frassineti, Giovanni Luca
   Marchetti, Paolo
   Antoniotti, Carlotta
   Leone, Francesco
   Zaniboni, Alberto
   Aprile, Giuseppe
   Zilocchi, Chiara
   Sobrero, Alberto
   Bordonaro, Roberto
TI Aflibercept Plus FOLFIRI in the Real-life Setting: Safety and Quality of
   Life Data From the Italian Patient Cohort of the Aflibercept Safety and
   Quality-of-Life Program Study
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE Antiangiogenesis; Antivascular endothelial growth factor agents; HRQL;
   Metastatic colorectal cancer; Targeted therapy
ID METASTATIC COLORECTAL-CANCER; ANGIOGENESIS; SURVIVAL; EUROQOL
AB The Italian subset of the real-life Aflibercept Safety and Quality-of-Life Program study evaluated the safety and health-related quality of life (HRQL) of aflibercept plus FOLFIRI (folinic acid, 5-fluorouracil, irinotecan) in 200 patients with pretreated metastatic colorectal cancer (mCRC). No significant worsening of HRQL occurred, and the safety profile was consistent with the reported data. The combination was well tolerated as second-line treatment for patients with mCRC in a real-life setting.
   Background: Aflibercept combined with FOLFIRI (folinic acid, 5-fluorouracil, irinotecan) as second-line treatment of metastatic colorectal cancer (mCRC) significantly improved survival compared with FOLFIRI alone in the pivotal VELOUR (aflibercept vs. placebo in combination with irinotecan and 5-fluorouracil in the treatment of patients with metastatic colorectal cancer after failure of an oxaliplatin-based regimen) trial. No quality-of-life assessment was performed in VELOUR; therefore, the ASQoP (Aflibercept Safety and Quality-of-Life Program) trial was designed to capture the safety and health-related quality of life (HRQL). Patients and Methods: ASQoP was an international, open-label, single-arm trial evaluating the safety and HRQL of aflibercept combined with FOLFIRI administered in a real-life setting to 781 patients with mCRC, pretreated with an oxaliplatin-based regimen with or without bevacizumab. The Italian subset of ASQoP enrolled 200 patients from 28 institutions. The primary endpoint was safety; HRQL was a secondary endpoint, assessed by validated questionnaires (European quality of life 5-dimension instrument 3-level; European Organization for Research and Treatment for Cancer Quality of Life Questionnaire Core 30, version 3; and EORTC-CR29) at baseline, during treatment, and at the end of treatment. Results: The median age of the Italian ASQoP population was 63 years; the median number of aflibercept and FOLFIRI cycles was 7. Treatment-emergent adverse events were reported in 97.5% of patients. Hypertension (28.5%), neutropenia (27.5%; from laboratory data), asthenic conditions (20.0%), diarrhea (17.0%), and stomatitis (13.0%) were the most frequent (incidence, >= 5%) grade 3/4 toxicities. One toxic death occurred during the study period due to sepsis, without neutropenic complications. No significant worsening of HRQL was shown during treatment. Conclusion: Aflibercept combined with FOLFIRI was well tolerated when administered as second-line treatment for patients with mCRC in a real-life setting. It did not affect HRQL and showed similar rates of treatment-emergent adverse events as those observed in the VELOUR trial. No new safety signals were identified. (C) 2018 The Authors. Published by Elsevier Inc.
C1 [Pastorino, Alessandro] Osped S Andrea, Dept Med Oncol, Via Vittorio Veneto 197, I-19121 La Spezia, Italy.
   [Di Bartolomeo, Maria] Fdn IRCCS Ist Nazl Tumori, Dept Med Oncol, Milan, Italy.
   [Maiello, Evaristo] IRCCS Casa Sollievo Sofferenza, Dept Oncol, San Giovanni Rotondo, Italy.
   [Iaffaioli, Vincenzo] Ist Nazl Tumori Fdn G Pascale IRCCS, Dept Abdominal Oncol, Naples, Italy.
   [Ciuffreda, Libero] AOU Citta Salute & Sci Molinette Hosp, Dept Med Oncol, Turin, Italy.
   [Fasola, Gianpiero] Univ & Gen Hosp, Dept Oncol, Udine, Italy.
   [Di Costanzo, Francesco] Azienda Osped Univ Careggi, Dept Med Oncol, Florence, Italy.
   [Frassineti, Giovanni Luca] IRCCS Ist Sci Romagnolo & Cura Tumori, Med Oncol Unit, Meldola, Italy.
   [Marchetti, Paolo] St Andrea Hosp Rome, Med Oncol Unit, Rome, Italy.
   [Marchetti, Paolo] IDI IRCCS, Rome, Italy.
   [Antoniotti, Carlotta] Univ Hosp Pisa, Dept Oncol, Pisa, Italy.
   [Leone, Francesco] Candiolo Canc Inst FPO IRCCS, Med Oncol Unit, Turin, Italy.
   [Zaniboni, Alberto] Fdn Poliambulanza, Med Oncol Unit, Brescia, Italy.
   [Aprile, Giuseppe] San Bortolo Gen Hosp, Dept Oncol, Vicenza, Italy.
   [Zilocchi, Chiara] Sanofi, Milan, Italy.
   [Sobrero, Alberto] IRCCS San Martino IST, Dept Med Oncol, Genoa, Italy.
   [Bordonaro, Roberto] ARNAS Garibaldi, Med Oncol Unit, Catania, Italy.
C3 Fondazione IRCCS Istituto Nazionale Tumori Milan; IRCCS Casa Sollievo
   Della Sofferenza; IRCCS Fondazione Pascale; A.O.U. Citta della Salute e
   della Scienza di Torino; AOU San Giovanni Battista-Molinette; University
   of Udine; University Hospital of Udine; University of Florence; Azienda
   Ospedaliero Universitaria Careggi; Sapienza University Rome; Azienda
   Ospedaliera Sant'Andrea; IRCCS Istituto Dermopatico dell'Immacolata
   (IDI); University of Pisa; Azienda Ospedaliero Universitaria Pisana;
   IRCCS Fondazione del Piemonte per l'Oncologia; ULSS 8 Berica; Ospedale
   San Bortolo di Vicenza; Sanofi-Aventis; University of Genoa; IRCCS AOU
   San Martino IST
RP Pastorino, A (corresponding author), Osped S Andrea, Dept Med Oncol, Via Vittorio Veneto 197, I-19121 La Spezia, Italy.
EM alessandro.pastorino@asl5.liguria.it
RI Fasola, Gianpiero/AAC-3629-2022; Bordonaro, Roberto/AAA-8138-2022;
   Sobrero, Alberto/AAF-9742-2019; Antoniotti, Carlotta/KIC-8096-2024; Di
   Costanzo, Francesco/HMV-6214-2023; Leone, Francesco/AAB-2355-2022;
   Marchetti, Paolo/J-9890-2018; Di Bartolomeo, Maria/D-1655-2017; LEONE,
   Francesco/R-3248-2016; Maiello, Evaristo/C-5224-2017
OI Marchetti, Paolo/0000-0002-9064-8761; Di Costanzo,
   Francesco/0000-0002-6858-7827; Fasola, Gianpiero/0000-0002-1254-4705;
   Frassineti, Giovanni Luca/0000-0002-0277-5622; Di Bartolomeo,
   Maria/0000-0002-7954-6609; LEONE, Francesco/0000-0001-5422-9706;
   Maiello, Evaristo/0000-0003-3890-3435; Bordonaro,
   Roberto/0000-0001-5005-0880
FU Sanofi; Regeneron Pharmaceuticals, Inc.; Sanofi (Italy)
FX The present study was supported by Sanofi in collaboration with
   Regeneron Pharmaceuticals, Inc. Editorial support in the preparation of
   our report was provided by Ray Hill, an independent medical writer, for
   English language editing and medical writing support before submission
   on behalf of Health Publishing & Services Srl, which was funded by
   Sanofi (Italy). We wish to thank all the patients who participated in
   our study and the following ASQoP study investigators: Massimo Aglietta,
   Candiolo, Turin; Giuseppe Altavilla, Messina; Antonio Avallone, Naples;
   Giovanni Baldino, Alghero; Maria Banzi, Reggio Emilia; Carlo Barone,
   Rome; Stefano Cascinu, Modena; Antonino Cassata, Naples; Stefano Cordio,
   Catania; Francesca Di Fabio, Bologna; Alfredo Falcone, Pisa; Vinera
   Gindulina, Naples; Sara Lonardi, Padua; Stefania Mosconi, Bergamo; Maria
   Emanuela Negru, Novara; Fausto Roila, Terni; Monica Ronzoni, Milan;
   Salvatore Siena, Milan; Pierosandro Tagliaferri, Catanzaro; Giuseppe
   Tonini, Rome; and Giampaolo Tortora, Verona. We also thank Dr Paolo
   Bruzzi (Unit of Clinical Epidemiology, IRCCS AOU San Martino IST, Genoa,
   Italy) and Dr Massimiliano Grassi (freelance MD) for supporting the
   statistical analysis of the quality of life data. This service was
   financed by Sanofi (Italy).
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NR 16
TC 18
Z9 18
U1 0
U2 2
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1533-0028
EI 1938-0674
J9 CLIN COLORECTAL CANC
JI Clin. Colorectal Canc.
PD SEP
PY 2018
VL 17
IS 3
BP E457
EP E470
DI 10.1016/j.clcc.2018.03.002
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GR5KI
UT WOS:000442669400003
PM 29605592
OA Green Published, hybrid
DA 2025-01-04
ER

PT B
AU Dlamini, Z
   Khoza, T
   Hull, R
   Choene, M
   Mkhize-Kwitshana, Z
AF Dlamini, Zodwa
   Khoza, Thandeka
   Hull, Rodney
   Choene, Mpho
   Mkhize-Kwitshana, Zilungile
BE Rodrigo, L
TI Current Immunotherapeutic Treatments in Colon Cancer
SO COLORECTAL CANCER - FROM PATHOGENESIS TO TREATMENT
LA English
DT Article; Book Chapter
DE Cancer vaccines; Monoclonal antibodies; Bispecific antibodies;
   Cytokines; Immune checkpoint inhibitors; Adoptive therapy; Immunotherapy
ID METASTATIC COLORECTAL-CANCER; HERPES-SIMPLEX-VIRUS; HEAT-SHOCK PROTEINS;
   T-CELLS; ANTITUMOR IMMUNITY; ONCOLYTIC VIRUSES; MONOCLONAL-ANTIBODIES;
   PEPTIDE VACCINE; DENDRITIC CELLS; REGULATORY T
AB The immune system is able to act against cancer cells and consequently these cells have developed a range of responses to evade or suppress the immune systems anticancer responses. The concept of cancer immunotherapy is based on techniques developed to restore or boost the ability of the immune system to recognize and target tumor cells. It is known that colon cancer does initiate an immune response and that this type of cancer initiates pathways and responses to evade or suppress the immune system. This chapter will discuss some of the dominant therapies being developed to treat colon cancer based on the concept of cancer immunotherapy. Cancer vaccines are based on the concept of providing the immune system with antigen targets derived from tumor-specific molecules, while monoclonal antibodies involve the development of antibodies specifically targeting proteins expressed on the surface of tumor cells. Antibodybased immunotherapy has further applications in the use of bispecific antibodies (BsAb), which are synthetic antibodies designed to be able to recognize two different antigens or epitopes and in this way can increase the immunoresponse and limit immune evasion observed in mono-targeted therapy. Immune checkpoint inhibitors target proteins that are responsible for keeping immune responses in check. Tumor cells overexpress these proteins in order to evade the immune response. Blocking these proteins will lead to an increased immune response against these cells. Cytokine-based immunotherapies involve the use of the immune systems' own molecular messengers that are responsible for a robust immune response, to boost the antitumor response of the immune system. Oncolytic viral therapy is based on the use of viruses that selectively infect and replicate in cancer and associated endothelial cells and subsequently kills these cells. Adoptive immunotherapy involves the use of immune cells from the patient to be cultured and altered in the laboratory and then reintroduced to boost the immune response. This is normally performed with T cells. Immunotherapy may be the next logical step in the development of an effective therapy for colon cancer and other cancers. The combination of these therapies with traditional chemotherapy or radiotherapy has shown promise in cancer treatment.
C1 [Dlamini, Zodwa; Khoza, Thandeka; Hull, Rodney; Choene, Mpho; Mkhize-Kwitshana, Zilungile] Mangosuthu Univ Technol, Res Innovat & Engagements Portfolio, Durban, South Africa.
C3 Mangosuthu University of Technology
RP Dlamini, Z (corresponding author), Mangosuthu Univ Technol, Res Innovat & Engagements Portfolio, Durban, South Africa.
EM dlaminiz@mut.ac.za
RI Hull, Rodney/HJP-0275-2023; Mkhize-Kwitshana, Zilungile/ISU-0265-2023;
   Dlamini, Zodwa/HNB-6090-2023
OI Mkhize-Kwitshana, Zilungile/0000-0002-0373-9973; Dlamini,
   Zodwa/0000-0002-8012-3646
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NR 112
TC 0
Z9 0
U1 0
U2 2
PU INTECH EUROPE
PI RIJEKA
PA JANEZA TRDINE9, RIJEKA, 51000, CROATIA
BN 978-953-51-2545-7; 978-953-51-2544-0
PY 2016
BP 211
EP 239
DI 10.5772/63212
D2 10.5772/61359
PG 29
WC Oncology; Gastroenterology & Hepatology
WE Book Citation Index – Science (BKCI-S)
SC Oncology; Gastroenterology & Hepatology
GA BK3WD
UT WOS:000435598000011
OA hybrid
DA 2025-01-04
ER

PT J
AU Quénet, F
   Elias, D
   Roca, L
   Goéré, D
   Ghouti, L
   Pocard, M
   Facy, O
   Arvieux, C
   Lorimier, G
   Pezet, D
   Marchal, F
   Loi, V
   Meeus, P
   Juzyna, B
   de Forges, H
   Paineau, J
   Glehen, O
AF Quenet, Francois
   Elias, Dominique
   Roca, Lise
   Goere, Diane
   Ghouti, Laurent
   Pocard, Marc
   Facy, Olivier
   Arvieux, Catherine
   Lorimier, Gerard
   Pezet, Denis
   Marchal, Frederic
   Loi, Valeria
   Meeus, Pierre
   Juzyna, Beata
   de Forges, Helene
   Paineau, Jacques
   Glehen, Olivier
CA UNICANCER-GI Grp
   BIG Renape Grp
TI Cytoreductive surgery plus hyperthermic intraperitoneal chemotherapy
   versus cytoreductive surgery alone for colorectal peritoneal metastases
   (PRODIGE 7): a multicentre, randomised, open-label, phase 3 trial
SO LANCET ONCOLOGY
LA English
DT Article
AB Background The addition of hyperthermic intraperitoneal chemotherapy (HIPEC) to cytoreductive surgery has been associated with encouraging survival results in some patients with colorectal peritoneal metastases who were eligible for complete macroscopic resection. We aimed to assess the specific benefit of adding HIPEC to cytoreductive surgery compared with receiving cytoreductive surgery alone.
   Methods We did a randomised, open-label, phase 3 trial at 17 cancer centres in France. Eligible patients were aged 18-70 years and had histologically proven colorectal cancer with peritoneal metastases, WHO performance status of 0 or 1, a Peritoneal Cancer Index of 25 or less, and were eligible to receive systemic chemotherapy for 6 months (ie, they had adequate organ function and life expectancy of at least 12 weeks). Patients in whom complete macroscopic resection or surgical resection with less than 1 mm residual tumour tissue was completed were randomly assigned (1:1) to cytoreductive surgery with or without oxaliplatin-based HIPEC. Randomisation was done centrally using minimisation, and stratified by centre, completeness of cytoreduction, number of previous systemic chemotherapy lines, and timing of protocol-mandated systemic chemotherapy. Oxaliplatin HIPEC was administered by the closed (360 mg/m(2)) or open (460 mg/m(2)) abdomen techniques, and systemic chemotherapy (400 mg/m(2) fluorouracil and 20 mg/m(2) folinic acid) was delivered intravenously 20 min before HIPEC. All individuals received systemic chemotherapy (of investigators' choosing) with or without targeted therapy before or after surgery, or both. The primary endpoint was overall survival, which was analysed in the intention-to-treat population. Safety was assessed in all patients who received surgery. This trial is registed with ClinicalTrials.gov, NCT00769405, and is now completed.
   Findings Between Feb 11, 2008, and Jan 6, 2014, 265 patients were included and randomly assigned, 133 to the cytoreductive surgery plus HIPEC group and 132 to the cytoreductive surgery alone group. After median follow-up of 63.8 months (IQR 53.0-77.1), median overall survival was 41.7 months (95% CI 36.2-53.8) in the cytoreductive surgery plus HIPEC group and 41.2 months (35.1-49.7) in the cytoreductive surgery group (hazard ratio 1.00 [95.37% CI 0.63-1.58]; stratified log-rank p=0.99). At 30 days, two (2%) treatment-related deaths had occurred in each group. Grade 3 or worse adverse events at 30 days were similar in frequency between groups (56 [42%] of 133 patients in the cytoreductive surgery plus HIPEC group vs 42 [32%] of 132 patients in the cytoreductive surgery group; p=0.083); however, at 60 days, grade 3 or worse adverse events were more common in the cytoreductive surgery plus HIPEC group (34 [26%] of 131 vs 20 [15%] of 130; p=0.035). Interpretation Considering the absence of an overall survival benefit after adding HIPEC to cytoreductive surgery and more frequent postoperative late complications with this combination, our data suggest that cytoreductive surgery alone should be the cornerstone of therapeutic strategies with curative intent for colorectal peritoneal metastases. Funding Institut National du Cancer, Programme Hospitalier de Recherche Clinique du Cancer, Ligue Contre le Cancer. Copyright (c) 2021 Elsevier Ltd. All rights reserved.
C1 [Quenet, Francois] Univ Montpellier, Dept Surg Oncol, Inst Canc Montpellier, Montpellier, France.
   [Roca, Lise] Univ Montpellier, Biometr Unit, Inst Canc Montpellier, Montpellier, France.
   [de Forges, Helene] Univ Montpellier, Dept Clin Res & Innovat, Montpellier, France.
   [Elias, Dominique; Goere, Diane] Gustave Roussy, Dept Surg, Villejuif, France.
   [Ghouti, Laurent] Ctr Hosp Purpan, Dept Surg, Toulouse, France.
   [Pocard, Marc] Paris Univ, Surg Oncol & Digest Unit, U1275, CAP Paris Tech, Paris, France.
   [Facy, Olivier] Ctr Hosp Univ Bocage, Dept Digest Surg & Oncol, Dijon, France.
   [Arvieux, Catherine] Ctr Hosp Univ Grenoble, Dept Oncol Surg, La Tronche, France.
   [Lorimier, Gerard] Ctr Paul Papin, Dept Surg, Angers, France.
   [Pezet, Denis] Hop Hotel Dieu, Dept Digest & Hepatobiliary Surg, Clermont Ferrand, France.
   [Marchal, Frederic] Inst Cancerol Lorraine, Dept Surg Oncol, Vandoeuvre Les Nancy, France.
   [Loi, Valeria] Hop Tenon, Dept Digest & Visceral Surg, Paris, France.
   [Meeus, Pierre] Ctr Leon Berard, Dept Oncol Surg, Lyon, France.
   [Juzyna, Beata] UNICANCER, Dept Res & Dev, Paris, France.
   [Paineau, Jacques] Inst Cancerol Ouest, Dept Surg, St Herblain, France.
   [Glehen, Olivier] Ctr Hosp Lyon Sud, Dept Digest Surg, Pierre Benite, France.
C3 UNICANCER; Universite de Montpellier; Institut Regional du Cancer
   Montpellier / Val d'Aurelle (ICM); UNICANCER; Universite de Montpellier;
   Institut Regional du Cancer Montpellier / Val d'Aurelle (ICM);
   Universite de Montpellier; UNICANCER; Gustave Roussy; CHU de Toulouse;
   Universite Paris Cite; CHU Dijon Bourgogne; CHU Grenoble Alpes;
   Communaute Universite Grenoble Alpes; Universite Grenoble Alpes (UGA);
   UNICANCER; Institut de Cancerologie de l'Ouest (ICO); CHU Clermont
   Ferrand; UNICANCER; Institut de cancerologie de Lorraine (ICL);
   Assistance Publique Hopitaux Paris (APHP); Sorbonne Universite; Hopital
   Universitaire Tenon - APHP; UNICANCER; Centre Leon Berard; UNICANCER;
   UNICANCER; Institut de Cancerologie de l'Ouest (ICO); CHU Lyon
RP Quénet, F (corresponding author), Inst Canc Montpellier, Dept Surg Oncol, F-34298 Montpellier, France.
EM francois.quenet@icm.unicancer.fr
RI Arvieux, Catherine/AAQ-3128-2021; facy, olivier/AAQ-2293-2021
OI facy, olivier/0000-0002-5619-8963
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NR 32
TC 483
Z9 504
U1 4
U2 38
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1470-2045
EI 1474-5488
J9 LANCET ONCOL
JI Lancet Oncol.
PD FEB
PY 2021
VL 22
IS 2
BP 256
EP 266
DI 10.1016/S1470-2045(20)30599-4
EA FEB 2021
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QE0SN
UT WOS:000615917800032
PM 33476595
OA Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Maroto, P
   Porta, C
   Capdevila, J
   Apolo, AB
   Viteri, S
   Rodriguez-Antona, C
   Martin, L
   Castellano, D
AF Maroto, Pablo
   Porta, Camillo
   Capdevila, Jaume
   Apolo, Andrea B.
   Viteri, Santiago
   Rodriguez-Antona, Cristina
   Martin, Lidia
   Castellano, Daniel
TI Cabozantinib for the treatment of solid tumors: a systematic review
SO THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
LA English
DT Review
DE cabozantinib; hepatocellular carcinoma; renal cell carcinoma; solid
   tumor; tyrosine kinase inhibitor; vascular endothelial growth factor
ID RENAL-CELL CARCINOMA; ADVANCED HEPATOCELLULAR-CARCINOMA; PHASE-II TRIAL;
   RANDOMIZED DISCONTINUATION TRIAL; DIFFERENTIATED THYROID-CANCER;
   CLINICAL-OUTCOMES CO; REAL-WORLD DATA; PATIENTS PTS; CELESTIAL TRIAL;
   TARGETED THERAPY
AB Background: Cabozantinib is approved, in various settings, for the treatment of renal cell carcinoma, medullary thyroid cancer, and hepatocellular carcinoma, and it has been investigated for the treatment of other cancers. With the available evidence and the real-world performance of cabozantinib compared with clinical trial data, we performed a systematic review of cabozantinib monotherapy as treatment for solid tumors in adults. Methods: This study was designed in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses and registered with PROSPERO (CRD42020144680). We searched for clinical and observational studies of cabozantinib monotherapy for solid tumors using Embase, MEDLINE, and Cochrane databases (October 2020), and screened relevant congress abstracts. Eligible studies reported clinical or safety outcomes, or biomarker data. Small studies (n < 25) and studies of cabozantinib combination therapies were excluded. Quality was assessed using National Institute for Health and Care Excellence methodology, and study characteristics were described qualitatively. Results: Of 2888 citations, 114 were included (52 randomized studies, 29 observational studies, 32 nonrandomized phase I or II studies or pilot trials, and 1 analysis of data from a randomized study and a nonrandomized study). Beyond approved indications, other tumors studied were castration-resistant prostate cancer, urothelial carcinoma, Ewing sarcoma, osteosarcoma, uveal melanoma, non-small-cell lung cancer, Merkel cell carcinoma, glioblastoma, pheochromocytomas and paragangliomas, cholangiocarcinoma, gastrointestinal stromal tumor, colorectal cancer, salivary gland cancer, carcinoid and pancreatic neuroendocrine tumors, and breast, endometrial and ovarian cancers. The most common adverse events were hypertension, diarrhea, and fatigue. Conclusion: The identified evidence demonstrates the positive efficacy/effectiveness of cabozantinib monotherapy in various solid tumor types, with safety findings being consistent with those observed with other VEGFR-targeting tyrosine kinase inhibitors. When available, real-world findings were consistent with the data reported from clinical trials. A limitation of this review is the high proportion of abstracts; however, this allowed us to capture the most up-to-date findings.
C1 [Maroto, Pablo] Hosp Santa Creu & Sant Pau, Med Oncol Serv, Barcelona 08025, Spain.
   [Porta, Camillo] Univ Bari Aldo Moro, Interdisciplinary Dept Med, Bari, Italy.
   [Capdevila, Jaume] Vall dHebron Univ Hosp, Vall dHebron Inst Oncol VHIO, Dept Med Oncol, Barcelona, Spain.
   [Apolo, Andrea B.] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Viteri, Santiago] UOMI Canc Ctr, Clin Mi Tres Torres, Barcelona, Spain.
   [Rodriguez-Antona, Cristina] Natl Canc Res Ctr, Madrid, Spain.
   [Martin, Lidia] Ipsen Pharma, Barcelona, Spain.
   [Castellano, Daniel] Univ Hosp 12 Octubre, Dept Med Oncol, Madrid, Spain.
C3 Hospital of Santa Creu i Sant Pau; Universita degli Studi di Bari Aldo
   Moro; Hospital Universitari Vall d'Hebron; Vall d'Hebron Institut
   d'Oncologia (VHIO); National Institutes of Health (NIH) - USA; NIH
   National Cancer Institute (NCI); Ipsen; Hospital Universitario 12 de
   Octubre
RP Maroto, P (corresponding author), Hosp Santa Creu & Sant Pau, Med Oncol Serv, Barcelona 08025, Spain.
EM JMaroto@santpau.cat
RI Viteri, Santiago/ABE-4563-2020; Porta, Camillo/AAB-9482-2020;
   Rodriguez-Antona, Cristina/E-1073-2011
OI MAROTO REY, PABLO/0000-0002-0030-0412; Rodriguez-Antona,
   Cristina/0000-0001-8750-7338; Viteri, Santiago/0000-0002-7572-1123
FU Ipsen; National Cancer Institute [ZIABC011351] Funding Source: NIH
   RePORTER
FX The authors disclosed receipt of the following financial support for the
   research, authorship, and/or publication of this article: This study was
   funded by Ipsen.
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NR 131
TC 33
Z9 34
U1 1
U2 10
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1758-8340
EI 1758-8359
J9 THER ADV MED ONCOL
JI Ther. Adv. Med. Oncol.
PD JUL
PY 2022
VL 14
AR 17588359221107112
DI 10.1177/17588359221107112
PG 28
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3B1QB
UT WOS:000827721700001
PM 35847482
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Crudden, C
   Shibano, T
   Song, DW
   Dragomir, MP
   Cismas, S
   Serly, J
   Nedelcu, D
   Fuentes-Mattei, E
   Tica, A
   Calin, GA
   Girnita, A
   Girnita, L
AF Crudden, Caitrin
   Shibano, Takashi
   Song, Dawei
   Dragomir, Mihnea P.
   Cismas, Sonia
   Serly, Julianna
   Nedelcu, Daniela
   Fuentes-Mattei, Enrique
   Tica, Andrei
   Calin, George A.
   Girnita, Ada
   Girnita, Leonard
TI Inhibition of G Protein-Coupled Receptor Kinase 2 Promotes Unbiased
   Downregulation of IGF1 Receptor and Restrains Malignant Cell Growth
SO CANCER RESEARCH
LA English
DT Article
ID FACTOR-I RECEPTOR; ARRESTIN-BIASED AGONISM; BETA-ARRESTIN;
   COLORECTAL-CANCER; INSULIN; UBIQUITINATION; ACTIVATION; PAROXETINE;
   MDM2; GRKS
AB The ability of a receptor to preferentially activate only a subset of available downstream signal cascades is termed biased signaling. Although comprehensively recognized for the G protein-coupled receptors (GPCR), this process is scarcely explored down-stream of receptor tyrosine kinases (RTK), including the cancer-relevant insulin-like growth factor-1 receptor (IGF1R). Successful IGF1R targeting requires receptor downregulation, yet therapy-mediated removal from the cell surface activates cancer-protective beta-arrestin-biased signaling (beta-arr-BS). As these overlapping processes are initiated by the beta-arr/IGF1R interaction and controlled by GPCR-kinases (GRK), we explored GRKs as potential anticancer therapeutic targets to disconnect IGF1R downregulation and beta-arr-BS. Transgenic modulation demonstrated that GRK2 inhibition or GRK6 overexpression enhanced degradation of IGF1R, but both scenarios sustained IGF1-induced beta-arr-BS. Pharmacologic inhibition of GRK2 by the clinically approved antidepressant, serotonin reuptake inhibitor paroxetine (PX), recapitulated the effects of GRK2 silencing with dose- and time-dependent IGF1R downregulation without associated beta-arr-BS. In vivo, PX treatment caused substantial downregulation of IGF1R, suppressing the growth of Ewing's sarcoma xenografts. Functional studies reveal that PX exploits the antagonism between beta-arrestin isoforms; in low ligand conditions, PX favored beta-arrestin 1/Mdm2-mediated ubiquitination/degradation of IGF1R, a scenario usually exclusive to ligand abundancy, making PX more effective than antibody-mediated IGF1R downregulation. This study provides the rationale, molecular mechanism, and validation of a clinically feasible concept for "system bias" targeting of the IGF1R to uncouple downregulation from signaling. Demonstrating system bias as an effective anticancer approach, our study reveals a novel strategy for the rational design or repurposing of therapeutics to selectively cross-target the IGF1R or other RTK.
   Significance: This work provides insight into the molecular and biological roles of biased signaling downstream RTK and provides a novel "system bias" strategy to increase the efficacy of anti-IGF1R-targeted therapy in cancer.
C1 [Crudden, Caitrin; Shibano, Takashi; Song, Dawei; Cismas, Sonia; Serly, Julianna; Nedelcu, Daniela; Girnita, Ada; Girnita, Leonard] Karolinska Inst, BioClinicum, Dept Oncol & Pathol, Stockholm, Sweden.
   [Crudden, Caitrin; Shibano, Takashi; Song, Dawei; Cismas, Sonia; Serly, Julianna; Nedelcu, Daniela; Girnita, Ada; Girnita, Leonard] Karolinska Univ Hosp, Stockholm, Sweden.
   [Crudden, Caitrin] Vrije Univ Amsterdam, Amsterdam UMC, Canc Ctr Amsterdam, Dept Pathol, Amsterdam, Netherlands.
   [Dragomir, Mihnea P.; Fuentes-Mattei, Enrique; Calin, George A.] Univ Texas MD Anderson Canc Ctr, Dept Expt Therapeut, Houston, TX 77030 USA.
   [Tica, Andrei] Univ Med & Pharm Craiova, Dept Pharmacol, Craiova, Romania.
   [Girnita, Ada] Karolinska Univ Hosp, Dept Dermatol, Stockholm, Sweden.
   [Dragomir, Mihnea P.] Charite, Inst Pathol, D-10117 Berlin, Germany.
   [Fuentes-Mattei, Enrique] Univ Texas MD Anderson Canc Ctr, Immunotherapy Radiat Oncol Strateg Initiat, Div Radiat Oncol, Houston, TX 77030 USA.
   [Calin, George A.] Univ Texas MD Anderson Canc Ctr, Dept Translat Mol Pathol, Houston, TX 77030 USA.
C3 Karolinska Institutet; Karolinska Institutet; Karolinska University
   Hospital; University of Amsterdam; Vrije Universiteit Amsterdam;
   University of Texas System; UTMD Anderson Cancer Center; University of
   Medicine & Pharmacy of Craiova; Karolinska Institutet; Karolinska
   University Hospital; Berlin Institute of Health; Free University of
   Berlin; Humboldt University of Berlin; Charite Universitatsmedizin
   Berlin; University of Texas System; UTMD Anderson Cancer Center;
   University of Texas System; UTMD Anderson Cancer Center
RP Girnita, L (corresponding author), Karolinska Inst, Dept Oncol Pathol, Karolinska Hosp, BioClinicum,NKS, J6 20,Akad Straket 1, S-17164 Stockholm, Sweden.
EM Leonard.Girnita@ki.se
RI Dragomir, Mihnea/ABB-8207-2020; TICA, ANDREI/AAK-8573-2020; 柴野,
   卓志/AHB-7015-2022; Song, Dawei/HGC-7852-2022; Crudden,
   Caitrin/Q-5172-2018; Girnita, Leonard/A-4168-2008
OI Calin, George/0000-0002-7427-0578; Crudden, Caitrin/0000-0002-7786-112X;
   Dragomir, Mihnea P./0000-0002-5550-3516; Song,
   Dawei/0000-0001-7707-7207; Girnita, Leonard/0000-0003-0280-9500
FU Swedish Research Council; Swedish Cancer Society; Swedish Childhood
   Cancer Foundation; Crown Princess Margareta's Foundation for the
   Visually Impaired; Welander Finsen Foundation; King Gustaf V Jubilee
   Foundation; SINF StratCan; Stockholm Cancer Society; Stockholm County;
   Karolinska Institute; NIH (NIH/NCATS) grant through the NIH Common Fund
   [UH3TR00943-01]; Office of Strategic Coordination (OSC); NCI grants
   [1R01 CA182905-01, 1R01CA222007-01A1]; NIGMS [1R01GM122775-01]; U54
   grant-UPR/MDACC Partnership for Excellence in Cancer Research 2016 Pilot
   Project [CA096297/CA096300]; Team DOD grant [CA160445P1]; Chronic
   Lymphocytic Leukemia Moonshot Flagship project; CLL Global Research
   Foundation 2019 grant; CLL Global Research Foundation 2020 grant;
   National Cancer Institute [R01CA222007, U54CA096297, U54CA096300]
   Funding Source: NIH RePORTER; CDMRP [917395, CA160445P1] Funding Source:
   Federal RePORTER
FX We thank Drs. R.J. Lefkowitz, R. Baserga, and V. Gurivech for generously
   providing reagents and cell lines. We thank Anna Malmerfelt at the
   histology core facility, Karolinska Institutet, for technical
   assistance. Research support was received from the Swedish Research
   Council, Swedish Cancer Society, The Swedish Childhood Cancer
   Foundation, Crown Princess Margareta's Foundation for the Visually
   Impaired, Welander Finsen Foundation, King Gustaf V Jubilee Foundation,
   SINF StratCan, Stockholm Cancer Society, Stockholm County, and
   Karolinska Institute.Dr. G.A. Calin is the Felix L. Haas Endowed
   Professor in Basic Science. Work in Dr. G.A. Calin's laboratory is
   supported by NIH (NIH/NCATS) grant UH3TR00943-01 through the NIH Common
   Fund, Office of Strategic Coordination (OSC), the NCI grants 1R01
   CA182905-01 and 1R01CA222007-01A1, an NIGMS 1R01GM122775-01 grant, a U54
   grant #CA096297/CA096300-UPR/MDACC Partnership for Excellence in Cancer
   Research 2016 Pilot Project, a Team DOD (CA160445P1) grant, a Chronic
   Lymphocytic Leukemia Moonshot Flagship project, a CLL Global Research
   Foundation 2019 grant, a CLL Global Research Foundation 2020 grant, and
   the Estate of C.G. Johnson, Jr.
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NR 64
TC 15
Z9 16
U1 0
U2 18
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD JAN 15
PY 2021
VL 81
IS 2
BP 501
EP 514
DI 10.1158/0008-5472.CAN-20-1662
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PX4WN
UT WOS:000611357000024
PM 33158816
OA Bronze
DA 2025-01-04
ER

PT J
AU Totzeck, M
   Mincu, RI
   Mrotzek, S
   Schadendorf, D
   Rassaf, T
AF Totzeck, Matthias
   Mincu, Raluca-Ileana
   Mrotzek, Simone
   Schadendorf, Dirk
   Rassaf, Tienush
TI Cardiovascular diseases in patients receiving small molecules with
   anti-vascular endothelial growth factor activity: A meta-analysis of
   approximately 29,000 cancer patients
SO EUROPEAN JOURNAL OF PREVENTIVE CARDIOLOGY
LA English
DT Article
DE Tyrosine kinase inhibitors; cardiovascular adverse events; meta-analysis
ID RANDOMIZED-PHASE-II; CELL LUNG-CANCER; TYROSINE KINASE INHIBITORS;
   METASTATIC COLORECTAL-CANCER; ARTERIAL THROMBOEMBOLIC EVENTS;
   GASTROINTESTINAL STROMAL TUMORS; DIFFERENTIATED THYROID-CANCER; ADVANCED
   PANCREATIC-CANCER; VANDETANIB PLUS DOCETAXEL; PLACEBO-CONTROLLED TRIAL
AB Background Targeted therapy with tyrosine kinase inhibitors with anti-vascular endothelial growth factor activity improves survival of cancer patients. Cardiovascular complications are critical and it is unknown whether these require specific treatment strategies. We aimed to clarify the associated risk of cardiovascular adverse events in patients treated with tyrosine kinase inhibitors.
   Design The design of this study was a meta-analysis of randomised controlled trials.
   Methods We searched PubMed, Cochrane, EMBASE and Web of Science databases for randomised controlled trials published until January 2017 that assessed patients with different types of cancer treated with or without tyrosine kinase inhibitors in addition to standard chemotherapy.
   Results A total of 29,252 patients from 71 randomised controlled trials were included. Tyrosine kinase inhibitor treatment was associated with a higher cardiac ischaemia relative risk (relative risk=1.69; 95% confidence interval: 1.12-2.57; p=0.01), with the highest risks observed for sorafenib and patients with renal cancer. Risk of thrombocytopaenia (relative risk=2.2; 95% confidence interval: 1.73-2.79; p<0.001) was highest for regorafenib and patients with breast cancer. Left ventricular systolic dysfunction was increased after tyrosine kinase inhibitor therapy (relative risk=2.53; 95% confidence interval:1.79 - 3.57; p<0.001), with the highest risks reported for sunitinib and hepatocellular cancer. QT corrected interval prolongation (relative risk=6.25; 95% confidence interval: 3.44-11.38; p<0.001) and arterial hypertension (relative risk=3.78; 95% confidence interval: 3.15-4.54; p<0.001) were reported. The relative risks of arterial adverse events, cerebral ischaemia, venous adverse events and pulmonary embolism were similar across groups.
   Conclusion Tyrosine kinase inhibitors increase the risk of severe cardiovascular and particularly thrombotic adverse events. Specific treatment regimens when prescribing tyrosine kinase inhibitor therapies appear desirable.
C1 [Totzeck, Matthias; Mincu, Raluca-Ileana; Mrotzek, Simone; Rassaf, Tienush] Univ Hosp Essen, Dept Cardiol & Vasc Med, Essen, Germany.
   [Schadendorf, Dirk] Univ Hosp Essen, Dept Dermatol, Essen, Germany.
C3 University of Duisburg Essen; University of Duisburg Essen
RP Totzeck, M (corresponding author), Univ Hosp Essen, Dept Cardiol & Vasc Med, West German Heart & Vasc Ctr, Hufelandstr 55, D-45147 Essen, Germany.
EM Matthias.Totzeck@uk-essen.de
RI Mincu, Raluca-Ileana/ABH-3141-2021; Schadendorf, Dirk/AAE-8206-2019
OI Schadendorf, Dirk/0000-0003-3524-7858
FU European Society of Cardiology [R-2016-013]; Medical Faculty of the
   University Duisburg-Essen
FX The author(s) disclosed receipt of the following financial support for
   the research, authorship, and/or publication of this article: RIM was
   supported through a research grant from the European Society of
   Cardiology (R-2016-013). TR received a grant from the Medical Faculty of
   the University Duisburg-Essen.
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NR 101
TC 65
Z9 68
U1 0
U2 9
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 2047-4873
EI 2047-4881
J9 EUR J PREV CARDIOL
JI Eur. J. Prev. Cardiol.
PD MAR
PY 2018
VL 25
IS 5
BP 482
EP 494
DI 10.1177/2047487318755193
PG 13
WC Cardiac & Cardiovascular Systems
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology
GA GC5BL
UT WOS:000429800300008
PM 29376753
DA 2025-01-04
ER

PT J
AU Liang, Y
   Xu, WH
   Liu, SH
   Chi, JW
   Zhang, JS
   Sui, AH
   Wang, LP
   Liang, ZJ
   Li, D
   Chen, YB
   Niu, HT
AF Liang, Ye
   Xu, Wenhua
   Liu, Shihai
   Chi, Jingwei
   Zhang, Jisheng
   Sui, Aihua
   Wang, Liping
   Liang, Zhijuan
   Li, Dan
   Chen, Yuanbin
   Niu, Haitao
TI N-Acetyl-Glucosamine Sensitizes Non-Small Cell Lung Cancer Cells to
   TRAIL-Induced Apoptosis by Activating Death Receptor 5
SO CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
LA English
DT Article
DE N-acetyl-glucosamine; TRAIL; Non-small cell lung cancer; Death receptor
ID CHITOSAN OLIGOSACCHARIDE; ENHANCES TRAIL; LIPID RAFTS;
   COLORECTAL-CANCER; EXPRESSION; NANOPARTICLES; GLYCOSYLATION;
   SUPPRESSION; PROGRESSION; MECHANISMS
AB Background/Aims: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potential anticancer agent due to its selective toxicity. However, many human non-small cell lung cancer (NSCLC) cells are partially resistant to TRAIL, thereby limiting its clinical application. Therefore, there is a need for the development of novel adjuvant therapeutic agents to be used in combination with TRAIL. Methods: In this study, the effect of N-acetyl-glucosamine (GIcNAc), a type of monosaccharide derived from chitosan, combined with TRAIL was evaluated in vitro and in vivo. Thirty NSCLC clinical samples were used to detect the expression of death receptor (DR) 4 and 5. After GIcNAc and TRAIL co-treatment, DR expression was determined by real-time PCR and western blotting. Cycloheximide was used to detect the protein half-life to further understand the correlation between GIcNAc and the metabolic rate of DR. Non-reducing sodium dodecyl sulfate-polyacrylamide gel electrophoresis was used to detect receptor clustering, and the localization of DR was visualized by immunofluorescence under a confocal microscope. Furthermore, a co-immunoprecipitation assay was performed to analyze the formation of death-inducing signaling complex (DISC). O-linked glycan expression levels were evaluated following DR5 overexpression and RNA interference mediated knockdown. Results: We found that the clinical samples expressed higher levels of DRS than DR4, and GIcNAc co-treatment improved the effect of TRAIL-induced apoptosis by activating DR5 accumulation and clustering, which in turn recruited the apoptosis-initiating protease caspase-8 to form DISC, and initiated apoptosis. Furthermore. GIcNAc promoted DR5 clustering by improving its O-glycosylation. Conclusion: These results uncovered the molecular mechanism by which GIcNAc sensitizes cancer cells to TRAIL-induced apoptosis, thereby highlighting a novel effective agent for TRAIL-mediated NSCLC-targeted therapy. (C) 2018 The Author(s) Published by S. Karger AG, Basel.
C1 [Liang, Ye; Wang, Liping; Liang, Zhijuan; Li, Dan; Chen, Yuanbin; Niu, Haitao] Qingdao Univ, Affiliated Hosp, Dept Urol & Androl, Key Lab, Qingdao, Peoples R China.
   [Liu, Shihai] Qingdao Univ, Affiliated Hosp, Lab Anim Ctr, Qingdao, Peoples R China.
   [Chi, Jingwei] Qingdao Univ, Affiliated Hosp, Dept Thyroid Surg, Key Lab, Qingdao, Peoples R China.
   [Zhang, Jisheng] Qingdao Univ, Affiliated Hosp, Key Lab, Dept Otolaryngol Head & Neck Surg, Qingdao, Peoples R China.
   [Sui, Aihua] Qingdao Univ, Affiliated Hosp, Cent Lab, Qingdao, Peoples R China.
   [Liang, Ye; Niu, Haitao] Qingdao Univ, Affiliated Hosp, Dept Urol, Qingdao, Peoples R China.
   [Xu, Wenhua] Qingdao Univ, Dept Inspect, Qingdao, Peoples R China.
C3 Qingdao University; Qingdao University; Qingdao University; Qingdao
   University; Qingdao University; Qingdao University; Qingdao University
RP Liang, Y; Niu, HT (corresponding author), Qingdao Univ, Affiliated Hosp, 16 Jiangsu Rd, Qingdao, Peoples R China.
EM liangye82812@163.com; niuht0532@126.com
RI Zhang, Jisheng/AAT-6495-2020; wenhua, xu/AAV-4853-2021; liang,
   ye/GZA-3319-2022; Wang, Liping/JRY-1318-2023
FU National Natural Science Foundations of China [81401899, 81472411,
   81772713, 81372752, 81672662]; Taishan Scholar Program of Shandong
   Province [tsqn20161077]; China Postdoctoral Science Foundation
   [2017M622144]; Qingdao Postdoctoral Application Research Project;
   Qingdao Young Scientist Applied Basic Research Fund [15-9-1-51-jch,
   16-6-2-28-NSH]; Natural Science Foundation [ZR2014HM088, ZR2014CM040];
   Key Research and Development Program of Shandong Province
   [2017GSF18193]; Science and Technology Development Foundation of
   Shandong Province [2014GHY115025]
FX This study was financially supported by the National Natural Science
   Foundations of China (81401899, 81472411, 81772713, 81372752, 81672662);
   Taishan Scholar Program of Shandong Province (tsqn20161077); China
   Postdoctoral Science Foundation (2017M622144) and Qingdao Postdoctoral
   Application Research Project; Qingdao Young Scientist Applied Basic
   Research Fund (15-9-1-51-jch, 16-6-2-28-NSH); Natural Science Foundation
   (ZR2014HM088, ZR2014CM040), Key Research and Development Program of
   Shandong Province (2017GSF18193) and the Science and Technology
   Development Foundation (2014GHY115025) of Shandong Province.
CR [Anonymous], SCI REP UK
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NR 51
TC 12
Z9 12
U1 1
U2 11
PU Cell Physiol Biochem Press GmbH & Co
PI Dsseldorf
PA Herzogstr. 85, Dsseldorf, GERMANY
SN 1015-8987
EI 1421-9778
J9 CELL PHYSIOL BIOCHEM
JI Cell. Physiol. Biochem.
PY 2018
VL 45
IS 5
BP 2054
EP 2070
DI 10.1150/000488042
PG 17
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA GB3IJ
UT WOS:000428950000028
PM 29533936
DA 2025-01-04
ER

PT J
AU Pappas, L
   Baiev, I
   Reyes, S
   Bocobo, AG
   Jain, A
   Spencer, K
   Le, TM
   Rahma, OE
   Maurer, J
   Stanton, J
   Zhang, K
   De Armas, AD
   Deleon, TT
   Roth, M
   Peters, MLB
   Zhu, AX
   Boyhen, K
   Vancott, C
   Patel, T
   Roberts, LR
   Lindsey, S
   Horick, N
   Lennerz, JK
   Iafrate, AJ
   Goff, LW
   Mody, K
   Borad, MJ
   Shroff, RT
   Javle, MM
   Kelley, RK
   Goyal, L
AF Pappas, Leontios
   Baiev, Islam
   Reyes, Stephanie
   Bocobo, Andrea Grace
   Jain, Apurva
   Spencer, Kristen
   Le, Tri Minh
   Rahma, Osama E.
   Maurer, Jordan
   Stanton, Jen
   Zhang, Karen
   De Armas, Anaemy Danner
   Deleon, Thomas T.
   Roth, Marc
   Peters, Mary Linton B.
   Zhu, Andrew X.
   Boyhen, Kylie
   Vancott, Christine
   Patel, Tushar
   Roberts, Lewis R.
   Lindsey, Stacie
   Horick, Nora
   Lennerz, Jochen K.
   Iafrate, A. John
   Goff, Laura Williams
   Mody, Kabir
   Borad, Mitesh J.
   Shroff, Rachna T.
   Javle, Milind M.
   Kelley, R. Katie
   Goyal, Lipika
TI The Cholangiocarcinoma in the Young (CITY) Study: Tumor Biology,
   Treatment Patterns, and Survival Outcomes in Adolescent Young Adults
   With Cholangiocarcinoma
SO JCO PRECISION ONCOLOGY
LA English
DT Article
ID COLORECTAL-CANCER; BREAST-CANCER; ONSET; VALIDATION; VARIANTS; FEATURES;
   DISEASE; IMPACT; ASSAY; AGE
AB PURPOSE Increased awareness of the distinct tumor biology for adolescents and young adults (AYAs) with cancer has led to improvement in outcomes for this population. However, in cholangiocarcinoma (CCA), a paucity of data exist on the AYA population. To our knowledge, we present the largest study to date on AYA disease biology, treatment patterns, and survival outcomes in CCA. METHODSA multi-institutional cohort of patients with CCA diagnosed with intrahepatic cholangiocarcinoma (ICC) or extrahepatic cholangiocarcinoma (ECC) was used for analysis. Retrospective chart review was conducted on patients who were 50 years old and younger (young; n = 124) and older than 50 years (older; n = 723). RESULTS Among 1,039 patients screened, 847 patients met eligibility (72% ICC, 28% ECC). Young patients had a larger median tumor size at resection compared with older patients (4.2 v 3.6 cm; P = .048), more commonly had N1 disease (65% v 43%; P = .040), and were more likely to receive adjuvant therapy (odds ratio, 4.0; 95% CI, 1.64 to 9.74). Tumors of young patients were more likely to harbor an FGFR2 fusion, BRAF mutation, or ATM mutation (P < .05 for each). Young patients were more likely to receive palliative systemic therapy (96% v 69%; P < .001), targeted therapy (23% v 8%; P < .001), and treatment on a clinical trial (31% v 19%; P = .004). Among patients who presented with advanced disease, young patients had a higher median overall survival compared with their older counterparts (17.7 v 13.5 months; 95% CI, 12.6 to 22.6 v 11.4 to 14.8; P = .049). CONCLUSION Young patients with CCA had more advanced disease at resection, more commonly received both adjuvant and palliative therapies, and demonstrated improved survival compared with older patients. Given the low clinical trial enrollment and poor outcomes among some AYA cancer populations, data to the contrary in CCA are highly encouraging.
C1 [Pappas, Leontios; Baiev, Islam; Maurer, Jordan; Stanton, Jen; Horick, Nora; Goyal, Lipika] Massachusetts Gen Hosp, Dept Med, Canc Ctr, Boston, MA USA.
   [Pappas, Leontios; Goyal, Lipika] Harvard Med Sch, Boston, MA USA.
   [Reyes, Stephanie] Duke Univ, Sch Med, Durham, NC USA.
   [Bocobo, Andrea Grace; Zhang, Karen; Kelley, R. Katie] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA USA.
   [Jain, Apurva; De Armas, Anaemy Danner; Javle, Milind M.] Univ Texas MD Anderson Canc Ctr, Div Canc Med, Dept Gastrointestinal Med Oncol, Houston, TX USA.
   [Spencer, Kristen] NYU Langone Hlth Perlmutter Canc Ctr, NYU Sch Med, Dept Med, New York, NY USA.
   [Le, Tri Minh] Univ Virginia, Dept Med, Comprehens Canc Ctr, Charlottesville, VA USA.
   [Rahma, Osama E.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA USA.
   [Deleon, Thomas T.; Borad, Mitesh J.] Div Hematol Oncol, Mayo Clin, Scottsdale, AZ USA.
   [Roth, Marc] St Lukes Canc Inst, Dept Med Oncol, Kansas City, MO USA.
   [Peters, Mary Linton B.] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA USA.
   [Zhu, Andrew X.] Jiahui Int Canc Ctr, Jiahui Hlth, Shanghai, Peoples R China.
   [Zhu, Andrew X.] I MAB Biopharm, Shanghai, Peoples R China.
   [Boyhen, Kylie] Yale Univ, New Haven, CT USA.
   [Vancott, Christine] HCA Florida South Tampa Hosp, Dept Med, Tampa, FL USA.
   [Patel, Tushar] Dept Transplantat, Mayo Clin, Jacksonville, FL USA.
   [Roberts, Lewis R.] Div Gastroenterol & Hepatol, Mayo Clin, Rochester, MN USA.
   [Lindsey, Stacie] Cholangiocarcinoma Fdn, Herriman, UT USA.
   [Lennerz, Jochen K.; Iafrate, A. John] Massachusetts Gen Hosp, Ctr Integrated Diagnost, Harvard Med Sch, Dept Pathol, Boston, MA USA.
   [Goff, Laura Williams] Vanderbilt Ingram Canc Ctr, Dept Med, Nashville, TN USA.
   [Mody, Kabir] Div Hematol Oncol, Mayo Clin, Jacksonville, FL USA.
   [Shroff, Rachna T.] Univ Arizona, Canc Ctr, Tucson, AZ USA.
   [Goyal, Lipika] Stanford Canc Ctr, Dept Med, Div Oncol, Palo Alto, CA USA.
   [Goyal, Lipika] Stanford Canc Ctr, 875 Blake Wilbur Dr, Palo Alto, CA 94304 USA.
C3 Harvard University; Massachusetts General Hospital; Harvard University;
   Harvard Medical School; Duke University; University of California
   System; University of California San Francisco; UCSF Medical Center;
   UCSF Helen Diller Family Comprehensive Cancer Center; University of
   Texas System; UTMD Anderson Cancer Center; New York University;
   University of Virginia; Harvard University; Dana-Farber Cancer
   Institute; Mayo Clinic; Mayo Clinic Phoenix; Harvard University; Beth
   Israel Deaconess Medical Center; Yale University; Mayo Clinic; Mayo
   Clinic; Harvard University; Harvard Medical School; Massachusetts
   General Hospital; Vanderbilt University; Mayo Clinic; University of
   Arizona; Stanford Cancer Institute; Stanford University; Stanford
   University; Stanford Cancer Institute
RP Goyal, L (corresponding author), Stanford Canc Ctr, 875 Blake Wilbur Dr, Palo Alto, CA 94304 USA.
EM lgoyal@stanford.edu
RI Horick, Nora/JLK-8769-2023; le, minh/HNQ-4216-2023; Goff,
   Laura/JKI-6730-2023; Peters, Mary Linton/HHS-7771-2022
OI Spencer, Kristen/0000-0001-5577-3439
FU Cholangiocarcinoma Foundation (CCF); International Cholangiocarcinoma
   Research Network (ICRN)
FX We would like to acknowledge support from The Cholangiocarcinoma
   Foundation (CCF), the International Cholangiocarcinoma Research Network
   (ICRN), and Jacqui Lewis and the Rare Initiative, and Joe and Katie
   Comeau.
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NR 48
TC 6
Z9 6
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
EI 2473-4284
J9 JCO PRECIS ONCOL
JI JCO Precis. Oncol.
PY 2023
VL 7
AR e2200594
DI 10.1200/PO.22.00594
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA NA3W8
UT WOS:001197689200005
PM 37561981
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Adua, D
   Di Fabio, F
   Ercolani, G
   Fiorentino, M
   Gruppioni, E
   Altimari, A
   Limpe, FLR
   Normanno, N
   Pinna, AD
   Pinto, C
AF Adua, Daniela
   Di Fabio, Francesca
   Ercolani, Giorgio
   Fiorentino, Michelangelo
   Gruppioni, Elisa
   Altimari, Annalisa
   Limpe, Fabiola Lorena Rojas
   Normanno, Nicola
   Pinna, Antonio Daniele
   Pinto, Carmine
TI Heterogeneity in the colorectal primary tumor and the synchronous
   resected liver metastases prior to and after treatment with an anti-EGFR
   monoclonal antibody
SO MOLECULAR AND CLINICAL ONCOLOGY
LA English
DT Article
DE intratumor heterogeneity; metastatic colorectal cancer; liver
   metastasis; next-generation sequencing; cetuximab
ID PIK3CA MUTATIONS; CANCER; CETUXIMAB; KRAS; RESISTANCE; BRAF; THERAPY
AB Molecular heterogeneity between primary tumors (PTs) and synchronous resected liver metastasis in colorectal cancer (CRC) has potential relevance in treatment strategies. Next-generation sequencing (NGS) may be able to increase the chances of identifying multiple molecular driver alterations, calling for therapy. The aim of the present study was to evaluate mutations in PT and synchronous resected liver metastases for patients with Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) exon 2 wild-type metastatic (m)CRC who underwent chemotherapy (CT) featuring an anti-epidermal growth factor receptor (EGFR) monoclonal antibody. Genomic analysis was performed on 54 lesions from 7 patients with mCRC. For each patient, a PT biopsy or a surgical specimen was obtained prior to CT, and the PT and all liver metastases resected following CT were analyzed. DNA libraries were generated using the Ion AmpliSeq Colon and Lung Cancer Panel, assessing the most frequent somatic mutations in 22 genes involved in colon tumorigenesis, and sequencing was performed on an Ion Personal Genome Machine system. A partial response was achieved in all the patients, with a median progression free survival time of 11 months (range, 3-21 months). All the patients were subjected to surgical liver metastasis resection. The median overall survival time was 31 months (range, 4-46 months). Molecular analysis of the genes correlated with the target therapy, suggesting significant intratumor heterogeneity, as revealed by the different mutational landscape of certain PTs and synchronous resected liver metastases following systemic therapy when compared with the PT prior to treatment. In particular, the loss and acquisition of mutations in KRAS, neuroblastoma RAS viral oncogene homolog (NRAS), tumor protein p53 (TP53), the p110 alpha catalytic subunit of phosphoinositide 3-kinase (PIK3CA), F-box/WD repeat-containing protein 7 (FBXW7) and phosphatase and tensin homolog (PTEN) were observed. In addition, one patient developed a mucinous pattern following systemic CT. Taken together, the results of the present study demonstrated that intratumor heterogeneity is likely to affect the response to therapy, and to drive acquired resistance to targeted agents. The preliminary data also suggest a potential role for NGS in the evaluation of biological drug resistance, affecting future sequential treatment strategies.
C1 [Adua, Daniela] Univ Bologna, Dept Expt Diagnost & Specialty Med, Via P Albertoni 15, I-40126 Bologna, Italy.
   [Adua, Daniela; Di Fabio, Francesca; Limpe, Fabiola Lorena Rojas] Univ Bologna, St Orsola Malpighi Hosp, Med Oncol Unit, Bologna, Italy.
   [Ercolani, Giorgio; Pinna, Antonio Daniele] Univ Bologna, St Orsola Malpighi Hosp, Dept Gen Surg & Transplantat, Bologna, Italy.
   [Fiorentino, Michelangelo; Gruppioni, Elisa; Altimari, Annalisa] Univ Bologna, St Orsola Malpighi Hosp, Addarii Inst, Pathol Unit, I-40138 Bologna, Italy.
   [Normanno, Nicola] Fdn Giovanni Pascale, IRCCS, Ist Nazl Tumori, CROM,Cell Biol & Biotherapy Unit, I-80131 Naples, Italy.
   [Normanno, Nicola] Fdn Giovanni Pascale, IRCCS, Ist Nazl Tumori, Lab Pharmacogen,CROM, I-80131 Naples, Italy.
   [Pinto, Carmine] IRCCS Arcispedale S Maria Nuova, Ctr Clin Canc, Med Oncol Unit, I-42123 Reggio Emilia, Italy.
C3 University of Bologna; University of Bologna; IRCCS Azienda
   Ospedaliero-Universitaria di Bologna; University of Bologna; IRCCS
   Azienda Ospedaliero-Universitaria di Bologna; University of Bologna;
   IRCCS Azienda Ospedaliero-Universitaria di Bologna; IRCCS Fondazione
   Pascale; Fondazione IRCCS Istituto Nazionale Tumori Milan; Fondazione
   IRCCS Istituto Nazionale Tumori Milan; IRCCS Fondazione Pascale; IRCCS
   Arcispedale S. Maria Nuova
RP Adua, D (corresponding author), Univ Bologna, Dept Expt Diagnost & Specialty Med, Via P Albertoni 15, I-40126 Bologna, Italy.
EM aduadani@hotmail.com
RI ercolani, giorgio/AAD-1462-2022; Fiorentino, Michelangelo/AAB-8056-2022;
   Pinna, Antonio/AAC-6685-2019; Di Fabio, Francesca/AAC-9288-2021;
   Normanno, Nicola/AAT-1107-2021; Gruppioni, Elisa/AFV-2110-2022; Pinto,
   Carmine/AAC-2184-2020
OI Pinto, Carmine/0000-0002-3159-5268
CR Adua D, 2014, J CLIN ONCOL S, V32, p5S
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NR 22
TC 13
Z9 15
U1 0
U2 3
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 2049-9450
EI 2049-9469
J9 MOL CLIN ONCOL
JI Mol. Clin. Oncol.
PD JUL
PY 2017
VL 7
IS 1
BP 113
EP 120
DI 10.3892/mco.2017.1270
PG 8
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA HE2RS
UT WOS:000453174500021
PM 28685087
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Lu, YJ
   Deng, SZ
   Dou, QY
   Pan, W
   Liu, QQ
   Ji, HC
   Wang, XW
   Zhang, HM
AF Lu, Yajie
   Deng, Shizhou
   Dou, Qiongyi
   Pan, Wei
   Liu, Qingqing
   Ji, Hongchen
   Wang, Xiaowen
   Zhang, Hong-Mei
TI Treatment-Related Coronary Disorders of Fluoropyrimidine Administration:
   A Systematic Review and Meta-Analysis
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE coronary disorder; 5-FU; capecitabine; meta-analysis; fluoropyrimidine
ID METASTATIC COLORECTAL-CANCER; PHASE-II TRIAL; 1ST-LINE TREATMENT;
   BREAST-CANCER; PLUS CAPECITABINE; MYOCARDIAL-ISCHEMIA; RECTAL-CANCER;
   FOLINIC ACID; GASTROESOPHAGEAL JUNCTION; RADIATION-THERAPY
AB Background: Coronary disorders are recognized as the most common manifestation of fluoropyrimidine-related cardiotoxicity in clinical practice. However, there are limited and conflicting data on the incidence and profiles of fluoropyrimidine-related coronary disorders. In this meta-analysis, we aimed to systematically assess the incidence of all-grade and grade 3 or higher fluoropyrimidine-related coronary disorders, and further explore the factors that influence its occurrence.Methods: Studies reporting the fluoropyrimidine-related coronary disorders were retrieved from a systematic search of English literature in the PubMed, Web of Science, Medline, and Cochrane database from 1 Jan 2001, to 1 Jan 2022. The NIH assessment tool was used to evaluate the quality of each study. The data of basic study characteristics, treatment details, and results of coronary toxicities were extracted. According to the results of the heterogeneity test (I-2 and p-value statistic), a random-effect model or fixed-effect model was selected for the pooled analysis of the incidence of adverse coronary events. Subgroup analysis was conducted to further explore the risks influencing the occurrence of fluoropyrimidine-related coronary disorders. The stability and publication bias of our results were evaluated by sensitivity analysis and Egger test, respectively.Results: A total of 63 studies were finally included in our pooled analysis, involving 25,577 patients. The pooled cumulative incidence of all-grade and grade 3 or higher coronary disorders was 2.75% (95% CI 1.89%-3.76%) and 1.00% (95% CI 0.62%-1.47%), respectively. The coronary disorders were most reported as myocardial ischemia (1.28%, 95% CI 0.42%-2.49%) and angina/chest pain (1.1%, 95% CI 0.54%-1.81%). Subgroup analysis revealed that studies in the female-only population seemed to have a lower incidence of fluoropyrimidine-related coronary disorders. The occurrence of adverse coronary events varied among different tumor types. Patients with esophageal cancer have the highest coronary toxicity (6.32%), while those with breast cancer have a relatively lower incidence (0.5%). Coronary disorders induced by 5-FU monotherapy are more frequent than that induced by capecitabine (3.31% vs. 1.21%, p < 0.01). Fluoropyrimidine combination therapy, whether combined with other chemotherapy drugs, targeted therapy drugs, or radiotherapy, significantly increased the incidence of coronary complications (p < 0.01).Conclusion: This meta-analysis has defined the incidence of fluoropyrimidine-related coronary disorders and depicted its epidemiological profiles for the first time, which may provide a reference for clinical practice in cancer management.
C1 [Lu, Yajie; Deng, Shizhou; Dou, Qiongyi; Pan, Wei; Liu, Qingqing; Ji, Hongchen; Wang, Xiaowen; Zhang, Hong-Mei] Air Force Med Univ PLA, Xijing Hosp, Dept Clin Oncol, Xian, Shaanxi, Peoples R China.
C3 Air Force Military Medical University
RP Zhang, HM (corresponding author), Air Force Med Univ PLA, Xijing Hosp, Dept Clin Oncol, Xian, Shaanxi, Peoples R China.
EM zhm@fmmu.edu.cn
RI zhang, xueying/JMB-7808-2023
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NR 93
TC 7
Z9 7
U1 0
U2 13
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD MAY 13
PY 2022
VL 13
AR 885699
DI 10.3389/fphar.2022.885699
PG 14
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 1W2AM
UT WOS:000806580400001
PM 35645806
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Dias, DD
   Machado, M
   Trabulo, C
   Gosalbez, B
   Ravasco, P
AF da Silva Dias, David
   Machado, Mafalda
   Trabulo, Carolina
   Gosalbez, Beatriz
   Ravasco, Paula
TI Impact of Body Composition on Prognosis and Dose-Limiting Toxicities on
   Metastatic Colorectal Cancer
SO FRONTIERS IN NUTRITION
LA English
DT Article
DE body composition; body mass index; skeletal muscle index; sarcopenia;
   metastatic colorectal cancer; dose limiting toxicities;
   neutrophil-to-lymphocyte ratio; systemic inflammation
ID SKELETAL-MUSCLE; SARCOPENIA; CHEMOTHERAPY; PREVALENCE; RESECTION; SLICE;
   MASS
AB Sarcopenia is a progressive skeletal muscle disease, often present in oncological patients, that is associated with multiple adverse events such as worse prognosis, physical performance, and quality of life. Body composition evaluation by CT cross-section at the L3 vertebrae region appears to be a precise method to quantify skeletal muscle. The optimal cut-off for the definition of sarcopenia is not yet established, therefore the incidence of sarcopenia varies according to different studies. The main goal was to evaluate the presence of sarcopenia in patients with metastatic colorectal cancer (mCRC) and its impact on overall survival (OS) and dose-limiting toxicities (DLT). A retrospective cohort study of 178 patients with mCRC under first-line chemotherapy (ChT) in association with target therapy, in two hospital units, between January 2015 and December 2018. Skeletal mass area (SMA) was quantified with the NIH ImageJ software in CT cross-sectional images at the L3 vertebrae region. Statistical analysis was performed with IBM SPSS v25 software https://www.ibm.com/analytics/spss-statistics-software. The median age was 62 (SD & PLUSMN; 11) years old, 65% were men and 62.9% had an Eastern Cooperative Oncology Group (ECOG) performance status of 0. The cut-off value was established based on ROC analysis, with sarcopenia defined as SMI < 49.12 cm(2)/m(2) for men and < 35.85 cm(2)/m(2) for women. Despite the mean body mass index (BMI) of 25.71 (& PLUSMN; 4.71) kg/m(2), half of the patients presented sarcopenia. In a multivariate analysis using a Cox regression model, an association was observed between OS and higher ECOG PS (p = 0.014; HR 5.46, CI 95% [1.42-21.10]), neutrophil-to-lymphocyte ratio (NLR) > 2.80 (p = 0.038; HR 2.20, CI 95% [1,05-4.62]), and sarcopenia (p = 0.01; HR 4.73, CI 95% [1.85-12.09]). Additionally, in a logistic regression model, age (p = 0.014; OR 1.09, IC 95% [1.02-1.16]) and sarcopenia (p= 0.030, OR 4.13, IC 95% [1.15-14.8]) were associated with higher incidence of DLT. The CT evaluation of the body composition at the L3 region allows for the quantification of sarcopenia, providing prognostic information and predictive value of DLT in patients with mCRC, although the establishment of optimal cut-off values are required for implementation in clinical practice. A multimodal strategy to delay muscle waste should be considered in these patients.
C1 [da Silva Dias, David; Gosalbez, Beatriz] Ctr Hosp Univ Algarve, Med Oncol Dept, Faro, Portugal.
   [da Silva Dias, David; Trabulo, Carolina; Ravasco, Paula] Univ Catolica Portuguesa, Ctr Interdisciplinary Res Hlth, Lisbon, Portugal.
   [Machado, Mafalda] Ctr Hosp Univ Algarve, Radiol Dept, Faro, Portugal.
   [Trabulo, Carolina] Ctr Hosp Barreiro Montijo, Med Oncol Dept, Barreiro, Portugal.
   [Ravasco, Paula] Univ Catolica Portuguesa, Catolica Med Sch, Lisbon, Portugal.
   [Ravasco, Paula] Inst Univ Egas Moniz IUEM, Ctr Invest Interdisciplinar Egas Moniz CiiEM, Caparica, Portugal.
C3 Universidade Catolica Portuguesa; Universidade Catolica Portuguesa;
   Instituto Superior de Ciencias da Saude Egas Moniz
RP Dias, DD (corresponding author), Ctr Hosp Univ Algarve, Med Oncol Dept, Faro, Portugal.; Dias, DD (corresponding author), Univ Catolica Portuguesa, Ctr Interdisciplinary Res Hlth, Lisbon, Portugal.
EM daviddias_77@hotmail.com
OI Ravasco, Paula/0000-0002-6056-8269
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NR 30
TC 12
Z9 12
U1 0
U2 7
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-861X
J9 FRONT NUTR
JI Front. Nutr.
PD JAN 27
PY 2022
VL 8
AR 671547
DI 10.3389/fnut.2021.671547
PG 7
WC Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Nutrition & Dietetics
GA YX0WJ
UT WOS:000753829400001
PM 35155507
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Baucom, RB
   Maguire, LH
   Kavalukas, SL
   Geiger, TM
   Ford, MM
   Muldoon, RL
   Hopkins, MB
   Hawkins, AT
AF Baucom, Rebeccah B.
   Maguire, Lillias H.
   Kavalukas, Sandra L.
   Geiger, Timothy M.
   Ford, Molly M.
   Muldoon, Roberta L.
   Hopkins, M. Benjamin
   Hawkins, Alexander T.
TI Nodal Disease in Rectal Cancer Patients With Complete Tumor Response
   After Neoadjuvant Chemoradiation: Danger Below Calm Waters
SO DISEASES OF THE COLON & RECTUM
LA English
DT Article; Proceedings Paper
CT Annual Scientific Meeting of the
   American-Society-of-Colon-and-Rectal-Surgeons
CY JUN 10-14, 2017
CL Seattle, WA
SP Amer Soc Colon & Rectal Surg
DE Complete tumor response; Neoadjuvant chemoradiation therapy; Nodal
   disease; Rectal cancer; Watchful waiting
AB BACKGROUND: A subset of patients with rectal cancer who undergo neoadjuvant chemoradiation therapy will develop a complete pathologic tumor response. Complete nodal response is not universal in these patients and is difficult to assess clinically. Quantifying the risk of nodal disease would allow for targeted therapy with either radical resection or "watchful waiting."
   OBJECTIVE: This study aimed to identify risk factors for residual nodal disease in ypT0 rectal adenocarcinoma.
   DESIGN: This is a retrospective case control study.
   SETTINGS: The National Cancer Database 2006 to 2014 was used to identify patients for this study.
   PATIENTS: Patients with stage II/III rectal adenocarcinoma who completed chemoradiation therapy followed by resection and who had ypT0 tumors were included. Patients with metastatic disease and <2 lymph nodes evaluated were excluded. Patients were divided into 2 groups: node positive and node negative.
   MAIN OUTCOME MEASURES: The main outcome was nodal disease. The secondary outcome was overall survival.
   RESULTS: A total of 42,257 patients with stage II/III rectal cancer underwent chemoradiation therapy and radical resection; 4170 (9.9%) patients had ypT0 tumors and 395 (9.5%) were node positive. Of patients with clinically node-negative disease (ie, pretreatment imaging), 6.2% were node positive after chemoradiation therapy and resection. In multivariable analysis, factors predictive of nodal disease included increasing (pretreatment) clinical N-stage, high tumor grade (3/4), perineural invasion, and lymphovascular invasion. Higher clinical T-stage was inversely associated with residual nodal disease. Overall 5-year survival was significantly different between patients with ypN0, ypN1, and ypN2 disease (87.4%, 82.2%, and 62.5%, p = 0.002).
   LIMITATIONS: This study was limited by the lack of clinical detail in the database and the inability to assess recurrence.
   CONCLUSIONS: Ten percent of patients with ypT0 tumors had positive nodes after chemoradiation therapy and resection. Factors associated with residual nodal disease included clinical nodal disease at diagnosis and poor histologic features. Patients with any of these features should consider radical resection regardless of tumor response. Others could be suitable for "watchful waiting" strategies. See Video Abstract at http://links.lww.com/DCR/A458.
C1 [Baucom, Rebeccah B.; Kavalukas, Sandra L.; Geiger, Timothy M.; Ford, Molly M.; Muldoon, Roberta L.; Hopkins, M. Benjamin; Hawkins, Alexander T.] Vanderbilt Univ, Med Ctr, Div Gen Surg, Nashville, TN 37232 USA.
   [Maguire, Lillias H.] Univ Minnesota, Div Colon & Rectal Surg, Minneapolis, MN USA.
C3 Vanderbilt University; University of Minnesota System; University of
   Minnesota Twin Cities
RP Hawkins, AT (corresponding author), Vanderbilt Univ, Sect Colon & Rectal Surg, 1161 21st Ave South,Rm D5248 MCN, Nashville, TN 37232 USA.
EM alexander.t.hawkins@vanderbilt.edu
RI Kavalukas, Sandra/AAN-9117-2020; Hawkins, Alexander/O-1163-2016
OI Hawkins, Alexander/0000-0002-8531-7247
NR 0
TC 17
Z9 17
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0012-3706
EI 1530-0358
J9 DIS COLON RECTUM
JI Dis. Colon Rectum
PD DEC
PY 2017
VL 60
IS 12
BP 1260
EP 1266
DI 10.1097/DCR.0000000000000947
PG 7
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Gastroenterology & Hepatology; Surgery
GA FN7ZI
UT WOS:000416237400011
PM 29112561
DA 2025-01-04
ER

PT J
AU Katoh, M
   Katoh, M
AF Katoh, Masuko
   Katoh, Masaru
TI Molecular genetics and targeted therapy of WNT-related human diseases
SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
LA English
DT Review
DE Alzheimer's disease; angiogenesis; cancer stem cells;
   epithelial-to-mesenchymal transition; FGF; myeloid-derived suppressor
   cells; Notch; regulatory T cells; tumor microenvironment; WNT5A
ID PLANAR CELL POLARITY; CANCER STEM-CELLS; RECEPTOR TYROSINE KINASES;
   ENDOTHELIAL GROWTH-FACTOR; NEURAL-TUBE DEFECTS; BETA-CATENIN;
   AUTOSOMAL-DOMINANT; SIGNALING PATHWAY; BREAST-CANCER; NASOPHARYNGEAL
   CARCINOMA
AB Canonical WNT signaling through Frizzled and LRP5/6 receptors is transduced to the WNT/beta-catenin and WNT/stabilization of proteins (STOP) signaling cascades to regulate cell fate and proliferation, whereas non-canonical WNT signaling through Frizzled or ROR receptors is transduced to the WNT/planar cell polarity (PCP), WNT/G protein-coupled receptor (GPCR) and WNT/receptor tyrosine kinase (RTK) signaling cascades to regulate cytoskeletal dynamics and directional cell movement. WNT/beta-catenin signaling cascade crosstalks with RTK/SRK and GPCR-cAMP-PKA signaling cascades to regulate beta-catenin phosphorylation and beta-catenin-dependent transcription. Germline mutations in WNT signaling molecules cause hereditary colorectal cancer, bone diseases, exudative vitreoretinopathy, intellectual disability syndrome and PCP-related diseases. APC or CTNNB1 mutations in colorectal, endometrial and prostate cancers activate the WNT/beta-catenin signaling cascade. RNF43, ZNRF3, RSPO2 or RSPO3 alterations in breast, colorectal, gastric, pancreatic and other cancers activate the WNT/beta-catenin, WNT/STOP and other WNT signaling cascades. ROR1 upregulation in B-cell leukemia and solid tumors and ROR2 upregulation in melanoma induce invasion, metastasis and therapeutic resistance through Rho-ROCK, Rac-JNK, PI3K-AKT and YAP signaling activation. WNT signaling in cancer, stromal and immune cells dynamically orchestrate immune evasion and antitumor immunity in a cell context-dependent manner. Porcupine (PORCN), RSPO3, WNT2B, FZD5, FZD10, ROR1, tankyrase and beta-catenin are targets of anti-WNT signaling therapy, and ETC-159, LGK974, OMP-18R5 (vantictumab), OMP-54F28 (ipafricept), OMP-131R10 (rosmantuzumab), PRI-724 and UC-961 (cirmtuzumab) are in clinical trials for cancer patients. Different classes of anti-WNT signaling therapeutics are necessary for the treatment of APC/CTNNB1-, RNF43/ZNRF3/RSPO2/RSPO3- and ROR1-types of human cancers. By contrast, Dickkopf-related protein 1 (DKK1), SOST and glycogen synthase kinase 3 beta (GSK3 beta) are targets of pro-WNT signaling therapy, and anti-DKK1 (BHQ880 and DKN-01) and anti-SOST (blosozumab, BPS804 and romosozumab) monoclonal antibodies are being tested in clinical trials for cancer patients and osteoporotic post-menopausal women. WNT-targeting therapeutics have also been applied as reagents for in vitro stem-cell processing in the field of regenerative medicine.
C1 [Katoh, Masuko] M&M Med BioInformat, Tokyo 1130033, Japan.
   [Katoh, Masaru] Natl Canc Ctr, Dept Om Network, 5-1-1 Tsukiji,Chuo Ward, Tokyo 1040045, Japan.
C3 National Cancer Center - Japan
RP Katoh, M (corresponding author), Natl Canc Ctr, Dept Om Network, 5-1-1 Tsukiji,Chuo Ward, Tokyo 1040045, Japan.
EM mkatoh-kkr@umin.ac.jp
OI Katoh, Masaru/0000-0003-3274-4066
FU M. Katoh's Fund
FX This study was financially supported in part by a Grant-in-Aid for the
   knowledge base project from M. Katoh's Fund.
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NR 281
TC 165
Z9 200
U1 3
U2 89
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1107-3756
EI 1791-244X
J9 INT J MOL MED
JI Int. J. Mol. Med.
PD SEP
PY 2017
VL 40
IS 3
BP 587
EP 606
DI 10.3892/ijmm.2017.3071
PG 20
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA FE0JS
UT WOS:000407907200001
PM 28731148
OA Green Published, hybrid, Green Submitted
DA 2025-01-04
ER

PT J
AU Stec, R
   Semeniuk-Wojtas, A
   Charkiewicz, R
   Bodnar, L
   Korniluk, J
   Smoter, M
   Chyczewski, L
   Niklinski, J
   Szczylik, C
AF Stec, Rafal
   Semeniuk-Wojtas, Aleksandra
   Charkiewicz, Radoslaw
   Bodnar, Lubomir
   Korniluk, Jan
   Smoter, Marta
   Chyczewski, Lech
   Niklinski, Jacek
   Szczylik, Cezary
TI Mutation of the <i>PIK3CA</i> gene as a prognostic factor in patients
   with colorectal cancer
SO ONCOLOGY LETTERS
LA English
DT Article
DE colorectal cancer; phosphatidylinositol-4,5-bisphosphate 3-kinase
   catalytic subunit alpha mutations; prognostic factor
ID TARGETED THERAPY; KRAS MUTATION; BRAF; CETUXIMAB; BIOMARKERS; BENEFIT;
   PTEN; EXPRESSION
AB Colorectal cancer (CRC) is one of the most common cancers worldwide, with similar to 700,000 mortalities Occurring due to CRC in 2012. The treatment options are effective in a small percentage of patients, and it is important to identify specific biomaiters in order to determine patients for whom the available therapies will be beneficial. It has been hypothesised that the PIK3CA gene mutation may affect the response to therapy of patients with metastatic CRC. In the present study, primary tumour specimens were collected from 156 patients with CRC who were treated in the Military Institute of Medicine in Warsaw (Warsaw, Poland). Codons 12 and 13 of exon 1 of KRAS, exans 11 and 15 of BRAT and exons 9 and 20 of PIK3CA were analysed for imitation using direct sequencing. The prognostic value of each mutation and the clinical and pathological variables of these tumours were estimated. The results revealed that PIK3CA mutations were present in 15 patients (9.6%), of whom seven (46.7%) possessed mutations in codon 9 and eight (53.3%) possessed mutations in codon 20. Mutation in the PIK3CA gene was detected in six patients with KRAS gene mutations, which accounted for 40% of PIK3CA-mutated tumours, and in one patient with BRAF mutations, which accounted for 6.6% of PEK3CA-mutated tumours. No significant differences were identified between the overall survival (OS) rates of patients with PIK3CA mutations (median OS, 56.7 months) and those with wild-type PIK3CA genes (median OS, 47.6 months) (P=0.1270). Univariate analysis identified that the following prognostic factors affected the OS rate in the current patient cohort: Gender, female patients survived for 57.5 months compared with 39.3 months for male patients (P=0.0111); and lymph node involvement grade, as survival of patients without lymph node metastases was 61.4 months compared with 45.4 months in patients presenting with metastases (P=0.0122). The findings of the present analysis indicate that PIK3CA mutation status is not a prognostic factor in CRC patients. In addition, no statistically significant association exists between tumours with PIK3CA mutations and clinical or pathological factors.
C1 [Stec, Rafal; Semeniuk-Wojtas, Aleksandra; Bodnar, Lubomir; Korniluk, Jan; Smoter, Marta; Szczylik, Cezary] Mil Inst Med, Dept Oncol, PL-04141 Warsaw, Poland.
   [Charkiewicz, Radoslaw; Niklinski, Jacek] Med Univ Bialystok, Dept Clin Mol Biol, PL-15089 Bialystok, Poland.
   [Chyczewski, Lech] Med Univ Bialystok, Dept Clin Pathol, PL-15089 Bialystok, Poland.
C3 Military Institute of Aviation Medicine; Medical University of
   Bialystok; Medical University of Bialystok
RP Semeniuk-Wojtas, A (corresponding author), Mil Inst Med, Dept Oncol, 128 Szaserow St, PL-04141 Warsaw, Poland.
EM osemeniuk@wp.pl
RI Stec, Rafal/V-3025-2018
OI Stec, Rafal/0000-0002-3291-6422; Szczylik, Cezary/0000-0002-2524-2810;
   Charkiewicz, Radoslaw/0000-0001-7864-6483
CR Baldus SE, 2010, CLIN CANCER RES, V16, P790, DOI 10.1158/1078-0432.CCR-09-2446
   Cathomas G, 2014, FRONT ONCOL, V4, DOI 10.3389/fonc.2014.00035
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   Domagala P, 2012, POL J PATHOL, V63, P145, DOI 10.5114/PJP.2012.31499
   Eisenhauer EA, 2009, EUR J CANCER, V45, P228, DOI 10.1016/j.ejca.2008.10.026
   Ferlay J., 2012, Globocan 2012, estimated cancer incidence, mortality and preval in 2012
   German S, 2013, HERED CANCER CLIN PR, V11, DOI 10.1186/1897-4287-11-5
   Herreros-Villanueva M, 2011, MOL BIOL REP, V38, P1347, DOI 10.1007/s11033-010-0236-6
   Huang LL, 2014, ARCH MED SCI, V10, P1, DOI 10.5114/aoms.2014.40728
   Ikenoue T, 2005, CANCER RES, V65, P4562, DOI 10.1158/0008-5472.CAN-04-4114
   Karapetis CS, 2014, CLIN CANCER RES, V20, P744, DOI 10.1158/1078-0432.CCR-13-0606
   Li VSW, 2005, BMC CANCER, V5, DOI 10.1186/1471-2407-5-29
   Liao XY, 2012, CLIN CANCER RES, V18, P2257, DOI 10.1158/1078-0432.CCR-11-2410
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   Stec R, 2012, CANCER BIOL THER, V13, P1235, DOI 10.4161/cbt.21813
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NR 31
TC 9
Z9 11
U1 0
U2 3
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD SEP
PY 2015
VL 10
IS 3
BP 1423
EP 1429
DI 10.3892/ol.2015.3398
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CQ9GZ
UT WOS:000360923000030
PM 26622684
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Wang, Y
   Yuan, YF
   Lin, HC
   Li, BK
   Wang, FH
   Wang, ZQ
   Ding, PR
   Chen, G
   Wu, XJ
   Lu, ZH
   Pan, ZZ
   Wan, DS
   Sun, P
   Yan, SM
   Xu, RH
   Li, YH
AF Wang, Yun
   Yuan, Yun-Fei
   Lin, Hao-Cheng
   Li, Bin-Kui
   Wang, Feng-Hua
   Wang, Zhi-Qiang
   Ding, Pei-Rong
   Chen, Gong
   Wu, Xiao-Jun
   Lu, Zhen-Hai
   Pan, Zhi-Zhong
   Wan, De-Sen
   Sun, Peng
   Yan, Shu-Mei
   Xu, Rui-Hua
   Li, Yu-Hong
TI Pathologic response after preoperative therapy predicts prognosis of
   Chinese colorectal cancer patients with liver metastases
SO CHINESE JOURNAL OF CANCER
LA English
DT Article
DE Colorectal cancer; Liver metastases; Chemotherapy; Pathologic response
ID HEPATIC RESECTION; PRIMARY TUMOR; CHEMOTHERAPY; BEVACIZUMAB;
   CHEMORADIOTHERAPY; CARCINOMA
AB Background: Pathologic response is evaluated according to the extent of tumor regression and is used to estimate the efficacy of preoperative treatment. Several studies have reported the association between the pathologic response and clinical outcomes of colorectal cancer patients with liver metastases who underwent hepatectomy. However, to date, no data from Chinese patients have been reported. In this study, we aimed to evaluate the association between the pathologic response to pre-hepatectomy chemotherapy and prognosis in a cohort of Chinese patients.
   Patients and methods: In this retrospective study, we analyzed the data of 380 liver metastases in 159 patients. The pathologic response was evaluated according to the tumor regression grade (TRG). The prognostic role of pathologic response in recurrence-free survival (RFS) and overall survival (OS) was assessed using Kaplan-Meier curves with the log-rank test and multivariate Cox models. Factors that had potential influence on pathologic response were also analyzed using multivariate logistic regression and Kruskal-Wallis/Mann-Whitney U tests.
   Results: Patients whose tumors achieved pathologic response after preoperative chemotherapy had significant longer RFS and OS than patients whose tumor had no pathologic response to chemotherapy (median RFS: 9.9 vs. 6.5 months, P = 0.009; median OS: 40.7 vs. 28.1 months, P = 0.040). Multivariate logistic regression and Kruskal-Wallis/Mann-Whitney U tests showed that metastases with small diameter, metastases from the left-side primary tumors, and metastases from patients receiving long-duration chemotherapy had higher pathologic response rates than their control metastases (all P < 0.05). A decrease in the serum carcinoembryonic antigen (CEA) level after preoperative chemotherapy predicted an increased pathologic response rate (P < 0.05). Although the application of targeted therapy did not significantly influence TRG scores of all cases of metastases, the addition of cetuximab to chemotherapy resulted in a higher pathologic response rate when combined with irinotecan-based regimens rather than with oxaliplatin-based regimens.
   Conclusions: We found that the evaluation of pathologic response may predict the prognosis of Chinese colorectal cancer patients with liver metastases after preoperative chemotherapy. Small tumor diameter, long-duration chemotherapy, left primary tumor, and decreased serum CEA level after chemotherapy are associated with increased pathologic response rates.
C1 [Wang, Yun; Yuan, Yun-Fei; Lin, Hao-Cheng; Li, Bin-Kui; Wang, Feng-Hua; Wang, Zhi-Qiang; Ding, Pei-Rong; Chen, Gong; Wu, Xiao-Jun; Lu, Zhen-Hai; Pan, Zhi-Zhong; Wan, De-Sen; Sun, Peng; Yan, Shu-Mei; Xu, Rui-Hua; Li, Yu-Hong] Sun Yat Sen Univ, Ctr Canc, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Guangzhou 510060, Guangdong, Peoples R China.
   [Wang, Yun; Lin, Hao-Cheng; Wang, Feng-Hua; Wang, Zhi-Qiang; Xu, Rui-Hua; Li, Yu-Hong] Sun Yat Sen Univ, Ctr Canc, Dept Med Oncol, Guangzhou 510060, Guangdong, Peoples R China.
   [Yuan, Yun-Fei; Li, Bin-Kui] Sun Yat Sen Univ, Ctr Canc, Dept Hepatobiliary Surg, Guangzhou 510060, Guangdong, Peoples R China.
   [Ding, Pei-Rong; Chen, Gong; Wu, Xiao-Jun; Lu, Zhen-Hai; Pan, Zhi-Zhong; Wan, De-Sen] Sun Yat Sen Univ, Ctr Canc, Dept Colorectal Surg, Guangzhou 510060, Guangdong, Peoples R China.
   [Sun, Peng; Yan, Shu-Mei] Sun Yat Sen Univ, Ctr Canc, Dept Pathol, Guangzhou 510060, Guangdong, Peoples R China.
C3 State Key Lab Oncology South China; Sun Yat Sen University; Sun Yat Sen
   University; Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen
   University
RP Xu, RH; Li, YH (corresponding author), Sun Yat Sen Univ, Ctr Canc, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Guangzhou 510060, Guangdong, Peoples R China.
EM xurh@sysucc.org.cn; liyh@sysucc.org.cn
RI Sun, Peng/KDO-4243-2024; Liu, Xiaoling/HGD-3566-2022; Xu,
   Rui-Hua/AAW-4766-2021
OI Li, Yu-hong/0000-0002-5710-9096; Xu, Rui-Hua/0000-0001-9771-8534
CR Abdalla EK, 2004, ANN SURG, V239, P818, DOI 10.1097/01.sla.0000128305.90650.71
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   Ajani JA, 2004, J CLIN ONCOL, V22, P2774, DOI 10.1200/JCO.2004.01.015
   Blazer DG, 2008, J CLIN ONCOL, V26, P5344, DOI 10.1200/JCO.2008.17.5299
   Brandi G, 2016, WORLD J GASTROENTERO, V22, P519, DOI 10.3748/wjg.v22.i2.519
   Carrasco J, 2015, BRIT J CANCER, V113, P1298, DOI 10.1038/bjc.2015.321
   Chen WQ, 2016, CA-CANCER J CLIN, V66, P115, DOI 10.3322/caac.21338
   Chun YS, 2011, ANN SURG ONCOL, V18, P3601, DOI 10.1245/s10434-011-2086-4
   Dai Zhen, 2012, Zhonghua Yu Fang Yi Xue Za Zhi, V46, P598
   Eisenhauer EA, 2009, EUR J CANCER, V45, P228, DOI 10.1016/j.ejca.2008.10.026
   Fu S, 2015, CHIN J CANCER, V34, DOI [10.1186/s40880-015-0032-8, 10.1186/s40880-015-0022-x]
   Gruenberger T, 2012, SURG ONCOL, V21, P309, DOI 10.1016/j.suronc.2012.07.003
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NR 30
TC 12
Z9 12
U1 0
U2 3
PU SUN YAT SEN UNIV MED SCI WHO
PI GUANGZHOU
PA 651 DONGFENG RD E, GUANGZHOU, GUANGDONG 510060, PEOPLES R CHINA
SN 1000-467X
EI 1944-446X
J9 CHIN J CANCER
JI Chin. J. Cancer
PD OCT 2
PY 2017
VL 36
AR 78
DI 10.1186/s40880-017-0244-1
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FI7RV
UT WOS:000412196300001
PM 28969708
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Serayssol, C
   Maulat, C
   Breibach, F
   Mokrane, FZ
   Selves, J
   Guimbaud, R
   Otal, P
   Suc, B
   Berard, E
   Muscari, F
AF Serayssol, Chloe
   Maulat, Charlotte
   Breibach, Florence
   Mokrane, Fatima-Zohra
   Selves, Janick
   Guimbaud, Rosine
   Otal, Philippe
   Suc, Bertrand
   Berard, Emilie
   Muscari, Fabrice
TI Predictive factors of histological response of colorectal liver
   metastases after neoadjuvant chemotherapy
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Colorectal liver metastasis; Tumor regression grade; Neoadjuvant
   chemotherapy; Liver surgery; Histological response; Hepatectomy
ID LONG-TERM OUTCOMES; HEPATIC RESECTION; 2-STAGE HEPATECTOMY;
   PROGNOSTIC-FACTORS; RAS MUTATION; PREOPERATIVE CHEMOTHERAPY; CANCER
   INCIDENCE; EARLY RECURRENCE; TUMOR-RESPONSE; RISK-FACTORS
AB BACKGROUND
   Colorectal cancer is the third most common cancer in men and the second most common in women worldwide. Almost a third of the patients has or will develop liver metastases. Neoadjuvant chemotherapy (NAC) has recently become nearly systematic prior to surgery of colorectal livers metastases (CRLMs). The response to NAC is evaluated by radiological imaging according to morphological criteria. More recently, the response to NAC has been evaluated based on histological criteria of the resected specimen. The most often used score is the tumor regression grade (TRG), which considers the necrosis, fibrosis, and number of viable tumor cells.
   AIM
   To analyze the predictive factors of the histological response, according to the TRG, on CRLM surgery performed after NAC.
   METHODS
   From January 2006 to December 2013, 150 patients who had underwent surgery for CRLMs after NAC were included. The patients were separated into two groups based on their histological response, according to Rubbia-Brandt TRG. Based on their TRG, each patient was either assigned to the responder (R) group (TRG 1, 2, and 3) or to the non-responder (NR) group (TRG 4 and 5). All of the histology slides were re-evaluated in a blind manner by the same specialized pathologist. Univariate and multivariate analyses were performed.
   RESULTS
   Seventy-four patients were classified as responders and 76 as non-responders. The postoperative mortality rate was 0.7%, with a complication rate of 38%. Multivariate analysis identified five predictive factors of histological response. Three were predictive of non-response: More than seven NAC sessions, the absence of a radiological response after NAC, and a repeat hepatectomy (P < 0.005). Two were predictive of a good response: A rectal origin of the primary tumor and a liver-first strategy (P < 0.005). The overall survival was 57% at 3 yr and 36% at 5 yr. The disease-free survival rates were 14% at 3 yr and 11% at 5 yr. The factors contributing to a poor prognosis for disease-free survival were: No histological response after NAC, largest metastasis > 3 cm, more than three preoperative metastases, R1 resection, and the use of a targeted therapy with NAC (P < 0.005).
   CONCLUSION
   A non-radiological response and a number of NAC sessions > 7 are the two most pertinent predictive factors of non-histological response (TRG 4 or 5).
C1 [Serayssol, Chloe; Maulat, Charlotte; Suc, Bertrand; Muscari, Fabrice] Toulouse Rangueil Univ Hosp, Dept Digest Surg & Liver Transplantat, F-31059 Toulouse, France.
   [Breibach, Florence; Selves, Janick] Toulouse Univ Hosp, Dept Pathol, F-31059 Toulouse, France.
   [Mokrane, Fatima-Zohra; Otal, Philippe] Toulouse Rangueil Univ Hosp, Dept Radiol, F-31059 Toulouse, France.
   [Guimbaud, Rosine] Toulouse Rangueil Univ Hosp, Dept Oncol, F-31059 Toulouse, France.
   [Berard, Emilie] Toulouse Univ Hosp, Toulouse Res Methodol Support Unit, F-31000 Toulouse, France.
C3 CHU de Toulouse; Universite de Toulouse; Universite Toulouse III - Paul
   Sabatier; CHU de Toulouse; CHU de Toulouse; CHU de Toulouse; Universite
   de Toulouse; Universite Toulouse III - Paul Sabatier; CHU de Toulouse
RP Maulat, C (corresponding author), CHU Rangueil, Toulouse Rangueil Univ Hosp, Dept Digest Surg & Liver Transplantat, 1 Ave J Poulhes, F-31059 Toulouse, France.
EM charlotte.maulat@gmail.com
RI Maulat, Charlotte/Y-3926-2019; BERARD, EMILIE/LWK-6604-2024; muscari,
   fabrice/AAQ-3856-2020
OI Mokrane, Fatima-Zohra/0000-0003-1610-1474; Serayssol,
   Chloe/0000-0001-9965-0908
CR Adam R, 2004, ANN SURG, V240, P1052, DOI 10.1097/01.sla.0000145964.08365.01
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NR 77
TC 8
Z9 9
U1 0
U2 2
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD APR 15
PY 2019
VL 11
IS 4
BP 295
EP 309
DI 10.4251/wjgo.v11.i4.295
PG 15
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA HU2UJ
UT WOS:000465126900003
PM 31040895
OA hybrid, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Wang, QY
   Shen, XF
   An, R
   Bai, JC
   Dong, JH
   Cai, HY
   Zhu, HY
   Zhong, WT
   Chen, WL
   Liu, AJ
   Du, JF
AF Wang, Qianyu
   Shen, Xiaofei
   An, Ran
   Bai, Junchao
   Dong, Junhua
   Cai, Huiyun
   Zhu, Hongyan
   Zhong, Wentao
   Chen, Wenliang
   Liu, Aijun
   Du, Junfeng
TI Peritumoral tertiary lymphoid structure and tumor stroma percentage
   predict the prognosis of patients with non-metastatic colorectal cancer
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE colorectal cancer; tumor immune microenvironment; tertiary lymphoid
   structures (TLS); tumor stroma percentage; nomogram; prognosis
ID T-CELL INFILTRATION; B-CELLS; SURVIVAL; IMMUNOTHERAPY; HALLMARKS;
   DEFINES
AB BackgroundTertiary lymphoid structures (TLSs) are crucial in promoting and maintaining positive anti-tumor immune responses. The tumor stroma has a powerful immunosuppressive function that could exclude tumor-infiltrating lymphocytes from the tumor beds and lead to a "cold" phenotype. TLSs and tumor stroma percentage (TSP) are significantly associated with the prognosis of patients with certain cancers. However, the exact roles of TLSs and TSP and their intrinsic relationship are still largely unknown in colorectal cancer (CRC). MethodsTLSs and TSP were assessed using hematoxylin-eosin (H&E) and/or immunohistochemistry (IHC) staining from 114 CRC patients in the training set and 60 CRC patients in the external validation set. The correlation between TILs, TLS and clinicopathological characteristics and their prognostic values were assessed. Finally, we plotted a Nomogram including the TLS, TSP and tumor-node-metastasis (TNM) stage to predict the probability of recurrence-free survival (RFS) at 2- and 5-years in non-metastatic colorectal cancer (nmCRC) patients. ResultsPeritumoral TLS (P-TLS), intratumoral TLS (In-TLS) and high TSP (H-TSP, >50%) were present in 99.1%, 26.3% and 41.2% patients, respectively. H-TSP tumor tends to be associated with lower P-TLS density (P =0.0205). The low P-TLS density (< 0.098/mm(2)) was significantly associated with reduced RFS (HR=6.597 95% CI: 2.882-15.103, P <0.001) and reduced overall survival (OS) (HR=6.628 95% CI: 2.893-15.183, P < 0.001) of nmCRC patients. In-TLS was not of significance in evaluating the clinical outcomes of nmCRC patients. H-TSP was significantly associated with reduced RFS (HR=0.126 95% CI: 0.048-0.333, P <0.001) and reduced OS (HR=0.125 95% CI: 0.047-0.332, P <0.001) of nmCRC patients. The 5-year RFS of the high P-TLS, low-TLS, H-TSP, and L-TSP groups were 89.7%, 47.2%, 53.2%, and 92.5%, respectively. The P-TLS density, TSP and TNM stage were independent prognosis factors of nmCRC patients. The Nomogram, including the P-TLS density, TSP and TNM stage, outperformed the TNM stage. ConclusionsHigh P-TLS density and low TSP (L-TSP) were independent and favorable prognostic factors of nmCRC patients, which might provide new directions for targeted therapy in the CRC tumor microenvironment, especially the tumor immune microenvironment.
C1 [Wang, Qianyu; Chen, Wenliang] Shanxi Med Univ, Sch Clin Med 2, Taiyuan, Peoples R China.
   [Shen, Xiaofei] Nanjing Univ, Affiliated Drum Tower Hosp, Med Sch, Dept Gen Surg, Nanjing, Peoples R China.
   [An, Ran; Zhu, Hongyan; Liu, Aijun] Chinese Peoples Liberat Army Gen Hosp, Med Ctr 7, Dept Pathol, Beijing, Peoples R China.
   [Bai, Junchao; Dong, Junhua; Cai, Huiyun; Zhong, Wentao; Du, Junfeng] Chinese Peoples Liberat Army PLA Gen Hosp, Med Ctr 7, Dept Gen Surg, Beijing, Peoples R China.
   [Zhong, Wentao; Du, Junfeng] Southern Med Univ, Sch Clin Med 2, Guangzhou, Peoples R China.
   [Chen, Wenliang] Shanxi Med Univ, Affiliated Hosp 2, Dept Gen Surg, Taiyuan, Peoples R China.
   [Du, Junfeng] Chinese Peoples Liberat Army PLA Gen Hosp, Med Ctr 1, Med Dept Gen Surg, Beijing, Peoples R China.
C3 Shanxi Medical University; Nanjing University; Chinese People's
   Liberation Army General Hospital; Seventh Medical Center of Chinese PLA
   General Hospital; Southern Medical University - China; Shanxi Medical
   University
RP Chen, WL (corresponding author), Shanxi Med Univ, Sch Clin Med 2, Taiyuan, Peoples R China.; Liu, AJ (corresponding author), Chinese Peoples Liberat Army Gen Hosp, Med Ctr 7, Dept Pathol, Beijing, Peoples R China.; Du, JF (corresponding author), Chinese Peoples Liberat Army PLA Gen Hosp, Med Ctr 7, Dept Gen Surg, Beijing, Peoples R China.; Du, JF (corresponding author), Southern Med Univ, Sch Clin Med 2, Guangzhou, Peoples R China.; Chen, WL (corresponding author), Shanxi Med Univ, Affiliated Hosp 2, Dept Gen Surg, Taiyuan, Peoples R China.; Du, JF (corresponding author), Chinese Peoples Liberat Army PLA Gen Hosp, Med Ctr 1, Med Dept Gen Surg, Beijing, Peoples R China.
EM sxmu66@126.com; aliu301@126.com; dujf66@126.com
RI Shen, Xiaofei/HDL-7300-2022; Chen, Wenliang/S-5405-2016
OI Wang, Qianyu/0000-0001-7048-8847; Shen, Xiaofei/0000-0002-5816-1814; du,
   junfeng/0000-0002-8482-4271; Zhong, Wentao/0000-0002-6268-1898
FU National Natural Science Foundation of China;  [81870393];  [81970500]
FX Funding This work was supported by the National Natural Science
   Foundation of China (No. 81870393, JFD, and 81970500, XFS).
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NR 49
TC 26
Z9 29
U1 0
U2 6
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD SEP 16
PY 2022
VL 13
AR 962056
DI 10.3389/fimmu.2022.962056
PG 16
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 4Z8GK
UT WOS:000862439700001
PM 36189233
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Konopleva, MY
   Dail, M
   Daver, NG
   Garcia, JS
   Jonas, BA
   Yee, KWL
   Kelly, KR
   Vey, N
   Assouline, S
   Roboz, GJ
   Paolini, S
   Pollyea, DA
   Tafuri, A
   Brandwein, JM
   Pigneux, A
   Powell, BL
   Fenaux, P
   Olin, RL
   Visani, G
   Martinelli, G
   Onishi, M
   Wang, J
   Huang, WZ
   Dunshee, DR
   Hamidi, H
   Ott, MG
   Hong, WJ
   Andreeff, M
AF Konopleva, Marina Y.
   Dail, Monique
   Daver, Naval G.
   Garcia, Jacqueline S.
   Jonas, Brian A.
   Yee, Karen W. L.
   Kelly, Kevin R.
   Vey, Norbert
   Assouline, Sarit
   Roboz, Gail J.
   Paolini, Stefania
   Pollyea, Daniel A.
   Tafuri, Agostino
   Brandwein, Joseph M.
   Pigneux, Arnaud
   Powell, Bayard L.
   Fenaux, Pierre
   Olin, Rebecca L.
   Visani, Giuseppe
   Martinelli, Giovanni
   Onishi, Maika
   Wang, Jue
   Huang, Weize
   Dunshee, Diana R.
   Hamidi, Habib
   Ott, Marion G.
   Hong, Wan-Jen
   Andreeff, Michael
TI Venetoclax and Cobimetinib in Relapsed/Refractory AML: A Phase 1b Trial
SO CLINICAL LYMPHOMA MYELOMA & LEUKEMIA
LA English
DT Article
DE Biomarker; Mitogen-activated protein kinase pathway; Targeted therapy;
   B-cell lymphoma-2
ID REFRACTORY AML; DOUBLE-BLIND; INHIBITOR; APOPTOSIS; LEUKEMIA;
   AZACITIDINE; INDUCTION; PATHWAYS; TRAMETINIB; MELANOMA
AB Treatment options for patients who have acute myeloid leukemia (AML) which has come back (relapsed) or stopped responding to treatment (refractory) are limited. In this study, 30 patients with relapsed/refractory AML received 2 drugs (venetoclax and cobimetinib). Venetoclax-cobimetinib had limited responses with unwanted side effects, compared with venetoclax alone. However, these findings will help future trials of similar drug combinations. Background: Therapies for relapsed/refractory acute myeloid leukemia remain limited and outcomes poor, especially amongst patients who are ineligible for cytotoxic chemotherapy or targeted therapies. Patients and Methods: This phase 1b trial evaluated venetoclax, a B-cell lymphoma-2 (BCL-2) inhibitor, plus cobimetinib, a MEK1/2 inhibitor, in patients with relapsed/refractory acute myeloid leukemia, ineligible for cytotoxic chemotherapy. Two-dimensional doseescalation was performed for venetoclax dosed daily, and for cobimetinib dosed on days 1-21 of each 28-day cycle. Results: Thirty patients (median [range] age: 71.5 years [60-84]) received venetoclax-cobimetinib. The most common adverse events (AEs; in >= 40.0% of patients) were diarrhea (80.0%), nausea (60.0%), vomiting (40.0%), febrile neutropenia (40.0%), and fatigue (40.0%). Overall, 66.7% and 23.3% of patients experienced AEs leading to dose modification/interruption or treatment withdrawal, respectively. The composite complete remission (CRc) rate (complete remission [CR] + CR with incomplete blood count recovery + CR with incomplete platelet recovery) was 15.6%; antileukemic response rate (CRc + morphologic leukemia -free state/partial remission) was 18.8%. For the recommended phase 2 dose (venetoclax: 600 mg; cobimetinib: 40 mg), CRc and antileukemic response rates were both 12.5%. Failure to achieve an antileukemic response was associated with elevated baseline phosphorylated ERK and MCL-1 levels, but not BCL-xL. Baseline mutations in >= 1 signaling gene or TP53 were noted in nonresponders and emerged on treatment. Pharmacodynamic biomarkers revealed inconsistent, transient inhibition of the mitogen-activated protein kinase (MAPK) pathway. Conclusion: Venetoclax-cobimetinib showed limited preliminary efficacy similar to single -agent venetoclax, but with added toxicity. Our findings will inform future trials of BCL-2/MAPK pathway inhibitor combinations.
C1 [Konopleva, Marina Y.; Daver, Naval G.; Andreeff, Michael] Univ Texas MD Anderson Canc Ctr, Houston, TX USA.
   [Dail, Monique; Onishi, Maika; Wang, Jue; Huang, Weize; Dunshee, Diana R.; Hamidi, Habib] Genentech Inc, South San Francisco, CA USA.
   [Garcia, Jacqueline S.] Dana Farber Canc Inst, Boston, MA USA.
   [Jonas, Brian A.] Univ Calif Davis, Comprehens Canc Ctr, Sacramento, CA USA.
   [Yee, Karen W. L.] Princess Margaret Canc Ctr, Toronto, ON, Canada.
   [Kelly, Kevin R.] Univ Southern Calif, Los Angeles, CA USA.
   [Vey, Norbert] Inst Paoli Calmettes, Hematol Clin, Marseille, France.
   [Assouline, Sarit] Jewish Gen Hosp, Montreal, PQ, Canada.
   [Roboz, Gail J.] New York Presbyterian, Weill Cornell Med Coll, New York, NY USA.
   [Paolini, Stefania] Ist Ematol Seragnoli, IRCCS Azienda Osped Univ Bologna, Bologna, Italy.
   [Pollyea, Daniel A.] Univ Colorado, Div Hematol, Aurora, CO USA.
   [Tafuri, Agostino] Univ Hosp St Andrea Sapienza, Dept Clin & Mol Med, Rome, Italy.
   [Brandwein, Joseph M.] Univ Alberta, Div Hematol, Edmonton, AB, Canada.
   [Pigneux, Arnaud] Bordeaux Haut Leveque Univ Hosp, Pessac, France.
   [Powell, Bayard L.] Atrium Hlth Wake Forest Baptist Comprehens Canc Ct, Winston Salem, NC USA.
   [Fenaux, Pierre] Univ Paris Diderot, Hop St Louis, Paris, France.
   [Olin, Rebecca L.] Univ Calif San Francisco, San Francisco, CA USA.
   [Visani, Giuseppe] Osped San Salvatore, Hematol, Pesaro, Italy.
   [Martinelli, Giovanni] IRCCS Ist Romagnolo Studio Tumori IRST Dino Amador, Meldola, Italy.
   [Ott, Marion G.] F Hoffmann La Roche Ltd, Basel, Switzerland.
   [Hong, Wan-Jen] Prelude Therapeut, Wilmington, DE USA.
   [Konopleva, Marina Y.] Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Div Canc Med, 1400 Holcombe Blvd, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; Roche Holding;
   Genentech; Harvard University; Dana-Farber Cancer Institute; University
   of California System; University of California Davis; University of
   Toronto; University Health Network Toronto; Princess Margaret Cancer
   Centre; University of Southern California; UNICANCER; Institut
   Paoli-Calmette (IPC); McGill University; NewYork-Presbyterian Hospital;
   Cornell University; Weill Cornell Medicine; IRCCS Azienda
   Ospedaliero-Universitaria di Bologna; University of Colorado System;
   University of Colorado Anschutz Medical Campus; University of Alberta;
   CHU Bordeaux; Universite de Bordeaux; Assistance Publique Hopitaux Paris
   (APHP); Universite Paris Cite; Hopital Universitaire Saint-Louis - APHP;
   University of California System; University of California San Francisco;
   Roche Holding; University of Texas System; UTMD Anderson Cancer Center
RP Konopleva, MY (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Div Canc Med, 1400 Holcombe Blvd, Houston, TX 77030 USA.
EM mkonople@mdanderson.org
RI Jonas, Brian/AAS-3639-2020; Daver, Naval/AFU-9643-2022; Hamidi,
   Habib/H-8030-2016; Martinelli, Giovanni/AAK-9211-2020; Vey,
   Norbert/AGE-3573-2022
OI Garcia, Jacqueline/0000-0003-2118-6302; Jonas,
   Brian/0000-0002-4921-5809; Vey, Norbert/0000-0001-7027-040X
FU Genentech, Inc.
FX Venetoclax is being developed in a collaboration between Genen-tech,
   Inc. and AbbVie, Inc. Genentech, Inc. provided financial support for the
   study and participated in the design, study conduct, analysis, and
   interpretation of data, as well as the writing, review, and approval of
   the manuscript. We thank the participating patients and their families,
   investigators, and trial staff. Denise Cheung, B. Pharm, of Genentech,
   Inc., provided support in analysis of the data, and Cherie Green and
   Connie Ma provided flow cytometry and data analysis support. Third-party
   medical writing assistance, under the direction of Maika Onishi, was
   provided by Roisin Weaver, MSc, of Ashfield MedComms, an Inizio company,
   and was funded by F. Hoffmann-La Roche Ltd.
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NR 57
TC 2
Z9 2
U1 0
U2 0
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 2152-2650
EI 2152-2669
J9 CL LYMPH MYELOM LEUK
JI Clin. Lymphoma Myeloma Leuk.
PD JUN
PY 2024
VL 24
IS 6
DI 10.1016/j.clml.2024.01.007
EA MAY 2024
PG 11
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA UQ1D5
UT WOS:001249423700001
PM 38378362
OA Green Published
DA 2025-01-04
ER

PT J
AU Palmieri, LJ
   Mineur, L
   Tougeron, D
   Rousseau, B
   Granger, V
   Gornet, JM
   Smith, D
   Lievre, A
   Galais, MP
   Doat, S
   Pernot, S
   Bignon-Bretagne, AL
   Metges, JP
   Baba-Hamed, N
   Michel, P
   Obled, S
   Vitellius, C
   Bouche, O
   Saban-Roche, L
   Buecher, B
   des Guetz, G
   Locher, C
   Trouilloud, I
   Goujon, G
   Dior, M
   Manfredi, S
   Soularue, E
   Phelip, JM
   Henriques, J
   Vernery, D
   Coriat, R
AF Palmieri, Lola-Jade
   Mineur, Laurent
   Tougeron, David
   Rousseau, Benoit
   Granger, Victoire
   Gornet, Jean-Marc
   Smith, Denis
   Lievre, Astrid
   Galais, Marie-Pierre
   Doat, Solene
   Pernot, Simon
   Bignon-Bretagne, Anne-Laure
   Metges, Jean-Philippe
   Baba-Hamed, Nabil
   Michel, Pierre
   Obled, Stephane
   Vitellius, Carole
   Bouche, Olivier
   Saban-Roche, Lea
   Buecher, Bruno
   des Guetz, Gaetan
   Locher, Christophe
   Trouilloud, Isabelle
   Goujon, Gael
   Dior, Marie
   Manfredi, Sylvain
   Soularue, Emilie
   Phelip, Jean-Marc
   Henriques, Julie
   Vernery, Dewi
   Coriat, Romain
TI Withholding the Introduction of Anti-Epidermal Growth Factor Receptor:
   Impact on Outcomes in <i>RAS</i> Wild-Type Metastatic Colorectal Tumors:
   A Multicenter AGEO Study (the WAIT or ACT Study)
SO ONCOLOGIST
LA English
DT Article
DE Metastatic colorectal cancer; RAS status; Anti-epidermal growth factor
   receptor; Bevacizumab
ID FOLFIRI PLUS CETUXIMAB; CANCER FIRE-3; OPEN-LABEL; BEVACIZUMAB;
   CHEMOTHERAPY; MUTATIONS; THERAPY
AB Background Patients with RAS wild-type (WT) nonresectable metastatic colorectal cancer (mCRC) may receive either bevacizumab or an anti-epidermal growth factor receptor (EGFR) combined with first-line, 5-fluorouracil-based chemotherapy. Without the RAS status information, the oncologist can either start chemotherapy with bevacizumab or wait for the introduction of the anti-EGFR. Our objective was to compare both strategies in a routine practice setting. Materials and Methods This multicenter, retrospective, propensity score-weighted study included patients with a RAS WT nonresectable mCRC, treated between 2013 and 2016 by a 5-FU-based chemotherapy, with either delayed anti-EGFR or immediate anti-vascular endothelial growth factor (VEGF). Primary criterion was overall survival (OS). Secondary criteria were progression-free survival (PFS) and objective response rate (ORR). Results A total of 262 patients (129 in the anti-VEGF group and 133 in the anti-EGFR group) were included. Patients receiving an anti-VEGF were more often men (68% vs. 56%), with more metastatic sites (>2 sites: 15% vs. 9%). The median delay to obtain the RAS status was 19 days (interquartile range: 13-26). Median OS was not significantly different in the two groups (29 vs. 30.5 months, p = .299), even after weighting on the propensity score (hazard ratio [HR] = 0.86, 95% confidence interval [CI], 0.69-1.08, p = .2024). The delayed introduction of anti-EGFR was associated with better median PFS (13.8 vs. 11.0 months, p = .0244), even after weighting on the propensity score (HR = 0.74, 95% CI, 0.61-0.90, p = .0024). ORR was significantly higher in the anti-EGFR group (66.7% vs. 45.6%, p = .0007). Conclusion Delayed introduction of anti-EGFR had no deleterious effect on OS, PFS, and ORR, compared with doublet chemotherapy with anti-VEGF. Implications for Practice For RAS/RAF wild-type metastatic colorectal cancer, patients may receive 5-fluorouracil-based chemotherapy plus either bevacizumab or an anti-epidermal growth factor receptor (EGFR). In daily practice, the time to obtain the RAS status might be long enough to consider two options: to start the chemotherapy with bevacizumab, or to start without a targeted therapy and to add the anti-EGFR at reception of the RAS status. This study found no deleterious effect of the delayed introduction of an anti-EGFR on survival, compared with the introduction of an anti-vascular endothelial growth factor from cycle 1. It is possible to wait one or two cycles to introduce the anti-EGFR while waiting for RAS status.
C1 [Palmieri, Lola-Jade; Coriat, Romain] Cochin Hosp, Dept Gastroenterol, Paris, France.
   [Mineur, Laurent] Inst St Catherine, Dept Oncol, Avignon, France.
   [Tougeron, David] Univ Poitiers Hosp, Dept Oncol, Poitiers, France.
   [Rousseau, Benoit] Mondor Hosp, Dept Oncol, Paris, France.
   [Granger, Victoire] Grenoble Univ Hosp, Dept Gastroenterol, Grenoble, France.
   [Gornet, Jean-Marc] St Louis Hosp, Dept Gastroenterol, Paris, France.
   [Smith, Denis] Bordeaux Univ Hosp, Dept Med Oncol, Bordeaux, France.
   [Lievre, Astrid] Rennes Univ Hosp, Dept Gastroenterol, Rennes, France.
   [Galais, Marie-Pierre] Francois Baclesse Ctr, Dept Med Oncol, Caen, France.
   [Doat, Solene] Hop La Pitie Salpetriere, Dept Gastroenterol, Paris, France.
   [Pernot, Simon] Georges Pompidou European Hosp, Dept Digest Oncol, Paris, France.
   [Bignon-Bretagne, Anne-Laure] Caen Univ Hosp, Dept Gastroenterol, Caen, France.
   [Metges, Jean-Philippe] Brest Univ Hosp, Dept Med Oncol, Brest, France.
   [Baba-Hamed, Nabil] St Joseph Hosp, Dept Med Oncol, Paris, France.
   [Michel, Pierre] Normandie Univ, Rouen Univ Hosp, Dept Hepatogastroenterol, UNIROUEN,Inserm 1245,IRON Grp, Rouen, France.
   [Obled, Stephane] Nimes Univ Hosp, Dept Med Oncol, Nimes, France.
   [Vitellius, Carole] Angers Univ Hosp, Dept Gastroenterol, Angers, France.
   [Bouche, Olivier] Reims Univ Hosp, Dept Digest Oncol, Reims, France.
   [Saban-Roche, Lea] Ctr Cancerol Loire, Dept Med Oncol, St Etienne, France.
   [Buecher, Bruno] Inst Curie, Dept Med Oncol, Paris, France.
   [des Guetz, Gaetan] Delafontaine Hosp, Dept Med Oncol, St Denis, Reunion, France.
   [Locher, Christophe] Meaux Gen Hosp, Dept Gastroenterol, Meaux, France.
   [Trouilloud, Isabelle] St Antoine Hosp, Dept Med Oncol, Paris, France.
   [Goujon, Gael] Hop Xavier Bichat, Dept Gastroenterol, Paris, France.
   [Dior, Marie] Louis Mourier Hosp, Dept Gastroenterol, Colombes, France.
   [Manfredi, Sylvain] Dijon Univ Hosp, Dept Gastroenterol, Dijon, France.
   [Soularue, Emilie] Kremlin Bicetre Hosp, Dept Gastroenterol, Le Kremlin Bicetre, France.
   [Phelip, Jean-Marc] St Etienne Univ Hosp, Dept Gastroenterol, St Etienne, France.
   [Henriques, Julie; Vernery, Dewi] Besancon Univ Hosp, Methodol & Qual Life Oncol Unit, INSERM UMR 1098, Besancon, France.
C3 Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Cochin - APHP; Universite de Poitiers; CHU
   Poitiers; Assistance Publique Hopitaux Paris (APHP); Universite
   Paris-Est-Creteil-Val-de-Marne (UPEC); Hopital Universitaire
   Henri-Mondor - APHP; CHU Grenoble Alpes; Communaute Universite Grenoble
   Alpes; Universite Grenoble Alpes (UGA); Assistance Publique Hopitaux
   Paris (APHP); Universite Paris Cite; Hopital Universitaire Saint-Louis -
   APHP; CHU Bordeaux; Universite de Rennes; CHU Rennes; UNICANCER; Centre
   Francois Baclesse; Assistance Publique Hopitaux Paris (APHP); Hopital
   Universitaire Pitie-Salpetriere - APHP; Sorbonne Universite; Assistance
   Publique Hopitaux Paris (APHP); Universite Paris Cite; Hopital
   Universitaire Europeen Georges-Pompidou - APHP; CHU de Caen NORMANDIE;
   Universite de Caen Normandie; CHU Brest; Universite Paris Cite; Hopital
   Paris Saint-Joseph; Universite de Rouen Normandie; CHU de Rouen;
   Institut National de la Sante et de la Recherche Medicale (Inserm);
   Universite de Montpellier; CHU de Nimes; Universite d'Angers; Centre
   Hospitalier Universitaire d'Angers; Universite de Reims
   Champagne-Ardenne; CHU de Reims; Institut de Cancerologie de la Loire;
   UNICANCER; Universite PSL; Institut Curie; Assistance Publique Hopitaux
   Paris (APHP); Sorbonne Universite; Hopital Universitaire Saint-Antoine -
   APHP; Universite Paris Cite; Assistance Publique Hopitaux Paris (APHP);
   Hopital Universitaire Bichat-Claude Bernard - APHP; Universite Paris
   Cite; Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
   Louis-Mourier - APHP; CHU Dijon Bourgogne; Universite Paris Saclay;
   Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire Bicetre
   - APHP; CHU de St Etienne; Institut National de la Sante et de la
   Recherche Medicale (Inserm); Universite de Franche-Comte; CHU Besancon
RP Coriat, R (corresponding author), Cochin Hosp, Dept Gastroenterol & Digest Oncol, 27 Rue Faubourg St Jacques, F-75014 Paris, France.
EM romain.coriat@aphp.fr
RI tougeron, david/ABF-3217-2020; Rousseau, Benoit/K-5651-2017
OI Palmieri, Lola-Jade/0000-0002-8540-9344
CR Allegra CJ, 2016, J CLIN ONCOL, V34, P179, DOI 10.1200/JCO.2015.63.9674
   Arnold D, 2017, ANN ONCOL, V28, P1713, DOI 10.1093/annonc/mdx175
   Bachet JB, 2018, ANN ONCOL, V29, P1211, DOI 10.1093/annonc/mdy061
   Douillard JY, 2013, NEW ENGL J MED, V369, P1023, DOI 10.1056/NEJMoa1305275
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NR 21
TC 4
Z9 5
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PD FEB
PY 2020
VL 25
IS 2
BP E266
EP E275
DI 10.1634/theoncologist.2019-0328
EA OCT 2019
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KK0QF
UT WOS:000488424600001
PM 32043796
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU El Omari, N
   Bakrim, S
   Khalid, A
   Albratty, M
   Abdalla, AN
   Lee, LH
   Goh, KW
   Ming, LC
   Bouyahya, A
AF El Omari, Nasreddine
   Bakrim, Saad
   Khalid, Asaad
   Albratty, Mohammed
   Abdalla, Ashraf N.
   Lee, Learn-Han
   Goh, Khang Wen
   Ming, Long Chiau
   Bouyahya, Abdelhakim
TI Anticancer clinical efficiency and stochastic mechanisms of belinostat
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE Melanoma; Cancer; HDACi; Apoptosis; Cell cycle arrest; Molecular
   pathways; Drug; Medicine
ID DEACETYLASE INHIBITOR BELINOSTAT; PHASE-II TRIAL; ENHANCED ANTITUMOR
   EFFICACY; HEPATOCELLULAR-CARCINOMA; COLORECTAL-CANCER; HDAC INHIBITOR;
   COMBINATION; DOXORUBICIN; PXD101; CYCLOPHOSPHAMIDE
AB Cancer progression is strongly affected by epigenetic events in addition to genetic modifications. One of the key elements in the epigenetic control of gene expression is histone modification through acetylation, which is regulated by the synergy between histone acetyltransferases (HATs) and histone deacetylases (HDACs). HDACs are thought to offer considerable potential for the development of anticancer medications, particularly when used in conjunction with other anticancer medications and/or radiotherapy. Belinostat (Beleodaq, PXD101) is a pan-HDAC unsaturated hydroxamate inhibitor with a sulfonamide group that has been approved by the U.S. Food and Drug Administration (FDA) for the treatment of refractory or relapsed peripheral T-cell lymphoma (PTCL) and solid malignancies or and other hematological tissues. This drug modifies histones and epigenetic pathways. Because HDAC and HAT imbalance can lead to downregulation of regulatory genes, resulting in tumorigenesis. Inhibition of HDACs by belinostat indirectly promotes anti-cancer therapeutic effect by provoking acetylated histone accumulation, re-establishing normal gene expressions in cancer cells and stimulating other routes such as the immune response, p27 signaling cascades, caspase 3 activation, nuclear protein poly (ADPribose) polymerase-1 (PARP-1) degradation, cyclin A (G2/M phase), cyclin E1 (G1/S phase) and other events. In addition, belinostat has already been discovered to increase p21WAF1 in a number of cell lines (melanoma, prostate, breast, lung, colon, and ovary). This cyclin-dependent kinase inhibitor actually has a role in processes that cause cell cycle arrest and apoptosis. Belinostat's clinical effectiveness, comprising Phase I and II studies within the areas of solid and hematological cancers, has been evidenced through several investigative trials that have supported its potential to be a valuable anti-cancer drug. The purpose of this research was to provide insight on the specific molecular processes through which belinostat inhibits HDAC. The ability to investigate new therapeutic options employing targeted therapy and acquire a deeper understanding of cancer cell abnormalities may result from a better understanding of these particular routes.
C1 [El Omari, Nasreddine] Mohammed V Univ Rabat, Fac Med & Pharm, Lab Histol Embryol & Cytogenet, Rabat 10100, Morocco.
   [Bakrim, Saad] Ibn Zohr Univ, Polydisciplinary Fac Taroudant, Geobioenvironment Engn & Innovat Lab, Biotechnol & Innovat Team,Molecular Engineering,Bi, Agadir 80000, Morocco.
   [Khalid, Asaad] Jazan Univ, Subst Abuse & Toxicol Res Ctr, POB 114, Jazan 45142, Saudi Arabia.
   [Albratty, Mohammed] Jazan Univ, Coll Pharm, Dept Pharmaceut Chem & Pharmacognosy, POB 114, Jazan 45142, Saudi Arabia.
   [Abdalla, Ashraf N.] Umm Al Qura Univ, Coll Pharm, Dept Pharmacol & Toxicol, Mecca 21955, Saudi Arabia.
   [Lee, Learn-Han] Sunway Univ, Sunway Microbi Ctr, Sch Med & Life Sci, Sunway City 47500, Malaysia.
   [Lee, Learn-Han] Monash Univ Malaysia, Jeffrey Cheah Sch Med & Hlth Sci, Novel Bacteria & Drug Discovery Res Grp NBDD, Microbiome & Bioresource Res Strength MBRS, Subang Jaya, Malaysia.
   [Goh, Khang Wen] INTI Int Univ, Fac Data Sci & Informat Technol, Nilai, Malaysia.
   [Ming, Long Chiau; Bouyahya, Abdelhakim] Sunway Univ, Sch Med & Life Sci, Sunway City 47500, Malaysia.
   [El Omari, Nasreddine; Bakrim, Saad; Khalid, Asaad; Albratty, Mohammed; Lee, Learn-Han; Ming, Long Chiau; Bouyahya, Abdelhakim] Mohammed V Univ Rabat, Fac Sci, Dept Biol, Lab Human Pathol Biol, Rabat 10106, Morocco.
C3 Mohammed V University in Rabat; Ibn sina University Hospital Center of
   Rabat; Ibn Zohr University of Agadir; Jazan University; Jazan
   University; Umm Al Qura University; Sunway University; Monash
   University; Monash University Malaysia; INTI International University;
   Sunway University; Mohammed V University in Rabat
RP Khalid, A; Lee, LH; Ming, LC; Bouyahya, A (corresponding author), Mohammed V Univ Rabat, Fac Sci, Dept Biol, Lab Human Pathol Biol, Rabat 10106, Morocco.
EM nasrelomari@gmail.com; s.bakrim@uiz.ac.ma; akahmed@jazanu.edu.sa;
   malbratty@jazanu.edu.sa; anabdrabo@uqu.edu.sa; learnhanl@sunway.edu.my;
   khangwen.goh@newinti.edu.my; chiaumingl@sunway.edu.my;
   a.bouyahya@um5r.ac.ma
RI Albratty, Mohammed/AHD-1350-2022; Goh, Khang Wen/HCH-4693-2022;
   Abdelhakim, BOUYAHYA/Y-5725-2019; BAKRIM, SAAD/HPC-6347-2023; El Omari,
   Nasreddine/ABG-6138-2021; KHALID, ASAAD/HJH-6413-2023; Ming, Long
   Chiau/J-5210-2015; Lee, Learn-Han/I-5331-2015
OI Ahmed, Asaad Khalid/0000-0001-8734-2588; Ming, Long
   Chiau/0000-0002-6971-1383; Saad, Bakrim/0000-0002-4521-3515; Lee,
   Learn-Han/0000-0002-8589-7456
FU Deputyship for Research and Innovation, Ministry of Education in Saudi
   Arabia [ISP22-15]
FX Deputyship for Research and Innovation, Ministry of Education in Saudi
   Arabia (project number ISP22-15)
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NR 56
TC 11
Z9 11
U1 2
U2 4
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD SEP
PY 2023
VL 165
AR 115212
DI 10.1016/j.biopha.2023.115212
EA AUG 2023
PG 10
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA P6EP6
UT WOS:001051590500001
PM 37541175
OA gold
DA 2025-01-04
ER

PT J
AU Jakobsen, AK
   Yuusufi, S
   Madsen, LB
   Meldgaard, P
   Knudsen, BR
   Stougaard, M
AF Jakobsen, Ann-Katrine
   Yuusufi, Sakineh
   Madsen, Line Bille
   Meldgaard, Peter
   Knudsen, Birgitta R.
   Stougaard, Magnus
TI TDP1 and TOP1 as targets in anticancer treatment of NSCLC: Activity and
   protein level in normal and tumor tissue from 150 NSCLC patients
   correlated to clinical data
SO LUNG CANCER
LA English
DT Article
DE Non-small cell lung cancer; Tyrosyl-DNA phosphodiesterase 1;
   Topoisomerase 1; Precision medicine; Targeted therapy; Biosensor
ID DNA TOPOISOMERASE-I; HUMAN-CELLS; COLORECTAL-CANCER; CELLULAR ROLES;
   REPAIR; PHOSPHORYLATION; DEFICIENCY; KINASE; DAMAGE; MECHANISMS
AB Objectives: Topoisomerase 1 (TOP1) is a drug target used in anticancer treatment of various cancer types. The effect of the TOP1 drugs can be counteracted by the enzymatic activity of tyrosyl-DNA phosphodiesterase 1 (TDP1). Thus, to elucidate the relevance of combining TDP1 and TOP1 as drug targets for anticancer treatment in NSCLC, TDP1 and TOP1 was for the first time quantified in a large cohort of paired normal and tumor tissue from NSCLC patients, and data were correlated between the two enzymes and to clinical data. Materials and methods: TDP1 and TOP1 activity and protein concentration were measured in paired normal and tumor tissue from 150 NSCLC patients using TDP1 and TOP1 specific biosensors and ELISA. TDP1 and TOP1 activity and protein concentration were correlated to clinical data.Results: TDP1 and TOP1 activity and protein concentration were significantly upregulated from normal to tumor tissue for the individual patients, but did not correlate to any of the clinical data. TDP1 and TOP1 activity were upregulated in 89.3% and 82.7% of the patients, respectively, and correlated in both normal and tumor tissue. The same tendency was observed for protein concentration with an upregulation of TDP1 and TOP1 in 73.0% and 84.4% of the patients, respectively. The activity and protein concentration correlated in normal and tumor tissue for both TDP1 and TOP1. Conclusion: The upregulations of TDP1 and TOP1 from normal to tumor tissue combined with the observation that TDP1 and TOP1 did not correlate to any of the clinical data indicate that both proteins are important for development or maintenance of the tumor cells in NSCLC. Correlations between TDP1 and TOP1 indicate a biological dependency and potential co-regulation of the enzymes. These observations is encouraging in relation to using TOP1 and TDP1 as targets in anticancer treatment of NSCLC.
C1 [Jakobsen, Ann-Katrine; Yuusufi, Sakineh; Stougaard, Magnus] Aarhus Univ, Dept Clin Med, DK-8200 Aarhus N, Denmark.
   [Jakobsen, Ann-Katrine; Yuusufi, Sakineh; Madsen, Line Bille; Stougaard, Magnus] Aarhus Univ Hosp, Dept Pathol, DK-8200 Aarhus N, Denmark.
   [Meldgaard, Peter] Aarhus Univ Hosp, Dept Oncol, DK-8200 Aarhus N, Denmark.
   [Knudsen, Birgitta R.] Aarhus Univ, Dept Mol Biol & Genet, DK-8000 Aarhus C, Denmark.
C3 Aarhus University; Aarhus University; Aarhus University; Aarhus
   University
RP Stougaard, M (corresponding author), Aarhus Univ, Dept Clin Med, DK-8200 Aarhus N, Denmark.; Stougaard, M (corresponding author), Aarhus Univ Hosp, Dept Pathol, DK-8200 Aarhus N, Denmark.
OI Knudsen, Birgitta Ruth/0000-0002-3484-3802; Meldgaard,
   Peter/0000-0002-5788-4463; Stougaard, Magnus/0000-0001-7456-902X;
   Jakobsen, Ann-Katrine/0000-0001-9922-7819
FU Kobmand Sven Hansen og hustru Ina Hansens Fond; Agnes og Poul Friis Fond
   [81008-003]; Fabrikant Einar Willumsens Mindelegat [500028]
FX This work was supported by Kobmand Sven Hansen og hustru Ina Hansens
   Fond, Agnes og Poul Friis Fond [81008-003], and Fabrikant Einar
   Willumsens Mindelegat [500028].
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NR 54
TC 4
Z9 4
U1 1
U2 15
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0169-5002
EI 1872-8332
J9 LUNG CANCER
JI Lung Cancer
PD FEB
PY 2022
VL 164
BP 23
EP 32
DI 10.1016/j.lungcan.2021.12.010
PG 10
WC Oncology; Respiratory System
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Respiratory System
GA 0Y0VP
UT WOS:000790115600004
PM 34974222
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Chen, QC
   Wu, CR
   Zhao, H
   Wu, JX
   Zhao, JJ
   Bi, XY
   Li, ZY
   Huang, Z
   Zhang, YF
   Zhou, JG
   Cai, JQ
AF Chen, Qichen
   Wu, Chaorui
   Zhao, Hong
   Wu, Jianxiong
   Zhao, Jianjun
   Bi, Xinyu
   Li, Zhiyu
   Huang, Zhen
   Zhang, Yefan
   Zhou, Jianguo
   Cai, Jianqiang
TI Neo-adjuvant Chemotherapy-Induced Neutropenia Is Associated with
   Histological Responses and Outcomes after the Resection of Colorectal
   Liver Metastases
SO JOURNAL OF GASTROINTESTINAL SURGERY
LA English
DT Article
DE Colorectal cancer liver metastasis; Liver resection; Neo-adjuvant
   chemotherapy; Neutropenia; Histological response; Prognosis
ID TREATMENT EFFICACY; HEPATIC RESECTION; CANCER PATIENTS; SOLID TUMORS;
   SURVIVAL; SARCOPENIA; TOXICITY; SURGERY; ADULTS
AB Background Neutropenia, the major adverse event in chemotherapy, is associated with favourable clinical outcome in several solid tumours. We aimed to investigate the predictive value of neo-adjuvant chemotherapy (NAC)-induced neutropenia for the pathological response and prognosis in colorectal liver metastases (CRLM) patients. Methods A retrospective review was performed in 141 CRLM patients receiving NAC followed by liver resection. A logistic regression was applied to analyse potential predictors. A Cox proportional hazards analysis was used to analyse survival. Results Neutropenia due to NAC was observed in 42.6% (60/141) of all patients, and grade 3/4 neutropenia was noted in 31.7% (19/60). A pathological response (tumour regression grade (TRG) 1-3) was reported in 46.1% (65/141) of patients. Multivariate analysis showed that neutropenia significantly predicted the favourable pathological response (OR = 3.718, 95% CI 1.716-8.329, P = 0.001), as well as targeted therapy, good differentiation and preoperative CEA < 10 ng/ml as independent predictors of favourable histological response. Of the patients, 54.6% (77/141) had postoperative complications, including 28 major complications (28/77, 36.4%). Severe neutropenia significantly predicted postoperative major complications in multivariate analysis (OR = 4.077, 95% CI 1.184-14.038, P = 0.026). Compared to patients without neutropenia, patients with neutropenia had significantly better progression-free survival (PFS) (P = 0.007; mPFS, 10.2 months vs. 6.7 months). Patients with histological response had significantly better PFS than patients with no histological response (P = 0.001; mPFS, 10.0 months vs. 5.5 months). According to multivariate analyses, neutropenia was a significant predictor for better PFS (HR = 0.613, 95% CI 0.406-0.925, P = 0.020) but not OS. Conclusions For CRLM patients receiving NAC followed by liver resection, NAC-induced neutropenia was a significant predictor of favourable pathological response, postoperative major complications and better prognosis, which makes it useful for CRLM patients in guiding treatment approaches and prognosis assessments.
C1 [Chen, Qichen; Zhao, Hong; Wu, Jianxiong; Zhao, Jianjun; Bi, Xinyu; Li, Zhiyu; Huang, Zhen; Zhang, Yefan; Zhou, Jianguo; Cai, Jianqiang] Chinese Acad Med Sci & Peking Union Med Coll, Natl Clin Res Ctr Canc, Dept Hepatobiliary Surg, Natl Canc Ctr,Canc Hosp, Beijing 100021, Peoples R China.
   [Wu, Chaorui] Chinese Acad Med Sci & Peking Union Med Coll, Natl Clin Res Ctr Canc, Dept Pancreat & Gastr Surg, Natl Canc Ctr,Canc Hosp, Beijing 100021, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Cancer Institute & Hospital - CAMS; Peking Union Medical College;
   Chinese Academy of Medical Sciences - Peking Union Medical College;
   Cancer Institute & Hospital - CAMS; Peking Union Medical College
RP Zhou, JG (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Natl Clin Res Ctr Canc, Dept Hepatobiliary Surg, Natl Canc Ctr,Canc Hosp, Beijing 100021, Peoples R China.
EM zjgty@hotmail.com
RI Cai, Jun/GLS-4538-2022; Zhang, Hongyang/IAR-1565-2023; Zhao,
   Jianjun/ABE-2301-2021; li, zy/HZM-1892-2023; Zhao, Hong/IUQ-0043-2023
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NR 41
TC 14
Z9 14
U1 2
U2 6
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1091-255X
EI 1873-4626
J9 J GASTROINTEST SURG
JI J. Gastrointest. Surg.
PD MAR
PY 2020
VL 24
IS 3
BP 659
EP 670
DI 10.1007/s11605-019-04202-3
PG 12
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA LE0ZC
UT WOS:000526452000020
PM 30937711
DA 2025-01-04
ER

PT J
AU Zmigrodzka, M
   Rzepecka, A
   Krzyzowska, M
   Witkowska-Pilaszewicz, O
   Cywinska, A
   Winnicka, A
AF Zmigrodzka, M.
   Rzepecka, A.
   Krzyzowska, M.
   Witkowska-Pilaszewicz, O.
   Cywinska, A.
   Winnicka, A.
TI THE CYCLOOXYGENASE-2/PROSTAGLANDIN E<sub>2</sub> PATHWAY AND ITS ROLE IN
   THE PATHOGENESIS OF HUMAN AND DOG HEMATOLOGICAL MALIGNANCIES
SO JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
LA English
DT Review
DE cyclooxygenase 2; prostaglandin E-2; hematologic malignances; cancer
   stem cells; cell proliferation; apoptosis; leukemia
ID ACUTE MYELOID-LEUKEMIA; NF-KAPPA-B; REGULATORY T-CELLS; NONSTEROIDAL
   ANTIINFLAMMATORY DRUGS; ACUTE LYMPHOBLASTIC-LEUKEMIA; TUMOR-ASSOCIATED
   MACROPHAGES; PROSTAGLANDIN E-2; COLORECTAL-CANCER; COX-2 INHIBITORS;
   TARGETED THERAPY
AB The overexpression of cyclooxygenase-2 (COX-2) has been documented in many types of cancer occurring in humans and animals. Increasing evidences have shown that the overexpression of COX-2 and increased production of prostaglandin E-2 (PGE(2)) correlate with poor prognosis in human solid tumours and hematological malignancies. Both, in vitro and in vivo studies have demonstrated that increased proliferation of cancer cells as well as an impairment of anti-tumour immunity are influenced by the overexpression of this enzyme. In leukemia and lymphoma, an increased activity of COX-2 and subsequent increase in prostaglandins (PGs) concentration allow cancer cells to evade immune response and contribute to metastases. Cancer stem cells (CSCs) in tumour microenvironment, suppression of innate and adaptive immunity depends on COX-2/PGE(2) axis activity which increases in hematological malignancies. Cyclooxygenases inhibitors block the formation of PGs, consequently inhibiting angiogenesis, and in some malignancies they decrease cancer cells proliferation and tumour invasiveness. They also increase apoptosis of CSCs and cancer cells, decrease their drug resistance as well as enhance the host immune response. Therefore COX-2/PGE(2) axis suppressors: selective COX-2 inhibitors or PG receptors antagonists have been considered as promising anticancer drugs. In comparative oncology dogs are increasingly used as a large animal model because they share the same environmental conditions with people and are exposed to the same environmental factors and also due to their relatively short life span. In dogs, spontaneously occurring non-Hodgkin lymphomas and leukemias have a large number of genetic and morphological features that are similar to those of humans' corresponding cancers. This, additionally makes the species a useful model for the study of new therapeutic strategies in human oncology. While the influence of COX-2 activity and PGE(2) receptors have been evaluated extensively in human cancer, their role in veterinary oncology still needs to be elucidated.
C1 [Zmigrodzka, M.; Rzepecka, A.; Witkowska-Pilaszewicz, O.; Cywinska, A.; Winnicka, A.] Warsaw Univ Life Sci, Dept Pathol & Vet Diagnost, Fac Vet Med, 159C Nowoursynowska St, PL-02776 Warsaw, Poland.
   [Krzyzowska, M.] Mil Inst Hyg & Epidemiol, Warsaw, Poland.
   [Witkowska-Pilaszewicz, O.] Poznan Univ Life Sci, Fac Vet Med & Anim Sci, Dept Internal Dis & Vet Diagnost, Poznan, Poland.
C3 Warsaw University of Life Sciences; Military Institute of Hygiene &
   Epidemiology (MIHE); Poznan University of Life Sciences
RP Zmigrodzka, M (corresponding author), Warsaw Univ Life Sci, Dept Pathol & Vet Diagnost, Fac Vet Med, 159C Nowoursynowska St, PL-02776 Warsaw, Poland.
EM mzmigro@gmail.com
RI Cywinska, Anna/AAD-2890-2020; Krzyzowska, Malgorzata/KTI-0649-2024
OI Krzyzowska, Malgorzata/0000-0002-8409-3974; Cywinska,
   Anna/0000-0002-5365-9218; Winnicka, Anna/0000-0001-9918-3430;
   Zmigrodzka, Magdalena/0000-0003-0880-9093; Witkowska-Pilaszewicz,
   Olga/0000-0002-3541-5914
FU Department of Pathology and Veterinary Diagnostic, Faculty of Veterinary
   Medicine, Warsaw University of Life Science (WULS SGGW); NCN (National
   Science Centre, Poland) MINIATURA [2017/01/X/NZ5/01481]; NCN (National
   Science Centre, Poland) [2015/17/N/NZ5/00663]
FX The financial assistance of the Department of Pathology and Veterinary
   Diagnostic, Faculty of Veterinary Medicine, Warsaw University of Life
   Science (WULS SGGW), NCN (National Science Centre, Poland) MINIATURA
   grant number 2017/01/X/NZ5/01481 (to M.Z) and NCN (National Science
   Centre, Poland) grant number 2015/17/N/NZ5/00663 (to A.R.).
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NR 119
TC 23
Z9 24
U1 0
U2 3
PU POLISH PHYSIOLOGICAL SOC
PI GRZEGORZECKA
PA JAGIELLONIAN UNIV SCHOOL MED, INST PHYSIOLOGY, 31-531 KRAKOW, 16
   GRZEGORZECKA, POLAND
SN 0867-5910
J9 J PHYSIOL PHARMACOL
JI J. Physiol. Pharmacol.
PD OCT
PY 2018
VL 69
IS 5
BP 653
EP 661
DI 10.26402/jpp.2018.5.01
PG 9
WC Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Physiology
GA HJ3LN
UT WOS:000457073300001
PM 30683818
DA 2025-01-04
ER

PT J
AU Mourtzikou, A
   Stamouli, M
   Karakitsos, P
   Athanasas, G
AF Mourtzikou, Antonia
   Stamouli, Marilena
   Karakitsos, Petros
   Athanasas, Georgios
TI Colorectal Cancer CTCs Detection Using Two FCM Protocol Approaches
SO CLINICAL LABORATORY
LA English
DT Article
DE CTCs (Circulating Tumor Cells); DTCs (Disseminating Tumor Cells);
   Colorectal Cancer (CRC); PBMCs (Peripheral Blood Mononuclear Cells);
   RT-PCR; PCR; Flow Cytometry; WBC (White Blood Cells)
ID CIRCULATING TUMOR-CELLS; FLOW-CYTOMETRY; BREAST-CANCER; ENUMERATION;
   CAPTURE; BLOOD
AB Background: The presence and quantification of circulating tumor cells (CTCs) could minimize the mortality among cancer patients by tailored, personalized, and targeted therapy and could also help in the field of investigation about new therapeutic targets. Identification of CTCs has been performed using molecular techniques and more advanced automated techniques such as CellSearch (R) and Amnis (R). Our aim was to test the possibility of identifying CTCs in colorectal cancer patients using a lower cost and less complex flow cytometry-based method.
   Methods: Besides the CellSearch (R) system for CTCs enumeration and Amnis (R) Imaging Flow Cytometers, which are both commercially available, we tested and developed two FCM protocol approaches after immunomagnetic enrichment for CTCs enumeration in the blood of colorectal cancer patients. The CTCs numbers were assessed at baseline before anesthesia and the curative surgery and day one after the curative surgery. Blood from healthy donors was used as negative control. The research was performed by the Cyflow (R) Space cytometer (Partec, Munster, Germany).
   Results: In the patient group, the enumeration using the direct protocol with a threshold 3 cells/mL, showed a mean of CTCs before surgery of 32, while after surgery it was 20, with sensitivity (SN) of 49.2% and specificity (SP) of 58.3%. On the other hand, using the intracellular protocol with a threshold of 1 cell/mL in patients' group, the mean of CTCs before surgery was 65 and after surgery it was 60, with a sensitivity (SN) of 62.7% and specificity (SP) of 70%.
   In the intracellular protocol the most significant correlation identified was for the expression of CKs with adenocarcinomas (r = 0.256, p = 0.044), with the existence of lymph node infiltration (r = 0.380, p = 0.008), and with the stage of the disease (r = 0.391, p = 0.003). For the direct protocol, considerable correlation was found with the samples of the right colon (r = 0.369, p = 0.002).
   Conclusions: Our findings demonstrate that we established two FCM low cost protocol approaches to detect and enumerate CTCs in colorectal cancer patients. In both FCM protocols (direct and intracellular) we observed a statistically significant increase (p < 0.05) of CTCs number in the patient group. No statistical significance (p < 0.05) of CTCs before and after surgery in patient group in both protocols was observed.
C1 [Mourtzikou, Antonia; Karakitsos, Petros] Univ Athens, Attikon Univ Hosp, Sch Med, Dept Cytopathol, Athens, Greece.
   [Stamouli, Marilena] Naval & Vet Hosp, Dept Biochem, Athens, Greece.
   [Athanasas, Georgios] Univ Athens, Attikon Univ Hosp, Sch Med, Surg Dept 4, Athens, Greece.
C3 University Hospital Attikon; National & Kapodistrian University of
   Athens; Athens Medical School; National & Kapodistrian University of
   Athens; Athens Medical School; University Hospital Attikon
RP Mourtzikou, A (corresponding author), Univ Gen Hosp Attikon, Haidari 12461, Greece.
EM antoniamour@med.uoa.gr
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NR 24
TC 2
Z9 2
U1 0
U2 1
PU CLIN LAB PUBL
PI HEIDELBERG
PA IM BREITSPIEL 15, HEIDELBERG, D-69126, GERMANY
SN 1433-6510
J9 CLIN LAB
JI Clin. Lab.
PY 2019
VL 65
IS 6
BP 989
EP 1000
DI 10.7754/Clin.Lab.2018.181035
PG 12
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA IE8LM
UT WOS:000472624900013
PM 31232030
DA 2025-01-04
ER

PT J
AU Gao, YY
   Kruithof-de Julio, M
   Peng, RW
   Dorn, P
AF Gao, Yanyun
   Kruithof-de Julio, Marianna
   Peng, Ren-Wang
   Dorn, Patrick
TI Organoids as a Model for Precision Medicine in Malignant Pleural
   Mesothelioma: Where Are We Today?
SO CANCERS
LA English
DT Review
DE mesothelioma; organoids; tumor model; drug screens; precision medicine
ID PLURIPOTENT STEM-CELLS; COLORECTAL-CANCER; IN-VITRO; LUNG-CANCER; MOUSE
   MODEL; HUMAN COLON; PATIENT; CULTURES; BIOLOGY; COMBINATION
AB Simple Summary Malignant pleural mesothelioma (MPM) is an extremely lethal cancer, notoriously known for its limited treatment options, lack of targeted therapies, and catastrophic survival rates. MPM tumors are highly heterogeneous and exhibit substantial variance in the genome landscape among individual patients, characterized by widespread loss-of-function mutations of tumor suppressor genes (TSGs) that are difficult to target. Therefore, there is an urgent and unmet need for novel therapeutic targets and strategies for personalized treatment. Patient-derived organoids (PDOs), the next generation tumor models that have significantly influenced the discovery of anticancer drugs and biomarkers of response to therapies in many other cancers, are emerging and promise to play a critical role in understanding the biology of MPM and, importantly, in identifying and developing precision oncology approaches tailored to specific subsets of MPM patients. MPM is an aggressive tumor originating from pleural mesothelial cells. A characteristic feature of the disease is the dominant prevalence of therapeutically intractable inactivating alterations in TSGs, making MPM one of the most difficult cancers to treat and the epitome of a cancer characterized by a significant lack of therapy options and an extremely poor prognosis (5-year survival rate of only 5% to 10%). Extensive interpatient heterogeneity poses another major challenge for targeted therapy of MPM, warranting stratified therapy for specific subgroups of MPM patients. Accurate preclinical models are critical for the discovery of new therapies and the development of personalized medicine. Organoids, an in vitro 'organ-like' 3D structure derived from patient tumor tissue that faithfully mimics the biology and complex architecture of cancer and largely overcomes the limitations of other existing models, are the next-generation tumor model. Although organoids have been successfully produced and used in many cancers, the development of MPM organoids is still in its infancy. Here, we provide an overview of recent advances in cancer organoids, focusing on the progress and challenges in MPM organoid development. We also elaborate the potential of MPM organoids for understanding MPM pathobiology, discovering new therapeutic targets, and developing personalized treatments for MPM patients.
C1 [Gao, Yanyun; Peng, Ren-Wang; Dorn, Patrick] Univ Bern, Univ Hosp Bern, Dept Gen Thorac Surg, Inselspital, CH-3008 Bern, Switzerland.
   [Gao, Yanyun; Peng, Ren-Wang; Dorn, Patrick] Univ Bern, Dept BioMed Res DBMR, Oncol Thorac Malignancies OTM, CH-3008 Bern, Switzerland.
   [Kruithof-de Julio, Marianna] Univ Bern, Dept BioMed Res DBMR, Urol Res Lab, CH-3008 Bern, Switzerland.
   [Kruithof-de Julio, Marianna] Univ Bern, Dept BioMed Res DBMR, Translat Organoid Res, CH-3008 Bern, Switzerland.
   [Kruithof-de Julio, Marianna] Univ Hosp Bern, Dept Urol, Inselspital, CH-3008 Bern, Switzerland.
C3 University of Bern; University Hospital of Bern; University of Bern;
   University of Bern; University of Bern; University of Bern; University
   Hospital of Bern
RP Peng, RW; Dorn, P (corresponding author), Univ Bern, Univ Hosp Bern, Dept Gen Thorac Surg, Inselspital, CH-3008 Bern, Switzerland.; Peng, RW; Dorn, P (corresponding author), Univ Bern, Dept BioMed Res DBMR, Oncol Thorac Malignancies OTM, CH-3008 Bern, Switzerland.
EM yanyun.gao@dbmr.unibe.ch; marianna.kruithofdejulio@dbmr.unibe.ch;
   renwang.peng@insel.ch; patrick.dorn@insel.ch
RI Gao, Yanyun/JJE-5144-2023; Peng, Ren-Wang/AAM-8542-2021
OI Kruithof-de Julio, Marianna/0000-0002-6085-7706; PENG,
   REN-WANG/0000-0003-1199-6520; Gao, Yanyun/0000-0002-1226-3073
FU Swiss Cancer League [KFS-4851-273 08-2019]; Swiss National Science
   Foundation [310030_192648]; Swiss National Science Foundation (SNF)
   [310030_192648] Funding Source: Swiss National Science Foundation (SNF)
FX This work was supported by grants from the Swiss Cancer League
   (#KFS-4851-273 08-2019; to R-W.P.) and the Swiss National Science
   Foundation (SNSF; #310030_192648; to R.-W.P.).
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NR 111
TC 5
Z9 5
U1 1
U2 9
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD AUG
PY 2022
VL 14
IS 15
AR 3758
DI 10.3390/cancers14153758
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3R7RH
UT WOS:000839104800001
PM 35954422
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Alig, AHS
   Modest, DP
   Stintzing, S
   Heinrich, K
   Geissler, M
   von Weikersthal, LF
   Decker, T
   Vehling-Kaiser, U
   Held, S
   Moosmann, N
   Stahler, A
   Tannapfel, A
   Giessen-Jung, C
   Jung, A
   Weiss, L
   Heinemann, V
AF Alig, A. H. S.
   Modest, D. P.
   Stintzing, S.
   Heinrich, K.
   Geissler, M.
   von Weikersthal, L. Fischer
   Decker, T.
   Vehling-Kaiser, U.
   Held, S.
   Moosmann, N.
   Stahler, A.
   Tannapfel, A.
   Giessen-Jung, C.
   Jung, A.
   Weiss, L.
   Heinemann, V.
TI Impact of primary tumor sidedness and sex on prognosis and
   anti-epidermal growth factor receptor antibody efficacy in<i>
   BRAF</i>-mutant metastatic colorectal cancer: a pooled analysis of AIO
   studies FIRE-1, CIOX, FIRE-3, XELAVIRI, and VOLFI
SO ESMO OPEN
LA English
DT Article
DE BRAF mutation; EGFR antibody; metastatic colorectal cancer; primary
   tumor location; primary tumor sidedness
ID FOLFIRI PLUS BEVACIZUMAB; PROGRESSION-FREE SURVIVAL; 1ST-LINE TREATMENT;
   OPEN-LABEL; MICROSATELLITE INSTABILITY; RAS MUTATIONS; KRAS MUTATION;
   CETUXIMAB; CHEMOTHERAPY; METAANALYSIS
AB Background: Primary tumor (PT) sidedness is an established prognostic marker in metastatic colorectal cancer (mCRC) and has a predictive impact on the efficacy fi cacy of anti-epidermal growth factor receptor (anti-EGFR) antibody [monoclonal antibody (mAb)] in patients with RAS wild-type mCRC. This investigation focuses on patients with BRAF V600E-mutated (BRAFmt) BRAF mt) mCRC and examines the efficacy fi cacy of anti-EGFR mAbs in relation to primary tumor sidedness (PTS). Patient and methods: This pooled analysis was carried out using individual patient data from fi ve randomized studies in the fi rst-line setting of mCRC. The population of interest was limited to patients with BRAFmt mt mCRC and known PTS. For analysis, treatment was stratified fi ed into two groups: those treated with anti-EGFR mAbs and those without. Dichotomous variables, such as overall response rate and objective response rate (ORR), were compared using chi-square or Fisher's ' s exact test. Time-to-event endpoints [progression-free survival (PFS) and overall survival (OS)] were analyzed using the Kaplan- Meier method, log-rank test, and Cox regression. An interaction test was carried out via Cox regression. Results: A total of 102 patients with BRAFmt mt mCRC were identified. fi ed. The type of targeted therapy (anti-EGFR-based versus non-anti-EGFR) did not significantly fi cantly impact the outcome. However, in patients with left-sided primary tumors, anti-EGFR mAb-based treatment, compared with non-anti-EGFR, was associated with a higher ORR (58% versus 34%; P < 0.01), trended toward improved PFS [hazard ratio (HR) 0.62; 95% confidence fi dence interval (CI) 0.341.13; P = 0.12], and demonstrated prolonged OS (HR 0.38; 95% CI 0.20-0.72; P < 0.01). In patients with right-sided primary tumors, anti-EGFR-based therapy had no effect on ORR (33% versus 36%; P > 0.99), induced inferior PFS (HR 1.97; 95% CI 1.12-3.47; P = 0.02), and trended toward a worse OS (HR 1.76; 95% CI 0.99-3.13; P = 0.05). Conclusion: This analysis suggests that PTS has predictive value for the efficacy fi cacy of anti-EGFR mAb in the fi rst-line treatment of BRAFmt mt mCRC.
C1 [Alig, A. H. S.; Modest, D. P.; Stintzing, S.; Stahler, A.; Giessen-Jung, C.] Charite Univ Med Berlin, Berlin, Germany.
   [Alig, A. H. S.; Modest, D. P.; Stintzing, S.; Stahler, A.; Giessen-Jung, C.] Free Univ Berlin, Berlin, Germany.
   [Alig, A. H. S.; Modest, D. P.; Stintzing, S.; Stahler, A.; Giessen-Jung, C.] Humboldt Univ, Dept Hematol Onol & Tumorimmunol, Berlin, Germany.
   [Heinrich, K.; Weiss, L.; Heinemann, V.] Ludwig Maximilians Univ Munchen, Dept Med 3, Univ Hosp, Munich, Germany.
   [Heinrich, K.; Weiss, L.; Heinemann, V.] Ludwig Maximilians Univ Munchen, Univ Hosp, Comprehens Canc Ctr, Munich, Germany.
   [Heinrich, K.; Decker, T.; Jung, A.; Heinemann, V.] German Canc Consortium DKTK, DKFZ, Munich, Germany.
   [Geissler, M.] Hosp Karlsruhe, Karlsruhe, Germany.
   [von Weikersthal, L. Fischer] Gesundheitszentrum St Marien, Amberg, Germany.
   [Vehling-Kaiser, U.] UBAG MVZ Dr Vehling Kaiser GmbH, Landshut, Germany.
   [Held, S.] ClinAssess GmbH, Leverkusen, Germany.
   [Moosmann, N.] Clin Barmherzige Brider Regensburg, Regensburg, Germany.
   [Tannapfel, A.] Ruhr Univ Bochum, Inst Pathol, Bochum, Germany.
   [Jung, A.] Univ Munich, Inst Pathol, Munich, Germany.
C3 Berlin Institute of Health; Free University of Berlin; Humboldt
   University of Berlin; Charite Universitatsmedizin Berlin; Free
   University of Berlin; Humboldt University of Berlin; University of
   Munich; University of Munich; Helmholtz Association; German Cancer
   Research Center (DKFZ); Municipal Hospital Karlsruhe; Ruhr University
   Bochum; University of Munich
RP Alig, AHS (corresponding author), Charite Univ Med Berlin, Dept Hematol Oncol & Tumorimmunol, Campus Charite Mitte, Charitepl 1, D-10117 Berlin, Germany.
EM annabel.alig@charite.de
RI Stintzing, Sebastian/I-4538-2016
OI Stintzing, Sebastian/0000-0002-3297-5801; Alig,
   Annabel/0000-0002-3922-3450; Held, Swantje/0000-0002-1344-9056
FU LMU by Pfizer; CIOX by Merck-Darmstadt; CIOX by Roche; CIOX by Pfizer;
   FIRE-3 by Merck-Darmstadt; FIRE-3 by Pfizer; XELAVIRI by Roche; AIO
   Studien gGmbH by Amgen
FX This work was supported by the hospital of the university (LMU) which
   was the legal sponsor of FIRE-1 (supported by Pfizer) , CIOX (supported
   by Merck-Darmstadt; Roche and Pfizer) , FIRE-3 (supported by
   Merck-Darmstadt and Pfizer) , and XELAVIRI (supported by Roche) (no
   grant number) . The AIO Studien gGmbH was the legal sponsor of VOLFI
   (supported by Amgen) . The supporting parties had no role in the design,
   analyses, or decision to submit the data for publication.
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NR 49
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2059-7029
J9 ESMO OPEN
JI ESMO Open
PD SEP
PY 2024
VL 9
IS 9
AR 103677
DI 10.1016/j.esmoop.2024.103677
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA E1Y4E
UT WOS:001301027900001
PM 39173562
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU McLean, J
   Rho, YS
   Kuruba, G
   Mamo, A
   Gilabert, M
   Kavan, T
   Panasci, L
   Melnychuk, D
   Batist, G
   Kavan, P
AF McLean, James
   Rho, Young Soo
   Kuruba, Gayathri
   Mamo, Aline
   Gilabert, Marine
   Kavan, Tomas
   Panasci, Lawrence
   Melnychuk, David
   Batist, Gerald
   Kavan, Petr
TI Clinical Practice Patterns in Chemotherapeutic Treatment Regimens for
   Metastatic Colorectal Cancer
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE Attrition; Biologic; Discontinuation of therapy; Longitudinal; Real
   world
ID SURVIVAL; FOLFIRI; FLUOROURACIL; AVAILABILITY; BEVACIZUMAB; OXALIPLATIN;
   IRINOTECAN; FOLFOXIRI; THERAPY
AB Patients with metastatic colorectal cancer are now being exposed to an increasing number of therapeutic agents. The present observational retrospective study reports the clinical practice patterns and characterizes how these agents were used and why they were discontinued in the longitudinal course of patient treatment. FOLFOX (5-fluorouracil, leucovorin, oxaliplatin), FOLFIRI (irinotecan, 5-fluorouracil, leucovorin), and bevacizumab were most frequently used. Most patients discontinued treatment because of disease progression.
   Background: The treatment of patients with metastatic colorectal cancer (mCRC) has evolved during the past 2 decades, and patient survival has increased. Consequently, patients are exposed to more chemotherapeutic agents and regimens. Little is known about therapeutic drug sequencing and the factors influencing these choices. Materials and Methods: An observational, retrospective medical record review was conducted of patients with newly diagnosed adult mCRC from January 2002 to September 2013 identified in the McGill University-Jewish General Hospital's local tumor registry. All patients presented with mCRC (stage IV) and received >= 2 cycles and/ or >= 28 days of first-line chemotherapy. The patient demographics, CRC characteristics, treatment patterns, and outcomes were recorded. The reason for changing or halting therapy was also reported. Results: Of the 215 patients who underwent treatment, 74.4% received second-line, 36% third-line, and 16.3% fourth-line treatment. In total, 88% received >= 3 classes of cytotoxic chemotherapy and 80% received >= 1 biologic agent. The most common first-line treatment was FOLFOX (5-fluorouracil, leucovorin, oxaliplatin) (47.4%) or CAPOX (capecitabine, oxaliplatin) (28.8%), and more than one half received bevacizumab (56%). Among the second-and third-line treatments, FOLFIRI (irinotecan, 5-fluorouracil, leucovorin) was the most common (40.3% and 30.3%, respectively), and bevacizumab was the most frequently used biologic agent (48.1% and 39.2%, respectively). For fourth-line treatment and beyond, most patients participated in clinical trials (45.7%) or received panitumumab monotherapy (31.4%). Across the first 4 therapy lines, disease progression was the primary motive for discontinuation (39.5%, 53.8%, 58.2%, and 37.1%). Conclusion: FOLFOX was the most common first-line and FOLFIRI the most common second-and third-line mCRC therapy. Bevacizumab was the most frequently used targeted therapy across all 3 treatment lines. Therapy discontinuation was primarily due to disease progression.
C1 [McLean, James; Rho, Young Soo; Kuruba, Gayathri; Mamo, Aline; Gilabert, Marine; Kavan, Tomas; Panasci, Lawrence; Melnychuk, David; Batist, Gerald; Kavan, Petr] McGill Univ, Sir Mortimer B Davis Jewish Gen Hosp, Segal Canc Ctr, Dept Med Oncol, Montreal, PQ H3T 1E2, Canada.
   [Panasci, Lawrence; Melnychuk, David; Batist, Gerald; Kavan, Petr] McGill Univ, Faulty Med, Dept Oncol, Montreal, PQ H3T 1E2, Canada.
C3 McGill University; McGill University
RP Kavan, P (corresponding author), McGill Univ, Sir Mortimer B Davis Jewish Gen Hosp, Segal Canc Ctr, Dept Oncol, 3755 Cote Ste Catherine, Montreal, PQ H3T 1E2, Canada.
EM petr.kavan@mcgill.ca
OI Rho, Young Soo/0000-0003-0296-9950
CR Abrams TA, 2014, JNCI-J NATL CANCER I, V106, DOI 10.1093/jnci/djt371
   Adam R, 2004, ANN SURG, V240, P1052, DOI 10.1097/01.sla.0000145964.08365.01
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NR 14
TC 28
Z9 29
U1 1
U2 3
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1533-0028
EI 1938-0674
J9 CLIN COLORECTAL CANC
JI Clin. Colorectal Canc.
PD JUN
PY 2016
VL 15
IS 2
BP 135
EP 140
DI 10.1016/j.clcc.2015.10.003
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DN9NR
UT WOS:000377407000014
PM 26553578
DA 2025-01-04
ER

PT J
AU Sever, T
   Ellidokuz, EB
   Basbinar, Y
   Ellidokuz, H
   Yilmaz, ÖH
   Calibasi-Kocal, G
AF Sever, Tolga
   Ellidokuz, Ender Berat
   Basbinar, Yasemin
   Ellidokuz, Hulya
   Yilmaz, Omer H.
   Calibasi-Kocal, Gizem
TI Beta-Hydroxybutyrate Augments Oxaliplatin-Induced Cytotoxicity by
   Altering Energy Metabolism in Colorectal Cancer Organoids
SO CANCERS
LA English
DT Article
DE colorectal cancer; organoid; beta-hydroxybutyrate; oxaliplatin; reactive
   oxygen species; metabolic targeted therapy
ID HUMAN COLON; IN-VITRO; CELLS; MELATONIN; ANTIOXIDANT
AB Simple Summary One of the hallmarks of cancer is the deregulation of cellular metabolism. The study investigates the potency of the administration of beta-hydroxybutyrate (BOHB) to elevate oxaliplatin's cytotoxic effect in colorectal cancer. The study employed an in vitro organoid model to assess this dual treatment. The results exhibited that non-toxic doses (7.5 and 10mM) of BOHB with oxaliplatin treatment significantly increased the cytotoxic effect of oxaliplatin in colorectal cancer organoids by altering energy metabolism, leading to higher levels of reactive oxygen species (ROS). Opposingly, healthy colon organoids were not affected by the dual treatment as in colorectal cancer organoids. Melatonin was found to neutralize this effect by protecting cancer cells from oxidative stress. The study suggests that BOHB may improve the effectiveness of chemotherapy, particularly with drugs that have a similar mechanism of action to oxaliplatin, in treating colorectal cancer, potentially leading to better outcomes for patients.Abstract Deregulation of cellular metabolism has recently emerged as a notable cancer characteristic. This reprogramming of key metabolic pathways supports tumor growth. Targeting cancer metabolism demonstrates the potential for managing colorectal cancer. Beta-hydroxybutyrate (BOHB) acts as an acetyl-CoA source for the tricarboxylic acid (TCA) cycle, possibly redirecting energy metabolic pathways towards the TCA cycle that could enhance sensitivity to oxaliplatin, through the generation of reactive oxygen species (ROS). This study explores the potential of BOHB to enhance oxaliplatin's cytotoxic effect by altering the energy metabolism in colorectal cancer. The study employed advanced in vitro organoid technology, which successfully emulates in vivo physiology. The combination treatment efficacy of BOHB and oxaliplatin was evaluated via cell viability assay. The levels of key proteins involved in energy metabolism, apoptotic pathways, DNA damage markers, and histone acetylation were analyzed via Western Blot. ROS levels were evaluated via flow cytometer. Non-toxic doses of BOHB with oxaliplatin significantly amplified cytotoxicity in colorectal cancer organoids. Treatment with BOHB and/or melatonin resulted in significantly decreased lactate dehydrogenase A and increased mitochondrial carrier protein 2 levels, indicating inhibited aerobic glycolysis and an increased oxidative phosphorylation rate. This metabolic shift induced apoptotic cell death mediated by oxaliplatin, owing to high levels of ROS. Melatonin counteracted this effect by protecting cancer cells from high oxidative stress conditions. BOHB may enhance the efficacy of chemotherapeutics with a similar mechanism of action to oxaliplatin in colorectal cancer treatment. These innovative combinations could improve treatment outcomes for colorectal cancer patients.
C1 [Sever, Tolga] Dokuz Eylul Univ, Inst Hlth Sci, Dept Translat Oncol, TR-35340 Izmir, Turkiye.
   [Ellidokuz, Ender Berat] Dokuz Eylul Univ, Fac Med, Dept Internal Dis, Gastroenterol, TR-35340 Izmir, Turkiye.
   [Basbinar, Yasemin; Calibasi-Kocal, Gizem] Dokuz Eylul Univ, Inst Oncol, Dept Translat Oncol, TR-35340 Izmir, Turkiye.
   [Ellidokuz, Hulya] Dokuz Eylul Univ, Inst Oncol, Dept Prevent Oncol, TR-35340 Izmir, Turkiye.
   [Yilmaz, Omer H.; Calibasi-Kocal, Gizem] MIT, David H Koch Inst Integrat Canc Res, Dept Biol, Cambridge, MA 02139 USA.
   [Yilmaz, Omer H.] Broad Inst MIT & Harvard, Cambridge, MA 02142 USA.
   [Yilmaz, Omer H.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
   Harvard Med Sch, Boston, MA USA.
C3 Dokuz Eylul University; Dokuz Eylul University; Dokuz Eylul University;
   Dokuz Eylul University; Massachusetts Institute of Technology (MIT);
   Harvard University; Massachusetts Institute of Technology (MIT); Broad
   Institute; Harvard University; Massachusetts General Hospital; Harvard
   University; Harvard Medical School
RP Calibasi-Kocal, G (corresponding author), Dokuz Eylul Univ, Inst Oncol, Dept Translat Oncol, TR-35340 Izmir, Turkiye.; Calibasi-Kocal, G (corresponding author), MIT, David H Koch Inst Integrat Canc Res, Dept Biol, Cambridge, MA 02139 USA.
EM ohyilmaz@mit.edu; gizem.calibasi@deu.edu.tr
RI Sever, Tolga/ABB-1222-2020; Ellidokuz, Hülya/Q-4049-2019; Basbinar,
   Yasemin/AFW-2981-2022; Calibasi Kocal, Gizem/G-1761-2014
OI Calibasi Kocal, Gizem/0000-0002-3201-4752
FU Dokuz Eylul University, Scientific Research Projects Coordination Unit
   [TDK-2021-2610]; Domestic Doctoral Scholarship Program [TUBITAK 2211A];
   Overseas Doctoral Research Scholarship Program [2214]; Council of Higher
   Education 100/2000 scholarship in priority field program
FX The study was supported with project number TDK-2021-2610 by Dokuz Eylul
   University, Scientific Research Projects Coordination Unit. TS was
   supported by TUBITAK 2211A Domestic Doctoral Scholarship Program, 2214
   Overseas Doctoral Research Scholarship Program, and Council of Higher
   Education 100/2000 scholarship in priority field program.
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NR 36
TC 1
Z9 1
U1 2
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD DEC
PY 2023
VL 15
IS 24
AR 5724
DI 10.3390/cancers15245724
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DG6B2
UT WOS:001130903200001
PM 38136270
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Segelov, E
   Waring, P
   Desai, J
   Wilson, K
   Gebski, V
   Thavaneswaran, S
   Elez, E
   Underhill, C
   Pavlakis, N
   Chantrill, L
   Nott, L
   Jefford, M
   Khasraw, M
   Day, F
   Wasan, H
   Ciardiello, F
   Karapetis, C
   Joubert, W
   van Hazel, G
   Haydon, A
   Price, T
   Tejpar, S
   Tebbutt, N
   Shapiro, J
AF Segelov, Eva
   Waring, Paul
   Desai, Jayesh
   Wilson, Kate
   Gebski, Val
   Thavaneswaran, Subotheni
   Elez, Elena
   Underhill, Craig
   Pavlakis, Nick
   Chantrill, Lorraine
   Nott, Louise
   Jefford, Michael
   Khasraw, Mustafa
   Day, Fiona
   Wasan, Harpreet
   Ciardiello, Fortunato
   Karapetis, Chris
   Joubert, Warren
   van Hazel, Guy
   Haydon, Andrew
   Price, Tim
   Tejpar, Sabine
   Tebbutt, Niall
   Shapiro, Jeremy
TI ICECREAM: randomised phase II study of cetuximab alone or in combination
   with irinotecan in patients with metastatic colorectal cancer with
   either <i>KRAS</i>, <i>NRAS</i>, <i>BRAF</i> and <i>PI3KCA</i> wild
   type, or G13D mutated tumours
SO BMC CANCER
LA English
DT Article
DE Colorectal tumours; Cetuximab; Irinotecan; Clinical trial; Tumour
   mutations
ID PLUS; MUTATIONS
AB Background: Patients with metastatic colorectal cancer whose disease has progressed on oxaliplatin-and irinotecan-containing regimens may benefit from EGFR-inhibiting monoclonal antibodies if they do not contain mutations in the KRAS gene (are "wild type"). It is unknown whether these antibodies, such as cetuximab, are more efficacious in refractory metastatic colorectal cancer as monotherapy, or in combination with irinotecan. Lack of mutation in KRAS, BRAF and PIK3CA predicts response to EFGR-inhibitors. The ICECREAM trial examines the question of monotherapy versus combination with chemotherapy in two groups of patients: those with a "quadruple wild type" tumour genotype (no mutations in KRAS, NRAS, PI3KCA or BRAF genes) and those with the specific KRAS mutation in codon G13D, for whom possibly EGFR-inhibitor efficacy may be equivalent.
   Methods and design: ICECREAM is a randomised, phase II, open-label, controlled trial comparing the efficacy of cetuximab alone or with irinotecan in patients with "quadruple wild type" or G13D-mutated metastatic colorectal cancer, whose disease has progressed on, or who are intolerant of oxaliplatin-and fluoropyrimidine-based chemotherapy. The primary endpoint is the 6-month progression-free survival benefit of the treatment regimen. Secondary endpoints are response rate, overall survival, and quality of life. The tertiary endpoint is prediction of outcome with further biological markers. International collaboration has facilitated recruitment in this prospective trial of treatment in these infrequently found molecular subsets of colorectal cancer.
   Discussion: This unique trial will yield prospective information on the efficacy of cetuximab and whether this is further enhanced with chemotherapy in two distinct populations of patients with metastatic colorectal cancer: the "quadruple wild type", which may 'superselect' for tumours sensitive to EGFR-inhibition, and the rare KRAS G13D mutated tumours, which are also postulated to be sensitive to the drug. The focus on establishing both positive and negative predictive factors for the response to targeted therapy is an attempt to improve outcomes, reduce toxicity and contain treatment costs. Tissue and blood will yield a resource for molecular studies. Recruitment, particularly of patients with the rare G13D mutation, will demonstrate the ability for international collaboration to run prospective trials in small colorectal cancer molecular subgroups.
C1 [Segelov, Eva] Univ New S Wales, St Vincents Clin Sch, Sydney, NSW, Australia.
   [Waring, Paul] Univ Melbourne, Melbourne, Vic, Australia.
   [Desai, Jayesh] Royal Melbourne Hosp, Melbourne, Vic, Australia.
   [Desai, Jayesh; Jefford, Michael] Peter MacCallum Canc Ctr, Melbourne, Vic, Australia.
   [Wilson, Kate; Gebski, Val; Thavaneswaran, Subotheni; Khasraw, Mustafa] Univ Sydney, NHMRC Clin Trials Ctr, Sydney, NSW 2006, Australia.
   [Elez, Elena] Vall dHebron Univ Hosp, Barcelona, Spain.
   [Underhill, Craig] Border Med Oncol, Albury, NSW, Australia.
   [Pavlakis, Nick] Univ Sydney, Royal N Shore Hosp, Northern Canc Inst, Sydney, NSW 2006, Australia.
   [Chantrill, Lorraine] Campbelltown Hosp, Macarthur Canc Therapy Ctr, Sydney, NSW, Australia.
   [Chantrill, Lorraine] Kinghorn Canc Ctr, Sydney, NSW, Australia.
   [Nott, Louise] Royal Hobart Hosp, Hobart, Tas, Australia.
   [Khasraw, Mustafa] Andrew Love Canc Ctr, Geelong, Vic, Australia.
   [Day, Fiona] Univ Newcastle, Calvary Mater Newcastle, Newcastle, NSW 2300, Australia.
   [Wasan, Harpreet] Hammersmith Hosp, London, England.
   [Ciardiello, Fortunato] Univ Naples 2, Oncol Med, Naples, Italy.
   [Karapetis, Chris] Flinders Med Ctr, Adelaide, SA, Australia.
   [Joubert, Warren] Princess Alexandra Hosp, Brisbane, Qld 4102, Australia.
   [van Hazel, Guy] Sir Charles Gairdner Hosp, Perth, WA 6000, Australia.
   [Haydon, Andrew] Alfred Hosp, Melbourne, Vic, Australia.
   [Price, Tim] Lyell McEwin Hosp, Queen Elizabeth Hosp, Adelaide, SA, Australia.
   [Tejpar, Sabine] Univ Hosp Leuven, Campus Gasthuisberg, Leuven, Belgium.
   [Tebbutt, Niall] Austin Hosp, Melbourne, Vic 3084, Australia.
   [Shapiro, Jeremy] Cabrini Hosp, Melbourne, Vic, Australia.
C3 University of New South Wales Sydney; University of Melbourne; Melbourne
   Health; Royal Melbourne Hospital; Peter Maccallum Cancer Center;
   University of Sydney; Hospital Universitari Vall d'Hebron; Royal North
   Shore Hospital; University of Sydney; Northern Cancer Institute; NSW
   Health; Campbelltown Hospital; The Kinghorn Cancer Centre; Royal Hobart
   Hospital; Calvary Mater Newcastle Hospital; University of Newcastle;
   Imperial College London; Universita della Campania Vanvitelli; Flinders
   Medical Centre; Princess Alexandra Hospital; University of Western
   Australia; Sir Charles Gairdner Hospital; Florey Institute of
   Neuroscience & Mental Health; Lyell McEwin Hospital; KU Leuven;
   University Hospital Leuven; Florey Institute of Neuroscience & Mental
   Health; Austin Research Institute; Cabrini Health
RP Segelov, E (corresponding author), Univ New S Wales, St Vincents Clin Sch, Sydney, NSW, Australia.
EM e.segelov@unsw.edu.au
RI Segelov, Eva/Q-7611-2019; Élez, Elena/AAH-2945-2019; Underhill,
   Craig/ABB-8092-2020; Chantrill, Lorraine/GXF-5117-2022; Desai,
   Jayesh/AAV-1237-2021; Price, Timothy/G-1404-2012; Khasraw,
   Mustafa/ABH-5962-2020; Gebski, Val/HNJ-2164-2023
OI Chantrill, Lorraine/0000-0002-5790-0208; Desai,
   Jayesh/0000-0003-4246-9344; Segelov, Eva/0000-0002-4410-6144; Gebski,
   Val/0000-0001-8748-1844; Karapetis, Christos/0000-0003-1741-996X;
   Jefford, Michael/0000-0002-8792-7807; Day, Fiona/0000-0002-5905-9408;
   Wilson, Kate/0000-0003-1886-4280; Elez, Elena/0000-0002-4653-6324;
   Wasan, Harpreet/0000-0002-6268-2030; Underhill,
   Craig/0000-0001-9335-2678; Khasraw, Mustafa/0000-0003-3249-9849
FU Merck Serono Australia Pty Ltd.
FX Unrestricted educational grant to AGITG from Merck Serono Australia Pty
   Ltd.
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NR 20
TC 14
Z9 14
U1 1
U2 9
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD MAY 31
PY 2016
VL 16
AR 339
DI 10.1186/s12885-016-2389-8
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DN3KB
UT WOS:000376959700001
PM 27246726
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Rebersek, M
   Mesti, T
   Boc, M
   Ocvirk, J
AF Rebersek, Martina
   Mesti, Tanja
   Boc, Marko
   Ocvirk, Janja
TI Molecular biomarkers and histological parameters impact on survival and
   response to first- line systemic therapy of metastatic colorectal cancer
   patients
SO RADIOLOGY AND ONCOLOGY
LA English
DT Article
DE metastatic colorectal cancer; chemotherapy; targeted therapy;
   histological parameters; biomarkers
ID CETUXIMAB PLUS IRINOTECAN; BRAF V600E MUTATION; KRAS CODON 12;
   MONOCLONAL-ANTIBODIES; SLOVENE PATIENTS; STAGE-II; CHEMOTHERAPY; COLON;
   ASSOCIATION; MANAGEMENT
AB Background. Histological parameters of primary tumour and nodal metastases are prognostic factors for survival of operable colorectal (CRC) patients, but not predictive for response rate of systemic therapy. KRAS mutations in codons 12 and 13 were first recognized as a predictive factor for resistance to anti-EGFR monoclonal antibodies. Not all patients with wild-type KRAS (wtKRAS) respond to anti-EGFR antibody treatment. Additional mechanisms of resistance may activate mutations of the other main EGFR effectors pathway, such as other mutations in RAS gene, mutations in P13K and PTEN expression.
   Patients and methods. In the prospective study prognostic and predictive impact of histological parameters of primary tumour, KRAS and BRAF mutations on overall survival (OS) and objective response (OR) rate of metastatic CRC (mCRC) patients treated with 1ST line systemic therapy were analysed. We additionally retrospectively analysed other mutations in RAS genes and their impact on survival and time to progression.
   Results. From November 2010 to December 2012, we enrolled 154 patients in the study, 95 men and 59 women. Mutations in KRAS gene and V600E BRAF gene were found in 42% and in 3% of patients, respectively. Median OS of the patients with T1, T2 and T3 tumour was 65.4 months (95% CI, 55.7-75.6) while in patients with T4 tumour, lymphangiosis, vascular and perineural invasion it has not been reached yet. Median OS of the patients with G1, G2 and G3 of tumour differentiation was 65.6 (95% CI, 53.7-77.5) and 25.3 months (95% CI, 16.6-34.1), respectively. Median OS of the patients with stage N0, N1 and N2 was 65.6 (95% CI, 56.4-74.8) and 58.0 months (95% CI, 21.9-94.2), respectively. Median OS of wtKRAS and mutated KRAS patients was 56.5 (95% CI, 48.2-64.9) and 58 months (95% CI, 52.6-63.4), respectively. Median OS of mutated codon 12 and codon 13 patients was 57 (95% CI, 50.9-64.4) and 44 months (95% CI, 40.1-48.4), respectively. Median OS of wtBRAF and of mutated BRAF patients was 59.2 (95% CI, 52.5-65.9) and 27.6 months (95% CI, 12.6-42.5), respectively. wtKRAS significantly affected the response to the first systemic therapy (p = 0.028), while other parameters did not affected it, p= 0.07. In 14 patients (17%), additional mutations in NRAS gene, codon 61 and codon 146 were found. Median OS of wtNRAS, codon 61 and 146 patients was 67.1 months (50.3-67.6) while median OS of mutated NRAS patients has not been reached yet (p = 0.072). Median time to progression of wtNRAS, codon 61 and 146 patients was 11.7 months (10.4-14.5) while median time to progression of mutated NRAS patients was 7.9 months (6.1-11.0), (p = 0.025).
   Conclusions. Mutated BRAF, N2 and G3 of primary tumour were poor prognostic factors for OS in mCRC patients. wtKRAS significantly affected the response to the first line systemic therapy. Histological parameters included in the analysis and mutated BRAF did not affect significantly the efficacy of line systemic therapy in mCRC patients.
C1 [Rebersek, Martina; Mesti, Tanja; Boc, Marko; Ocvirk, Janja] Inst Oncol Ljubljana, Dept Med Oncol, Zaloska 2, SI-1000 Ljubljana, Slovenia.
C3 Institute of Oncology - Slovenia
RP Ocvirk, J (corresponding author), Inst Oncol Ljubljana, Dept Med Oncol, Zaloska 2, SI-1000 Ljubljana, Slovenia.
EM jocvirk@onko-i.si
FU Slovenian Research Ageny (ARRS) [P3-0321]
FX The research was founded by Slovenian Research Ageny (ARRS), grant
   number P3-0321.
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NR 48
TC 4
Z9 5
U1 1
U2 3
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1318-2099
EI 1581-3207
J9 RADIOL ONCOL
JI Radiol. Oncol.
PD MAR
PY 2019
VL 53
IS 1
BP 85
EP 95
DI 10.2478/raon-2019-0013
PG 11
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA HM2YP
UT WOS:000459337800011
PM 30840593
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kalantzis, I
   Nonni, A
   Pavlakis, K
   Delicha, EM
   Miltiadou, K
   Kosmas, C
   Ziras, N
   Gkoumas, K
   Gakiopoulou, H
AF Kalantzis, Ioannis
   Nonni, Afroditi
   Pavlakis, Kitty
   Delicha, Eumorphia-Maria
   Miltiadou, Konstantinos
   Kosmas, Christos
   Ziras, Nikolaos
   Gkoumas, Konstantinos
   Gakiopoulou, Harikleia
TI Clinicopathological differences and correlations between right and left
   colon cancer
SO WORLD JOURNAL OF CLINICAL CASES
LA English
DT Article
DE Colorectal neoplasm; Epidermal growth factor; Vascular endothelial
   growth factor; Histology; Molecular biology; Metabolic syndrome
ID PLUS CHEMOTHERAPY
AB BACKGROUND The differences in histopathology and molecular biology between right colon cancer (RCC) and left colon cancer (LCC) were first reported in the literature by Bufill in 1990. Since then, a large number of studies have confirmed their differences in epidemiology, clinical presentation, comorbidities and biological behaviours, which may be related to the difference in prognosis and overall survival (OS) between the two groups.
   AIM To investigate statistically significant differences between Greek patients with LCC and RCC.
   METHODS The present observational study included 144 patients diagnosed with colon cancer of any stage who received chemotherapy in a Greek tertiary oncology hospital during a 2.5-year period. Clinical information, comorbidities, histopathologic characteristics and molecular biomarkers were collected from the patients' medical records retrospectively, while administered chemotherapy regimens, targeted agents, progression-free survival (PFS) periods with first- and second-line chemotherapy and OS were recorded retroactively and prospectively. Data analysis was performed with the SPSS statistical package.
   RESULTS Eighty-six males and 58 females participated in the study. One hundred (69.4%) patients had a primary lesion in the left colon, and 44 (30.6%) patients had a primary lesion in the right colon. Patients with RCC were more likely to display anaemia than patients with LCC [odds ratio (OR) = 3.09], while LCC patients were more likely to develop rectal bleeding (OR = 3.37) and a feeling of incomplete evacuation (OR = 2.78) than RCC patients. Considering comorbidities, RCC patients were more likely to suffer from diabetes (OR = 3.31) and coronary artery disease (P = 0.056) than LCC patients. The mucinous differentiation rate was higher in the right-sided group than in the left-sided group (OR = 4.49), as was the number of infiltrated lymph nodes (P = 0.039), while the percentage of high-grade differentiation was higher in the group of patients with left-sided colon cancer than in RCC patients (OR = 2.78). RAS wild-type patients who received anti-epidermal growth factor receptor (EGFR): Treatment experienced greater benefit (PFS: 16.5 mo) than those who received anti-vascular endothelial growth factor treatment (PFS: 13.7 mo) (P = 0.05), while among RAS wild-type patients who received anti-EGFR treatment, LCC patients experienced greater benefit (PFS: 15.8 mo) than the RCC subgroup (PFS: 5.5 mo) in the first-line chemotherapy setting (P = 0.034). BRAF-mutant patients had shorter PFS (9.3 mo) than BRAF wild-type patients (14.5 mo) (P = 0.033). RCC patients showed a shorter tumour recurrence period (7.7 mo) than those with LCC (14.5 mo) (P < 0.001), as well as shorter (OS) (58.4 mo for RCC patients; 82.4 mo for LCC patients) (P = 0.018).
   CONCLUSION RCC patients present more comorbidities, worse histological and molecular characteristics and a consequently higher probability of tumour recurrence, poor response to targeted therapy and shorter OS than LCC patients.
C1 [Kalantzis, Ioannis; Gkoumas, Konstantinos] Korgialenio Mpenakeio Hellen Red Cross Hosp, Dept Gastroenterol, 2 Athanasaki St, Athens 11526, Greece.
   [Kalantzis, Ioannis; Miltiadou, Konstantinos; Kosmas, Christos; Ziras, Nikolaos] Metaxa Anticanc Hosp, Dept Oncol, Piraeus 18537, Greece.
   [Nonni, Afroditi; Pavlakis, Kitty; Gakiopoulou, Harikleia] Natl & Kapodistrian Univ Athens, Med Sch, Dept Pathol 1, Athens 11527, Greece.
   [Delicha, Eumorphia-Maria] ASTAT, Stat Clin Res, Glifadha 16675, Greece.
   [Miltiadou, Konstantinos] Attikon Univ, Gen Hosp, Hepatogastroenterol Unit, Dept Internal Med 2, Athens 12462, Greece.
C3 National & Kapodistrian University of Athens; University Hospital
   Attikon
RP Kalantzis, I (corresponding author), Korgialenio Mpenakeio Hellen Red Cross Hosp, Dept Gastroenterol, 2 Athanasaki St, Athens 11526, Greece.
EM johnkalantzis@hotmail.com
RI Gkoumas, Konstantinos/JCE-0450-2023; Kosmas, Christos/ABG-4070-2021;
   Kosmas, Christos/HKV-7389-2023
OI Kosmas, Christos/0000-0001-6790-5785
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NR 39
TC 17
Z9 17
U1 1
U2 5
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 2307-8960
J9 WORLD J CLIN CASES
JI World J. Clin. Cases
PD APR 26
PY 2020
VL 8
IS 8
BP 1424
EP 1443
DI 10.12998/wjcc.v8.i8.1424
PG 20
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA LO4HQ
UT WOS:000533590700008
PM 32368535
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Majumder, A
AF Majumder, Avisek
TI HER3: Toward the Prognostic Significance, Therapeutic Potential, Current
   Challenges, and Future Therapeutics in Different Types of Cancer
SO CELLS
LA English
DT Review
DE targeted therapy; structure-function analyses; small-molecule
   inhibitors; monoclonal antibody; antibody-drug conjugate (ADC);
   epidermal growth factor receptor (EGFR); human epidermal growth factor
   receptor 2 (HER2); non-small cell lung cancers (NSCLC); breast cancer
ID GROWTH-FACTOR-RECEPTOR; HUMAN-BREAST-CANCER; SQUAMOUS-CELL CARCINOMA;
   ANTI-HER3 MONOCLONAL-ANTIBODY; PHASE-1 DOSE-ESCALATION; TYROSINE KINASE;
   PATIENTS PTS; PHOSPHATIDYLINOSITOL 3-KINASE; COLORECTAL-CANCER;
   METASTATIC BREAST
AB Human epidermal growth factor receptor 3 (HER3) is the only family member of the EGRF/HER family of receptor tyrosine kinases that lacks an active kinase domain (KD), which makes it an obligate binding partner with other receptors for its oncogenic role. When HER3 is activated in a ligand-dependent (NRG1/HRG) or independent manner, it can bind to other receptors (the most potent binding partner is HER2) to regulate many biological functions (growth, survival, nutrient sensing, metabolic regulation, etc.) through the PI3K-AKT-mTOR pathway. HER3 has been found to promote tumorigenesis, tumor growth, and drug resistance in different cancer types, especially breast and non-small cell lung cancer. Given its ubiquitous expression across different solid tumors and role in oncogenesis and drug resistance, there has been a long effort to target HER3. As HER3 cannot be targeted through its KD with small-molecule kinase inhibitors via the conventional method, pharmaceutical companies have used various other approaches, including blocking either the ligand-binding domain or extracellular domain for dimerization with other receptors. The development of treatment options with anti-HER3 monoclonal antibodies, bispecific antibodies, and different combination therapies showed limited clinical efficiency for various reasons. Recent reports showed that the extracellular domain of HER3 is not required for its binding with other receptors, which raises doubt about the efforts and applicability of the development of the HER3-antibodies for treatment. Whereas HER3-directed antibody-drug conjugates showed potentiality for treatment, these drugs are still under clinical trial. The currently understood model for dimerization-induced signaling remains incomplete due to the absence of the crystal structure of HER3 signaling complexes, and many lines of evidence suggest that HER family signaling involves more than the interaction of two members. This review article will significantly expand our knowledge of HER3 signaling and shed light on developing a new generation of drugs that have fewer side effects than the current treatment regimen for these patients.
C1 [Majumder, Avisek] Univ Calif San Francisco, Dept Med, San Francisco, CA 94158 USA.
C3 University of California System; University of California San Francisco
RP Majumder, A (corresponding author), Univ Calif San Francisco, Dept Med, San Francisco, CA 94158 USA.
EM avisek.majumder@ucsf.edu
RI Majumder, Avisek/AAO-9296-2020
OI Majumder, Avisek/0000-0002-6761-2242
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NR 205
TC 12
Z9 12
U1 2
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD NOV
PY 2023
VL 12
IS 21
AR 2517
DI 10.3390/cells12212517
PG 29
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA X7NK8
UT WOS:001100271600001
PM 37947595
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Myint, ZW
   Sun, RMC
   Hensley, PJ
   James, AC
   Wang, P
   Strup, SE
   McDonald, RJ
   Yan, DL
   St Clair, WH
   Allison, DB
AF Myint, Zin W.
   Sun, Ramon C.
   Hensley, Patrick J.
   James, Andrew C.
   Wang, Peng
   Strup, Stephen E.
   McDonald, Robert J.
   Yan, Donglin
   St Clair, William H.
   Allison, Derek B.
TI Evaluation of Glutaminase Expression in Prostate Adenocarcinoma and
   Correlation with Clinicopathologic Parameters
SO CANCERS
LA English
DT Article
DE glutaminase; immunohistochemistry; in situ methods; prostate; prognosis
ID TUMOR MICROENVIRONMENT; COLORECTAL-CANCER; CELL-GROWTH; METABOLISM;
   INHIBITOR; HYPOXIA; CB-839
AB Simple Summary
   High expression levels of glutaminase (GLS1) are reported for several cancers, and correlate with parameters of disease status. GLS1, the rate-limiting enzyme in the glutamine pathway, is involved in DNA/RNA and amino acid synthesis and contributes to other pathways (e.g., TCA cycle). Inhibition of GLS1 has shown anti-tumor activity in both solid tumors and hematological malignancies. The CB-839 agent, a novel GLS1 inhibitor, has been under investigation clinically. GLS1 expression by immunohistochemical (IHC) staining in prostate has not been definitively demonstrated. We present a retrospective study evaluating GLS1 expression utilizing The Cancer Genome Atlas (TCGA) RNA-Seq data and by IHC in formalin-fixed paraffin embedded radical prostatectomy samples. The study showed a significant difference in GLS1 levels between cancer and non-cancer, but fell short as a prognostic marker. As the study cohort was skewed to less aggressive localized prostate cancer, we support further studies that incorporate high-risk and very high-risk localized and metastatic prostate cancers.
   High Glutaminase (GLS1) expression may have prognostic implications in colorectal and breast cancers; however, high quality data for expression in prostate cancer (PCa) are lacking. The purpose of this study is to investigate the status of GLS1 expression in PCa and correlated expression levels with clinicopathologic parameters. This study was conducted in two phases: an exploratory cohort analyzing RNA-Seq data for GLS1 from The Cancer Genome Atlas (TCGA) data portal (246 PCa samples) and a GLS1 immunohistochemical protein expression cohort utilizing a tissue microarray (TMA) (154 PCa samples; 41 benign samples) for correlation with clinicopathologic parameters. In the TCGA cohort, GLS1 mRNA expression did not show a statistically significant difference in disease-free survival (DFS) but did show a small significant difference in overall survival (OS). In the TMA cohort, there was no correlation between GLS1 expression and stage, Gleason score, DFS and OS. GLS1 expression did not significantly correlate with the clinical outcomes measured; however, GLS1 expression was higher in PCa cells compared to benign epithelium. Future studies are warranted to evaluate expression levels in greater numbers of high-grade and advanced PCa samples to investigate whether there is a rational basis for GLS1 targeted therapy in a subset of patients with prostate cancer.
C1 [Myint, Zin W.; Wang, Peng] Univ Kentucky, Div Med Oncol, Dept Internal Med, Lexington, KY 40536 USA.
   [Myint, Zin W.; Sun, Ramon C.; James, Andrew C.; Wang, Peng; Strup, Stephen E.; Yan, Donglin; St Clair, William H.; Allison, Derek B.] Univ Kentucky, Markey Canc Ctr, Lexington, KY 40536 USA.
   [Sun, Ramon C.] Univ Kentucky, Coll Med, Dept Neurosci, Lexington, KY 40536 USA.
   [Hensley, Patrick J.] Univ Texas MD Anderson Canc Ctr, Dept Urol, Houston, TX 77030 USA.
   [James, Andrew C.; Strup, Stephen E.; Allison, Derek B.] Univ Kentucky, Dept Urol, Lexington, KY 40536 USA.
   [McDonald, Robert J.; Allison, Derek B.] Univ Kentucky, Dept Pathol & Lab Med, Lexington, KY 40536 USA.
   [Yan, Donglin] Univ Kentucky, Dept Internal Med Hlth Serv Res, Lexington, KY 40536 USA.
   [St Clair, William H.] Univ Kentucky, Dept Radiat Med, Lexington, KY 40536 USA.
C3 University of Kentucky; University of Kentucky; University of Kentucky;
   University of Texas System; UTMD Anderson Cancer Center; University of
   Kentucky; University of Kentucky; University of Kentucky; University of
   Kentucky
RP Myint, ZW (corresponding author), Univ Kentucky, Div Med Oncol, Dept Internal Med, Lexington, KY 40536 USA.; Myint, ZW (corresponding author), Univ Kentucky, Markey Canc Ctr, Lexington, KY 40536 USA.
EM zin.myint@uky.edu; ramon.sun@uky.edu; hpatrick1@mdanderson.org;
   andrew.james@uky.edu; p.wang@uky.edu; Stephen.Strup@uky.edu;
   rmcdonald@uky.edu; donglin.yan@uky.edu; stclair@email.uky.edu;
   Derek.Allison@uky.edu
RI wang, peng/AAV-1896-2020; James, Anna/AAY-9937-2021; ALLISON,
   Derek/AAL-8028-2021; Liu, XiaoYan/GQA-7216-2022
OI Allison, Derek/0000-0002-5119-2474; Hensley,
   Patrick/0000-0002-8098-901X; Myint, Zin/0000-0002-3479-4203; Yan,
   Donglin/0000-0002-5111-9437; Sun, Ramon/0000-0002-3009-1850
FU NCI Cancer Center Support Grant [P30 CA177558]
FX The University of Kentucky Markey Cancer Center's Research
   Communications Office assisted with manuscript preparation, the
   Biostatistics and Bioinformatics Shared Resource Facility provided
   statistical support, and the Biospecimen Procurement & Translational
   Pathology Shared Resource Facility provided IHC preparation and staining
   support; these Shared Resource Facilities are supported by NCI Cancer
   Center Support Grant (P30 CA177558).
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NR 31
TC 15
Z9 17
U1 1
U2 11
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD MAY
PY 2021
VL 13
IS 9
AR 2157
DI 10.3390/cancers13092157
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SB4MS
UT WOS:000649971100001
PM 33947068
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Golan, T
   Casolino, R
   Biankin, AV
   Hammel, P
   Whitaker, KD
   Hall, MJ
   Riegert-Johnson, DL
AF Golan, Talia
   Casolino, Raffaella
   Biankin, Andrew V.
   Hammel, Pascal
   Whitaker, Kristen D.
   Hall, Michael J.
   Riegert-Johnson, Douglas L.
TI Germline BRCA testing in pancreatic cancer: improving awareness, timing,
   turnaround, and uptake
SO THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
LA English
DT Review
DE genetic counseling; genetic testing; germline BRCA mutation; pancreatic
   ductal adenocarcinoma; referral; targeted therapy
ID RANDOMIZED NONINFERIORITY TRIAL; EPITHELIAL OVARIAN-CANCER;
   POPULATION-BASED SAMPLE; DNA-DAMAGE RESPONSE; BREAST-CANCER; TUMOR DNA;
   PRECISION MEDICINE; RACIAL DISPARITIES; COLORECTAL-CANCER; HIGH-GRADE
AB Prognosis is generally poor for patients with pancreatic ductal adenocarcinoma. However, patients with germline BRCA1 or BRCA2 mutations (gBRCAm) may benefit from first-line platinum-based chemotherapy and maintenance therapy with the poly(adenosine diphosphate-ribose) polymerase inhibitor olaparib following at least 16 weeks of first-line platinum-based chemotherapy without disease progression. Germline breast cancer gene (BRCA) testing is therefore important to ensure that patients receive the most effective treatment. In addition, testing for other DNA damage response gene mutations beyond gBRCAm may also guide treatment decisions. However, clinical pathways for genetic testing are often suboptimal, leading to delays in treatment initiation or missed opportunities for personalized therapy. Barriers to testing include low rates of referral and uptake, delays to referral and slow result turnaround times, cost, and biopsy and assay limitations if somatic testing is performed, leading to the requirement for subsequent dedicated germline testing. Low rates of referral may result from lack of awareness among physicians of the clinical value of testing, coupled with low confidence in interpreting test results and poor availability of genetic counseling services. Among patients, barriers to uptake may include similar lack of awareness of the clinical value of testing, anxiety regarding the implications of test results, lack of insurance coverage, fear of negative insurance implications, and socioeconomic factors. Potential solutions include innovative approaches to testing pathways, including 'mainstreaming' of testing in which BRCA tests are routinely arranged by the treating oncologist, with the involvement of genetic counselors if a patient is found to have a gBRCAm. More recently, the utility of multigene panel analyses has also been explored. Access to genetic counseling may also be improved through initiatives such as having a genetic counseling appointment for all new patient visits and telemedicine approaches, including the use of telephone consultations or DVD-assisted counseling. Educational programs will also be beneficial, and cost effectiveness is likely to improve as the number of targeted treatments increases and when the earlier detection of tumors in family members following cascade testing is considered.
C1 [Golan, Talia] Sheba Med Ctr, Inst Oncol, IL-52621 Tel Hashomer, Israel.
   [Golan, Talia] Tel Aviv Univ, Fac Med, IL-69978 Tel Aviv, Israel.
   [Casolino, Raffaella; Biankin, Andrew V.] Univ Glasgow, Inst Canc Sci, Wolfson Wohl Canc Res Ctr, Glasgow City, Scotland.
   [Casolino, Raffaella] Univ & Hosp Trust Verona, Dept Med, Verona, Italy.
   [Biankin, Andrew V.] Glasgow Royal Infirm, West Scotland Pancreat Unit, Glasgow City, Scotland.
   [Biankin, Andrew V.] Univ New South Wales, Fac Med, South Western Sydney Clin Sch, Liverpool, Australia.
   [Hammel, Pascal] Univ Paris Saclay, AP HP, Dept Digest & Med Oncol, Paul Brousse Hosp, Villejuif, France.
   [Whitaker, Kristen D.; Hall, Michael J.] Fox Chase Canc Ctr, Dept Clin Genet, Philadelphia, PA USA.
   [Whitaker, Kristen D.] Fox Chase Canc Ctr, Dept Clin Genet, Philadelphia, PA USA.
   [Riegert-Johnson, Douglas L.] Mayo Clin, Div Clin Genom & Gastroenterol & Hepatol, Jacksonville, FL USA.
C3 Chaim Sheba Medical Center; Tel Aviv University; University of Glasgow;
   University of Verona; Azienda Ospedaliera Universitaria Integrata
   Verona; University of New South Wales Sydney; Assistance Publique
   Hopitaux Paris (APHP); Hopital Universitaire Paul-Brousse - APHP;
   Universite Paris Saclay; Fox Chase Cancer Center; Fox Chase Cancer
   Center; Mayo Clinic
RP Golan, T (corresponding author), Sheba Med Ctr, Inst Oncol, IL-52621 Tel Hashomer, Israel.; Golan, T (corresponding author), Tel Aviv Univ, Fac Med, IL-69978 Tel Aviv, Israel.
EM Talia.Golan@sheba.health.gov.il
FU Medical writing support was provided by Abigail Woollard and Charlie
   Foster, both of Oxford PharmaGenesis, Oxford, UK, and was funded by
   AstraZeneca and Merck Sharp amp;amp; Dohme LLC, a subsidiary of Merck
   amp;amp; Co., Inc., Rahway, NJ, USA.; AstraZeneca; Merck Sharp amp;amp;
   Dohme LLC; Rahway, NJ, USA
FX Medical writing support was provided by Abigail Woollard and Charlie
   Foster, both of Oxford PharmaGenesis, Oxford, UK, and was funded by
   AstraZeneca and Merck Sharp & amp; Dohme LLC, a subsidiary of Merck &
   amp; Co., Inc., Rahway, NJ, USA.
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NR 95
TC 7
Z9 7
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1758-8340
EI 1758-8359
J9 THER ADV MED ONCOL
JI Ther. Adv. Med. Oncol.
PY 2023
VL 15
AR 17588359231189127
DI 10.1177/17588359231189127
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA R7JQ1
UT WOS:001066083900001
PM 37720496
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Gallois, C
   Bergen, ES
   Auclin, E
   Pernot, S
   Higué, J
   Trouilloud, I
   Touchefeu, Y
   Turpin, A
   Mazard, T
   Sartore-Bianchi, A
   Prenen, H
   Alberti, A
   Pilla, L
   Cuissy, S
   Wookey, V
   Perret, A
   Melchior, C
   Artru, P
   Dubreuil, O
   Drouillard, A
   Doat, S
   Lavolé, J
   Basile, D
   Perkins, G
   Jary, M
   Stintzing, S
   Jos, J
   Tougeron, D
   Taieb, J
AF Gallois, C.
   Bergen, E. S.
   Auclin, E.
   Pernot, S.
   Higue, J.
   Trouilloud, I.
   Touchefeu, Y.
   Turpin, A.
   Mazard, T.
   Sartore-Bianchi, A.
   Prenen, H.
   Alberti, A.
   Pilla, L.
   Cuissy, S.
   Wookey, V.
   Perret, A.
   Melchior, C.
   Artru, P.
   Dubreuil, O.
   Drouillard, A.
   Doat, S.
   Lavole, J.
   Basile, D.
   Perkins, G.
   Jary, M.
   Stintzing, S.
   Jos, J.
   Tougeron, D.
   Taieb, J.
TI Efficacy and safety of the combination of encorafenib/cetuximab with or
   without binimetinib in patients with BRAF V600E-mutated metastatic
   colorectal cancer: an AGEO real-world multicenter study
SO ESMO OPEN
LA English
DT Article
DE colorectal cancer; BRAF V600E mutation; encorafenib; targeted therapy;
   real-world study
ID OPEN-LABEL; CETUXIMAB; VEMURAFENIB; INHIBITION; SURVIVAL; MUTATION
AB Background: The combination of encorafenib with cetuximab has become the standard of care in patients with BRAF V600E-mutated metastatic colorectal cancer (mCRC) after a prior systemic therapy. This study aims to describe the efficacy and safety of encorafenib/cetuximab +/- binimetinib in patients with BRAF V600E-mutated mCRC in a real-world setting. Patients and methods: This retrospective study included patients with BRAF V600E-mutated mCRC who received this combination from January 2020 to June 2022 in 30 centers. Results: A total of 201 patients were included, with 55% of women, a median age of 62 years, and an Eastern Cooperative Oncology Group performance status (ECOG-PS) >1 in 20% of cases. The main tumor characteristics were 60% of right-sided primary tumor, 11% of microsatellite instability/mismatch repair deficient phenotype, and liver and peritoneum being the two main metastatic sites (57% and 51%). Encorafenib/cetuximab +/- binimetinib was prescribed in the first, second, third, and beyond third line in 4%, 56%, 29%, and 11%, respectively, of cases, with the encorafenib/cetuximab/binimetinib combination for 21 patients (10%). With encorafenib/cetuximab treatment, 21% of patients experienced grade >= 3 adverse events (AEs), with each type of grade >= 3 AE observed in <5% of patients. The objective response rate was 32.2% and the disease control rate (DCR) was 71.2%. The median progression-free survival (PFS) was 4.5 months [95% confidence interval (CI) 3.9-5.4 months] and the median overall survival (OS) was 9.2 months (95% CI 7.8-10.8 months). In multivariable analysis, factors associated with a shorter PFS were synchronous metastases [hazard ratio (HR) 1.66, P = 0.04] and ECOG-PS >1 (HR 1.88, P = 0.007), and those associated with a shorter OS were the same factors (HR 1.71, P = 0.03 and HR 2.36, P < 0.001, respectively) in addition to treatment beyond the second line (HR 1.74, P = 0.003) and high carcinoembryonic antigen level (HR 1.72, P = 0.003). Conclusion: This real-world study showed that in patients with BRAF V600E-mutated mCRC treated with encorafenib/cetuximab +/- binimetinib, efficacy and safety data confirm those reported in the BEACON registration trial. The main poor prognostic factors for this treatment are synchronous metastases and ECOG-PS >1.
C1 [Gallois, C.; Pilla, L.; Taieb, J.] Paris Cite Univ, Georges Pompidou European Hosp, Dept Gastroenterol & Digest Oncol, SIRIC CARPEM, Paris, France.
   [Bergen, E. S.] Med Univ Vienna, Dept Med 1, Div Oncol, Vienna, Austria.
   [Auclin, E.] Hop Europeen Georges Pompidou, Med & Thorac Oncol Dept, AP HP, Paris, France.
   [Pernot, S.] Inst Bergonie, Dept Med Oncol, Bordeaux, France.
   [Higue, J.] Ctr Hosp Univ Toulouse, Toulouse, France.
   [Trouilloud, I.] Hop St Antoine, Dept Med Oncol, AP HP, Paris, France.
   [Touchefeu, Y.] Ctr Hosp Univ Nantes, Inst Malad Appareil Digest, Digest Oncol, Nantes, France.
   [Turpin, A.] Univ Lille, Dept Med Oncol, Lille, France.
   [Turpin, A.] CHU Lille, CNRS UMR9020, Canther Canc Heterogene Plast & Resistance Therapi, UMR S1277,INSERM, Lille, France.
   [Mazard, T.] Montpellier Canc Inst ICM, Dept Med Oncol, Montpellier, France.
   [Mazard, T.] Univ Montpellier, Inst Rech Cancerol Montpellier IRCM, INSERM U1194, Montpellier, France.
   [Sartore-Bianchi, A.] Univ Milano Niguarda Canc Ctr, Grande Osped Metropolitano Niguarda, Dept Oncol & Hematooncol, Milan, Italy.
   [Prenen, H.] Univ Hosp Antwerp, Edegem, Belgium.
   [Alberti, A.] Univ Brescia, ASST Spedali Civili, Med Oncol, Brescia, Italy.
   [Cuissy, S.] Rouen Univ Hosp, Dept Hepatogastroenterol, Rouen, France.
   [Wookey, V.] Mayo Clin, Dept Oncol, Rochester, MN USA.
   [Perret, A.] Gustave Roussy Canc Ctr, Dept Med Oncol, Villejuif, France.
   [Melchior, C.] Ctr Leon Berard, Dept Med Oncol, Lyon, France.
   [Artru, P.] Hop Jean Mermoz, Hepatogastroenterol Dept, Lyon, France.
   [Dubreuil, O.] Grp Hosp Diaconesses Croix St Simon, Dept Digest Oncol, Paris, France.
   [Drouillard, A.] Dijon Hosp, Dept Hepatogastroenterol, Dijon, France.
   [Doat, S.] Hop La Pitie Salpetriere, Dept Hepatogastroenterol, Paris, France.
   [Lavole, J.] Begin Teaching Mil Hosp, Dept Hepatogastroenterol, St Mande, France.
   [Basile, D.] San Giovanni Dio Hosp, Dept Med Oncol, Crotone, Italy.
   [Perkins, G.] CHRU Pontchaillou, Dept Gastroenterol, Rennes, France.
   [Jary, M.] Univ Hosp Clermont Ferrand, Dept Surg & Med Oncol, Clermont Ferrand, France.
   [Stintzing, S.] Charite Univ Med Berlin, Dept Hematol Oncol & Canc Immunol CCM, Berlin, Germany.
   [Jos, J.] Vall dHebron Univ Hosp, Dept Med Oncol, Barcelona, Spain.
   [Tougeron, D.] Univ Poitiers Hosp, Dept Gastroenterol & Hepatol, Poitiers, France.
C3 Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Europeen Georges-Pompidou - APHP; Medical
   University of Vienna; Assistance Publique Hopitaux Paris (APHP);
   Universite Paris Cite; Hopital Universitaire Europeen Georges-Pompidou -
   APHP; UNICANCER; Institut Bergonie; CHU de Toulouse; Assistance Publique
   Hopitaux Paris (APHP); Sorbonne Universite; Hopital Universitaire
   Saint-Antoine - APHP; Nantes Universite; CHU de Nantes; Universite de
   Lille; Institut National de la Sante et de la Recherche Medicale
   (Inserm); Universite de Lille; CHU Lille; Universite de Montpellier;
   Institut National de la Sante et de la Recherche Medicale (Inserm);
   UNICANCER; Universite de Montpellier; Institut Regional du Cancer
   Montpellier / Val d'Aurelle (ICM); University of Antwerp; Hospital
   Spedali Civili Brescia; University of Brescia; Universite de Rouen
   Normandie; CHU de Rouen; Mayo Clinic; UNICANCER; Gustave Roussy;
   UNICANCER; Centre Leon Berard; Sorbonne Universite; Assistance Publique
   Hopitaux Paris (APHP); Hopital Universitaire Pitie-Salpetriere - APHP;
   Universite de Rennes; CHU Rennes; CHU Clermont Ferrand; Berlin Institute
   of Health; Free University of Berlin; Humboldt University of Berlin;
   Charite Universitatsmedizin Berlin; Hospital Universitari Vall d'Hebron;
   Vall d'Hebron Institut d'Oncologia (VHIO); Universite de Poitiers; CHU
   Poitiers
RP Taieb, J (corresponding author), Georges Pompidou European Hosp, Dept Gastroenterol & Digest Oncol, 20 Rue Leblanc, F-75015 Paris, France.
EM jtaieb75@gmail.com
RI Stintzing, Sebastian/I-4538-2016
OI Prenen, Hans/0000-0001-8802-7352; Ros, Javier/0000-0002-8137-5415
FU Pierre Fabre Laboratories
FX This work was supported by Pierre Fabre Laboratories (no grant number) .
   The sponsor had no involvement in the collection, analysis, or
   interpretation of data nor in the writing of the report or in the
   decision to submit the article for publication. Pierre Fabre
   Laboratories checked the manuscript for scientific fi c accuracy only.
CR André T, 2020, NEW ENGL J MED, V383, P2207, DOI 10.1056/NEJMoa2017699
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NR 36
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2059-7029
J9 ESMO OPEN
JI ESMO Open
PD SEP
PY 2024
VL 9
IS 9
AR 103696
DI 10.1016/j.esmoop.2024.103696
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA G0E7L
UT WOS:001313455200001
PM 39255538
OA gold
DA 2025-01-04
ER

PT J
AU Chen, Y
   Gao, ZT
   Mohd-Ibrahim, I
   Yang, H
   Wu, L
   Fu, YY
   Deng, YP
AF Chen, Yu
   Gao, Zitong
   Mohd-Ibrahim, Isam
   Yang, Hua
   Wu, Lang
   Fu, Yuanyuan
   Deng, Youping
TI Pan-cancer analyses of bromodomain containing 9 as a novel therapeutic
   target reveals its diagnostic, prognostic potential and biological
   mechanism in human tumours
SO CLINICAL AND TRANSLATIONAL MEDICINE
LA English
DT Article
DE BRD9; diagnosis; immune infiltration; m(6)A; PD-1; prognosis; SMARCD1
ID HUMAN PROTEIN ATLAS; SWI/SNF COMPLEX; BRD9; EXPRESSION; SUBUNIT; GENES;
   CELLS
AB Background; Mutations in one or more genes responsible for encoding subunits within the SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin-remodelling complexes are found in approximately 25% of cancer patients. Bromodomain containing 9 (BRD9) is a more recently identified protein coding gene, which can encode SWI/SNF chromatin-remodelling complexes subunits. Although initial evaluations of the potential of BRD9-based targeted therapy have been explored in the clinical application of a small number of cancer types, more detailed study of the diagnostic and prognostic potential, as well as the detailed biological mechanism of BRD9 remains unreported. Methods: We used various bioinformatics tools to generate a comprehensive, pan-cancer analyses of BRD9 expression in multiple disease types described in The Cancer Genome Atlas (TCGA). Experimental validation was conducted in tissue microarrays and cell lines derived from lung and colon cancers. Results: Our study revealed that BRD9 exhibited elevated expression in a wide range of tumours. Analysis of survival data and DNA methylation for BRD9 indicated distinct conclusions for multiple tumours. mRNA splicing and molecular binding were involved in the functional mechanism of BRD9. BRD9 may affect cancer progression through different phosphorylation sites or N6-methyladenosine site modifications. BRD9 could potentially serve as a novel biomarker for diagnosing different cancer types, especially could accurately forecast the prognosis of melanoma patients receiving anti-programmed cell death 1 immunotherapy. BRD9 has the potential to serve as a therapeutic target, when pairing with etoposide in patients with melanoma. The BRD9/SMARCD1 axis exhibited promising discriminative performance in forecasting the prognosis of patients afflicted with liver hepatocellular carcinoma (LIHC) and mesothelioma. Additionally, this axis appears to potentially influence the immune response in LIHC by regulating the programmed death-ligand 1 immune checkpoint. For experimental validation, high expression levels of BRD9 were observed in tumour tissue samples from both lung and colon cancer patients. Knocking down BRD9 led to the inhibition of lung and colon cancer development, likely via the Wnt/beta-catenin signalling pathway. Conclusions: These pan-cancer study revealed the diagnostic and prognostic potential, along with the biological mechanism of BRD9 as a novel therapeutic target in human tumours.
C1 [Chen, Yu; Gao, Zitong; Mohd-Ibrahim, Isam; Yang, Hua; Fu, Yuanyuan; Deng, Youping] Univ Hawaii Manoa, John A Burns Sch Med, Dept Quantitat Hlth Sci, Honolulu, HI USA.
   [Chen, Yu; Gao, Zitong; Mohd-Ibrahim, Isam] Univ Hawaii Manoa, Coll Trop Agr & Human Resources, Dept Mol Biosci & Bioengn, Agr Sci, Honolulu, HI USA.
   [Wu, Lang] Univ Hawaii Manoa, Univ Hawaii Canc Ctr, Populat Sci Pacific Program, Canc Epidemiol Div, Honolulu, HI 96813 USA.
   [Fu, Yuanyuan; Deng, Youping] Univ Hawaii Manoa, John A Burns Sch Med, Dept Quantitat Hlth Sci, 651Ilalo St, Honolulu, HI 96822 USA.
C3 University of Hawaii System; University of Hawaii Manoa; University of
   Hawaii System; University of Hawaii Manoa; University of Hawaii System;
   University of Hawaii Manoa; Cancer Research Center of Hawaii; University
   of Hawaii System; University of Hawaii Manoa
RP Fu, YY; Deng, YP (corresponding author), Univ Hawaii Manoa, John A Burns Sch Med, Dept Quantitat Hlth Sci, 651Ilalo St, Honolulu, HI 96822 USA.
EM fuy@hawaii.edu; dengy@hawaii.edu
RI FU, yuanyuan/LKL-5601-2024; Gao, Zitong/AAR-1723-2021
OI Chen, Yu/0000-0003-1348-8992
FU American Association for Cancer Research [R01CA223490, R01CA230514,
   P30GM114737, P20GM103466, U54MD007601, P30CA071789, P20GM139753,
   U54GM138062, U54HG013243, 1OT2OD032581-02-PP90]; National Institutes of
   Health [22-40-68-FU]; American Association for Cancer Research-Merck
   Cancer Disparities Fellowship
FX This work was supported by the National Institutes of Health grants
   (R01CA223490, R01CA230514, P30GM114737, P20GM103466, U54MD007601,
   P30CA071789, P20GM139753, U54GM138062, U54HG013243 and
   1OT2OD032581-02-PP90) to Youping Deng. This work was also supported by
   the 2022 American Association for Cancer Research-Merck Cancer
   Disparities Fellowship (22-40-68-FU) to Yuanyuan Fu.
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NR 62
TC 1
Z9 1
U1 3
U2 5
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
SN 2001-1326
J9 CLIN TRANSL MED
JI Clin. Transl. Med.
PD FEB
PY 2024
VL 14
IS 2
AR e1543
DI 10.1002/ctm2.1543
PG 24
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA GW9F7
UT WOS:001155821400001
PM 38303608
OA gold
DA 2025-01-04
ER

PT J
AU Lu, XA
   Li, YY
   Li, Y
   Zhang, XM
   Shi, J
   Feng, H
   Yu, Z
   Gao, YQ
AF Lu, Xiaona
   Li, Yuyao
   Li, Yue
   Zhang, Xuemei
   Shi, Jia
   Feng, Hai
   Yu, Zhuo
   Gao, Yueqiu
TI Prognostic and predictive biomarkers for anti-EGFR monoclonal antibody
   therapy in <i>RAS</i> wild-type metastatic colorectal cancer: a
   systematic review and meta-analysis
SO BMC CANCER
LA English
DT Review
DE Colorectal cancer; Prognostic; Predictive value; Biomarkers; Anti-EGFR
   monoclonal antibody
ID GENE COPY NUMBER; GROWTH-FACTOR; PLUS CETUXIMAB; PHASE-III; 1ST-LINE
   TREATMENT; CLINICAL IMPACT; EXPRESSION; PANITUMUMAB; MUTATIONS; BENEFIT
AB Background RAS mutations affect prognosis in patients with metastatic colorectal cancer (mCRC) and have been identified as strong negative predictive markers for anti-epidermal growth factor receptor monoclonal antibody (anti-EGFR mAb) therapy, but many tumors containing wild-type RAS genes still do not respond to these therapies. Some additional biomarkers may have prognostic or predictive roles, but conclusions remain controversial.Methods We performed a meta-analysis and systematic review of randomized controlled trials comparing anti-EGFR mAb therapy with alternative therapy that investigated the prognostic and predictive impact of additional biomarkers in RAS wild-type (wt) mCRC patients. Hazard ratios (HRs) and 95% confidence intervals (CIs) for progression-free survival (PFS) and overall survival (OS) and odds ratios (ORs) for objective response rate (ORR) were calculated. The prognostic value of biomarkers was investigated by separately pooling HR and OR for different treatment groups in an individual study. The predictive value was assessed by pooling study interactions between treatment effects and biomarker subgroups.Results Thirty publications reporting on eighteen trials were selected, including a total of 13,507 patients. In prognostic analysis, BRAF mutations were associated with poorer PFS [HRs = 3.76 (2.47-5.73) and 2.69 (1.82-3.98)] and OS [HRs = 2.66 (1.95-3.65) and 2.45 (1.55-3.88)] in both the experimental and control arms; low miR-31-3p expression appeared to have longer PFS and OS. In terms of predictive effect, a lack of response to anti-EGFR therapy was observed in patients with BRAF mutant tumors (P-interaction < 0.01 for PFS). Patients with tumors with any mutation in the KRAS/NRAS/BRAF/PIK3CA gene also showed similar results compared with all wild-type tumors (P-interaction for PFS, OS, and ORR were < 0.01, < 0.01 and 0.01, respectively). While low miR-31-3p expression could predict PFS (P-interaction = 0.01) and OS (P-interaction = 0.04) benefit. The prognostic and predictive value regarding PIK3CA mutations, PTEN mutations or deletions, EGFR, EREG/AREG, HER2, HER3, and HER4 expression remains uncertain.Conclusions In RAS wt mCRC patients receiving EGFR-targeted therapy, BRAF mutation is a powerful prognostic and therapy-predictive biomarker, with no effect found for PIK3CA mutation, PTEN mutation or deletion, but the combined biomarker KRAS/NRAS/BRAF/PIK3CA mutations predict resistance to anti-EGFR therapy. Low miR-31-3p expression may have positive prognostic and therapy predictive effects. Evidence on the prognostic and predictive roles of EGFR and its ligands, and HER2/3/4 is insufficient.
C1 [Lu, Xiaona; Li, Yuyao; Li, Yue; Zhang, Xuemei; Shi, Jia; Yu, Zhuo; Gao, Yueqiu] Shanghai Univ Tradit Chinese Med, Dept Liver Dis, Shuguang Hosp, Shanghai 201203, Peoples R China.
   [Feng, Hai; Gao, Yueqiu] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Inst Infect Dis, Shanghai 201203, Peoples R China.
C3 Shanghai University of Traditional Chinese Medicine; Shanghai University
   of Traditional Chinese Medicine
RP Yu, Z; Gao, YQ (corresponding author), Shanghai Univ Tradit Chinese Med, Dept Liver Dis, Shuguang Hosp, Shanghai 201203, Peoples R China.; Feng, H; Gao, YQ (corresponding author), Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Inst Infect Dis, Shanghai 201203, Peoples R China.
EM fogsea@163.com; zhuoyu@shutcm.edu.cn; gaoyueqiu@shutcm.edu.cn
RI Yu, Zhuo/AAQ-6164-2020
OI Yu, Zhuo/0000-0003-4100-8415
FU Not applicable.
FX Not applicable.
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NR 100
TC 6
Z9 6
U1 0
U2 1
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD NOV 16
PY 2023
VL 23
IS 1
AR 1117
DI 10.1186/s12885-023-11600-z
PG 27
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA Y6FY1
UT WOS:001106209400003
PM 37974093
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU von Arx, C
   De Placido, P
   Caltavituro, A
   Di Rienzo, R
   Buonaiuto, R
   De Laurentiis, M
   Arpino, G
   Puglisi, F
   Giuliano, M
   Del Mastro, L
AF von Arx, Claudia
   De Placido, Pietro
   Caltavituro, Aldo
   Di Rienzo, Rossana
   Buonaiuto, Roberto
   De Laurentiis, Michelino
   Arpino, Grazia
   Puglisi, Fabio
   Giuliano, Mario
   Del Mastro, Lucia
TI The evolving therapeutic landscape of trastuzumab-drug conjugates:
   Future perspectives beyond HER2-positive breast cancer
SO CANCER TREATMENT REVIEWS
LA English
DT Review
DE ADCs; HER2-low breast cancer; Colon -rectal cancer; Non -small -cell
   lung cancer; Gastric cancer; Trastuzumab
ID DERUXTECAN T-DXD; EMTANSINE T-DM1; OPEN-LABEL; PHASE-III; TAXANE;
   RESISTANCE; TRIAL; GATSBY; ADC; MBC
AB A novel class of drugs, antibody-drug conjugates (ADCs), are now rapidly emerging as highly effective treatments for solid tumours. ADCs conjugate conventional chemotherapeutics with highly selective targeted monoclonal antibodies. Anti-HER2 therapies selectively target cancer cells expressing human epidermal growth factor receptor 2 (HER2), among them trastuzumab has been the first HER2-targeting monoclonal antibody to achieve successful results that made it the backbone of anti-HER2 therapies. Trastuzumab drug conjugates (T-DCs), use trastuzumab as a selective antibody to lead cytotoxic drugs inside cancer cells. Trastuzumab-emtansine (T-DM1) and trastuzumab-deruxtecan (T-Dxd) are the two approved T-DCs. T-Dxd along with other five T-DCs represents "second generation ADCs" that has been firstly tested in HER2 positive breast cancer (BC) and then in HER2-low BC and other cancers showing promising results thanks to extraordinary and innovative pharmacokinetic and pharmacodynamic characteristics. The evidence generated so far are establishing them as a completely new class of agents effective in solid cancer treatments but also war-rants physicians against unconventional toxicity profiles. The role of T-DCs in HER2-positive BC has been largely reviewed, while in this review, we provided for the first time in literature an overview of trastuzumab drug conjugates (T-DCs) approved and/or in clinical devel-opment with a specific focus on their efficacy and safety profile in HER2-low BC and other solid tumours different from BC. We started by analysing T-DCs biological characteristics that underly the differences in T-DCs phar-macodynamics and safety profile, then presented the main evidence on the activity and efficacy of these emerging T-DCs in HER2-low BC and other HER2 overexpressing and/or mutated solid tumours and lastly, we provided an overview of the complex and still evolving scenario in which these compounds should be allocated. A specific focus on possible combination strategies with other drugs such as immunotherapy, chemotherapy and target therapy, to increase T-DCs activity and eventually overcome future upcoming resistance mechanisms, are here also critically reviewed.
C1 [von Arx, Claudia; De Laurentiis, Michelino] Ist Nazl Tumori IRCCS Fdn Pascale, Dept Breast & Thorac Oncol, Via Semmola, Naples, Italy.
   [De Placido, Pietro; Caltavituro, Aldo; Di Rienzo, Rossana; Buonaiuto, Roberto; Arpino, Grazia; Giuliano, Mario] Univ Naples Federico II, Dept Clin Med & Surg, Naples, Italy.
   [Puglisi, Fabio] Ctr Riferimento Oncol Aviano CRO IRCCS, Dept Med Oncol, Unit Med Oncol & Canc Prevent, Aviano, Italy.
   [Puglisi, Fabio] Univ Udine, Dept Med DAME, Udine, Italy.
   [Del Mastro, Lucia] IRCCS Osped Policlin San Martino, Dept Med Oncol, Breast Unit, Genoa, Italy.
   [Del Mastro, Lucia] Univ Genoa, Sch Med, Dept Internal Med & Med Specialties DIMI, Genoa, Italy.
C3 IRCCS Fondazione Pascale; University of Naples Federico II; University
   of Udine; University of Genoa
RP von Arx, C (corresponding author), Ist Nazl Tumori IRCCS Fdn Pascale, Dept Breast & Thorac Oncol, Via Semmola, Naples, Italy.
EM claudia.vonarx@istitutotumori.na.it
RI Del Mastro, Lucia/J-6163-2016; Puglisi, Fabio/N-3863-2017; De
   Laurentiis, Michelino/AAC-6321-2022; DE LAURENTIIS,
   Michelino/K-4934-2018
OI DE LAURENTIIS, Michelino/0000-0001-9009-1572; caltavituro,
   aldo/0000-0001-5952-4333; Arpino, Grazia/0000-0002-4074-2530; De
   Placido, Pietro/0000-0002-1979-5400
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NR 79
TC 43
Z9 43
U1 4
U2 9
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 0305-7372
EI 1532-1967
J9 CANCER TREAT REV
JI Cancer Treat. Rev.
PD FEB
PY 2023
VL 113
AR 102500
DI 10.1016/j.ctrv.2022.102500
EA DEC 2022
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 8H6PU
UT WOS:000921154000001
PM 36587473
DA 2025-01-04
ER

PT J
AU Gerard, JP
   Myint, AS
   Barbet, N
   Dejean, C
   Thamphya, B
   Gal, J
   Montagne, L
   Vuong, T
AF Gerard, Jean-Pierre
   Myint, Arthur Sun
   Barbet, Nicolas
   Dejean, Catherine
   Thamphya, Brice
   Gal, Jocelyn
   Montagne, Lucile
   Vuong, Te
TI Targeted Radiotherapy Using Contact X-ray Brachytherapy 50 kV
SO CANCERS
LA English
DT Article
DE targeted therapy; contact X-ray; brachytherapy; organ preservation
ID ADVANCED RECTAL-CANCER; ORGAN PRESERVATION; PREOPERATIVE
   CHEMORADIOTHERAPY; SPHINCTER PRESERVATION; LOCAL EXCISION; OPEN-LABEL;
   MULTICENTER; CHEMOTHERAPY; RECURRENCE; OUTCOMES
AB Simple Summary Organ preservation is becoming a topic of great interest for rectal cancer. Radiotherapy, often in association with chemotherapy, is playing a major role in achieving tumor sterilization and long-term local control. In order to achieve this goal, a high dose (>70 Gy) of radiotherapy is necessary. To avoid radiation toxicity of such a high dose, an endocavitary approach using contact X-ray 50 kV brachytherapy (CXB) is an attractive method. Historical series and two randomized trials in Europe give good evidence of the merit of CXB. The selection of early tumors is a key prognostic factor to achieve good results. A planned organ preservation treatment using CXB followed by chemoradiotherapy can be proposed to patients with T2-T3 a-b < 3 cm in diameter. At 3 years, the chance of local control should be close to 90% with good bowel function.
   Abstract Rectal adenocarcinoma is a quite radioresistant tumor. In order to achieve non-operative management (NOM) radiotherapy plays a major role. Targeted radiotherapy aiming at high precision 3D radiotherapy uses stereotactic image-guided external beam radiotherapy machines. To further safely increase the tumor dose, endocavitary brachytherapy (ECB) is an original approach. There are two different ways to perform such an ECB: contact X-ray brachytherapy (CXB) using a 50 kV X-ray generator with an X-ray tube positioned under eye guidance into the rectal cavity and high-dose-rate brachytherapy (HDRB) using iridium-192 sources positioned into the rectal cavity under image guidance. This study focused on CXB. CXB uses a small mobile generator that produces 50 kV X-rays with limited penetration. This technique is well adapted to accessible tumors of limited size and especially needs a high dose rate (<greater than or equal to>15 Gy/minutes) for rectal tumors. It is performed on an ambulatory basis. A total dose between 80-110 Gy is delivered in 3-4 fractions over 3 to 6 weeks into a small volume (5 cm(3)). CXB was pioneered in the 1970s by Papillon using the Philips RT 50(TM). Since 2009, the Papillon P50(TM) has been used in 11 institutions in Europe. The OPERA Phase III trial tested the hypothesis that a CXB boost (90 Gy/3 fr) compared to an EBRT boost (9 Gy/5 fr) for T2-T3 ab < 5 cm and N0-N1 < 8 mm will increase the 3-year organ preservation (OP) rate when combined with 45 Gy/5 weeks with concomitant capecitabine. Out of more than 300 patients with tumors < 3 cm (1962-1992), Papillon reported a long-term local control close to 85%. Similar results were published in Europe and USA at that time. The Lyon R96-2 Phase III trial (2004) demonstrated that, when combined with preoperative EBRT, a CXB boost (90 Gy/3 fr) significantly increased the rate of clinical complete response (cCR) and sphincter preservation, with some patients having OP at 10 years. With more than 2000 patients treated in Europe (2010-2020) using the Papillon 50(TM), organ preservation appears possible in close to 80% of cases in selected early T2-T3. The OPERA trial closed after 141 inclusions (2015-2020) after an independent data monitoring committee recommendation because of promising results. At the 2-year follow-up (blinded data), the rate of cCR and OP were 77% and 72%, respectively, for the 141 tumors, and for T < 3 cm (61 pts), they were 86% and 85%, respectively, with good bowel function. The final results should be available in 2022. Organ preservation using NOM appears to be a promising approach for rectal cancer. A CXB boost with chemoradiotherapy in selected early T2-T3 could become an attractive option to achieve a planned OP. This approach should be proposed to well-informed patients after discussion in an MDT.
C1 [Gerard, Jean-Pierre; Dejean, Catherine; Montagne, Lucile] Cote Azur Univ, Ctr Antoine Lacassagne, Dept Radiat Oncol, F-06000 Nice, France.
   [Myint, Arthur Sun] Univ Liverpool, Clatterbrige Canc Ctr, Liverpool L7 8YA, Merseyside, England.
   [Barbet, Nicolas] Bayard Lyon Villeurbanne, ORLAM, Dept Radiat Oncol, F-69100 Lyon, France.
   [Thamphya, Brice; Gal, Jocelyn] Cote Azur Univ, Ctr Antoine Lacassagne, Dept Clin Res Stat, F-06000 Nice, France.
   [Vuong, Te] McGill Univ, Jewish Gen Hosp, Montreal, PQ H3T 1E2, Canada.
C3 UNICANCER; Centre Antoine Lacassagne; Universite Cote d'Azur; University
   of Liverpool; UNICANCER; Centre Antoine Lacassagne; Universite Cote
   d'Azur; McGill University
RP Gerard, JP (corresponding author), Cote Azur Univ, Ctr Antoine Lacassagne, Dept Radiat Oncol, F-06000 Nice, France.
EM jean-pierre.gerard@nice.unicancer.fr; sun.myint@nhs.net;
   barbet71@wanadoo.fr; catherine.dejean@nice.unicancer.fr;
   brice.thamphya@nice.unicancer.fr; jocelyn.gal@nice.unicancer.fr;
   lucile.montagne@nice.unicancer.fr; te.vuong@mcgill.ca
RI Dejean, Catherine/AGA-1605-2022; Myint, Arthur/AAO-7695-2020
OI GERARD, Jean-Pierre/0000-0002-2599-8140; DEJEAN,
   Catherine/0000-0002-5158-7249; Gal, Jocelyn/0000-0002-1802-118X
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NR 29
TC 6
Z9 6
U1 2
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD MAR
PY 2022
VL 14
IS 5
AR 1313
DI 10.3390/cancers14051313
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZT1BE
UT WOS:000768890000001
PM 35267621
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Li, Y
   Xu, YL
   Cai, SF
   Li, JW
   Ruan, FY
   Xia, CR
   Luo, P
   Li, J
AF Li, Yun
   Xu, Yali
   Cai, Shifeng
   Li, Jingwen
   Ruan, Fangying
   Xia, Chaoran
   Luo, Peng
   Li, Jun
TI Combination of microwave ablation and systemic treatments achieve a long
   survival time for a patient with metachronous advanced double primary
   lung and colon adenocarcinoma: A case report
SO ONCOLOGY LETTERS
LA English
DT Article
DE metachronous advanced lung and colon adeno-carcinoma; EGFR 19 exon
   deletion; EGFR-TKI; microwave ablation; chemotherapy
ID CANCER; MUTATION
AB Despite significant improvements that have been made in terms of progression-free survival and overall survival rates brought about by targeted therapy in non-small cell lung cancer (NSCLC), the emergence of drug resistance remains a limiting factor. However, a previous study has shown promising results by combining local microwave ablation (MWA) with epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) therapy for patients with oligometastatic NSCLC. The current study presented the case of a Chinese female patient who was identified as having lung adenocarcinoma (LADC) with EGFR exon 19 deletions (Del) in January 2014, and who experienced multiple instances of oligoprogression but showed a positive response to a combination of chemotherapy, MWA and a TKI drug. First, the patient was treated with four cycles of chemotherapy (120 mg docetaxel on day 1 and 40 mg cisplatin on days 1, 2 and 3; every three weeks as one cycle) and gefitinib (Iressa; 250 mg/day), maintaining a partial response for 17 months. In August 2015, a new solitary lesion was identified in the right lung and erlotinib (Tarceva; 150 mg/day) was administered for 3 months thereafter. In response, the patient underwent ablation of both the new right lung lesion and the primary left lung lesion in January 2016. Subsequently, a treatment course consisting of six cycles of chemotherapy (0.8 g pemetrexed on day 1 and 70 mg nedaplatin on days 1 and 2; every three weeks as one cycle) resulted in stable disease. In May 2016, the patient began treatment with osimertinib (AZD9291; 80 mg/day), resulting in a rapid shrinkage of the mediastinal lymph node after one month, which has been providing a benefit for the patient for 82 months and counting. Of note, the patient also developed metachronous colon cancer in January 2020, followed by the identification of right posterior liver metastases in February 2020 and lung metastases in May 2021 and in February 2022. To address this, the patient underwent radical resection of colon cancer and liver metastasectomy and received a combination of chemotherapy with bevacizumab, along with MWA for lung metastases. Remarkably, the patient has achieved long-term survival of 110 months. In conclusion, this case highlights the promising potential of combining MWA with systemic therapy for a patient with advanced LADC harboring EGFR exon 19 Del and metachronous lung and liver-metastasized colon adenocarcinoma. MWA effectively controlled both in situ oligoprogression and new oligoprogression, thereby enhancing the efficacy of systematic chemotherapy/TKI therapy. Furthermore, this case report emphasizes the importance of repeated histologic biopsies and genetic testing as reliable indicators for adjusting treatment regimens. Physicians should also remain vigilant regarding the occurrence of secondary primary carcinomas, and timely and accurate adjustments to treatment plans will be of significant benefit to patients in terms of treatment efficacy and overall quality of life.
C1 [Li, Yun] Shandong First Med Univ, Shandong Prov Hosp, Dept Thorac Surg, Jinan 250021, Shandong, Peoples R China.
   [Xu, Yali] Shandong First Med Univ, Shandong Prov Hosp, Dept Pathol, Jinan 250021, Shandong, Peoples R China.
   [Cai, Shifeng] Shandong First Med Univ, Shandong Prov Hosp, Dept Radiol, Jinan 250021, Shandong, Peoples R China.
   [Li, Jingwen] Shandong First Med Univ, Shandong Prov Hosp, Dept Gastroenterol, Jinan 250021, Shandong, Peoples R China.
   [Ruan, Fangying; Xia, Chaoran; Luo, Peng] Zhejiang Shaoxing Topgen Biomed Technol Co Ltd, Shanghai 201321, Peoples R China.
   [Li, Jun] Shandong First Med Univ, Shandong Prov Hosp, Dept Oncol, 324 Jingwuweiqi Rd, Jinan 250021, Shandong, Peoples R China.
C3 Shandong First Medical University & Shandong Academy of Medical
   Sciences; Shandong First Medical University & Shandong Academy of
   Medical Sciences; Shandong First Medical University & Shandong Academy
   of Medical Sciences; Shandong First Medical University & Shandong
   Academy of Medical Sciences; Shandong First Medical University &
   Shandong Academy of Medical Sciences
RP Li, J (corresponding author), Shandong First Med Univ, Shandong Prov Hosp, Dept Oncol, 324 Jingwuweiqi Rd, Jinan 250021, Shandong, Peoples R China.
EM lijun201911@163.com
RI Luo, Peng/C-5323-2017; xu, yali/GWC-9971-2022
FU Project of the investigation of factors associated with the planning
   system for percutaneous pulmonary microwave ablation surgery [lj007]
FX The preparation of this study was funded by the Project of the
   investigation of factors associated with the planning system for
   percutaneous pulmonary microwave ablation surgery (grant no. lj007).
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NR 27
TC 0
Z9 0
U1 0
U2 0
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD SEP
PY 2024
VL 28
IS 3
AR 407
DI 10.3892/ol.2024.14540
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YL3D4
UT WOS:001268595200001
PM 38988445
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zhang, YZ
   Li, HR
   Lv, C
   Wu, BK
   Yu, Y
   Zhong, CL
   Lang, Q
   Liang, ZY
   Li, Y
   Shi, Y
   Zhang, J
   Xu, F
   Tian, Y
AF Zhang, Yizhou
   Li, Hanrong
   Lv, Chao
   Wu, Baokang
   Yu, Yang
   Zhong, Chongli
   Lang, Qi
   Liang, Zhiyun
   Li, Yang
   Shi, Yu
   Zhang, Jian
   Xu, Feng
   Tian, Yu
TI HHLA2 promotes tumor progression by long non-coding RNA H19 in human
   gallbladder cancer
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE human endogenous retrovirus-H long terminal repeat-associating protein
   2; target therapy; gallbladder cancer; epithelial-mesenchymal
   transition; TGF-beta 1; long non-coding RNA H19
ID EPITHELIAL-MESENCHYMAL TRANSITION; COLORECTAL-CANCER; B7 FAMILY;
   CARCINOMA; CELLS; EXPRESSION; RECEPTOR; MEMBER; PD-L1
AB Advanced gallbladder cancer (GBC) is one of the most malignant of all types of biliary tract cancers that is associated with poor prognosis and high mortality. Accumulating evidence suggest that the B7 family of proteins serve an essential role in various types of cancers, including GBC. However, the potential function and regulatory mechanism of human endogenous retrovirus-H long terminal repeat-associating protein 2 (HHLA2; also known as B7-H7 or B7H5) in GBC remain poorly understood. In the present study, immunohistochemistry was used to examine the expression pattern of HHLA2 in samples from 89 patients with GBC. The possible association between HHLA2 expression and the clinicopathological parameters, including prognosis, were then assessed. Using lentiviruses, overexpression of HHLA2 plasmid or short-hairpin RNA (shRNA) of HHLA2 were transfected into GBC-SD cells to overexpress or knock down HHLA2 expression, respectively. The effects of HHLA2 overexpression and knockdown on the epithelial-mesenchymal transition (EMT) process on GBC-SD cells were measured by the western blotting and immunofluorescence staining of collagen I, N-cadherin, E-cadherin, vimentin and alpha-SMA. By contrast, changes in cell proliferation were measured using EdU assay. Cell invasion and migration were assessed using Transwell and wound-healing assays, respectively. In addition, a xenograft mouse model was established to evaluate the tumorigenic ability of the GBC cell line in vivo after stable transfection with lentivirus for HHLA2 overexpression or shRNA for HHLA2 knockdown. The regulatory relationships among TGF-beta 1, long non-coding RNA (lncRNA) H19 (H19) and HHLA2 were then investigated. The mRNA expression of lncRNA H19 were assessed using reverse transcription-quantitative PCR, whereas the expression levels of HHLA2 were detected by western blotting and immunofluorescence staining. HHLA2 expression was found to gradually increase as the stages of the GBC samples become more advanced. In addition, the expression level of HHLA2 was calculated to be positively associated with the Nevin stage, American Joint Committee on Cancer stage, tumor invasion and regional lymph node metastasis but was negatively associated with the overall patient survival (OS). In vitro experiments demonstrated that overexpression of HHLA2 promoted GBC migration, invasion, proliferation and EMT, whereas in vivo experiments found a promoting role of HHLA2 overexpression on GBC tumor growth. After transfection with lentiviruses encoding the overexpression plasmid of lncRNA H19, GBC migration, invasion, proliferation and EMT were increased. By contrast, knocking down HHLA2 expression suppressed TGF-beta 1- or lncRNA H19 overexpression-induced GBC migration, invasion, proliferation and EMT. In addition, HHLA2 knockdown significantly reduced the sizes of the GBC tumors in vivo. These results suggest that HHLA2 overexpression can promote GBC progression. Conversely, ablation of HHLA2 expression inhibited both TGF-beta 1- and lncRNA H19-induced GBC progression, suggesting that HHLA2 is a potential therapeutic target for this disease.
C1 [Zhang, Yizhou; Lv, Chao; Wu, Baokang; Zhong, Chongli; Lang, Qi; Liang, Zhiyun; Li, Yang; Shi, Yu; Xu, Feng; Tian, Yu] China Med Univ, Dept Gen Surg, Shengjing Hosp, Shenyang 110004, Liaoning, Peoples R China.
   [Li, Hanrong] China Med Univ, Dept Ophthalmol, Affiliated Hosp 4, Shenyang 110005, Liaoning, Peoples R China.
   [Yu, Yang] Jinzhou Med Univ, Dept Surg, Jinzhou 121001, Liaoning, Peoples R China.
   [Zhang, Jian] China Med Univ, Dept Oncol, Liaoyang Cent Hosp, Liaoyang 111010, Liaoning, Peoples R China.
   [Tian, Yu] China Med Univ, Dept Gen Surg, Shengjing Hosp, 36 Sanhao St, Shenyang 110004, Liaoning, Peoples R China.
C3 China Medical University; China Medical University; Jinzhou Medical
   University; China Medical University; China Medical University
RP Tian, Y (corresponding author), China Med Univ, Dept Gen Surg, Shengjing Hosp, 36 Sanhao St, Shenyang 110004, Liaoning, Peoples R China.
EM yu.tian@cmu.edu.cn
RI Xu, Feng/L-8097-2019; Shi, Yu/D-2784-2018; Tian, Yu-Xin/H-1236-2018;
   zhang, xiaowei/GQH-5387-2022; liu, yichen/GVT-6262-2022
FU Natural Science Foundation of China; Scientific Research Project of
   Education Department of Liaoning Province [81974377]; 345 Talent Project
   of Shengjing Hospital [JC2019017];  [2019-2021]
FX The present study was supported by the Natural Science Foundation of
   China (grant no. 81974377 to YT), The Scientific Research Project of
   Education Department of Liaoning Province (grant no. JC2019017 to YT)
   and 345 Talent Project of Shengjing Hospital (grant no. 2019-2021 to
   YT).
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NR 54
TC 7
Z9 7
U1 1
U2 15
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1019-6439
EI 1791-2423
J9 INT J ONCOL
JI Int. J. Oncol.
PD SEP
PY 2022
VL 61
IS 3
AR 112
DI 10.3892/ijo.2022.5402
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 4P8LW
UT WOS:000855642600001
PM 35920182
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Wu, YX
   Du, ZY
   Mou, J
   Qiu, XY
   Chen, JL
   Cai, SJ
   Ren, DM
   Xiao, FX
   Zhou, G
   Yuan, CF
AF Wu, Yinxin
   Du, Zhuoying
   Mou, Jie
   Qiu, Xinyan
   Chen, Jinlan
   Cai, Sanjin
   Ren, Dongming
   Xiao, Fangxiang
   Zhou, Gang
   Yuan, Chengfu
TI The Functions of EphA1 Receptor Tyrosine Kinase in Several Tumors
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
DE RTK; EphA1; tumors; hepatocellular carcinoma; biomarkers; diagnosis;
   angiogenesis
ID SQUAMOUS-CELL CARCINOMA; PROGNOSTIC-SIGNIFICANCE; CANCER STATISTICS;
   EPHRIN LIGANDS; IN-VITRO; EXPRESSION; METASTASIS; PROGRESSION;
   KNOCKDOWN; INVASION
AB Background: Eph receptors tyrosine kinase (RTK) were identified in 1987 from hepatocellular carcinoma cell lines and were the largest known subfamily of RTK. Eph receptors can be divided into two categories, EphA and EphB, based on their structure and receptor-ligand specificity. EphA can be divided into 10 species (EphA 1-10) and EphB into 6 species (EphB1-6). Similarly, the ligands of Eph receptors are Ephrins. Ephrins also can be divided into Ephrin A and Ephrin B, of which there are five species(Ephrin-A1-5) and three species(Ephrin-B1-3). Among the Eph receptors, EphA1 has been the least studied so far. As far as we know, Eph receptors are involved in multiple pathologies, including cancer progression, tumor angiogenesis, intestinal environmental stability, the lymph node system, neurological disease, and inhibition of nerve regeneration after injury. There is a link between EphA1, integrin and ECM- related signal pathways. Ephrin-A1 is a ligand of the EphA1 receptor. EphA1 and ephrin-A1 functions are related to tumor angiogenesis. EphA1 and ephrin-A1 also play roles in gynecological diseases. Ephrin-A1 and EphA1 receptors regulate the follicular formation, ovulation, embryo transport, implantation and placental formation, which are of great significance for the occurrence of gynecological tumor diseases. EphA1 has been identified as an oncoprotein in various tumors and has been associated with the prognosis of various tumors in recent years. EphA1 is considered a driver gene in tumor genomics. There are significant differences in EphA1 expression levels in different types of normal tissues and tumors and even in different stages of tumor development, suggesting its functional diversity. Changes at the gene level in cell biology are often used as biological indicators of cancer, known as biomarkers, which can be used to provide diagnostic or prognostic information and are valuable for improving the detection, monitoring and treatment of tumors. However, few prognostic markers can selectively predict clinically significant tumors with poor prognosis. These malignancies are more likely to progress and lead to death, requiring more aggressive treatment. Currently available treatments for advanced cancer are often ineffective, and treatment options are mainly palliative. Therefore, early identification and treatment of those at risk of developing malignant tumors are crucial. Although pieces of evidence have shown the role of EphA1 in tumorigenesis and development, its specific mechanism is still unknown to a great extent. Objective: This review reveals the changes and roles of EphA1 in many tumors and cancers. The change of EphA1 expression can be used as a biological marker of cancer, which is valuable for improving tumor detection, monitoring and treatment and can be applied to imaging. Studies have shown that structural modification of EphA1 could make it an effective new drug. EphA1 is unique in that it can be considered a prognostic marker in many tumors and is of important meaning for clinical diagnosis and operative treatment. At the same time, the study of the specific mechanism of EphA1 in tumors can provide a new way for targeted therapy. Methods: Relevant studies were retrieved and collected through the PubMed system.
   After determining EphA1 as the research object, by analyzing research articles on EphA1 in the PubMed system in recent 10 years, we found that EphA1 was closely connected with the occurrence and development of tumors and further determined the references according to the influencing factors for review and analysis.
   Results: EphA1 has been identified as a cancer protein in various tumors, such as hepatocellular carcinoma, nasopharyngeal carcinoma, ovarian cancer, gastric cancer, colorectal cancer, clear cell renal cell carcinoma, esophageal squamous cell carcinoma, breast cancer, prostate cancer and uveal melanoma. EphA1 is abnormally expressed in these tumor cells, which mainly plays a role in cancer progression, tumor angiogenesis, intestinal environmental stability, the lymph node system, nervous system diseases and gynecological diseases. In a narrow sense, EphA1 is especially effective in breast cancer in terms of gynecological diseases. However, the specific mechanism of EphA1 leading to the change of cancer cells in some tumors is not clear, which needs further research and exploration. Conclusion: RTK EphA1 can be used as a biomarker for tumor diagnosis (especially a prognostic marker), an indispensable therapeutic target for new anti-tumor therapies, and a novel anti-tumor drug.
C1 [Wu, Yinxin; Du, Zhuoying; Mou, Jie; Qiu, Xinyan; Chen, Jinlan; Yuan, Chengfu] China Three Gorges Univ, Third Grade Pharmacol Lab Tradit Chinese Med, State Adm Tradit Chinese Med, Yichang 443002, Peoples R China.
   [Wu, Yinxin; Du, Zhuoying; Mou, Jie; Qiu, Xinyan; Chen, Jinlan; Cai, Sanjin; Ren, Dongming; Xiao, Fangxiang; Yuan, Chengfu] China Three Gorges Univ, Coll Basic Med Sci, Yichang 443002, Peoples R China.
   [Zhou, Gang] China Three Gorges Univ, Coll Tradit Chinese Med, Yichang 443002, Peoples R China.
   [Zhou, Gang] Yichang Hosp Tradit Chinese Med, Yichang 443002, Peoples R China.
C3 China Three Gorges University; China Three Gorges University; China
   Three Gorges University
RP Yuan, CF (corresponding author), China Three Gorges Univ, Third Grade Pharmacol Lab Tradit Chinese Med, State Adm Tradit Chinese Med, Yichang 443002, Peoples R China.; Zhou, G (corresponding author), China Three Gorges Univ, Coll Tradit Chinese Med, Yichang 443002, Peoples R China.
EM 13661880@qq.com; yuancf46@ctgu.edu.cn
RI Du, Zhuoying/HJY-2279-2023
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NR 75
TC 3
Z9 3
U1 1
U2 10
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 0929-8673
EI 1875-533X
J9 CURR MED CHEM
JI Curr. Med. Chem.
PY 2023
VL 30
IS 20
BP 2340
EP 2353
DI 10.2174/0929867329666220820125638
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
   Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA H8WP6
UT WOS:000998702000005
PM 35996244
DA 2025-01-04
ER

PT J
AU Wu, YX
AF Wu, Yinxin
TI SNHG11: A New Budding Star in Tumors and Inflammatory Diseases
SO MINI-REVIEWS IN MEDICINAL CHEMISTRY
LA English
DT Review
DE LncRNA; SNHG11; tumors; ceRNA; miRNA; biomarkers
ID PROMOTES CELL-PROLIFERATION; NONCODING RNA SNHG11; COLORECTAL-CANCER;
   PANCREATIC-CANCER; PROSTATE-CANCER; BREAST-CANCER; EXPRESSION;
   MIGRATION; METASTASIS; INVASION
AB Background Long non-coding RNAs (lncRNAs) are transcripts that are over 200 nucleotides in length and lack protein-coding potential. Despite their name, lncRNAs have important regulatory roles in transcription, translation, and protein function by interacting with DNA, RNA, and protein molecules. Small nucleolar RNAs (snoRNAs), found in various tumors, are encoded by lncRNAs and have gained attention in recent research. The lncRNAs, encoding snoRNAs are known as small nucleolar RNA host genes (SNHGs), a newly identified class of lncRNAs. SNHG11, a specific SNHG, is a critical regulatory factor involved in various biological processes. Accumulating evidence suggests that SNHG11 can impact tumor development and inflammatory diseases by modulating downstream gene expression through chromatin modification, transcription, or post-transcriptional mechanisms. The expression levels of SNHG11 vary significantly in different normal tissues, tumors, and stages of tumor development. Currently, treatment options for advanced cancers are mainly palliative and lack curative potential.Objectives This review aims to explore the modifications and functions of lncRNA SNHG11 in various tumors and inflammatory diseases. Through a comprehensive analysis of relevant literature on SNHG11 in PubMed, the review aims to provide a comprehensive description of the roles of SNHG11 in known tumors and inflammatory diseases and elucidate the specific mechanism's underlying functions. The changes in SNHG11 expression in tumors and inflammatory diseases can serve as early biomarkers, therapeutic targets, and prognostic indicators. Improving the clinical detection, staging, treatment, and prognosis of tumors is of great value. Additionally, the structural modifications of SNHG11 can potentially enhance its function as a drug carrier to maximize the therapeutic potential of drugs. Furthermore, understanding the specific mechanisms of SNHG11 in tumors and inflammatory diseases may provide new ways for targeted therapy.Materials and Methods Relevant studies were retrieved and collected from the PubMed system. SNHG11 was identified as the research object, and research literature on SNHG11 in the past ten years was analyzed to determine its strong association with the onset and progression of various diseases. The precise mechanisms of SNHG11's mode of action were reviewed, and references were further determined based on their impact factors for comprehensive analysis.Results Through review and analysis, it was found that SNHG11 is involved in a wide range of tumors and inflammatory diseases through its high expression, including lung cancer, colorectal cancer, prostate cancer, hepatocellular carcinoma, triple-negative breast cancer, gastric cancer, glioma, ovarian cancer, pancreatic cancer, acute pancreatitis, and ischemic stroke, but with lower expression in virus myocarditis. SNHG11 is abnormally expressed in cells of these tumors and inflammatory diseases mainly contributes to disease proliferation, metastasis, ceRNA activity, miRNA sponging, drug resistance, and tumor prognosis. However, the specific mechanisms of SNHG11 in tumors and inflammatory diseases require further detailed exploration. Understanding the known regulatory mechanisms can expand the scope of clinical applications and promote early clinical detection, monitoring, and treatment.Conclusion LncRNA SNHG11 can serve as an early diagnostic biomarker, therapeutic target, and prognostic indicator in various diseases, particularly tumors.
   SNHG11 plays a crucial role in the occurrence and development of tumors and inflammatory diseases through various mechanisms, which has significant implications for clinical diagnosis and treatment.
C1 [Wu, Yinxin] China Three Gorges Univ, Med Coll Basic Sci, Yichang 443002, Peoples R China.
C3 China Three Gorges University
RP Wu, YX (corresponding author), China Three Gorges Univ, Med Coll Basic Sci, Yichang 443002, Peoples R China.
EM Wuuuyxin777@163.com
OI Wu, Yinxin/0000-0001-9429-4983
FU Declared none.
FX Declared none.
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NR 91
TC 1
Z9 1
U1 4
U2 5
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1389-5575
EI 1875-5607
J9 MINI-REV MED CHEM
JI Mini-Rev. Med. Chem.
PY 2023
VL 23
IS 20
BP 1993
EP 2006
DI 10.2174/1389557523666230509122402
PG 14
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA T5ZZ8
UT WOS:001078782500005
PM 37165588
DA 2025-01-04
ER

PT J
AU Bellio, H
   Bertaut, A
   Hervieu, A
   Zanetta, S
   Hennequin, A
   Vincent, J
   Palmier, R
   Bengrine-Lefevre, L
   Ghiringhelli, F
   Fumet, JD
AF Bellio, Helene
   Bertaut, Aurelie
   Hervieu, Alice
   Zanetta, Sylvie
   Hennequin, Audrey
   Vincent, Julie
   Palmier, Remi
   Bengrine-Lefevre, Leila
   Ghiringhelli, Francois
   Fumet, Jean-David
TI Phase I Dose-Escalation Trial of an Innovative Chemotherapy Regimen
   Combining a Fractionated Dose of Irinotecan Plus Bevacizumab,
   Oxaliplatin, 5-Fluorouracil, and Folinic Acid (bFOLFIRINOX-3) in
   Chemorefractory Metastatic Colorectal Cancer
SO CANCERS
LA English
DT Article
DE 5-fluorouracil; irinotecan; oxaliplatin; bevacizumab; chemotherapy
   metastatic colorectal cancer
ID 1ST-LINE TREATMENT; III TRIAL; PANITUMUMAB PLUS; SUPPORTIVE CARE;
   OPEN-LABEL; FLUOROURACIL; THERAPY; FOLFIRI; MONOTHERAPY; RECHALLENGE
AB Simple Summary: Treatment of non-resectable metastatic colorectal cancer (mCRC) involves chemotherapy based on 5-fluorouracil, oxaliplatin and irinotecan and monoclonal antibodies targeting VEGF or EGFR. After an initial progression, it is usual to change the chemotherapy regimen and targeted therapy, with rather moderate results. Several studies have focused on the interest of using again already used molecules and rechallenge with oxaliplatin and irinotecan bi fractionation (FOLFIRI3) have previously shown efficacy in chemorefractory patients, but desynchronized triplet chemotherapy was never tested. The aim of this study was to evaluate the safety and efficacy of a new regimen so-called: FOLFIRINOX-3 bevacizumab in chemorefractory metastatic colorectal cancer.
   The care of metastatic colorectal cancers is based on combination chemotherapies including 5-fluorouracil, oxaliplatin, irinotecan, and monoclonal antibodies targeting the epidermal growth factor receptor or vascular endothelial growth factor. The regimen is determined based on the patient's molecular biology and general condition. Irinotecan bifractionation showed efficacy in chemorefractory patients in a previous study, FOLFIRI-3, but a desynchronized triplet has never been tested. The aim of bFOLFIRINOX-3 is to determine the safety, tolerance, and efficacy of a new regimen (FOLFIRINOX-3 bevacizumab) in chemorefractory patients. The aim of this study was to evaluate the safety and efficacy of FOLFIRINOX-3 bevacizumab in chemorefractory metastatic colorectal cancer (mCRC). A standard phase I, "3 + 3" design study was performed. The standard protocol comprised simplified FOLFOX 4 (folinic acid 400 mg/m(2)), 5-fluorouracil (a 400 mg/m(2) bolus followed by 2400 mg/m(2) for 46 h), oxaliplatin (85 mg/m(2)) and irinotecan (administered before and after 5-fluorouracil infusion), plus bevacizumab (5 mg/kg). In a "3 + 3" design, three different doses of irinotecan were tested: 60, 70 and 90 mg/m(2). The primary endpoint was the maximum tolerable dose (MTD) of irinotecan. The secondary endpoints included the objective response (at 8 and 16 weeks) according to the RECIST 1.1 criteria and progression free survival. Thirteen patients were enrolled, and twelve patients were finally evaluated for dose-limiting toxicity (DLT). The dose level defined was 70 mg/m(2) irinotecan. A total of three DLTs were observed (grade 3 diarrhea): two DLTs at the 90 mg/m(2) dose level and one at the 70 mg/m(2) dose level. The most frequently described adverse events were asthenia (93%), diarrhea (77%), nausea (62%) and peripheral sensory neuropathy (46%). The most frequent biological event was thrombopenia (54%). Regarding efficacy, among the 11 evaluable patients, no progression was observed at 8 weeks, and the partial response rate was 18.2%. At 16 weeks, a partial response rate of 27.3% was observed, and five patients had a stable disease. The new regimen of bFOLFIRINOX-3 with irinotecan at 70 mg/m(2) was well tolerated. In chemorefractory patients, this protocol shows a high response rate.
C1 [Bellio, Helene; Bertaut, Aurelie; Hervieu, Alice; Zanetta, Sylvie; Hennequin, Audrey; Vincent, Julie; Palmier, Remi; Bengrine-Lefevre, Leila; Ghiringhelli, Francois; Fumet, Jean-David] Georges Francois Leclerc Canc Ctr UNICANCER, Platform Transfer Biol Oncol, 1 Rue Prof Marion, F-21000 Dijon, France.
   [Bellio, Helene; Bertaut, Aurelie; Hervieu, Alice; Zanetta, Sylvie; Hennequin, Audrey; Vincent, Julie; Palmier, Remi; Bengrine-Lefevre, Leila; Ghiringhelli, Francois; Fumet, Jean-David] Georges Francois Leclerc Canc Ctr UNICANCER, Dept Med Oncol, 1 Rue Prof Marion, F-21000 Dijon, France.
   [Bellio, Helene; Bertaut, Aurelie; Hervieu, Alice; Zanetta, Sylvie; Hennequin, Audrey; Vincent, Julie; Palmier, Remi; Bengrine-Lefevre, Leila; Ghiringhelli, Francois; Fumet, Jean-David] Univ Burgundy Franche Comte, Maison Univ Esplanade Erasme, F-21000 Dijon, France.
   [Ghiringhelli, Francois] UMR INSERM 1231, 7 Blvd Jeanne dArc, F-21000 Dijon, France.
C3 Universite de Bourgogne; Institut Agro; AgroSup Dijon; Universite de
   Bourgogne; Universite de Bourgogne; Institut National de la Sante et de
   la Recherche Medicale (Inserm); Institut Agro; AgroSup Dijon
RP Bellio, H; Fumet, JD (corresponding author), Georges Francois Leclerc Canc Ctr UNICANCER, Platform Transfer Biol Oncol, 1 Rue Prof Marion, F-21000 Dijon, France.; Bellio, H; Fumet, JD (corresponding author), Georges Francois Leclerc Canc Ctr UNICANCER, Dept Med Oncol, 1 Rue Prof Marion, F-21000 Dijon, France.; Bellio, H; Fumet, JD (corresponding author), Univ Burgundy Franche Comte, Maison Univ Esplanade Erasme, F-21000 Dijon, France.
EM bellio.helene@gmail.com; abertaut@cgfl.fr; ahervieu@cgfl.fr;
   szanetta@cgfl.fr; ahennequin@cgfl.fr; jvincent@cgfl.fr;
   rpalmier@cgfl.fr; lbengrine@cgfl.fr; fghiringhelli@cgfl.fr;
   jdfumet@cgfl.fr
OI ghiringhelli, francois/0000-0002-5465-8305; bertaut,
   Aurelie/0000-0002-7934-9509
FU ARCAD foundation
FX This research was funded by the ARCAD foundation.
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NR 39
TC 0
Z9 0
U1 0
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD NOV
PY 2021
VL 13
IS 21
AR 5472
DI 10.3390/cancers13215472
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 0A4HB
UT WOS:000773916100015
PM 34771635
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Higami, S
   Mukai, M
   Yokoyama, D
   Uda, S
   Abe, R
   Mamuro, N
   Kishima, K
   Hasegawa, S
   Tajima, T
   Nomura, E
   Makuuchi, H
   Yokoyama, D
AF Higami, Shigeo
   Mukai, Masaya
   Yokoyama, Daiki
   Uda, Syuji
   Abe, Rin
   Mamuro, Nana
   Kishima, Kyoko
   Hasegawa, Sayuri
   Tajima, Takayuki
   Nomura, Eiji
   Makuuchi, Hiroyasu
   Yokoyama, D.
TI A single-center retrospective analysis of the efficacy and safety of a
   modified regimen of irinotecan plus S-1 (IRIS) with molecular targeting
   agents as second-line chemotherapy in Japanese patients with recurrent
   or nonresectable colorectal cancer
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Colorectal cancer; chemotherapy; molecular targeting therapy; irinotecan
   plus S-1 (IRIS); recurrent; non-resectable cancer
ID BRAF-MUTATION; ADJUVANT CHEMOTHERAPY; 1ST-LINE TREATMENT; POOLED
   ANALYSIS; COLON-CANCER; WILD-TYPE; BEVACIZUMAB; PANITUMUMAB;
   FLUOROURACIL; OXALIPLATIN
AB Background: As the second-line chemotherapy for stage IV recurrent or nonresectable colorectal cancer, our hospital started a modified treatment regimen comprising of irinotecan plus S-1 (IRIS) [tegafur/ gimeracil/oteracil (S-1)] plus molecular targeting agents (MTAs), i.e., an epidermal growth factor receptor (EGFR) inhibitor such as panitumumab (P-mab) or cetuximab (C-mab) or vascular endothelial growth factor (VEGF) inhibitor such as bevacizumab (B-mab) since October 2012. The purpose of this study is to evaluate the efficacy and safety of this modified regimen.Methods: This retrospective study included 41 patients with advanced recurrent colorectal cancer at our hospital whom at least 3 courses of chemotherapy were conducted from January 2015 to December 2021. Based on the location of the primary tumor, patients were classified into two group (right-sided group, proximal to the splenic curve, and left-sided, distal to the splenic curve). We assessed archived data on RAS and BRAF status and UGT1A1 polymorphisms and use of the VEGF inhibitor bevacizumab (B-mab) and the EGFR inhibitors panitumumab (P-mab) and cetuximab (C-mab). In addition, progression-free survival rate (36M-PFS) and the overall survival rate (36M-OS) were calculated. Furthermore, the respective median survival time (MST), the median number of treatment courses; the objective response rate (ORR) and clinical benefit rate (CBR) and the incidence of adverse events (AEs) were assessed as well.Results: There were 11 patients (26.8%) in the right-sided group, and 30 patients (73.2%) in the left-sided group. There were 19 patients with RAS wild type (46.3%) (1 in the right sided group and 18 in the left sided group). P-mab was used for 16 of these patients (84.2%), C-mab for 2 (10.5%), and B-mab for 1 (5.3%); the remaining 22 patients (53.7%). Ten (10 patients) in the right group and 12 patients in the left group were a mutated type and received B-mab. BRAF testing was performed in 17 patients (41.5%); as more than 50% of patients (58.5%) were included before the assay's introduction. 5 patients in the right-sided group and 12 patients in the left-sided group had wild type. There was no mutated type. UGT1A1 polymorphism was tested in 16/41 patients: Eight were wild type (8/41 patients, 19.5%) and 8, mutated type. Regarding the *6/*28 double heterozygous type, there was only 1 patient in the right-sided group and the remaining 7 patients were in the left-sided group. The total number of chemotherapy courses was 299, and the median number, 6.0 (range, 3-20). PFS, OS, and MST were as follows: 36M-PFS (total/Rt/Lt), 6.2%/0.0%/8.5% (MST; 7.6/6.3/8.9 months); and 36M-OS (total/Rt/Lt), 32.1%/0.0%/44.0% (MST; 22.1/18.8/28.6 months). The ORR and CBR were 24.4% and 75.6%, respectively. The majority of AEs were grades 1 or 2 and were improved with conservative treatment. Grade 3 leukopenia was observed in 2 cases (4.9%), neutropenia in 4 cases (9.8%), and malaise/nausea/diarrhea/perforation in 1 case each (2.4%). Grade 3 leukopenia (2 patients) and neutropenia (3 patients) were more commonly observed in the left-sided group. Diarrhea and Conclusions: This second-line modified IRIS regimen with MTAs is safe and effective and results in good ps and os
C1 [Higami, Shigeo; Mukai, Masaya; Yokoyama, Daiki; Uda, Syuji; Abe, Rin; Mamuro, Nana; Kishima, Kyoko; Hasegawa, Sayuri; Tajima, Takayuki; Nomura, Eiji; Makuuchi, Hiroyasu; Yokoyama, D.] Tokai Univ, Dept Surg, Hachioji Hosp, Hachioji, Tokyo 1920032, Japan.
   [Higami, Shigeo] Tokai Univ, Hachioji Hosp, Dept Surg, Surg, 1838 Ishikawa Machi, Hachioji, Tokyo 1920032, Japan.
C3 Tokai University; Tokai University
RP Higami, S (corresponding author), Tokai Univ, Dept Surg, Hachioji Hosp, Hachioji, Tokyo 1920032, Japan.; Higami, S (corresponding author), Tokai Univ, Hachioji Hosp, Dept Surg, Surg, 1838 Ishikawa Machi, Hachioji, Tokyo 1920032, Japan.
EM s.higami@is.icc.u-tokai.ac.jp
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NR 38
TC 0
Z9 0
U1 0
U2 1
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD APR 29
PY 2023
VL 14
IS 2
BP 663
EP 675
DI 10.21037/jgo-22-899
EA APR 2023
PG 13
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA O2WM1
UT WOS:000969645800001
PM 37201062
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Starska-Kowarska, K
AF Starska-Kowarska, Katarzyna
TI Role of Vitamin D in Head and Neck Cancer-Immune Function, Anti-Tumour
   Effect, and Its Impact on Patient Prognosis
SO NUTRIENTS
LA English
DT Review
DE anti-cancer therapy; apoptosis; cancer pathogenesis; cancer prevention;
   cellular signalling; cell-cycle progression; head and neck cancer (HNC);
   head and neck squamous cell carcinoma (HNSCC); vitamin D
ID SQUAMOUS-CELL CARCINOMA; SERUM 25-HYDROXYVITAMIN D; NF-KAPPA-B;
   HUMAN-COLON-CANCER; D-RECEPTOR; 1-ALPHA,25-DIHYDROXYVITAMIN D-3;
   ORAL-CANCER; E-CADHERIN; 1,25-DIHYDROXYVITAMIN D-3; D SUPPLEMENTATION
AB Head and neck squamous cell carcinoma (HNSCC) describes a heterogeneous group of human neoplasms of the head and neck with high rates of morbidity and mortality, constituting about 3% of all cancers and similar to 1.5% of all cancer deaths. HNSCC constituted the seventh most prevalent human malignancy and the most common human cancer in the world in 2020, according to multi-population observations conducted by the GLOBOCAN group. Since approximately 60-70% of patients present with stage III/IV neoplastic disease, HNSCC is still one of the leading causes of death in cancer patients worldwide, with an overall survival rate that is too low, not exceeding 40-60% of these patients. Despite the application of newer surgical techniques and the implementation of modern combined oncological treatment, the disease often follows a fatal course due to frequent nodal metastases and local neoplastic recurrences. The role of micronutrients in the initiation, development, and progression of HNSCC has been the subject of considerable research. Of particular interest has been vitamin D, the pleiotropic biologically active fat-soluble family of secosteroids (vitamin-D-like steroids), which constitutes a key regulator of bone, calcium, and phosphate homeostasis, as well as carcinogenesis and the further development of various neoplasms. Considerable evidence suggests that vitamin D plays a key role in cellular proliferation, angiogenesis, immunity, and cellular metabolism. A number of basic science, clinical, and epidemiological studies indicate that vitamin D has multidirectional biological effects and influences anti-cancer intracellular mechanisms and cancer risk, and that vitamin D dietary supplements have various prophylactic benefits. In the 20th century, it was reported that vitamin D may play various roles in the protection and regulation of normal cellular phenotypes and in cancer prevention and adjunctive therapy in various human neoplasms, including HNSCC, by regulating a number of intracellular mechanisms, including control of tumour cell expansion and differentiation, apoptosis, intercellular interactions, angio- and lymphogenesis, immune function, and tumour invasion. These regulatory properties mainly occur indirectly via epigenetic and transcriptional changes regulating the function of transcription factors, chromatin modifiers, non-coding RNA (ncRNAs), and microRNAs (miRs) through protein-protein interactions and signalling pathways. In this way, calcitriol enhances intercellular communication in cancer biology, restores the connection with the extracellular matrix, and promotes the epithelial phenotype; it thus counteracts the tumour-associated detachment from the extracellular matrix and inhibits the formation of metastases. Furthermore, the confirmation that the vitamin D receptor (VDR) is present in many human tissues confirmed the physiopathological significance of vitamin D in various human tumours. Recent studies indicate quantitative associations between exposure to vitamin D and the incidence of HNC, i.e., cancer risk assessment included circulating calcidiol plasma/serum concentrations, vitamin D intake, the presence of the VDR gene polymorphism, and genes involved in the vitamin D metabolism pathway. Moreover, the chemopreventive efficacy of vitamin D in precancerous lesions of the head and neck and their role as predictors of mortality, survival, and recurrence of head and neck cancer are also widely discussed.
   As such, it may be considered a promising potential anti-cancer agent for developing innovative methods of targeted therapy. The proposed review discusses in detail the mechanisms regulating the relationship between vitamin D and HNSCC. It also provides an overview of the current literature, including key opinion-forming systematic reviews as well as epidemiological, prospective, longitudinal, cross-sectional, and interventional studies based on in vitro and animal models of HNSCC, all of which are accessible via the PubMed/Medline/EMBASE/Cochrane Library databases. This article presents the data in line with increasing clinical credibility.
C1 [Starska-Kowarska, Katarzyna] Med Univ Lodz, Dept Physiol Pathophysiol & Clin Immunol, Zeligowskiego 7-9, PL-90752 Lodz, Poland.
   [Starska-Kowarska, Katarzyna] Med Univ Lodz, Dept Clin Physiol, Zeligowskiego 7-9, PL-90752 Lodz, Poland.
   [Starska-Kowarska, Katarzyna] EnelMed Ctr Expert Lodz, Dept Otorhinolaryngol, Drewnowska 58, PL-91001 Lodz, Poland.
C3 Medical University Lodz; Medical University Lodz
RP Starska-Kowarska, K (corresponding author), Med Univ Lodz, Dept Physiol Pathophysiol & Clin Immunol, Zeligowskiego 7-9, PL-90752 Lodz, Poland.; Starska-Kowarska, K (corresponding author), Med Univ Lodz, Dept Clin Physiol, Zeligowskiego 7-9, PL-90752 Lodz, Poland.; Starska-Kowarska, K (corresponding author), EnelMed Ctr Expert Lodz, Dept Otorhinolaryngol, Drewnowska 58, PL-91001 Lodz, Poland.
EM katarzyna.starska@umed.lodz.pl
RI Starska-Kowarska, Katarzyna/S-9327-2016
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NR 348
TC 8
Z9 7
U1 0
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6643
J9 NUTRIENTS
JI Nutrients
PD MAY 31
PY 2023
VL 15
IS 11
AR 2592
DI 10.3390/nu15112592
PG 60
WC Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Nutrition & Dietetics
GA I8AR3
UT WOS:001004963100001
PM 37299554
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Adam, R
   Piedvache, C
   Chiche, L
   Adam, JP
   Salamé, E
   Bucur, P
   Cherqui, D
   Scatton, O
   Granger, V
   Ducreux, M
   Cillo, U
   Cauchy, F
   Mabrut, JY
   Verslype, C
   Coubeau, L
   Hardwigsen, J
   Boleslawski, E
   Muscari, F
   Jeddou, H
   Pezet, D
   Heyd, B
   Lucidi, V
   Geboes, K
   Lerut, J
   Majno, P
   Grimaldi, L
   Levi, F
   Lewin, M
   Gelli, M
AF Adam, Rene
   Piedvache, Celine
   Chiche, Laurence
   Adam, Jean Philippe
   Salame, Ephrem
   Bucur, Petru
   Cherqui, Daniel
   Scatton, Olivier
   Granger, Victoire
   Ducreux, Michel
   Cillo, Umberto
   Cauchy, Francois
   Mabrut, Jean-Yves
   Verslype, Chris
   Coubeau, Laurent
   Hardwigsen, Jean
   Boleslawski, Emmanuel
   Muscari, Fabrice
   Jeddou, Heithem
   Pezet, Denis
   Heyd, Bruno
   Lucidi, Valerio
   Geboes, Karen
   Lerut, Jan
   Majno, Pietro
   Grimaldi, Lamiae
   Levi, Francis
   Lewin, Maite
   Gelli, Maximiliano
CA Collaborat TransMet grp
TI Liver transplantation plus chemotherapy versus chemotherapy alone in
   patients with permanently unresectable colorectal liver metastases
   (TransMet): results from a multicentre, open-label, prospective,
   randomised controlled trial
SO LANCET
LA English
DT Article
ID CANCER; PHASE-3; BEVACIZUMAB; PROGRESSION; RESECTION; SURVIVAL
AB Background Despite the increasing efficacy of chemotherapy, permanently unresectable colorectal liver metastases are associated with poor long-term survival. We aimed to assess whether liver transplantation plus chemotherapy could improve overall survival. Methods TransMet was a multicentre, open-label, prospective, randomised controlled trial done in 20 tertiary centres in Europe. Patients aged 18-65 years, with Eastern Cooperative Oncology Group performance score 0-1, permanently unresectable colorectal liver metastases from resected BRAF-non-mutated colorectal cancer responsive to systemic chemotherapy (>= 3 months, <= 3 lines), and no extrahepatic disease, were eligible for enrolment. Patients were randomised (1:1) to liver transplantation plus chemotherapy or chemotherapy alone, using block randomisation. The liver transplantation plus chemotherapy group underwent liver transplantation for 2 months or less after the last chemotherapy cycle. At randomisation, the liver transplantation plus chemotherapy group received a median of 21.0 chemotherapy cycles (IQR 18.0-29.0) versus 17.0 cycles (12.0-24.0) in the chemotherapy alone group, in up to three lines of chemotherapy. During first-line chemotherapy, 64 (68%) of 94 patients had received doublet chemotherapy and 30 (32%) of 94 patients had received triplet regimens; 76 (80%) of 94 patients had targeted therapy. Transplanted patients received tailored immunosuppression (methylprednisolone 10 mg/kg intravenously on day 0; tacrolimus 0<middle dot>1 mg/kg via gastric tube on day 0, 6-10 ng/mL days 1-14; mycophenolate mofetil 10 mg/kg intravenously day 0 to <2 months and switch to everolimus 5-8 ng/mL), and postoperative chemotherapy, and the chemotherapy group had continued chemotherapy. The primary endpoint was 5-year overall survival analysed in the intention to treat and per-protocol population. Safety events were assessed in the as-treated population. The study is registered with ClinicalTrials.gov (NCT02597348), and accrual is complete. Findings Between Feb 18, 2016, and July 5, 2021, 94 patients were randomly assigned and included in the intention-to- treat population, with 47 in the liver transplantation plus chemotherapy group and 47 in the chemotherapy alone group. 11 patients in the liver transplantation plus chemotherapy group and nine patients in the chemotherapy alone group did not receive the assigned treatment; 36 patients and 38 patients in each group, respectively, were included in the per-protocol analysis. Patients had a median age of 54.0 years (IQR 47.0-59.0), and 55 (59%) of 94 patients were male and 39 (41%) were female. Median follow-up was 59.3 months (IQR 42.4-60.2). In the intention-to-treat population, 5-year overall survival was 56.6% (95% CI 43.2-74.1) for liver transplantation plus chemotherapy and 12.6% (5.2-30.1) for chemotherapy alone (HR 0<middle dot>37 [95% CI 0<middle dot>21-0<middle dot>65]; p=0<middle dot>0003) and 73.3% (95% CI 59.6-90.0) and 9.3% (3.2-26.8), respectively, for the per-protocol population. Serious adverse events occurred in 32 (80%) of 40 patients who underwent liver transplantation (from either group), and 69 serious adverse events were observed in 45 (83%) of 54 patients treated with chemotherapy alone. Three patients in the liver transplantation plus chemotherapy group were retransplanted, one of whom died postoperatively of multi-organ failure.
   Interpretation In selected patients with permanently unresectable colorectal liver metastases, liver transplantation plus chemotherapy with organ allocation priority significantly improved survival versus chemotherapy alone. These results support the validation of liver transplantation as a new standard option for patients with permanently unresectable liver-only metastases. Funding French National Cancer Institute and Assistance Publique-H & ocirc;pitaux de Paris. Copyright (c) 2024 Elsevier Ltd. All rights reserved, including those for text and data mining, AI training, and similar technologies.
C1 [Adam, Rene; Cherqui, Daniel] Univ Paris Saclay, Hop Paul Brousse, AP HP, Dept Hepatobiliary Surg & Transplantat, F-94800 Villejuif, France.
   [Piedvache, Celine; Grimaldi, Lamiae] Univ Paris Saclay, Hop Kremlin Bictr, AP HP, Clin Res Unit, Paris, France.
   [Chiche, Laurence; Adam, Jean Philippe] Hop Haut Leveque, Dept Hepatobiliary Surg & Transplantat, Bordeaux, France.
   [Salame, Ephrem; Bucur, Petru] Reg Univ Hosp, Dept Digest Hepatobiliary & Pancreat Surg, Tours, France.
   [Scatton, Olivier] Hop La Pitie Salpetriere, AP HP, Dept Hepatobiliary Surg, Paris, France.
   [Granger, Victoire] Univ Grenoble Alpes, Univ Hosp Grenoble, Dept Gastroenterol & Digest Oncol, Grenoble, France.
   [Ducreux, Michel] Univ Paris Saclay, Dept Med Oncol, Gustave Roussy, Villejuif, France.
   [Cillo, Umberto] Univ Hosp Padua, Hepatobiliary Surg & Liver Transplant Unit, Padua, Italy.
   [Cauchy, Francois] Hop Beaujon, AP HP, Hepatobiliary Surg Unit, Clichy, France.
   [Mabrut, Jean-Yves] Hop Croix Rousse, Dept Hepatobiliary Surg & Liver Transplantat, Lyon, France.
   [Mabrut, Jean-Yves; Verslype, Chris] Univ Hosp Leuven, Dept Oncol, Leuven, Belgium.
   [Coubeau, Laurent] Univ Hosp St Luc, Dept Abdominal Surg & Transplantat, Brussels, Belgium.
   [Hardwigsen, Jean] Marseille Univ Hosp Timone, Dept Digest Hepatobiliary & Transplantat Surg, Marseilles, France.
   [Boleslawski, Emmanuel] Univ Hosp Lille, Dept Digest Surg & Transplantat, Lille, France.
   [Muscari, Fabrice] Univ Hosp Toulouse, Hop Rangueil, Dept Digest Surg, Toulouse, France.
   [Lerut, Jan] Catholic Univ Louvain, Inst Expt & Clin Res, Louvain, Belgium.
   [Adam, Rene; Levi, Francis; Lewin, Maite] Univ Paris Saclay, Fac Med, Dept Oncol, UPR Chronotherapy Canc & Transplantat, Villejuif, France.
   [Jeddou, Heithem] Univ Hosp, Dept Hepatobiliary & Digest Surg, Rennes, France.
   [Pezet, Denis] Univ Hosp Clermont Ferrand, Dept Gen Surg, Clermont Ferrand, France.
   [Heyd, Bruno] Reg Univ Hosp Besancon, Dept Digest & Oncol Surg, Besancon, France.
   [Lucidi, Valerio] Univ Libre Bruxelles, Hop Univ Bruxelles, Dept Digest Surg & Transplantat, Brussels, Belgium.
   [Geboes, Karen] Univ Hosp Ghent, Dept Gastroenterol Digest Oncol, Ghent, Belgium.
   [Majno, Pietro] Univ Italian Switzerland, Dept Biomed Sci, Lugano, Switzerland.
   [Lewin, Maite] Univ Paris Saclay, Hop Paul Brousse, Dept Radiol, Villejuif, France.
   [Gelli, Maximiliano] Univ Paris Saclay, Gustave Roussy Hosp, Dept Anaesthesia Surg & Intervent Radiol, Villejuif, France.
C3 Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
   Paul-Brousse - APHP; Universite Paris Saclay; Universite Paris Saclay;
   Assistance Publique Hopitaux Paris (APHP); CHU Bordeaux; CHU Tours;
   Sorbonne Universite; Assistance Publique Hopitaux Paris (APHP); Hopital
   Universitaire Pitie-Salpetriere - APHP; CHU Grenoble Alpes; Communaute
   Universite Grenoble Alpes; Universite Grenoble Alpes (UGA); Universite
   Paris Saclay; UNICANCER; Gustave Roussy; University of Padua; Azienda
   Ospedaliera - Universita di Padova; Assistance Publique Hopitaux Paris
   (APHP); Universite Paris Cite; Hopital Universitaire Beaujon - APHP; CHU
   Lyon; KU Leuven; University Hospital Leuven; Universite Catholique
   Louvain; Cliniques Universitaires Saint-Luc; Universite de Lille; CHU
   Lille; CHU de Toulouse; Universite de Toulouse; Universite Toulouse III
   - Paul Sabatier; Universite Catholique Louvain; Universite Paris Saclay;
   CHU Rennes; CHU Clermont Ferrand; Universite de Franche-Comte; CHU
   Besancon; Universite Libre de Bruxelles; Ghent University; Ghent
   University Hospital; Universita della Svizzera Italiana; Universite
   Paris Saclay; Assistance Publique Hopitaux Paris (APHP); Hopital
   Universitaire Paul-Brousse - APHP; UNICANCER; Gustave Roussy; Universite
   Paris Saclay
RP Adam, R (corresponding author), Univ Paris Saclay, Hop Paul Brousse, AP HP, Dept Hepatobiliary Surg & Transplantat, F-94800 Villejuif, France.
EM rene.adam@aphp.fr
RI Gelli, Maximiliano/K-8340-2019; Coubeau, Laurent/HKE-6301-2023;
   François, Cauchy/J-7031-2019; LEVI, Francis/J-7167-2019; Cillo,
   Umberto/AAC-2591-2019
OI Gelli, Maximiliano/0000-0001-9807-4021; LEVI,
   Francis/0000-0003-1364-7463; Verslype, Chris/0000-0003-3857-466X
FU French National Cancer Institute; Assistance Publique-Hppitaux de Paris
FX French National Cancer Institute and Assistance Publique-Hppitaux de
   Paris.
CR Adam R, 2004, ANN SURG, V240, P1052, DOI 10.1097/01.sla.0000145964.08365.01
   Adam R, 2004, ANN SURG, V240, P644, DOI 10.1097/01.sla.0000141198.92114.16
   Adam R, 2024, ECLINICALMEDICINE, V72, DOI 10.1016/j.eclinm.2024.102608
   Adam R, 2018, TRANSPL INT, V31, P1293, DOI 10.1111/tri.13358
   Battistella S, 2024, MEDICINA-LITHUANIA, V60, DOI 10.3390/medicina60030412
   Bond MJG, 2023, LANCET ONCOL, V24, P757, DOI 10.1016/S1470-2045(23)00219-X
   Bonney GK, 2021, LANCET GASTROENTEROL, V6, P933, DOI 10.1016/S2468-1253(21)00219-3
   Chavez-Villa M, 2024, J CLIN ONCOL, V42, DOI 10.1200/JCO.23.01781
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NR 31
TC 6
Z9 6
U1 7
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0140-6736
EI 1474-547X
J9 LANCET
JI Lancet
PD SEP 21
PY 2024
VL 404
IS 10458
BP 1107
EP 1118
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA H1T3B
UT WOS:001321327200001
PM 39306468
DA 2025-01-04
ER

PT J
AU Abdirahman, SM
   Christie, M
   Preaudet, A
   Burstroem, MCU
   Mouradov, D
   Lee, BD
   Sieber, OM
   Putoczki, TL
AF Abdirahman, Suad M.
   Christie, Michael
   Preaudet, Adele
   Burstroem, Marie C. U.
   Mouradov, Dmitri
   Lee, Belinda
   Sieber, Oliver M.
   Putoczki, Tracy L.
TI A Biobank of Colorectal Cancer Patient-Derived Xenografts
SO CANCERS
LA English
DT Article
DE colon cancer; chemotherapy; model; patient-derived; xenograft
ID EPITHELIAL OVARIAN-CANCER; COLON-CANCER; TUMOR XENOGRAFTS; CELL-LINE;
   1ST-LINE TREATMENT; STAGE-II; MODELS; ESTABLISHMENT; IDENTIFICATION;
   HETEROGENEITY
AB Colorectal cancer (CRC) is a challenging disease, with a high mortality rate and limited effective treatment options, particularly for late-stage disease. Patient-derived xenografts (PDXs) have emerged as an informative, renewable experimental resource to model CRC architecture and biology. Here, we describe the generation of a biobank of CRC PDXs from stage I to stage IV patients. We demonstrate that PDXs within our biobank recapitulate the histopathological and mutation features of the original patient tumor. In addition, we demonstrate the utility of this resource in pre-clinical chemotherapy and targeted treatment studies, highlighting the translational potential of PDX models in the identification of new therapies that will improve the overall survival of CRC patients.
C1 [Abdirahman, Suad M.; Christie, Michael; Preaudet, Adele; Burstroem, Marie C. U.; Mouradov, Dmitri; Lee, Belinda; Sieber, Oliver M.; Putoczki, Tracy L.] Walter & Eliza Hall Inst Med Res, Personalised Oncol Div, Parkville, Vic 3052, Australia.
   [Abdirahman, Suad M.; Mouradov, Dmitri; Sieber, Oliver M.; Putoczki, Tracy L.] Univ Melbourne, Dept Med Biol, Parkville, Vic 3010, Australia.
   [Christie, Michael] Univ Melbourne, Dept Pathol, Parkville, Vic 3010, Australia.
   [Sieber, Oliver M.; Putoczki, Tracy L.] Univ Melbourne, Dept Surg, Parkville, Vic 3010, Australia.
   [Sieber, Oliver M.] Monash Univ, Dept Biochem & Mol Biol, Clayton, Vic 3800, Australia.
C3 Walter & Eliza Hall Institute; University of Melbourne; University of
   Melbourne; University of Melbourne; Monash University
RP Putoczki, TL (corresponding author), Walter & Eliza Hall Inst Med Res, Personalised Oncol Div, Parkville, Vic 3052, Australia.; Putoczki, TL (corresponding author), Univ Melbourne, Dept Med Biol, Parkville, Vic 3010, Australia.; Putoczki, TL (corresponding author), Univ Melbourne, Dept Surg, Parkville, Vic 3010, Australia.
EM abdirahman.s@wehi.edu.au; christie.m@wehi.edu.au;
   preaudet.a@wehi.edu.au; burstroem.l@wehi.edu.au; Mouradov.d@wehi.edu.au;
   lee.b@wehi.edu.au; sieber.o@wehi.edu.au; Putoczki.t@wehi.edu.au
RI Sieber, Oliver/ABA-9211-2021; Sieber, Oliver/M-9473-2015
OI Putoczki, Tracy/0000-0003-1639-4932; Abdirahman,
   Suad/0000-0002-3276-9557; Sieber, Oliver/0000-0001-9480-0786; Mouradov,
   Dmitri/0000-0001-8149-816X; Lee, Belinda/0000-0002-0947-9834
FU Victorian Cancer Agency [MCRF16009]; Cancer Therapeutics (CTX); National
   Health and Medical Research Council (NHMRC) of Australia [1080498,
   1079362, 1136119]; WEHI Dyson Bequest Centenary Fellowship; National
   Health and Medical Research Council of Australia [1136119, 1080498,
   1079362] Funding Source: NHMRC
FX This project was funded by the Victorian Cancer Agency (MCRF16009 to
   T.L.P.) with additional support from Cancer Therapeutics (CTX to T.L.P.
   and O.M.S.), and the National Health and Medical Research Council
   (NHMRC) of Australia (project 1080498 to TLP, project 1079362 and
   fellowship 1136119 to O.M.S.), a WEHI Dyson Bequest Centenary Fellowship
   (T.L.P.). We gratefully acknowledge infrastructure support from the
   NHMRC IRIISS and the Victorian State Government Operational
   Infrastructure Support Program.
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NR 91
TC 10
Z9 12
U1 0
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD SEP
PY 2020
VL 12
IS 9
AR 2340
DI 10.3390/cancers12092340
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OD8UM
UT WOS:000580121600001
PM 32825052
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Bin, J
   Nie, SL
   Tang, ZY
   Kang, AD
   Fu, ZP
   Hu, YB
   Liao, QJ
   Xiong, W
   Zhou, YJ
   Tang, YY
   Jiang, JR
AF Bin, Jie
   Nie, Shaolin
   Tang, Ziyuan
   Kang, Anding
   Fu, Zhongping
   Hu, Yingbin
   Liao, Qianjin
   Xiong, Wei
   Zhou, Yujuan
   Tang, Yanyan
   Jiang, Jiarui
TI Long noncoding RNA EPB41L4A-AS1 functions as an oncogene by regulating
   the Rho/ROCK pathway in colorectal cancer
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Article
DE colorectal cancer; epithelial-mesenchymal transition; long noncoding RNA
ID HEPATOCELLULAR-CARCINOMA; CELL-PROLIFERATION; POOR-PROGNOSIS; INVASION;
   MIGRATION; CYTOSKELETON; PROGRESSION; METASTASIS; MECHANISMS; GROWTH
AB Colorectal cancer (CRC) is one of the most common malignant tumors worldwide. In terms of cancer-related death, colon cancer ranks second and third among men and women, respectively, and the incidence is increasing annually. Accumulating evidence have indicated that long noncoding RNA (lncRNA) plays an important role in tumorigenesis. In this study, we found that lncRNA EPB41L4A-AS1 was highly expressed in CRC tissues and was associated with poor prognosis and tumor metastasis in patients with CRC. In vitro studies showed that the knockdown of EPB41L4A-AS1 inhibited the proliferation, migration, invasion, and epithelial-mesenchymal transition of CRC cells. Mechanically, we found that EPB41L4A-AS1 may participate in the development of CRC by activating the Rho/Rho-associated protein kinase signaling pathway. Collectively, these results demonstrated that EPB41L4A-AS1 can promote the proliferation, invasion, and migration of CRC, and it may be a novel biomarker for the diagnosis and targeted treatment of CRC.
C1 [Bin, Jie; Nie, Shaolin; Tang, Ziyuan; Kang, Anding; Fu, Zhongping; Hu, Yingbin; Liao, Qianjin; Xiong, Wei; Zhou, Yujuan; Tang, Yanyan; Jiang, Jiarui] Cent South Univ, Hunan Canc Hosp, Affiliated Canc Hosp, Xiangya Sch Med, 283 Tongzipo Rd, Changsha 410013, Hunan, Peoples R China.
   [Bin, Jie; Nie, Shaolin; Tang, Ziyuan; Kang, Anding; Fu, Zhongping; Hu, Yingbin; Tang, Yanyan; Jiang, Jiarui] Cent South Univ, Hunan Canc Hosp, Affiliated Canc Hosp, Dept Colorectal Surg,Xiangya Sch Med, Changsha, Peoples R China.
   [Liao, Qianjin; Tang, Yanyan] Cent South Univ, Hunan Canc Hosp, Affiliated Canc Hosp, Cent Lab,Xiangya Sch Med, Changsha, Peoples R China.
   [Xiong, Wei] Cent South Univ, Canc Res Inst, Key Lab Carcinogenesis & Canc Invas, Chinese Minist Educ, Changsha, Hunan, Peoples R China.
C3 Central South University; Central South University; Central South
   University; Central South University
RP Tang, YY; Jiang, JR (corresponding author), Cent South Univ, Hunan Canc Hosp, Affiliated Canc Hosp, Xiangya Sch Med, 283 Tongzipo Rd, Changsha 410013, Hunan, Peoples R China.
EM yytang@csu.edu.cn; 15974241531@163.com
RI Hu, Yingbin/IQU-7644-2023; xiong, wei/GXZ-9586-2022
OI Hu, Yingbin/0000-0003-3645-7339
FU Funding for Hunan Science and Technology Plan Project [2016SK2043];
   Changsha Science and Technology Project [kq1901071]; Research Projects
   of Health Commission of Hunan Province [20201772]; Natural Science
   Foundation of Hunan Province [2018JJ3634]; Fundamental Research Funds
   for the Central Universities of Central South University, Changsha,
   China [502211904]
FX Funding for Hunan Science and Technology Plan Project, Grant/Award
   Number: 2016SK2043; The Changsha Science and Technology Project,
   Grant/Award Number: kq1901071; Research Projects of Health Commission of
   Hunan Province, Grant/Award Number: 20201772; Natural Science Foundation
   of Hunan Province, Grant/Award Number: 2018JJ3634; Fundamental Research
   Funds for the Central Universities of Central South University,
   Changsha, China, Grant/Award Number: 502211904
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NR 44
TC 26
Z9 27
U1 0
U2 9
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9541
EI 1097-4652
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD JAN
PY 2021
VL 236
IS 1
BP 523
EP 535
DI 10.1002/jcp.29880
EA JUN 2020
PG 13
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA OT9OU
UT WOS:000540703000001
PM 32557646
DA 2025-01-04
ER

PT J
AU Wu, XY
   Xu, JZ
   Yang, XY
   Wang, DP
   Xu, XX
AF Wu, Xinyu
   Xu, Jinzhao
   Yang, Xiaoying
   Wang, Danping
   Xu, Xiaoxi
TI Integrating Transcriptomics and Metabolomics to Explore the Novel
   Pathway of <i>Fusobacterium nucleatum</i> Invading Colon Cancer Cells
SO PATHOGENS
LA English
DT Article
DE Fusobacterium nucleatum; extracellular vesicles; colon cancer cells;
   transcriptomics; metabolomics
ID GUT MICROBIOTA; MICE; EXPRESSION; INHIBITOR; PROTEIN
AB Colorectal cancer (CRC) is a malignancy with a very high incidence and mortality rate worldwide. Fusobacterium nucleatum bacteria and their metabolites play a role in inducing and promoting CRC; however, no studies on the exchange of information between Fusobacterium nucleatum extracellular vesicles (Fnevs) and CRC cells have been reported. Our research shows that Fusobacterium nucleatum ATCC25586 secretes extracellular vesicles carrying active substances from parental bacteria which are endocytosed by colon cancer cells. Moreover, Fnevs promote the proliferation, migration, and invasion of CRC cells and inhibit apoptosis; they also improve the ability of CRC cells to resist oxidative stress and SOD enzyme activity. The genes differentially expressed after transcriptome sequencing are mostly involved in the positive regulation of tumor cell proliferation. After detecting differential metabolites using liquid chromatography-tandem mass spectrometry, Fnevs were found to promote cell proliferation by regulating amino acid biosynthesis in CRC cells and metabolic pathways such as central carbon metabolism, protein digestion, and uptake in cancer. In summary, this study not only found new evidence of the synergistic effect of pathogenic bacteria and colon cancer tumor cells, but also provides a new direction for the early diagnosis and targeted treatment of colon cancer.
C1 [Wu, Xinyu; Xu, Jinzhao; Yang, Xiaoying; Wang, Danping; Xu, Xiaoxi] Northeast Agr Univ, Key Lab Dairy Sci, Minist Educ, Harbin 150030, Peoples R China.
   [Wu, Xinyu; Xu, Jinzhao; Yang, Xiaoying; Wang, Danping; Xu, Xiaoxi] Northeast Agr Univ, Coll Food Sci, Harbin 150030, Peoples R China.
C3 Northeast Agricultural University - China; Northeast Agricultural
   University - China
RP Xu, XX (corresponding author), Northeast Agr Univ, Key Lab Dairy Sci, Minist Educ, Harbin 150030, Peoples R China.; Xu, XX (corresponding author), Northeast Agr Univ, Coll Food Sci, Harbin 150030, Peoples R China.
EM xiaoxi_xu01@163.com
RI Xu, Jinzhao/HSI-1253-2023
OI Xu, Jinzhao/0000-0003-4372-3295; Xu, Xiao-Xi/0000-0002-4350-0094; wu,
   xin yu/0000-0002-0253-6760
FU Major special project of "ten million" engineering science and
   technology in Heilongjiang Province [2020ZX07B01]
FX This research was funded by Major special project of "ten million"
   engineering science and technology in Heilongjiang Province
   (2020ZX07B01).
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NR 60
TC 2
Z9 2
U1 9
U2 34
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-0817
J9 PATHOGENS
JI Pathogens
PD FEB
PY 2023
VL 12
IS 2
AR 201
DI 10.3390/pathogens12020201
PG 18
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA 9K6EP
UT WOS:000940958900001
PM 36839472
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Jin, ZH
   Sinicrope, FA
AF Jin, Zhaohui
   Sinicrope, Frank A.
TI Advances in the therapy of BRAF<SUP>V600E</SUP> metastatic colorectal
   cancer
SO EXPERT REVIEW OF ANTICANCER THERAPY
LA English
DT Review
DE BRAF(V600E); colorectal cancer; targeted treatment; microsatellite
   instability; circulating tumor DNA
ID DNA MISMATCH REPAIR; III COLON-CANCER; FOLFOXIRI PLUS BEVACIZUMAB; CELL
   LUNG-CANCER; KRAS WILD-TYPE; MICROSATELLITE INSTABILITY; 1ST-LINE
   TREATMENT; BRAF MUTATION; OPEN-LABEL; CLINICAL VALIDATION
AB Introduction: BRAF(V600E) metastatic colorectal cancer (CRC) is an aggressive tumor subset with an approximate 8% incidence. In these patients, standard chemotherapy has limited efficacy, and the recent development of novel-targeted treatment regimens may significantly improve clinical outcome. Area covered: This review provides an overview of available data regarding advances in the first-line treatment of BRAF(V600E) metastatic CRC including patient tumors with microsatellite instability. The implications of BRAF(V600E) in earlier stage CRC are also discussed. Expert opinion: Recently, significant progress has been achieved in improving tumor response rates using a novel-targeted regimen in patients with BRAF(V600E) metastatic CRC. The implications of BRAF(V600E) in non-metastatic CRC are also becoming more evident and remains an area of ongoing investigation. The majority of CRCs with microsatellite instability high are sporadic and frequently harbor BRAF(V600E). All patients with microsatellite instability high metastatic CRCs, irrespective of BRAF(V600E), are candidates for immune checkpoint inhibitors. The optimal sequencing of treatment regimens for patients with BRAF(V600E) metastatic CRCs is an important area for future research.
C1 [Jin, Zhaohui; Sinicrope, Frank A.] Mayo Clin, Div Oncol, Rochester, MN 55905 USA.
   [Jin, Zhaohui; Sinicrope, Frank A.] Mayo Comprehens Canc Ctr, Rochester, MN 14642 USA.
C3 Mayo Clinic; Mayo Clinic
RP Sinicrope, FA (corresponding author), Mayo Clin, Div Oncol, Rochester, MN 55905 USA.; Sinicrope, FA (corresponding author), Mayo Comprehens Canc Ctr, Rochester, MN 14642 USA.
EM Sinicrope.Frank@mayo.edu
RI Jin, Zhaohui/AAI-5562-2020
OI Jin, Zhaohui/0000-0001-7844-5833
CR [Anonymous], J CLIN ONCOL S
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NR 65
TC 3
Z9 6
U1 0
U2 9
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1473-7140
EI 1744-8328
J9 EXPERT REV ANTICANC
JI Expert Rev. Anticancer Ther
PD SEP 2
PY 2019
VL 19
IS 9
BP 823
EP 829
DI 10.1080/14737140.2019.1661778
EA SEP 2019
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IY3JJ
UT WOS:000485014300001
PM 31455117
DA 2025-01-04
ER

PT J
AU Franzén, AS
   Boulifa, A
   Radecke, C
   Stintzing, S
   Raftery, MJ
   Pecher, G
AF Franzen, Alexander Sebastian
   Boulifa, Abdelhadi
   Radecke, Clarissa
   Stintzing, Sebastian
   Raftery, Martin J.
   Pecher, Gabriele
TI Next-Generation CEA-CAR-NK-92 Cells against Solid Tumors: Overcoming
   Tumor Microenvironment Challenges in Colorectal Cancer
SO CANCERS
LA English
DT Article
DE immunotherapy; CAR-NK; CEA; PD1-checkpoint inhibition (CPI); CCR4;
   colorectal carcinoma (CRC); NK-92-cell line; tumor microenvironment;
   trogocytosis; 3D tumor models
ID NATURAL-KILLER-CELLS; CARCINOEMBRYONIC ANTIGEN; NK CELLS; INFILTRATING
   LYMPHOCYTES; VIVO EXPANSION; SPHEROID MODEL; NK-92 CELLS; IMMUNE;
   RECEPTOR; SAFETY
AB Simple Summary Colon cancer is a solid tumor that is a prominent contributor to global mortality. Immune cells genetically engineered with a chimeric antigen receptor (CAR) that can recognize cancer-specific targets is a new innovative therapy approach that has had success in treating blood cancers but is still in development for treating solid tumors such as colon cancer. Part of the reason for the added difficulty in targeting solid tumors is the tumor microenvironment that acts as a protective barrier around a solid tumor. In this research paper, we have developed a new cellular approach for the targeted treatment of colon cancer that is designed to overcome the tumor microenvironment. We tested this new CAR cell therapy against multiple solid colon cancer models, and confirmed its efficacy and functionality in finding and eliminating solid tumors.Abstract Colorectal carcinoma (CRC) presents a formidable medical challenge, demanding innovative therapeutic strategies. Chimeric antigen receptor (CAR) natural killer (NK) cell therapy has emerged as a promising alternative to CAR T-cell therapy for cancer. A suitable tumor antigen target on CRC is carcinoembryonic antigen (CEA), given its widespread expression and role in tumorigenesis and metastasis. CEA is known to be prolifically shed from tumor cells in a soluble form, thus hindering CAR recognition of tumors and migration through the TME. We have developed a next-generation CAR construct exclusively targeting cell-associated CEA, incorporating a PD1-checkpoint inhibitor and a CCR4 chemokine receptor to enhance homing and infiltration of the CAR-NK-92 cell line through the TME, and which does not induce fratricidal killing of CAR-NK-92-cells. To evaluate this therapeutic approach, we harnessed intricate 3D multicellular tumor spheroid models (MCTS), which emulate key elements of the TME. Our results demonstrate the effective cytotoxicity of CEA-CAR-NK-92 cells against CRC in colorectal cell lines and MCTS models. Importantly, minimal off-target activity against non-cancerous cell lines underscores the precision of this therapy. Furthermore, the integration of the CCR4 migration receptor augments homing by recognizing target ligands, CCL17 and CCL22. Notably, our CAR design results in no significant trogocytosis-induced fratricide. In summary, the proposed CEA-targeting CAR-NK cell therapy could offer a promising solution for CRC treatment, combining precision and efficacy in a tailored approach.
C1 [Franzen, Alexander Sebastian; Boulifa, Abdelhadi; Raftery, Martin J.; Pecher, Gabriele] Univ Med Berlin, Berlin Inst Hlth Charite, Charitepl 1, D-10117 Berlin, Germany.
   [Franzen, Alexander Sebastian; Boulifa, Abdelhadi; Radecke, Clarissa; Stintzing, Sebastian; Raftery, Martin J.; Pecher, Gabriele] Charite Univ Med Berlin, Competence Ctr Immunooncol & Translat Cell Therapy, Dept Hematol Oncol & Tumor Immunol, CCM, Charitepl 1, D-10117 Berlin, Germany.
   [Franzen, Alexander Sebastian; Boulifa, Abdelhadi; Radecke, Clarissa; Stintzing, Sebastian; Raftery, Martin J.; Pecher, Gabriele] Univ Berlin, Charitepl 1, D-10117 Berlin, Germany.
   [Franzen, Alexander Sebastian; Boulifa, Abdelhadi; Radecke, Clarissa; Stintzing, Sebastian; Raftery, Martin J.; Pecher, Gabriele] Humboldt Univ, Charitepl 1, D-10117 Berlin, Germany.
C3 Berlin Institute of Health; Free University of Berlin; Humboldt
   University of Berlin; Charite Universitatsmedizin Berlin; Berlin
   Institute of Health; Free University of Berlin; Humboldt University of
   Berlin; Charite Universitatsmedizin Berlin; Berlin Institute of Health;
   Free University of Berlin; Humboldt University of Berlin; Charite
   Universitatsmedizin Berlin; Berlin Institute of Health; Free University
   of Berlin; Humboldt University of Berlin; Charite Universitatsmedizin
   Berlin
RP Pecher, G (corresponding author), Univ Med Berlin, Berlin Inst Hlth Charite, Charitepl 1, D-10117 Berlin, Germany.; Pecher, G (corresponding author), Charite Univ Med Berlin, Competence Ctr Immunooncol & Translat Cell Therapy, Dept Hematol Oncol & Tumor Immunol, CCM, Charitepl 1, D-10117 Berlin, Germany.; Pecher, G (corresponding author), Univ Berlin, Charitepl 1, D-10117 Berlin, Germany.; Pecher, G (corresponding author), Humboldt Univ, Charitepl 1, D-10117 Berlin, Germany.
EM gabriele.pecher@charite.de
RI ; Stintzing, Sebastian/I-4538-2016
OI Franzen, Alexander Sebastian/0000-0002-4169-6652; Stintzing,
   Sebastian/0000-0002-3297-5801; Pecher, Gabriele/0000-0003-0779-1493
FU Berlin Institute of Health @ Charit SPARK-Validation Track II program
FX No Statement Available
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NR 71
TC 5
Z9 5
U1 3
U2 9
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JAN
PY 2024
VL 16
IS 2
AR 388
DI 10.3390/cancers16020388
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FY1B4
UT WOS:001149310300001
PM 38254876
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zarour, LR
   Anand, S
   Billingsley, KG
   Bisson, WH
   Cercek, A
   Clarke, MF
   Coussens, LM
   Gast, CE
   Geltzeiler, CB
   Hansen, L
   Kelley, KA
   Lopez, CD
   Rana, SR
   Ruhl, R
   Tsikitis, VL
   Vaccaro, GM
   Wong, MH
   Mayo, SC
AF Zarour, Luai R.
   Anand, Sudarshan
   Billingsley, Kevin G.
   Bisson, William H.
   Cercek, Andrea
   Clarke, Michael F.
   Coussens, Lisa M.
   Gast, Charles E.
   Geltzeiler, Cristina B.
   Hansen, Lissi
   Kelley, Katherine A.
   Lopez, Charles D.
   Rana, Shushan R.
   Ruhl, Rebecca
   Tsikitis, V. Liana
   Vaccaro, Gina M.
   Wong, Melissa H.
   Mayo, Skye C.
TI Colorectal Cancer Liver Metastasis: Evolving Paradigms and Future
   Directions
SO CELLULAR AND MOLECULAR GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Review
DE Colorectal Cancer Liver Metastasis; Biomarkers; Hepatic Arterial
   Infusion; High-Risk Colorectal Cancer; Recurrence
ID HEPATIC ARTERIAL INFUSION; CIRCULATING TUMOR-CELLS; III COLON-CANCER;
   EXOSOME-MEDIATED TRANSFER; QUALITY-OF-LIFE; STAGE-II; MICROSATELLITE
   ALTERATIONS; CHROMOSOMAL INSTABILITY; CLINICAL-SIGNIFICANCE; ADJUVANT
   TREATMENT
AB Colorectal cancer ranks as the second leading cause of cancer-related deaths, with metastatic disease to the liver a common cause. Here we discuss exciting developments in the field that promise innovative approaches for early detection and treatment of metastatic colorectal cancer in the liver.
   In patients with colorectal cancer (CRC) that metasta-sizes to the liver, there are several key goals for improving outcomes including early detection, effective prognostic indicators of treatment response, and accurate identification of patients at high risk for recurrence. Although new therapeutic regimens developed over the past decade have increased survival, there is substantial room for improvement in selecting targeted treatment regimens for the patients who will derive the most benefit. Recently, there have been exciting developments in identifying high-risk patient cohorts, refinements in the understanding of systemic vs localized drug delivery to metastatic niches, liquid biomarker development, and dramatic advances in tumor immune therapy, all of which promise new and innovative approaches to tackling the problem of detecting and treating the metastatic spread of CRC to the liver. Our multidisciplinary group held a state-of-the-science symposium this past year to review advances in this rapidly evolving field. Herein, we present a discussion around the issues facing treatment of patients with CRC liver metastases, including the relationship of discrete gene signatures with prognosis. We also discuss the latest advances to maximize regional and systemic therapies aimed at decreasing intrahepatic recurrence, review recent insights into the tumor microenvironment, and summarize advances in noninvasive multimodal biomarkers for early detection of primary and recurrent disease. As we continue to advance clinically and technologically in the field of colorectal tumor biology, our goal should be continued refinement of predictive and prognostic studies to decrease recurrence after curative resection and minimize treatment toxicity to patients through a tailored multidisciplinary approach to cancer care.
C1 [Zarour, Luai R.; Billingsley, Kevin G.; Mayo, Skye C.] Oregon Hlth & Sci Univ, Div Surg Oncol, Portland, OR 97201 USA.
   [Geltzeiler, Cristina B.; Kelley, Katherine A.; Tsikitis, V. Liana] Oregon Hlth & Sci Univ, Dept Surg, Div Colorectal Surg, Portland, OR 97201 USA.
   [Anand, Sudarshan; Coussens, Lisa M.; Gast, Charles E.; Ruhl, Rebecca; Wong, Melissa H.] Oregon Hlth & Sci Univ, Dept Cell Dev & Canc Biol, Portland, OR 97201 USA.
   [Anand, Sudarshan; Billingsley, Kevin G.; Bisson, William H.; Coussens, Lisa M.; Hansen, Lissi; Lopez, Charles D.; Tsikitis, V. Liana; Vaccaro, Gina M.; Wong, Melissa H.; Mayo, Skye C.] Oregon Hlth & Sci Univ, Knight Canc Inst, Portland, OR 97201 USA.
   [Hansen, Lissi] Oregon Hlth & Sci Univ, Sch Nursing, Portland, OR 97201 USA.
   [Lopez, Charles D.; Vaccaro, Gina M.] Oregon Hlth & Sci Univ, Dept Med, Div Hematol & Med Oncol, Portland, OR 97201 USA.
   [Rana, Shushan R.] Oregon Hlth & Sci Univ, Dept Radiat Med, Portland, OR 97201 USA.
   [Bisson, William H.] Oregon State Univ, Environm & Mol Toxicol, Corvallis, OR 97331 USA.
   [Cercek, Andrea] Mem Sloan Kettering Canc Ctr, Solid Tumor Div, Dept Gastrointestinal Med Oncol, New York, NY 10021 USA.
   [Clarke, Michael F.] Stanford Univ, Stanford Inst Stem Cell & Regenerat Med, Stanford, CA 94305 USA.
   [Clarke, Michael F.] Stanford Univ, Dept Med, Div Oncol, Stanford, CA 94305 USA.
C3 Oregon Health & Science University; Oregon Health & Science University;
   Oregon Health & Science University; Oregon Health & Science University;
   Oregon Health & Science University; Oregon Health & Science University;
   Oregon Health & Science University; Oregon State University; Memorial
   Sloan Kettering Cancer Center; Stanford University; Stanford University
RP Mayo, SC (corresponding author), Oregon Hlth & Sci Univ, Dept Surg, 3181 SW Sam Jackson Pk Rd,Mailcode L223, Portland, OR 97239 USA.
EM mayos@ohsu.edu
RI Coussens, Lisa/ABH-9834-2020; Kelley, Katherine/U-5382-2019; ANAND,
   SUDARSHAN/I-5316-2019
OI Mayo, Skye/0000-0002-1631-9855; anand, sudarshan/0000-0002-4969-6884;
   Rana, Shushan/0000-0002-9298-1605; Geltzeiler,
   Cristina/0000-0003-0308-6308
FU Knight Cancer Institute at Oregon Health & Science University; Oregon
   State University
FX The State of the Science Symposium held on June 17, 2016, in Portland,
   Oregon, and this review was supported by a Team Building Pilot Project
   grant from the Knight Cancer Institute at Oregon Health & Science
   University and Oregon State University.
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NR 98
TC 203
Z9 224
U1 2
U2 43
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 2352-345X
J9 CELL MOL GASTROENTER
JI Cell. Mol. Gastroenterol. Hepatol.
PD MAR
PY 2017
VL 3
IS 2
BP 163
EP 173
DI 10.1016/j.jcmgh.2017.01.006
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA FV4IV
UT WOS:000424537700008
PM 28275683
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Martín-García, D
   García-Aranda, M
   Redondo, M
AF Martin-Garcia, Desiree
   Garcia-Aranda, Marilina
   Redondo, Maximino
TI Biomarker Identification through Proteomics in Colorectal Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE colorectal cancer; proteomics; biomarkers; personalized medicine;
   targeted treatment
ID LYMPH-NODE METASTASIS; EMBEDDED FFPE TISSUE; COLON-CANCER;
   MICROSATELLITE INSTABILITY; SERRATED PATHWAY; BREAST-CANCER; PROTEIN;
   SURVIVAL; POLYPS; MICROARRAYS
AB Colorectal cancer (CRC) is a devastating disease that ranks third in diagnosis and as the second leading cause of cancer-related deaths. The early detection of CRC has been shown to be the most effective strategy to improve treatment outcomes and patient survival. Therefore, current lines of research focus on the development of reliable diagnostic tools. Targeted therapies, in combination with standard chemotherapy and immune checkpoint inhibitors, have emerged as promising treatment protocols in CRC. However, their effectiveness is linked to the molecular characteristics of each patient. The importance of discovering biomarkers that help predict response to therapies and assess prognosis is evident as they allow for a fundamental step towards personalized care and successful treatments. Among the ongoing efforts to identify them, mass spectrometry-based translational proteomics presents itself as a unique opportunity as it enables the discovery and application of protein biomarkers that may revolutionize the early detection and treatment of CRC. Our objective is to show the most recent studies focused on the identification of CRC-related protein markers, as well as to provide an updated view of advances in the field of proteomics and cancer.
C1 [Martin-Garcia, Desiree; Redondo, Maximino] Univ Malaga, Fac Med, Biochem & Immunol Dept, Surg Specialties, Malaga 29010, Spain.
   [Martin-Garcia, Desiree; Garcia-Aranda, Marilina; Redondo, Maximino] Red Invest Cron Atenc Primaria & Promoc Salud RICA, Malaga 29590, Spain.
   [Martin-Garcia, Desiree; Garcia-Aranda, Marilina; Redondo, Maximino] Inst Invest Biomed Malaga & Plataforma Nanomed IBI, Malaga 29590, Spain.
   [Martin-Garcia, Desiree; Garcia-Aranda, Marilina; Redondo, Maximino] Hosp Univ Costa Sol, Res & Innovat Unit, Marbella 29602, Spain.
C3 Universidad de Malaga
RP Redondo, M (corresponding author), Univ Malaga, Fac Med, Biochem & Immunol Dept, Surg Specialties, Malaga 29010, Spain.; Redondo, M (corresponding author), Red Invest Cron Atenc Primaria & Promoc Salud RICA, Malaga 29590, Spain.; Redondo, M (corresponding author), Inst Invest Biomed Malaga & Plataforma Nanomed IBI, Malaga 29590, Spain.; Redondo, M (corresponding author), Hosp Univ Costa Sol, Res & Innovat Unit, Marbella 29602, Spain.
EM desirermg@uma.es; marilina.garcia.sspa@juntadeandalucia.es;
   maximino.redondo.sspa@juntadeandalucia.es
RI ARANDA, MARILINA/AAH-4730-2019
OI Martin-Garcia, Desiree/0009-0009-5007-0529; GARCIA ARANDA,
   MARILINA/0000-0003-3759-4044
FU European Social Fund-Operational Program of Andalusia 2014-2020
FX No Statement Available
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NR 106
TC 4
Z9 4
U1 1
U2 11
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD FEB
PY 2024
VL 25
IS 4
AR 2283
DI 10.3390/ijms25042283
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA IS6B2
UT WOS:001168348800001
PM 38396959
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Hasibuan, PAZ
   Simanjuntak, Y
   Hey-Hawkins, E
   Lubis, MF
   Rohani, AS
   Park, MN
   Kim, B
   Syahputra, RA
AF Hasibuan, Poppy Anjelisa Zaitun
   Simanjuntak, Yogi
   Hey-Hawkins, Evamarie
   Lubis, Muhammad Fauzan
   Rohani, Ade Sri
   Park, Moon Nyeo
   Kim, Bonglee
   Syahputra, Rony Abdi
TI Unlocking the potential of flavonoids: Natural solutions in the fight
   against colon cancer
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE Colon cancer; Flavonoids; Chemoprevention; Xenograft; Genetically
   engineered mouse; models (GEMMs); Inflammation
ID NF-KAPPA-B; SODIUM-INDUCED COLITIS; COLORECTAL-CANCER; IN-VITRO;
   DNA-DAMAGE; ANTICANCER ACTIVITY; OXIDATIVE STRESS; APC(MIN/+) MICE; GUT
   MICROBIOTA; MOUSE MODELS
AB Colorectal cancer (CRC) is a major cause of cancer-related deaths worldwide, underscoring the importance of understanding the diverse molecular and genetic underpinnings of CRC to improve its diagnosis, prognosis, and treatment. This review delves into the adenoma-carcinoma-metastasis model, emphasizing the "APC-KRAS-TP53" signature events in CRC development. CRC is categorized into four consensus molecular subtypes, each characterized by unique genetic alterations and responses to therapy, illustrating its complexity and heterogeneity. Furthermore, we explore the role of chronic inflammation and the gut microbiome in CRC progression, emphasizing the potential of targeting these factors for prevention and treatment. This review discusses the impact of dietary carcinogens and lifestyle factors and the critical role of early detection in improving outcomes, and also examines conventional chemotherapy options for CRC and associated challenges. There is significant focus on the therapeutic potential of flavonoids for CRC management, discussing various types of flavonoids, their sources, and mechanisms of action, including their antioxidant properties, modulation of cell signaling pathways, and effects on cell cycle and apoptosis. This article presents evidence of the synergistic effects of flavonoids with conventional cancer therapies and their role in modulating the gut microbiome and immune response, thereby offering new avenues for CRC treatment. We conclude by emphasizing the importance of a multidisciplinary approach to CRC research and treatment, incorporating insights from genetic, molecular, and lifestyle factors. Further research is needed on the preventive and therapeutic potential of natural compounds, such as flavonoids, in CRC, underscoring the need for personalized and targeted treatment strategies.
C1 [Hasibuan, Poppy Anjelisa Zaitun; Simanjuntak, Yogi; Rohani, Ade Sri; Syahputra, Rony Abdi] Univ Sumatera Utara, Fac Pharm, Dept Pharmacol, Sumatera Utara, Indonesia.
   [Hey-Hawkins, Evamarie] Univ Leipzig, Inst Bioanalyt Chem, Fac Chem & Mineral, Ctr Biotechnol & Biomed BBZ, Deutsch Pl 5, D-04103 Leipzig, Germany.
   [Lubis, Muhammad Fauzan] Univ Sumatera Utara, Fac Pharm, Dept Pharmaceut Biol, Sumatera Utara, Indonesia.
   [Park, Moon Nyeo; Kim, Bonglee] Kyung Hee Univ, Coll Korean Med, Dept Internal Med, Seoul 02447, South Korea.
   [Park, Moon Nyeo; Kim, Bonglee] Kyung Hee Univ, Coll Korean Med, Seoul 05253, South Korea.
C3 University of North Sumatra; Leipzig University; University of North
   Sumatra; Kyung Hee University; Kyung Hee University
RP Hasibuan, PAZ (corresponding author), Univ Sumatera Utara, Fac Pharm, Dept Pharmacol, Sumatera Utara, Indonesia.
EM poppyanjelisa@usu.ac.id
RI anjelisa zaitun hasibuan, poppy/JVZ-8785-2024; Kim,
   Bonglee/AAH-9077-2020; Rohani, Ade Sri/GPP-4887-2022
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NR 240
TC 2
Z9 2
U1 9
U2 9
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD JUL
PY 2024
VL 176
AR 116827
DI 10.1016/j.biopha.2024.116827
EA JUN 2024
PG 26
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA XT0V2
UT WOS:001263820300001
PM 38850646
OA gold
DA 2025-01-04
ER

PT J
AU Al Kattar, S
   Jurjus, R
   Pinon, A
   Leger, DY
   Jurjus, A
   Boukarim, C
   Diab-Assaf, M
   Liagre, B
AF Al Kattar, Sahar
   Jurjus, Rosalyn
   Pinon, Aline
   Leger, David Yannick
   Jurjus, Abdo
   Boukarim, Chawki
   Diab-Assaf, Mona
   Liagre, Bertrand
TI Metformin and Probiotics in the Crosstalk between Colitis-Associated
   Colorectal Cancer and Diabetes in Mice
SO CANCERS
LA English
DT Article
DE colorectal cancer; microbiota; inflammation; diabetes; oxidative stress;
   probiotics
ID INFLAMMATORY-BOWEL-DISEASE; NF-KAPPA-B; GUT MICROBIOTA; COLON-CANCER;
   TNF-ALPHA; MODEL; MELLITUS; SUPPLEMENTATION; INHIBITION; MECHANISMS
AB The co-occurrence of colorectal cancer (CRC) and diabetes mellitus along with inflammation and dismicrobism has been frequently reported. Several studies shed light on the antioncogenic potential of metformin on colorectal carcinogenesis. This study aimed to demonstrate that metformin in association with probiotics acts in a synergic effect in breaking the crosstalk, thus inhibiting CRC progression, improving diabetes, and reducing inflammation. Ninety-six male Balb/c mice, 6-8 weeks old, were divided into 16 control and experimental groups to assess the effect of the different treatments and combinations at the clinical, histological, and molecular levels. Metformin and probiotics showed beneficial outcomes on CRC and diabetes, alone and most importantly in combination. Their effects were exerted by inhibiting the inflammatory process whereby a downregulation of IL-6 and TNF-alpha as well as oxidative stress were depicted. The characterization of the effects of probiotics and metformin on CRC and diabetes sheds light on the role of inflammation and microbiota in this crosstalk. Deciphering the downstream signaling pathways elicited by these compounds will help in developing new effective targeted treatment modalities.
C1 [Al Kattar, Sahar; Pinon, Aline; Leger, David Yannick; Liagre, Bertrand] Univ Limoges, Fac Pharm, Lab PEIRENE EA 7500, 2 Rue Docteur Raymond Marcland, F-87025 Limoges, France.
   [Al Kattar, Sahar; Diab-Assaf, Mona] Lebanese Univ, Doctoral Sch Sci & Technol, Hadath 99000, Lebanon.
   [Al Kattar, Sahar; Jurjus, Rosalyn; Jurjus, Abdo] Amer Univ Beirut, Dept Anat Cell Biol & Physiol, Beirut 11072020, Lebanon.
   [Boukarim, Chawki] Lebanese Univ, Fac Sci 3, Dept Chem, Mt Michel Ras Maska 826, El Koura, Lebanon.
C3 Universite de Limoges; American University of Beirut
RP Liagre, B (corresponding author), Univ Limoges, Fac Pharm, Lab PEIRENE EA 7500, 2 Rue Docteur Raymond Marcland, F-87025 Limoges, France.; Jurjus, A (corresponding author), Amer Univ Beirut, Dept Anat Cell Biol & Physiol, Beirut 11072020, Lebanon.
EM sahar_kattar@hotmail.com; rj58@aub.edu.lb; aline.pinon@unilim.fr;
   david.leger@unilim.fr; aj00@aub.edu.lb; cboukarim@ul.edu.lb;
   mdiabassaf@ul.edu.lb; bertrand.liagre@unilim.fr
RI Liagre, Bertrand/G-2979-2013; Jurjus, Rosalyn/AAG-7853-2020
OI Pinon, Aline/0000-0002-3123-7495; Liagre, Bertrand/0000-0003-4148-2598
FU Ministere de l'Enseignement Superieur, de la Recherche et de
   l'Innovation through the European Fund of Regional Development FEDER
   2014-2020; Conseil Regional Nouvelle Aquitaine; Ligue contre le Cancer;
   American University of Beirut, Seed grant
FX The expenses of this work were defrayed in part by the Ministere de
   l'Enseignement Superieur, de la Recherche et de l'Innovation through the
   European Fund of Regional Development FEDER 2014-2020, by the Conseil
   Regional Nouvelle Aquitaine, and by the Ligue contre le Cancer; and by
   the American University of Beirut, Seed grant.
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NR 65
TC 16
Z9 17
U1 2
U2 23
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUL
PY 2020
VL 12
IS 7
AR 1857
DI 10.3390/cancers12071857
PG 31
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA MX2PD
UT WOS:000557567200001
PM 32664279
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU O'Connell, E
   Reynolds, IS
   McNamara, DA
   Burke, JP
   Prehn, JHM
AF O'Connell, Emer
   Reynolds, Ian S.
   McNamara, Deborah A.
   Burke, John P.
   Prehn, Jochen H. M.
TI Resistance to Cell Death in Mucinous Colorectal Cancer-A Review
SO CANCERS
LA English
DT Review
DE mucin; colorectal; apoptosis; chemo-resistance
AB Simple Summary
   Mucinous colorectal cancer is characterised by abundant mucin glycoprotein production and is associated with resistance to chemotherapy-based treatments. This review outlines mechanisms for cell death resistance present in mucinous colorectal cancer including glycoprotein interactions with cell survival and cell apoptotic pathways. Further mechanisms are explored, including alterations in the expression of chemotherapy metabolism and resistance genes. This review identifies directions for future investigation of mucinous colorectal cancer and novel treatment strategies.
   Mucinous colorectal cancer (CRC) is estimated to occur in approximately 10-15% of CRC cases and is characterized by abundant extracellular mucin. Mucinous CRC is frequently associated with resistance to apoptosis. Inferior prognosis is observed in mucinous CRC, particularly in rectal cancer and metastatic cases. Mucins are heavily glycosylated secretory or transmembrane proteins that participate in protection of the colonic epithelium. MUC2 overexpression is a hallmark of mucinous CRCs. Mucinous CRC is associated with KRAS and BRAF mutation, microsatellite instability and the CpG island methylator phenotype. Mutations of the APC gene and p53 mutations which are characteristic non-mucinous colorectal adenocarcinoma are less common in mucinous CRC. Both physical and anti-apoptotic properties of mucin provide mechanisms for resistance to cell death. Mucin glycoproteins are associated with decreased expression of pro-apoptotic proteins, increased expression of anti-apoptotic proteins and increased cell survival signaling. The role for BCL-2 proteins, including BCL-X-L, in preventing apoptosis in mucinous CRC has been explored to a limited extent. Additional mechanisms opposing cell death include altered death receptor expression and altered mutation rates in genes responsible for chemotherapy resistance. The roles of alternate cell death programs including necroptosis and pyroptosis are not well understood in mucinous CRC. While the presence of MUC2 is associated with an immunosuppressive environment, the tumor immune environment of mucinous CRC and the role of immune-mediated tumor cell death likewise require further investigation. Improved understanding of cell death mechanisms in mucinous CRC may allow modification of currently used regimens and facilitate targeted treatment.
C1 [O'Connell, Emer; Reynolds, Ian S.; McNamara, Deborah A.; Burke, John P.] Beaumont Hosp, Dept Colorectal Surg, Dublin 9, Ireland.
   [O'Connell, Emer; Reynolds, Ian S.; Prehn, Jochen H. M.] Royal Coll Surgeons Ireland, Dept Physiol & Med Phys, Dublin 2, Ireland.
   [McNamara, Deborah A.] Royal Coll Surgeons Ireland, Dept Surg, Dublin 2, Ireland.
   [Prehn, Jochen H. M.] Royal Coll Surgeons Ireland, Ctr Syst Med, Dublin 2, Ireland.
C3 Royal College of Surgeons - Ireland; Royal College of Surgeons -
   Ireland; Royal College of Surgeons - Ireland
RP Prehn, JHM (corresponding author), Royal Coll Surgeons Ireland, Dept Physiol & Med Phys, Dublin 2, Ireland.; Prehn, JHM (corresponding author), Royal Coll Surgeons Ireland, Ctr Syst Med, Dublin 2, Ireland.
EM emerpoconnell@rcsi.com; ianreynolds@rcsi.ie; deborahmcnamara@rcsi.ie;
   johnburke@rcsi.ie; Prehn@rcsi.ie
RI Reynolds, Ian/AAF-6332-2020; Prehn, Jochen/A-3928-2010
OI Prehn, Jochen/0000-0003-3479-7794; McNamara,
   Deborah/0000-0003-3975-0485; Reynolds, Ian Sean/0000-0002-8790-2538
FU RCSI StAR MD programme [19437]; Beaumont Hospital Colorectal Research
   Trust [19518]
FX This research was funded by the RCSI StAR MD programme, grant number
   19437 and the Beaumont Hospital Colorectal Research Trust, grant number
   19518.
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NR 96
TC 19
Z9 19
U1 1
U2 16
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD MAR
PY 2021
VL 13
IS 6
AR 1389
DI 10.3390/cancers13061389
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RE7PC
UT WOS:000634340100001
PM 33808549
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Hajjafari, A
   Sadr, S
   Rahdar, A
   Bayat, M
   Lotfalizadeh, N
   Dianaty, S
   Rezaei, A
   Moghaddam, SP
   Hajjafari, K
   Simab, PA
   Kharaba, Z
   Borji, H
   Pandey, S
AF Hajjafari, Ashkan
   Sadr, Soheil
   Rahdar, Abbas
   Bayat, Mansour
   Lotfalizadeh, Narges
   Dianaty, Shiva
   Rezaei, Arezou
   Moghaddam, Soroush Partovi
   Hajjafari, Khashayar
   Simab, Pouria Ahmadi
   Kharaba, Zelal
   Borji, Hassan
   Pandey, Sadanand
TI Exploring the integration of nanotechnology in the development and
   application of biosensors for enhanced detection and monitoring of
   colorectal cancer
SO INORGANIC CHEMISTRY COMMUNICATIONS
LA English
DT Article
DE Biosensors; Colorectal cancer; Biomarkers; Diagnosis; Nanotechnology
ID FUNCTIONAL COMPOSITE NANOFIBERS; ISLAND METHYLATOR PHENOTYPE; DOT-BASED
   NANOSENSOR; BOTTOM-UP SYNTHESIS; COLON-CANCER; ELECTROCHEMICAL
   BIOSENSORS; MICROSATELLITE INSTABILITY; CARCINOEMBRYONIC ANTIGEN;
   SENSITIVE DETECTION; TUMOR-MARKERS
AB As the third most severe cancer in the world, colorectal cancer (CRC) is of high concern to global health concerns. Aging, unhealthy lifestyles, and genetic factors contribute to CRC development. Early detection and intervention are crucial due to early-stage symptoms' subtle or absent nature. The interplay of genetic and environmental factors has identified potential CRC biomarkers for early detection and prognosis. Nanotechnology offers promising opportunities in CRC screening, detection, and treatment. A targeted nanoparticle enhances the accuracy of diagnosis and treatment effectiveness for CRC. PET, MRI, and fluorescence imaging are nanoparticlebased imaging techniques that have revolutionized cancer detection. Additionally, nanoparticles are used in biosensors, highly sensitive devices, to detect CRC-associated biomarkers, allowing for an early diagnosis. Nanoparticles have made significant contributions to cancer care due to these advancements. Drug delivery systems utilize nanoparticles to deliver anticancer drugs directly to CRC cells, improving drug efficacy and stability. This review examines CRC, covering clinical stages, pathogenic mechanisms, and potential biomarkers. Some CRC biomarkers include mutations in genes (KRAS, BRAF, TP53, APC, NRAS), Carcinoembryonic Antigen (CEA), DNA mismatch repair, CA19-9, Epidermal growth factor receptor (EGFR), microsatellite instability status, MicroRNAs (miRNAs), Interleukin-6 (IL-6), CpG island methylation, and Circulating Tumor Cells (CTCs). These biomarkers play a role in diagnosis, prognosis, and targeted treatment strategies for CRC. The review emphasizes the importance of early diagnosis for successful treatment and improved patient outcomes. It explores recent advancements in utilizing nanotechnology for CRC diagnosis and therapy. Integrating nanomedicine and personalized treatments in CRC management shows promise for enhancing patient care and prognosis. Investing in nanomaterials and nanotechnology will likely increase our ability to develop more effective treatment, prevention, and diagnosis strategies to combat CRC, ultimately reducing its impact.
C1 [Hajjafari, Ashkan; Bayat, Mansour; Moghaddam, Soroush Partovi] Islamic Azad Univ, Fac Vet Med Sci, Dept Pathobiol, Sci & Res Branch, Tehran, Iran.
   [Sadr, Soheil; Lotfalizadeh, Narges; Borji, Hassan] Ferdowsi Univ Mashhad, Fac Vet Med, Dept Pathobiol, Mashhad, Iran.
   [Rahdar, Abbas] Univ Zabol, Dept Phys, Zabol, Iran.
   [Dianaty, Shiva] Shahrekord Univ, Fac Vet Med, Dept Clin Sci, Shahrekord, Iran.
   [Rezaei, Arezou] Damghan Univ, Sch Biol, Damghan, Iran.
   [Hajjafari, Khashayar] Med Doctor Seyed Oshohada Gen Hosp, Kerman, Iran.
   [Simab, Pouria Ahmadi] Islamic Azad Univ, Fac Vet Med, Dept Pathobiol, Sanandaj Branch, Sanandaj, Iran.
   [Kharaba, Zelal] Univ Sharjah, Coll Pharm, Dept Pharm Practice & Pharmacotherapeut, Sharjah, U Arab Emirates.
   [Rahdar, Abbas; Bayat, Mansour; Kharaba, Zelal; Borji, Hassan; Pandey, Sadanand] Shoolini Univ, Fac Appl Sci & Biotechnol, Sch Bioengn & Food Technol, Solan 173229, Himachal Prades, India.
   [Pandey, Sadanand] Yeungnam Univ, Coll Nat Sci, Dept Chem, 280 Daehak Ro, Gyongsan 38541, Gyeongbuk, South Korea.
C3 Islamic Azad University; Ferdowsi University Mashhad; Shahrekord
   University; Damghan University; Islamic Azad University; University of
   Sharjah; Shoolini University; Yeungnam University
RP Rahdar, A; Bayat, M; Kharaba, Z; Borji, H; Pandey, S (corresponding author), Shoolini Univ, Fac Appl Sci & Biotechnol, Sch Bioengn & Food Technol, Solan 173229, Himachal Prades, India.
EM a.rahdar@uoz.ac.ir; m.bayat@srbiau.ac.ir; zkharaba@sharjah.ac.ae;
   hborji@um.ac.ir; sadanand.au@gmail.com
RI Sadr, Soheil/JNR-2873-2023; Borji, Hassan/AAB-4024-2020; Rahdar,
   Abbas/S-1816-2019; Hajjafari, Ashkan/JXX-2583-2024; Ahmadi Simab,
   Pouria/AEO-1058-2022
OI Kharaba, Zelal/0000-0001-8012-684X; Hajjafari,
   Ashkan/0000-0003-2849-9125
FU University of Zabol [UOZ- GR-8906]
FX Abbas Rahdar thanks from University of Zabol for funding (UOZ- GR-8906).
   The authors (Sadanand Pandey) express profound gratitude to Shoolini
   University for their invaluable support, which played a pivotal role in
   facilitating the completion of work.
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NR 351
TC 10
Z9 10
U1 6
U2 9
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1387-7003
EI 1879-0259
J9 INORG CHEM COMMUN
JI Inorg. Chem. Commun.
PD JUN
PY 2024
VL 164
AR 112409
DI 10.1016/j.inoche.2024.112409
EA APR 2024
PG 20
WC Chemistry, Inorganic & Nuclear
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA SJ6L0
UT WOS:001234124100001
DA 2025-01-04
ER

PT J
AU Frackowiak, M
   Lewandowski, T
   Stelmasiak, P
AF Frackowiak, Marta
   Lewandowski, Tomasz
   Stelmasiak, Pawel
TI Molecular subtypes of colorectal cancer as a potential prognostic and
   predictive factor in the selection of the optimal treatment strategy
SO ONCOLOGY IN CLINICAL PRACTICE
LA English
DT Review
DE colon cancer; CMS; chemotherapy; molecular-targeted treatment
ID COLON-CANCER; SURVIVAL
AB Colorectal cancer is one of the most common cancers and is the third cause of death from malignant tumours. In recent years, a consensus has been developed that distinguishes four subtypes of colon cancer (CMS, consensus molecular subtypes): CMS1 - immunological, CMS2 - canonical, CMS3 - metabolic, and CMS4 - mesenchymal. They differ in terms of clinical course and response to chemotherapy and biological treatment. The practical application of molecular classification can be helpful as a prognostic and predictive factor in the selection of an optimal and individualised strategy for the treatment of individual patients.
C1 [Frackowiak, Marta; Lewandowski, Tomasz; Stelmasiak, Pawel] Radom Oncol Ctr, Ul Uniwersytecka 6, PL-26600 Radom, Poland.
   [Lewandowski, Tomasz] Ctr Postgrad Med Educ, Warsaw, Poland.
C3 Centre of Postgraduate Medical Education - Poland
RP Frackowiak, M (corresponding author), Radom Oncol Ctr, Ul Uniwersytecka 6, PL-26600 Radom, Poland.
EM m.frackowiak@onkologiaradom.pl
RI Stelmasiak, Paweł/ITT-5377-2023
OI Stelmasiak, Pawel/0009-0000-5838-6215
CR Aderka D., 2018, ESMO WCGC
   [Anonymous], P AM SOC CLIN ONCO S
   [Anonymous], 2017, P AM SOC CLIN ONCO S
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NR 27
TC 1
Z9 1
U1 0
U2 4
PU VIA MEDICA
PI GDANSK
PA UL SWIETOKRZYSKA 73, 80-180 GDANSK, POLAND
SN 2450-1654
EI 2450-6478
J9 ONCOL CLIN PRACT
JI Oncol. Clin. Pract.
PY 2019
VL 15
IS 6
BP 320
EP 325
DI 10.5603/OCP.2019.0036
PG 6
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA KJ8GC
UT WOS:000512293100007
OA gold
DA 2025-01-04
ER

PT J
AU Akhoundova, D
   Hussung, S
   Sivakumar, S
   Töpfer, A
   Rechsteiner, M
   Kahraman, A
   Arnold, F
   Angst, F
   Britschgi, C
   Zoche, M
   Moch, H
   Weber, A
   Sokol, E
   Fritsch, RM
AF Akhoundova, Dilara
   Hussung, Saskia
   Sivakumar, Smruthy
   Topfer, Antonia
   Rechsteiner, Markus
   Kahraman, Abdullah
   Arnold, Fabian
   Angst, Florian
   Britschgi, Christian
   Zoche, Martin
   Moch, Holger
   Weber, Achim
   Sokol, Ethan
   Fritsch, Ralph M.
TI <i>ROS1</i> genomic rearrangements are rare actionable drivers in
   microsatellite stable colorectal cancer
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE acquired resistance; colorectal cancer; crizotinib; molecular subgroups;
   precision treatment; ROS1 rearrangement
ID CELL LUNG-CANCER; FUSIONS; RESISTANCE; MUTATIONS; ACTIVATION;
   CRIZOTINIB; THERAPY; GENE
AB c-Ros oncogene 1, receptor tyrosine kinase (ROS1) genomic rearrangements have been reported previously in rare cases of colorectal cancer (CRC), yet little is known about the frequency, molecular characteristics, and therapeutic vulnerabilities of ROS1-driven CRC. We analyzed a clinical dataset of 40 589 patients with CRC for ROS1 genomic rearrangements and their associated genomic characteristics (Foundation Medicine, Inc [FMI]). We moreover report the disease course and treatment response of an index patient with ROS1-rearranged metastatic CRC. ROS1 genomic rearrangements were identified in 34 (0.08%) CRC samples. GOPC-ROS1 was the most common ROS1 fusion identified (11 samples), followed by TTC28-ROS1 (3 samples). Four novel 5 ' gene partners of ROS1 were identified (MCM9, SRPK1, EPHA6, P4HA1). Contrary to previous reports on fusion-positive CRC, ROS1-rearrangements were found exclusively in microsatellite stable (MSS) CRCs. KRAS mutations were significantly less abundant in ROS1-rearranged vs ROS1 wild type cases. The index patient presented with chemotherapy-refractory metastatic right-sided colon cancer harboring GOPC-ROS1. Molecularly targeted treatment with crizotinib induced a rapid and sustained partial response. After 15 months on crizotinib disseminated tumor progression occurred and KRAS Q61H emerged in tissue and liquid biopsies. ROS1 rearrangements define a small, yet therapeutically actionable molecular subgroup of MSS CRC. In summary, the high prevalence of GOPC-ROS1 and noncanonical ROS1 fusions pose diagnostic challenges. We advocate NGS-based comprehensive molecular profiling of MSS CRCs that are wild type for RAS and BRAF and patient enrollment in precision trials.
C1 [Akhoundova, Dilara; Hussung, Saskia; Britschgi, Christian; Fritsch, Ralph M.] Univ Hosp Zurich, Dept Med Oncol & Hematol, Ramistr 100, CH-8091 Zurich, Switzerland.
   [Sivakumar, Smruthy; Sokol, Ethan] Fdn Med Inc, Canc Genom Res, Cambridge, MA USA.
   [Topfer, Antonia; Rechsteiner, Markus; Kahraman, Abdullah; Arnold, Fabian; Zoche, Martin; Moch, Holger; Weber, Achim] Univ Hosp Zurich, Dept Pathol & Mol Pathol, Zurich, Switzerland.
   [Angst, Florian] Univ Hosp Zurich, Inst Diagnost & Intervent Radiol, Zurich, Switzerland.
C3 University of Zurich; University Zurich Hospital; Foundation Medicine;
   University of Zurich; University Zurich Hospital; University of Zurich;
   University Zurich Hospital
RP Fritsch, RM (corresponding author), Univ Hosp Zurich, Dept Med Oncol & Hematol, Ramistr 100, CH-8091 Zurich, Switzerland.
EM ralph.fritsch@usz.ch
RI Fritsch, Ralph/KPB-7703-2024
OI Fritsch, Ralph/0000-0001-9639-3213; Hussung, Saskia/0000-0001-7987-0065;
   Britschgi, Christian/0000-0001-8831-1564; Kahraman,
   Abdullah/0000-0003-3523-4467; Akhoundova, Dilara/0000-0003-1639-3059
FU Universitat Zurich
FX The graphical abstract was created with BioRender.com. Open access
   funding provided by Universitat Zurich.
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NR 50
TC 8
Z9 9
U1 0
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD DEC 15
PY 2022
VL 151
IS 12
BP 2161
EP 2171
DI 10.1002/ijc.34257
EA AUG 2022
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 5L3NI
UT WOS:000847424000001
PM 36053834
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Tauriello, DVF
   Calon, A
   Lonardo, E
   Batlle, E
AF Tauriello, Daniele V. F.
   Calon, Alexandre
   Lonardo, Enza
   Batlle, Eduard
TI Determinants of metastatic competency in colorectal cancer
SO MOLECULAR ONCOLOGY
LA English
DT Review
DE cancer immunology; cancer stem cells; clonal diversity; combination
   therapy; dormancy; Heterogeneity; immunotherapy; stroma; TGF-beta;
   tumour microenvironment
ID MESENCHYMAL STEM-CELLS; HEPATOCYTE GROWTH-FACTOR; CIRCULATING
   TUMOR-CELLS; CCR1(+) MYELOID CELLS; TGF-BETA PATHWAY; CD8(+) T-CELLS;
   COLON-CANCER; SUPPRESSOR-CELLS; IMMUNE CELLS; CLINICAL-SIGNIFICANCE
AB Colorectal cancer (CRC) is one of the most common cancer types and represents a major therapeutic challenge. Although initial events in colorectal carcinogenesis are relatively well characterized and treatment for early-stage disease has significantly improved over the last decades, the mechanisms underlying metastasis - the main cause of death - remain poorly understood. Correspondingly, no effective therapy is currently available for advanced or metastatic disease. There is increasing evidence that colorectal cancer is hierarchically organized and sustained by cancer stem cells, in concert with various stromal cell types. Here, we review the interplay between cancer stem cells and their microenvironment in promoting metastasis and discuss recent insights relating to both patient prognosis and novel targeted treatment strategies. A better understanding of these topics may aid the prevention or reduction of metastatic burden.
C1 [Tauriello, Daniele V. F.; Lonardo, Enza; Batlle, Eduard] Barcelona Inst Sci & Technol, Inst Res Biomed IRB Barcelona, Baldiri & Reixac 10, Barcelona 08028, Spain.
   [Calon, Alexandre] Hosp del Mar Med Res Inst IMIM, MAR Hlth Pk Barcelona,Dr Aiguader 88, Barcelona 08003, Spain.
   [Batlle, Eduard] ICREA, Pg Lluis Companys 23, Barcelona 08010, Spain.
C3 Barcelona Institute of Science & Technology; Institute for Research in
   Biomedicine - IRB Barcelona; Hospital del Mar Research Institute;
   Hospital del Mar; ICREA
RP Tauriello, DVF; Batlle, E (corresponding author), Barcelona Inst Sci & Technol, Inst Res Biomed IRB Barcelona, Baldiri & Reixac 10, Barcelona 08028, Spain.; Calon, A (corresponding author), Hosp del Mar Med Res Inst IMIM, MAR Hlth Pk Barcelona,Dr Aiguader 88, Barcelona 08003, Spain.; Batlle, E (corresponding author), ICREA, Pg Lluis Companys 23, Barcelona 08010, Spain.
EM Daniele.Tauriello@irbbarcelona.org; ACalon@imim.es;
   Eduard.Batlle@irbbarcelona.org
RI Calon, Alexandre/GPK-2061-2022; lonardo, enza/AAI-5726-2020; Tauriello,
   Daniele V. F./H-4644-2018; Batlle, Eduard/K-8080-2014
OI Calon, Alexandre/0000-0002-3398-6131; Tauriello, Daniele V.
   F./0000-0003-1522-3496; Batlle, Eduard/0000-0003-2422-0326; Lonardo,
   Enza/0000-0001-6654-1043
FU Spanish Ministry of Economy and Competitiveness (MINECO); Fundacion Olga
   Torres; Asociacion Espanola contra el Cancer; Dr. Josef Steiner
   Foundation; Fundacion Botin, through Santander Universities; Banco
   Santander, through Santander Universities; Severo Ochoa Award of
   Excellence from the MINECO;  [SAF2014-53784_R]
FX Work by the authors has been supported by grant SAF2014-53784_R (EB) and
   Juan de la Cierva fellowships (DVFT and AC) from the Spanish Ministry of
   Economy and Competitiveness (MINECO), by fellowships from Fundacion Olga
   Torres (EL) and Asociacion Espanola contra el Cancer (EL) and by the Dr.
   Josef Steiner Foundation (EB). Work in the laboratory of EB is supported
   by Fundacion Botin and Banco Santander, through Santander Universities.
   IRB Barcelona is the recipient of a Severo Ochoa Award of Excellence
   from the MINECO. We would like to thank members of the laboratory of EB
   for fruitful discussions.
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NR 194
TC 173
Z9 181
U1 0
U2 19
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1574-7891
EI 1878-0261
J9 MOL ONCOL
JI Mol. Oncol.
PD JAN
PY 2017
VL 11
IS 1
SI SI
BP 97
EP 119
DI 10.1002/1878-0261.12018
PG 23
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FA8XO
UT WOS:000405730200007
PM 28085225
OA gold, Green Published, Green Accepted
DA 2025-01-04
ER

PT J
AU Zawawi, SSA
   Musa, M
AF Zawawi, Sahira Syamimi Ahmad
   Musa, Marahaini
TI Dynamic Co-Evolution of Cancer Cells and Cancer-Associated Fibroblasts:
   Role in Right- and Left-Sided Colon Cancer Progression and Its Clinical
   Relevance
SO BIOLOGY-BASEL
LA English
DT Review
DE colon cancer; activated fibroblast; evolution; heterogeneity; sidedness
ID COLORECTAL-CANCER; STEM-CELLS; CELLULAR HETEROGENEITY; SOMATIC
   EVOLUTION; PREDICTIVE MARKER; CLONAL EVOLUTION; TUMOR EVOLUTION;
   EXPRESSION; MYOFIBROBLASTS; INSTABILITY
AB Simple Summary The versatile crosstalk between cancer cells and cancer-associated fibroblasts (CAFs) of the tumour microenvironment (TME) drives colorectal carcinogenesis and heterogeneity. Colorectal cancer (CRC) can be classified by the anatomical sites from which the cancer arises, either from the right or left colon. Although the cancer cell-CAF interaction is being widely studied, its role in the progression of cancer in the right and left colon and cancer heterogeneity are still yet to be elucidated. Further insight into the complex interaction between different cellular components in the cancer niche, their evolutionary process and their influence on cancer progression would propel the discovery of effective targeted CRC therapy. Cancer is a result of a dynamic evolutionary process. It is composed of cancer cells and the tumour microenvironment (TME). One of the major cellular constituents of TME, cancer-associated fibroblasts (CAFs) are known to interact with cancer cells and promote colorectal carcinogenesis. The accumulation of these activated fibroblasts is linked to poor diagnosis in colorectal cancer (CRC) patients and recurrence of the disease. However, the interplay between cancer cells and CAFs is yet to be described, especially in relation to the sidedness of colorectal carcinogenesis. CRC, which is the third most commonly diagnosed cancer globally, can be classified according to the anatomical region from which they originate: left-sided (LCRC) and right-sided CRC (RCR). Both cancers differ in many aspects, including in histology, evolution, and molecular signatures. Despite occurring at lower frequency, RCRC is often associated with worse diagnosis compared to LCRC. The differences in molecular profiles between RCRC and LCRC also influence the mode of treatment that can be used to specifically target these cancer entities. A better understanding of the cancer cell-CAF interplay and its association with RCRC and LRCR progression will provide better insight into potential translational aspects of targeted treatment for CRC.
C1 [Zawawi, Sahira Syamimi Ahmad; Musa, Marahaini] Univ Sains Malaysia, Human Genome Ctr, Sch Med Sci, Kota Baharu 16150, Kelantan, Malaysia.
C3 Universiti Sains Malaysia
RP Musa, M (corresponding author), Univ Sains Malaysia, Human Genome Ctr, Sch Med Sci, Kota Baharu 16150, Kelantan, Malaysia.
EM sahirasyamimi002@gmail.com; marahaini.musa@usm.my
RI Sahira Syamimi, Ahmad Zawawi/HNC-0323-2023; Musa, Marahaini/E-9987-2019
OI Ahmad Zawawi, Sahira Syamimi/0000-0002-4963-8721
FU Ministry of Higher Education Malaysia [FRGS/1/2020/SKK0/USM/03/10];
   Universiti Sains Malaysia
FX This work was supported by the Ministry of Higher Education Malaysia for
   Fundamental Research Grant Scheme, project code
   FRGS/1/2020/SKK0/USM/03/10, and Universiti Sains Malaysia.
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NR 143
TC 6
Z9 6
U1 1
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2079-7737
J9 BIOLOGY-BASEL
JI Biology-Basel
PD JUL
PY 2022
VL 11
IS 7
AR 1014
DI 10.3390/biology11071014
PG 19
WC Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics
GA 3I1TH
UT WOS:000832506400001
PM 36101394
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Carmignani, A
   Battaglini, M
   Marino, A
   Pignatelli, F
   Ciofani, G
AF Carmignani, Alessio
   Battaglini, Matteo
   Marino, Attilio
   Pignatelli, Francesca
   Ciofani, Gianni
TI Drug-Loaded Polydopamine Nanoparticles for Chemo/Photothermal Therapy
   against Colorectal Cancer Cells
SO ACS APPLIED BIO MATERIALS
LA English
DT Article
DE polydopamine nanoparticles; colorectal cancer; chemotherapy;
   photothermal therapy; combinationtherapy
ID HEPATOCELLULAR-CARCINOMA CELLS; COLON-CANCER; SORAFENIB; APOPTOSIS;
   DELIVERY; INHIBITOR; AGENT; HEAT
AB Colorectal cancer (CRC) is a common and deadly malignancy, ranking second in terms of mortality and third in terms of incidence on a global scale. The survival rates for CRC patients are unsatisfactory primarily because of the absence of highly effective clinical strategies. The efficacy of existing CRC treatments, such as chemotherapy (CT), is constrained by issues such as drug resistance and damage to healthy tissues. Alternative approaches such as photothermal therapy (PTT), while offering advantages over traditional therapies, suffer instead from a low efficiency in killing tumor cells when used alone. In this context, nanostructures can efficiently contribute to a selective and targeted treatment. Here, we combined CT and PTT by developing a nanoplatform based on polydopamine nanoparticles (PDNPs), selected for their biocompatibility, drug-carrying capabilities, and ability to produce heat upon exposure to near-infrared (NIR) irradiation. As a chemotherapy drug, sorafenib has been selected, a multikinase inhibitor already approved for clinical use. By encapsulating sorafenib in polydopamine nanoparticles (Sor-PDNPs), we were able to successfully improve the drug stability in physiological media and the consequent uptake by CRC cells, thereby increasing its therapeutic effects. Upon NIR stimulus, Sor-PDNPs can induce a temperature increment of about 10 degrees C, encompassing both PTT and triggering a localized and massive drug release. Sor-PDNPs were tested on healthy colon cells, showing minimal adverse outcomes; conversely, they demonstrated excellent efficacy against CRC cells, with a strong capability to hinder cancer cell proliferation and induce apoptosis. Obtained findings pave the way to new synergistic chemo-photothermal approaches, maximizing the therapeutic outcomes against CRC while minimizing side effects on healthy cells.
C1 [Carmignani, Alessio; Battaglini, Matteo; Marino, Attilio; Pignatelli, Francesca; Ciofani, Gianni] Ist Italiano Tecnol, Smart Bio Interfaces, I-56025 Pontedera, Italy.
   [Carmignani, Alessio] Scuola Super Sant Anna, Biorobot Inst, I-56025 Pontedera, Italy.
C3 Istituto Italiano di Tecnologia - IIT; Scuola Superiore Sant'Anna
RP Carmignani, A; Ciofani, G (corresponding author), Ist Italiano Tecnol, Smart Bio Interfaces, I-56025 Pontedera, Italy.; Carmignani, A (corresponding author), Scuola Super Sant Anna, Biorobot Inst, I-56025 Pontedera, Italy.
EM alessio.carmignani@iit.it; gianni.ciofani@iit.it
RI Carmignani, Alessio/CAI-2405-2022; Marino, Attilio/LRU-3769-2024;
   Ciofani, Gianni/D-3761-2009
OI Marino, Attilio/0000-0002-3290-494X; Carmignani,
   Alessio/0000-0002-6316-3478; Ciofani, Gianni/0000-0003-1192-3647
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NR 70
TC 7
Z9 8
U1 4
U2 12
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 2576-6422
J9 ACS APPL BIO MATER
JI ACS Appl. Bio Mater.
PD MAR 15
PY 2024
VL 7
IS 4
BP 2205
EP 2217
DI 10.1021/acsabm.3c01203
EA MAR 2024
PG 13
WC Nanoscience & Nanotechnology; Materials Science, Biomaterials
WE Emerging Sources Citation Index (ESCI)
SC Science & Technology - Other Topics; Materials Science
GA NW0M1
UT WOS:001186375400001
PM 38489294
DA 2025-01-04
ER

PT J
AU Potocki, PM
   Wysocki, PJ
AF Potocki, Pawel M.
   Wysocki, Piotr J.
TI BRAF - a new therapeutic target in colorectal cancer
SO ONCOLOGY IN CLINICAL PRACTICE
LA English
DT Review
DE colorectal cancer; BRAF; V600E; FOLFOXIRI
ID FOLFOXIRI PLUS BEVACIZUMAB; RANDOMIZED CLINICAL-TRIALS; PHASE-III TRIAL;
   KRAS WILD-TYPE; 1ST-LINE TREATMENT; MUTATION STATUS; POOLED ANALYSIS;
   COLON-CANCER; MICROSATELLITE INSTABILITY; V600E MUTATION
AB The BRAF V600E mutation, already a well-established biomarker in the treatment of metastatic melanoma, has been extensively studied in patients with metastatic colorectal cancer (CRC) in recent years. It was revealed that this mutation occurs in about 10% of CRC patients. It has been proven to be a negative prognostic factor, although more recent studies indicate a complex association of this effect with the state of genes responsible for the repair of "mismatch" DNA damage. Although the predictive value of the BRAF V600E mutation for chemotherapy and targeted treatment remains the subject of controversy, the guidelines of international scientific societies highlight the need for a different approach to systemic treatment of patients in this population. Numerous treatment options are currently evaluated: from the intensification of the classic chemotherapy regimens administered in the first-line setting to the innovative combinations of targeted drugs aimed at eliminating the influence of BRAF V600E mutation on signal transduction pathways that are crucial for carcinogenesis. The following review is intended to bring this complex topic to the attention of oncologists who deal with the treatment of gastrointestinal cancer in clinical practice.
C1 [Potocki, Pawel M.; Wysocki, Piotr J.] Jagiellonian Univ, Med Coll, Oncol Dept, Krakow, Poland.
C3 Jagiellonian University; Collegium Medicum Jagiellonian University
RP Potocki, PM (corresponding author), Szpital Uniwersytecki, Klin Onkol, Ul Sniadeckich 10, PL-31501 Krakow, Poland.
EM pawel.potocki@uj.edu.p
RI Wysocki, Piotr/HKF-6762-2023; Potocki, Pawel/AAK-7272-2021
OI Potocki, Pawel/0000-0003-3627-5201
FU Amgen; Merck; Roche; Novartis
FX Pawel Potocki: received honoraria and travel grants from Amgen, Merck,
   Roche.Piotr Wysocki: received honoraria, travel grants from Roche,
   Merck, Amgen, Novartis.
CR [Anonymous], ANN ONCOL S6
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NR 55
TC 2
Z9 2
U1 0
U2 2
PU VIA MEDICA
PI GDANSK
PA UL SWIETOKRZYSKA 73, 80-180 GDANSK, POLAND
SN 2450-1654
EI 2450-6478
J9 ONCOL CLIN PRACT
JI Oncol. Clin. Pract.
PY 2018
VL 14
IS 2
BP 86
EP 95
DI 10.5603/OCP.2018.0013
PG 10
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA GM0AS
UT WOS:000437707300004
DA 2025-01-04
ER

PT J
AU Cotan, HT
   Emilescu, RA
   Iaciu, CI
   Orlov-Slavu, CM
   Olaru, MC
   Popa, AM
   Jinga, M
   Nitipir, C
   Schreiner, OD
   Ciobanu, RC
AF Cotan, Horia T.
   Emilescu, Radu A.
   Iaciu, Cristian I.
   Orlov-Slavu, Cristina M.
   Olaru, Mihaela C.
   Popa, Ana M.
   Jinga, Mariana
   Nitipir, Cornelia
   Schreiner, Oliver Daniel
   Ciobanu, Romeo Cristian
TI Prognostic and Predictive Determinants of Colorectal Cancer: A
   Comprehensive Review
SO CANCERS
LA English
DT Review
DE prognostic marker; predictive markers; biomarkers; molecular targeted
   treatment
ID III COLON-CANCER; DIHYDROPYRIMIDINE DEHYDROGENASE-DEFICIENCY;
   MICROSATELLITE-INSTABILITY STATUS; SEVERE 5-FLUOROURACIL TOXICITY;
   CIRCULATING TUMOR-CELLS; LYMPH-NODE METASTASES; RANDOMIZED PHASE-III;
   DNA MISMATCH REPAIR; STAGE-III; WILD-TYPE
AB Colorectal cancer (CRC) remains a significant global health burden, necessitating a thorough understanding of prognostic and predictive factors to enhance patient outcomes. This systematic review aims to comprehensively evaluate prognostic and predictive determinants in CRC, encompassing both traditional and emerging biomarkers. A systematic search of major electronic databases was conducted to identify relevant studies published from 1995 up to 2024. Eligible articles were critically appraised, and data extraction was performed according to predefined criteria. The prognostic determinants examined included clinicopathological features such as tumor stage, grade, and lymph node involvement, as well as molecular biomarkers including RAS, BRAF, and MSI status. Predictive determinants encompassed biomarkers influencing response to targeted therapies and immunotherapy, such as HER2 and Immunoscore. The review also explores novel prognostic and predictive markers, including tumor microenvironment characteristics and liquid biopsy-based biomarkers. Synthesizing evidence from diverse studies, this review provides insights into the prognostic and predictive landscape of CRC, highlighting the potential clinical implications of identified determinants. Understanding the multifaceted nature of prognostic and predictive factors in CRC is imperative for the advancement of personalized treatment strategies and improvement of patient outcomes.
C1 [Cotan, Horia T.; Emilescu, Radu A.; Iaciu, Cristian I.; Orlov-Slavu, Cristina M.; Olaru, Mihaela C.; Popa, Ana M.; Jinga, Mariana; Nitipir, Cornelia] Carol Davila Univ Med & Pharm, Gen Med Fac, 8 Sanit Heroes Blvd, Bucharest 050474, Romania.
   [Schreiner, Oliver Daniel] Reg Inst Oncol Iasi, 2-4 Gen Henri Mathias Berthelot St, Iasi 700483, Romania.
   [Schreiner, Oliver Daniel] Grigore T Popa Univ Med & Pharm, Dept Med Sci 3, 16 Univ St, Iasi 700115, Romania.
   [Schreiner, Oliver Daniel; Ciobanu, Romeo Cristian] Gheorghe Asachi Tech Univ, Dept Elect Measurements & Mat, Iasi 700050, Romania.
C3 Carol Davila University of Medicine & Pharmacy; Regional Institute of
   Oncology IASI; Grigore T Popa University of Medicine & Pharmacy; GH
   Asachi Technical University
RP Emilescu, RA (corresponding author), Carol Davila Univ Med & Pharm, Gen Med Fac, 8 Sanit Heroes Blvd, Bucharest 050474, Romania.; Ciobanu, RC (corresponding author), Gheorghe Asachi Tech Univ, Dept Elect Measurements & Mat, Iasi 700050, Romania.
EM horia-teodor.cotan@rez.umfcd.ro; raduemilescu66@gmail.com;
   cristian-ion.iaciu@rez.umfcd.ro; orlov.cristina@gmail.com;
   miha0611@yahoo.com; amy.popa@yahoo.com; mariana_jinga@yahoo.com;
   niti-pir2003@yahoo.com; oliver090598@yahoo.com; r.c.ciobanu@tuiasi.ro
RI POPA, ANA/AAL-3244-2021
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   US
NR 240
TC 0
Z9 0
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD DEC
PY 2024
VL 16
IS 23
AR 3928
DI 10.3390/cancers16233928
PG 35
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA P2E9F
UT WOS:001376119200001
PM 39682117
OA gold
DA 2025-01-04
ER

EF