﻿FN Clarivate Analytics Web of Science
VR 1.0
PT J
AU Kayser, A
   Wolff, A
   Berlin, P
   Duehring, L
   Henze, L
   Mundkowski, R
   Bergmann, W
   Mueller-Hilke, B
   Wagner, C
   Huehns, M
   Oehmcke-Hecht, S
   Maletzki, C
AF Kayser, Annika
   Wolff, Annabell
   Berlin, Peggy
   Duehring, Lara
   Henze, Larissa
   Mundkowski, Ralf
   Bergmann, Wendy
   Mueller-Hilke, Brigitte
   Wagner, Charlotte
   Huehns, Maja
   Oehmcke-Hecht, Sonja
   Maletzki, Claudia
TI Selective but not pan-CDK inhibition abrogates 5-FU-driven tissue factor
   upregulation in colon cancer
SO SCIENTIFIC REPORTS
LA English
DT Article
DE Epithelial-mesenchymal transition; Senescence; Targeted therapy; Cell
   sorting; Hypercoagulation; Microvesicles
ID HUMAN COLORECTAL-CARCINOMA; TO-MESENCHYMAL TRANSITION; VENOUS
   THROMBOEMBOLISM; FACTOR EXPRESSION; PROCOAGULANT ACTIVITY; TUMOR
   PROGRESSION; CELL-LINES; CHEMOTHERAPY; P27(KIP1); RISK
AB Thromboembolic events are complications in cancer patients and hypercoagulability has been linked to the tissue factor (TF) pathway, making this an attractive target. Here, we investigated the effects of chemotherapeutics and CDK inhibitors (CDKI) abemaciclib/palbociclib (CDK4/6), THZ-1 (CDK7/12/13), and dinaciclib (CDK1/2/5/9) alone and in combination regimens on TF abundance and coagulation. The human colorectal cancer (CRC) cell line HROC173 was treated with 5-FU or gemcitabine to stimulate TF expression. TF+ cells were sorted, recultured, and re-analyzed. The effect of treatment alone or in combination was assessed by functional assays. Low-dose chemotherapy induced a hypercoagulable state and significantly upregulated TF, even after reculture without treatment. Cells exhibited characteristics of epithelial-mesenchymal transition, including high expression of vimentin and mucin. Dinaciclib and THZ-1 also upregulated TF, while abemaciclib and palbociclib downregulated it. Similar results were observed in coagulation assays. The same anticoagulant activity of abemaciclib was seen after incubation with peripheral immune cells from healthy donors and CRC patients. Abemaciclib reversed 5-FU-induced TF upregulation and prolonged clotting times in second-line treatment. Effects were independent of cytotoxicity, senescence, and p27kip1 induction. TF-antibody blocking experiments confirmed the importance of TF in plasma coagulation, with Factor XII playing a minor role. Short-term abemaciclib counteracts 5-FU-induced hypercoagulation and eventually even prevents thromboembolic events.
C1 [Kayser, Annika; Wolff, Annabell; Duehring, Lara; Henze, Larissa; Wagner, Charlotte; Maletzki, Claudia] Rostock Univ, Dept Med, Clin Hematol Oncol Palliat Med 3, Med Ctr, Ernst Heydemann Str 6, D-18057 Rostock, Germany.
   [Berlin, Peggy] Rostock Univ, Med Ctr, Dept Med 2, Div Gastroenterol, D-18057 Rostock, Germany.
   [Wolff, Annabell; Duehring, Lara; Oehmcke-Hecht, Sonja] Rostock Univ, Inst Med Microbiol Virol & Hyg, Med Ctr, D-18057 Rostock, Germany.
   [Henze, Larissa] Asklepios Hosp Harz, Dept Internal Med 2, Goslar, Germany.
   [Mundkowski, Ralf] Rostock Univ, Inst Clin Pharmacol, Ctr Pharmacol & Toxicol, Med Ctr, D-18057 Rostock, Germany.
   [Bergmann, Wendy; Mueller-Hilke, Brigitte] Rostock Univ, Med Ctr, Lab Clin Immunol, Core Facil Cell Sorting & Cell Anal, D-18057 Rostock, Germany.
   [Huehns, Maja] Rostock Univ, Inst Pathol, Med Ctr, D-18057 Rostock, Germany.
C3 University of Rostock; University of Rostock; University of Rostock;
   University of Rostock; University of Rostock; University of Rostock
RP Maletzki, C (corresponding author), Rostock Univ, Dept Med, Clin Hematol Oncol Palliat Med 3, Med Ctr, Ernst Heydemann Str 6, D-18057 Rostock, Germany.; Oehmcke-Hecht, S (corresponding author), Rostock Univ, Inst Med Microbiol Virol & Hyg, Med Ctr, D-18057 Rostock, Germany.
EM sonja.oehmcke-hecht@med.uni-rostock.de;
   claudia.maletzki@med.uni-rostock.de
FU Universittsmedizin Rostock (8980) [FKZ 01ZX1903A]; Federal Ministry of
   Education and Research of Germany
FX The authors thank Jana Bull and Liane Krause for her excellent technical
   assistance. LH acknowledges the financial support by the Federal
   Ministry of Education and Research of Germany for the "SASKit" project
   (FKZ 01ZX1903A).
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NR 52
TC 0
Z9 0
U1 2
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 MAY 8
PY 2024
VL 14
IS 1
AR 10582
DI 10.1038/s41598-024-61076-5
PG 12
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA PU1P1
UT WOS:001216508100063
PM 38719932
OA gold
DA 2025-01-04
ER

PT J
AU Tang, F
   Min, L
   Seebacher, NA
   Li, XY
   Zhou, YB
   Hornicek, FJ
   Wei, YQ
   Tu, CQ
   Duan, ZF
AF Tang, Fan
   Min, Li
   Seebacher, Nicole A.
   Li, Xiaoyang
   Zhou, Yubin
   Hornicek, Francis J.
   Wei, Yuquan
   Tu, Chongqi
   Duan, Zhenfeng
TI Targeting mutant TP53 as a potential therapeutic strategy for the
   treatment of osteosarcoma
SO JOURNAL OF ORTHOPAEDIC RESEARCH
LA English
DT Article
DE osteosarcoma; gene mutation; TP53; CRISPR-Cas9; targeted therapy
ID COLORECTAL-CANCER; BCL-2 EXPRESSION; P53 MUTATIONS; IN-VITRO; CELL;
   GROWTH; CARCINOMA; SURVIVIN; PROLIFERATION; TUMORIGENESIS
AB Mutant TP53 is a promising therapeutic target in cancers. Considering the current challenges facing the clinical treatment of cancer, as well as the urgent need to identify novel therapeutic targets in osteosarcomas, we aimed to evaluate the clinical significance of mutant TP53 in osteosarcoma patients and to explore the therapeutic effect of targeting mutant TP53 in osteosarcomas. We performed a meta-analysis to investigate the relationship between mutant TP53 and the overall survival of patients with osteosarcoma. A CRISPR-Cas9 system and a TP53 inhibitor, NSC59984, were also used to specifically knock-out and inhibit mutant TP53 in the human osteosarcoma cell lines, KHOS, and KHOSR2. The meta-analysis demonstrated that mutations in the TP53 gene could be used to predict a poor 2-year survival in osteosarcoma patients. We also demonstrated that the expression of mutant TP53 in human osteosarcoma cell lines can be efficiently knocked-out using CRISPR-Cas9, and this decreased the proliferation, migration, and tumor formation activity of these osteosarcoma cells. Moreover, drug sensitivity to doxorubicin was increased in these TP53 knock-out osteosarcoma cells. NSC59984 also showed similar anti-tumor effects as CRISPR-Cas9 targeted TP53 in the osteosarcoma cells in vitro. We have also demonstrated that the knock-out or inhibition of mutant TP53 decreased the expression of the oncogene IGF-1R, anti-apoptotic proteins Bcl-2, and Survivin in osteosarcoma cells. Collectively, these results suggest that mutant TP53 is a promising therapeutic target in osteosarcomas. Therefore, further studies exploring novel strategies to target mutant TP53 may help improve the treatment outcomes of osteosarcoma patients in the clinic. (c) 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res
C1 [Tang, Fan; Min, Li; Tu, Chongqi] Sichuan Univ, Dept Orthoped, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.
   [Tang, Fan; Wei, Yuquan] Sichuan Univ, State Key Lab Biotherapy, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.
   [Tang, Fan; Wei, Yuquan] Collaborat Innovat Ctr, Chengdu 610041, Sichuan, Peoples R China.
   [Tang, Fan; Min, Li; Seebacher, Nicole A.; Li, Xiaoyang; Zhou, Yubin; Hornicek, Francis J.; Duan, Zhenfeng] Univ Calif Los Angeles, David Geffen Sch Med, Sarcoma Biol Lab, Dept Orthopaed Surg, Los Angeles, CA 90095 USA.
C3 Sichuan University; Sichuan University; University of California System;
   University of California Los Angeles; University of California Los
   Angeles Medical Center; David Geffen School of Medicine at UCLA
RP Tu, CQ (corresponding author), Sichuan Univ, Dept Orthoped, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.; Duan, ZF (corresponding author), Univ Calif Los Angeles, David Geffen Sch Med, Sarcoma Biol Lab, Dept Orthopaed Surg, Los Angeles, CA 90095 USA.
EM tcqbonetumor@163.com; zduan@mednet.ucla.edu
RI Duan, Zhenfeng/AAK-5587-2020; Zhou, Yubin/D-4748-2011
OI Hornicek, Francis/0000-0002-6916-8042; duan,
   zhenfeng/0000-0001-7276-3910
FU Sarcoma Foundation of America [222433]; National Natural Science
   Foundation of China [81702664]; National Cancer Institute [UO1,
   CA151452-01]
FX Grant sponsor: Sarcoma Foundation of America; Grant number: 222433;
   Grant sponsor: National Natural Science Foundation of China; Grant
   number: 81702664; Grant sponsor: National Cancer Institute; Grant
   number: UO1, CA151452-01.
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NR 50
TC 34
Z9 35
U1 0
U2 22
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0736-0266
EI 1554-527X
J9 J ORTHOP RES
JI J. Orthop. Res.
PD MAR
PY 2019
VL 37
IS 3
BP 789
EP 798
DI 10.1002/jor.24227
PG 10
WC Orthopedics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Orthopedics
GA HT2UM
UT WOS:000464419100028
PM 30667081
OA Bronze
DA 2025-01-04
ER

PT J
AU Bryja, A
   Zadka, L
   Farzaneh, M
   Zehtabi, M
   Ghasemian, M
   Dyszkiewicz-Konwinska, M
   Mozdziak, P
   Zabel, M
   Podhorska-Okolów, M
   Dziegiel, P
   Piotrowska-Kempisty, H
   Kempisty, B
AF Bryja, Artur
   Zadka, Lukasz
   Farzaneh, Maryam
   Zehtabi, Mojtaba
   Ghasemian, Majid
   Dyszkiewicz-Konwinska, Marta
   Mozdziak, Paul
   Zabel, Maciej
   Podhorska-Okolow, Marzenna
   Dziegiel, Piotr
   Piotrowska-Kempisty, Hanna
   Kempisty, Bartosz
TI Small extracellular vesicles - A host for advanced bioengineering and
   "Trojan Horse" of non-coding RNAs
SO LIFE SCIENCES
LA English
DT Review
DE Small extracellular vesicles; Non -coding RNAs; Therapeutic agent;
   Exosomes; cancer
ID COLORECTAL-CANCER; ENDOTHELIAL-CELLS; CIRCULAR RNA; EXOSOMES; PROMOTE;
   LNCRNA; MICRORNAS; CHEMORESISTANCE; FIBROBLASTS; RESISTANCE
AB Small extracellular vesicles (sEVs) are a type of membranous vesicles that can be released by cells into the extracellular space. The relationship between sEVs and non-coding RNAs (ncRNAs) is highly intricate and interdependent. This symbiotic relationship plays a pivotal role in facilitating intercellular communication and holds profound implications for a myriad of biological processes. The concept of sEVs and their ncRNA cargo as a "Trojan Horse" highlights their remarkable capacity to traverse biological barriers and surreptitiously deliver their cargo to target cells, evading detection by the host-immune system. Accumulating evidence suggests that sEVs may be harnessed as carriers to ferry therapeutic ncRNAs capable of selectively silencing disease-driving genes, particularly in conditions such as cancer. This approach presents several advantages over conventional drug delivery methods, opening up new possibilities for targeted therapy and improved treatment outcomes. However, the utilization of sEVs and ncRNAs as therapeutic agents raises valid concerns regarding the possibility of unforeseen consequences and unintended impacts that may emerge from their application. It is important to consider the fundamental attributes of sEVs and ncRNAs, including by an in-depth analysis of the practical and clinical potentials of exosomes, serving as a representative model for sEVs encapsulating ncRNAs.
C1 [Bryja, Artur; Kempisty, Bartosz] Wroclaw Med Univ, Dept Human Morphol & Embryol, Div Anat, Chalubinskiego 6a St, PL-50368 Wroclaw, Poland.
   [Zadka, Lukasz; Zabel, Maciej; Podhorska-Okolow, Marzenna] Wroclaw Med Univ, Div Ultrastruct Res, Wroclaw, Poland.
   [Farzaneh, Maryam] Ahvaz Jundishapur Univ Med Sci, Fertil Infertil & Perinatol Res Ctr, Ahvaz, Iran.
   [Zehtabi, Mojtaba] Tabriz Univ Med Sci, Hematol & Oncol Res Ctr, Tabriz, Iran.
   [Ghasemian, Majid] Ahvaz Jundishapur Univ Med Sci, Fac Med, Dept Clin Biochem, Ahvaz, Iran.
   [Dyszkiewicz-Konwinska, Marta] Poznan Univ Med Sci, Dept Diagnost, Poznan, Poland.
   [Mozdziak, Paul; Kempisty, Bartosz] North Carolina State Univ, Prestage Dept Poultry Sci, Raleigh, NC USA.
   [Zabel, Maciej; Dziegiel, Piotr] Wroclaw Med Univ, Dept Human Morphol & Embryol, Div Histol & Embryol, Wroclaw, Poland.
   [Zabel, Maciej] Univ Zielona Gora, Div Anat & Histol, Zielona Gora, Poland.
   [Piotrowska-Kempisty, Hanna] Poznan Univ Med Sci, Dept Toxicol, Poznan, Poland.
   [Piotrowska-Kempisty, Hanna] Nicolaus Copernicus Univ Torun, Inst Vet Med, Dept Basic & Preclin Sci, Torun, Poland.
   [Kempisty, Bartosz] Univ Hosp, Dept Obstet & Gynecol, Brno, Czech Republic.
   [Kempisty, Bartosz] Masaryk Univ, Brno, Czech Republic.
   [Kempisty, Bartosz] Nicolaus Copernicus Univ Torun, Inst Vet Med, Dept Vet Surg, Torun, Poland.
C3 Wroclaw Medical University; Wroclaw Medical University; Ahvaz
   Jundishapur University of Medical Sciences (AJUMS); Tabriz University of
   Medical Science; Ahvaz Jundishapur University of Medical Sciences
   (AJUMS); Poznan University of Medical Sciences; North Carolina State
   University; Wroclaw Medical University; University of Zielona Gora;
   Poznan University of Medical Sciences; Nicolaus Copernicus University;
   University Hospital Brno; Masaryk University Brno; Nicolaus Copernicus
   University
RP Kempisty, B (corresponding author), Wroclaw Med Univ, Dept Human Morphol & Embryol, Div Anat, Chalubinskiego 6a St, PL-50368 Wroclaw, Poland.
EM bartosz.kempisty@umw.edu.pl
RI Konwinska, Marta/AFQ-0541-2022; Bryja, Artur/HKV-5372-2023; Ghasemian,
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OI Podhorska-Okolow, Marzenna/0000-0003-2215-5997; Zabel,
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   Piotr/0000-0002-8292-1385; mozdziak, paul/0000-0002-1575-3123
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NR 151
TC 3
Z9 4
U1 2
U2 6
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0024-3205
EI 1879-0631
J9 LIFE SCI
JI Life Sci.
PD NOV 1
PY 2023
VL 332
AR 122126
DI 10.1016/j.lfs.2023.122126
EA SEP 2023
PG 10
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA X1BY6
UT WOS:001095882600001
PM 37769803
OA hybrid
DA 2025-01-04
ER

PT J
AU Migliore, C
   Morando, E
   Ghiso, E
   Anastasi, S
   Leoni, VP
   Apicella, M
   Cora', D
   Sapino, A
   Pietrantonio, F
   De Braud, F
   Columbano, A
   Segatto, O
   Giordano, S
AF Migliore, Cristina
   Morando, Elena
   Ghiso, Elena
   Anastasi, Sergio
   Leoni, Vera P.
   Apicella, Maria
   Cora', Davide
   Sapino, Anna
   Pietrantonio, Filippo
   De Braud, Filippo
   Columbano, Amedeo
   Segatto, Oreste
   Giordano, Silvia
TI miR-205 mediates adaptive resistance to MET inhibition via ERRFI1
   targeting and raised EGFR signaling
SO EMBO MOLECULAR MEDICINE
LA English
DT Article
DE EGFR; ERRFI1; MET; resistance; targeted therapy
ID GROWTH-FACTOR RECEPTOR; TYROSINE KINASE INHIBITORS; CELL LUNG-CANCER;
   ACQUIRED-RESISTANCE; COLORECTAL-CANCER; AMPLIFICATION; MECHANISMS;
   RATIONALE; MICRORNAS; THERAPIES
AB The onset of secondary resistance represents a major limitation to long-term efficacy of target therapies in cancer patients. Thus, the identification of mechanisms mediating secondary resistance is the key to the rational design of therapeutic strategies for resistant patients. MiRNA profiling combined with RNA-Seq in MET-addicted cancer cell lines led us to identify the miR-205/ERRFI1 (ERBB receptor feedback inhibitor-1) axis as a novel mediator of resistance to MET tyrosine kinase inhibitors (TKIs). In cells resistant to MET-TKIs, epigenetically induced miR-205 expression determined the downregulation of ERRFI1 which, in turn, caused EGFR activation, sustaining resistance to MET-TKIs. Anti-miR-205 transduction reverted crizotinib resistance invivo, while miR-205 over-expression rendered wt cells refractory to TKI treatment. Importantly, in the absence of EGFR genetic alterations, miR-205/ERRFI1-driven EGFR activation rendered MET-TKI-resistant cells sensitive to combined MET/EGFR inhibition. As a proof of concept of the clinical relevance of this new mechanism of adaptive resistance, we report that a patient with a MET-amplified lung adenocarcinoma displayed deregulation of the miR-205/ERRFI1 axis in concomitance with onset of clinical resistance to anti-MET therapy.
C1 [Migliore, Cristina; Cora', Davide; Giordano, Silvia] Univ Torino, Dept Oncol, Candiolo, Italy.
   [Migliore, Cristina; Morando, Elena; Ghiso, Elena; Apicella, Maria; Cora', Davide; Sapino, Anna; Giordano, Silvia] FPO IRCCS, Candiolo Canc Inst, Candiolo, Italy.
   [Anastasi, Sergio; Segatto, Oreste] IRCCS Regina Elena Natl Canc Inst, Unit Oncogen & Epigenet, Rome, Italy.
   [Leoni, Vera P.; Columbano, Amedeo] Univ Cagliari, Dept Biomed Sci, Unit Oncol & Mol Pathol, Cagliari, Italy.
   [Cora', Davide] Piemonte Orientale Univ Amedeo Avogadro, Dept Translat Med, Novara, Italy.
   [Sapino, Anna] Univ Torino, Dept Med Sci, Turin, Italy.
   [Pietrantonio, Filippo; De Braud, Filippo] Fdn IRCCS Ist Nazl Tumori, Med Oncol, Milan, Italy.
   [Pietrantonio, Filippo; De Braud, Filippo] Univ Milan, Dept Oncol & Hematooncol, Milan, Italy.
C3 University of Turin; IRCCS Fondazione del Piemonte per l'Oncologia;
   University of Cagliari; University of Eastern Piedmont Amedeo Avogadro;
   University of Turin; Fondazione IRCCS Istituto Nazionale Tumori Milan;
   University of Milan
RP Migliore, C; Giordano, S (corresponding author), Univ Torino, Dept Oncol, Candiolo, Italy.; Migliore, C (corresponding author), FPO IRCCS, Candiolo Canc Inst, Candiolo, Italy.; Segatto, O (corresponding author), IRCCS Regina Elena Natl Canc Inst, Unit Oncogen & Epigenet, Rome, Italy.
EM cristina.migliore@unito.it; oreste.segatto@ifo.gov.it;
   silvia.giordano@unito.it
RI Migliore, Cristina/ISB-9176-2023; Columbano, Amedeo/C-7463-2011; Leoni,
   Valerio/AAC-1652-2019; Sapino, Anna/AGY-9901-2022; anastasi,
   sergio/AAB-9585-2020; Pietrantonio, Filippo/C-2180-2017; Sapino,
   Anna/J-4113-2018; GIORDANO, Silvia/J-9858-2018; de Braud, Filippo
   Guglielmo Maria/B-9997-2017
OI Leoni, Vera Piera/0000-0002-2447-0547; Pietrantonio,
   Filippo/0000-0002-8530-8420; Sapino, Anna/0000-0003-3542-9571; Migliore,
   Cristina/0000-0003-3722-2814; GIORDANO, Silvia/0000-0003-1854-1086;
   Segatto, Oreste/0000-0003-2561-1142; Cora', Davide/0000-0003-4123-1705;
   de Braud, Filippo Guglielmo Maria/0000-0003-0103-730X; Columbano,
   Amedeo/0000-0002-6956-9030
FU Italian Association for Cancer Research (AIRC);  [20210];  [16726]; 
   [20176]
FX We thank all our colleagues for helpful scientific discussion; Daniela
   Conticelli for help in experiment execution; Barbara Martinoglio,
   Roberta Porporato, Daniela Cantarella, Michela Buscarino, Stefania
   Bolla, and Ivana Sarotto for providing technical support with real-time
   PCR, RNA extraction, Sanger sequencing, and IHC, respectively; Stefania
   Durando and Daniel Moya for animal care; we are indebted to S. Di
   Agostino for advice, L. Nardinocchi for cloning the Luc-ERRFI1 reporter
   and to Dr. Dragani for help for methylation experiments. JNJ-38877605
   was kindly provided by Janssen. This work was funded by the Italian
   Association for Cancer Research (AIRC); IG grants 20210 to SG, 16726 to
   OS and 20176 to AC.
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   Martin V, 2014, MOL ONCOL, V8, P1561, DOI 10.1016/j.molonc.2014.06.010
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NR 28
TC 22
Z9 24
U1 0
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1757-4676
EI 1757-4684
J9 EMBO MOL MED
JI EMBO Mol. Med.
PD SEP
PY 2018
VL 10
IS 9
AR e8746
DI 10.15252/emmm.201708746
PG 12
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA GT7BU
UT WOS:000444676000006
PM 30021798
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Xi, CL
   Wang, L
   Yu, J
   Ye, H
   Cao, LL
   Gong, ZL
AF Xi, Changlei
   Wang, Ling
   Yu, Jie
   Ye, Hui
   Cao, Longlei
   Gong, Zhilin
TI Inhibition of eukaryotic translation initiation factor 4E is effective
   against chemo-resistance in colon and cervical cancer
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE eIF4E; Ribavirin; VEGF; c-Myc; Chemoresistance; Cancer therapy
ID BREAST-CANCER; EIF4E PHOSPHORYLATION; RIBAVIRIN; TRANSFORMATION;
   CHEMOTHERAPY; PROGRESSION; CARCINOMA; CELLS; TUMORIGENESIS; SURVIVAL
AB Although cancer patients initially respond well to chemotherapy, they eventually develop resistance and relapse. In this work, we demonstrate that eIF4E-targeting therapy is a potential sensitizing strategy for overcoming chemoresistance and progression in cancer. We show that ribavirin, an anti-viral drug and pharmacological eIF4E inhibitor, effectively inhibits proliferation and decreases viability of paclitaxel-resistant cervical cancer and 5-FU-resistant colon cancer cells while is less toxic to human fibroblast cells. Importantly, oral administration of ribavirin significantly inhibits paclitaxel-resistant colon and 5-FU-resistant cervical cancer growth in xenograft mouse cancer model without causing significant toxicity in mice. Consistently, combination of ribavirin with paclitaxel or 5-FU sensitizes colon and cervical cancer cells to chemotherapeutic agents treatment in vitro and in vivo. We further confirm that the mechanism of the action of ribavirin in chemoresistant cancer cells is through suppressing eIF4E function. In addition, specific eIF4E knockdown via two independent siRNA mimics the effects of ribavirin in chemoresistant colon and cervical cancer cells. Cell cycle analysis indicate that ribavirin enhances the anti-proliferative effect of 5-FU by additionally arresting cells at G2/M phase via increasing cyclin B1, phistone H3(Ser10) and Mad2 levels. Our work demonstrates that eIF4E inhibition using inhibitor or siRNA, either as single agent or in combination, could sensitize chemoresistant cancer cells to paclitaxel or 5-FU treatment and thereby improving the efficacy of chemodrug. Our findings demonstrate the therapeutic value of inhibiting eIF4E, particularly in chemoresistant cancers. Our findings also suggest ribavirin as a promising sensitizing drug for cancer treatment. (C) 2018 Elsevier Inc. All rights reserved.
C1 [Xi, Changlei; Yu, Jie; Ye, Hui; Cao, Longlei; Gong, Zhilin] Jingzhou Cent Hosp, Dept Anorectal Surg, Renmin Rd 1, Jingzhou 434020, Peoples R China.
   [Wang, Ling] Jingzhou Cent Hosp, Dept Obstet & Gynaecol, Jingzhou, Peoples R China.
RP Gong, ZL (corresponding author), Jingzhou Cent Hosp, Dept Anorectal Surg, Renmin Rd 1, Jingzhou 434020, Peoples R China.
EM Doctor_gong434020@163.com
FU Jingzhou Central Hospital [201206606]
FX This work was supported by a research grant provided by Jingzhou Central
   Hospital (Grant No. 201206606).
CR Aljabr W, 2016, J VIROL, V90, P4876, DOI 10.1128/JVI.02349-15
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   Berden FAC, 2017, CLIN GASTROENTEROL H, V15, P349, DOI 10.1016/j.cgh.2016.10.034
   Borden KLB, 2010, LEUKEMIA LYMPHOMA, V51, P1805, DOI 10.3109/10428194.2010.496506
   Boussemart L, 2014, NATURE, V513, P105, DOI 10.1038/nature13572
   Chen YT, 2017, PATHOL RES PRACT, V213, P490, DOI 10.1016/j.prp.2017.02.004
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   Furic L, 2010, P NATL ACAD SCI USA, V107, P14134, DOI 10.1073/pnas.1005320107
   Grzmil M, 2016, CELL SIGNAL, V28, P1412, DOI 10.1016/j.cellsig.2016.06.005
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NR 31
TC 29
Z9 30
U1 0
U2 10
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 SEP 18
PY 2018
VL 503
IS 4
BP 2286
EP 2292
DI 10.1016/j.bbrc.2018.06.150
PG 7
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA GT8MM
UT WOS:000444791600014
PM 29959920
DA 2025-01-04
ER

PT J
AU El Guerrab, A
   Bamdad, M
   Kwiatkowski, F
   Bignon, YJ
   Penault-Llorca, F
   Aubel, C
AF El Guerrab, Abderrahim
   Bamdad, Mahchid
   Kwiatkowski, Fabrice
   Bignon, Yves-Jean
   Penault-Llorca, Frederique
   Aubel, Corinne
TI Anti-EGFR monoclonal antibodies and EGFR tyrosine kinase inhibitors as
   combination therapy for triple-negative breast cancer
SO ONCOTARGET
LA English
DT Article
DE triple-negative breast cancer; epidermal growth factor receptor;
   anti-EGFR targeted therapy; cytotoxicity; cell cycle
ID GROWTH-FACTOR RECEPTOR; METASTATIC COLORECTAL-CANCER; CETUXIMAB PLUS
   IRINOTECAN; RANDOMIZED PHASE-II; GENE COPY NUMBER; CELL LUNG-CANCER;
   TARGETED THERAPIES; 1ST-LINE TREATMENT; DRUG-RESISTANCE; BRCA1 MUTATIONS
AB Triple-negative breast cancer (TNBC) is characterized by overexpression of epidermal growth factor receptor (EGFR) and activation of its downstream signaling pathways. Dual targeting of EGFR using one monoclonal antibody (mAb; cetuximab or panitumumab) and one tyrosine kinase inhibitor (EGFR-TKI; gefitinib or erlotinib) is a potential therapeutic approach. We investigated the effect of these therapies in EGFR-expressing TNBC cell lines that do or do not harbor the main activating mutations of EGFR pathways. Cell lines were sensitive to EGFR-TKIs, whereas mAbs were active only in MDA-MB-468 (EGFR amplification) and SUM-1315 (KRAS and PTEN wild-type) cells. MDA-MB-231 (KRAS mutated) and HCC-1937 (PTEN deletion) cells were resistant to mAbs. The combined treatment resulted in a synergistic effect on cell proliferation and superior inhibition of the RAS/MAPK signaling pathway in mAb-sensitive cells. The anti-proliferative effect was associated with G1 cell cycle arrest followed by apoptosis. Sensitivity to therapies was characterized by induction of positive regulators and inactivation of negative regulators of cell cycle. These results suggest that dual EGFR inhibition might result in an enhanced antitumor effect in a subgroup of TNBC. The status of EGFR, KRAS and PTEN could be used as a molecular marker for predicting the response to this therapeutic strategy.
C1 [El Guerrab, Abderrahim; Kwiatkowski, Fabrice; Bignon, Yves-Jean; Penault-Llorca, Frederique; Aubel, Corinne] Ctr Jean Perrin, ERTICa EA4677, BP392, F-63011 Clermont Ferrand, France.
   [El Guerrab, Abderrahim; Bamdad, Mahchid; Bignon, Yves-Jean; Penault-Llorca, Frederique; Aubel, Corinne] Univ Auvergne, Clermont Univ, ERTICa EA4677, Fac Med, BP38, F-63001 Clermont Ferrand, France.
   [Bamdad, Mahchid] Ensemble Univ Cezeaux, Clermont Univ, Univ Auvergne, Inst Univ Technol,Dept Genie Biol,ERTICa EA4677, F-63172 Aubiere, France.
C3 UNICANCER; Centre Jean Perrin; Universite Clermont Auvergne (UCA);
   Universite Clermont Auvergne (UCA)
RP Bignon, YJ (corresponding author), Ctr Jean Perrin, ERTICa EA4677, BP392, F-63011 Clermont Ferrand, France.; Bignon, YJ (corresponding author), Univ Auvergne, Clermont Univ, ERTICa EA4677, Fac Med, BP38, F-63001 Clermont Ferrand, France.
EM Yves-Jean.bignon@cjp.fr
RI Bamdad, Mahchid/Y-1363-2019; aubel, corinne/Y-7143-2019
OI Bamdad, Mahchid/0000-0002-2474-6910; Aubel, Corinne/0000-0003-4500-6505
FU French Ligue Nationale Contre le Cancer
FX This study was supported by grants from the French Ligue Nationale
   Contre le Cancer.
CR [Anonymous], ASCO M
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NR 79
TC 81
Z9 90
U1 1
U2 26
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 8
PY 2016
VL 7
IS 45
BP 73618
EP 73637
DI 10.18632/oncotarget.12037
PG 20
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EB5WT
UT WOS:000387452100090
PM 27655662
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Rouyer, M
   Fourrier-Réglat, A
   Smith, D
   Becouarn, Y
   Guimbaud, R
   Tubiana-Mathieu, N
   Robinson, P
   Jové, J
   Grelaud, A
   Noize, P
   Moore, N
   Ravaud, A
AF Rouyer, Magali
   Fourrier-Reglat, Annie
   Smith, Denis
   Becouarn, Yves
   Guimbaud, Rosine
   Tubiana-Mathieu, Nicole
   Robinson, Philip
   Jove, Jeremy
   Grelaud, Angela
   Noize, Pernelle
   Moore, Nicholas
   Ravaud, Alain
TI Effectiveness and safety of first-line bevacizumab plus FOLFIRI in
   elderly patients with metastatic colorectal cancer: Results of the ETNA
   observational cohort
SO JOURNAL OF GERIATRIC ONCOLOGY
LA English
DT Article
DE Aged; Colorectal neoplasms; Secondary; Molecular targeted therapy;
   Bevacizumab; Cohort studies
ID CLINICAL-OUTCOMES; CHEMOTHERAPY; EFFICACY; TRIALS; MCRC
AB Objectives: Effectiveness of bevacizumab for metastatic colorectal cancer in elderly patients has been investigated in observational studies, mainly associated with oxaliplatin-based regimens. Here, using the ETNA cohort in which the majority of patients received bevacizumab + FOLFIRI, the effectiveness of this combination in elderly patients is explored.
   Materials and Methods: Patients initiating first-line therapy with bevacizumab between January 2006 and December 2007 were identified in 28 French centres and followed for 24 months. Vital status was collected over 36 months. In the present analysis those who received FOLFIRI were retained (85% of those included), and patients were stratified by age (<70/>= 70 years). The Kaplan-Meier method estimated progression-free survival (PFS) and overall survival (OS), and Cox models were used to assess the independent effect of age on survival outcomes.
   Results: Among the 351 patients who received bevacizumab + FOLFIRI, 33.9% were aged >= 70 years, 66.1% <70 years. Respectively 15.1% and 9.5% of patients had ECOG-PS >= 2; 49.6% and 40.1% used 'stop-and-go' treatment scheduling; and 56.3% and 44.4% experienced grade 3/4 adverse events. Overall response rate was 58.8% and 62.5%. Median [95% confidence interval, CI] OS was respectively 24.1 [20.4; 26.2] and 28.5 [25.0; 31.0] months; age >= 70 years and ECOG-PS >= 2 were significantly associated with death. Median PFS [95% CI] was respectively 10.9 [9.4; 12.6] and 9.8 [9.2; 11.2] months; hepatic metastases was associated with progression, and age >= 70 years was associated with progression after 14 months of follow-up but not before.
   Conclusions: The present study adds to the literature on the safe and beneficial effect of bevacizumab in the elderly receiving FOLFIRI regimen. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [Rouyer, Magali; Fourrier-Reglat, Annie; Robinson, Philip; Jove, Jeremy; Grelaud, Angela; Moore, Nicholas; Ravaud, Alain] Univ Bordeaux, F-33000 Bordeaux, France.
   [Rouyer, Magali; Fourrier-Reglat, Annie; Robinson, Philip; Jove, Jeremy; Grelaud, Angela; Noize, Pernelle; Moore, Nicholas; Ravaud, Alain] CIC Bordeaux, CIC1401, F-33000 Bordeaux, France.
   [Rouyer, Magali; Robinson, Philip; Jove, Jeremy; Grelaud, Angela] ADERA, F-33600 Pessac, France.
   [Fourrier-Reglat, Annie; Smith, Denis; Noize, Pernelle; Moore, Nicholas; Ravaud, Alain] CHU Bordeaux, F-33000 Bordeaux, France.
   [Fourrier-Reglat, Annie; Noize, Pernelle; Moore, Nicholas] INSERM, U1219, F-33000 Bordeaux, France.
   [Becouarn, Yves] Inst Bergonie, F-33076 Bordeaux, France.
   [Guimbaud, Rosine] CHU Toulouse, F-31059 Toulouse, France.
   [Tubiana-Mathieu, Nicole] CHU Limoges, F-87042 Limoges, France.
C3 Universite de Bordeaux; Universite de Bordeaux; CHU Bordeaux; Universite
   de Bordeaux; Institut National de la Sante et de la Recherche Medicale
   (Inserm); Universite de Bordeaux; UNICANCER; Institut Bergonie; CHU de
   Toulouse; Universite de Toulouse; Universite Toulouse III - Paul
   Sabatier; CHU Limoges
RP Fourrier-Réglat, A (corresponding author), Univ Bordeaux, INSERM, U1219, CIC1401, Case 36,146 Rue Leo Saignat, F-33076 Bordeaux, France.
EM annie.fourrier-reglat@u-bordeaux.fr
RI Noize, Pernelle/T-1955-2019; Moore, Nicholas/B-2368-2013
OI Ravaud, Alain/0000-0001-9455-6744; tubiana mathieu,
   nicole/0000-0001-7849-3667; Moore, Nicholas/0000-0003-1212-2817; Noize,
   Pernelle/0000-0001-5617-7954; Angela, Grelaud/0000-0002-3480-3405
FU French National Clinical Research Programme (Programme Hospitalier de
   Recherche Clinique) from the French Ministry of Health
   [2005/PHRC/INCa/DHOS]; Roche SAS, manufacturers of bevacizumab
FX This work was supported by partial funding from the French National
   Clinical Research Programme (Programme Hospitalier de Recherche
   Clinique) from the French Ministry of Health [grant number
   2005/PHRC/INCa/DHOS]; and an additional unconditional grant from Roche
   SAS, manufacturers of bevacizumab, who had no role in study design; in
   the collection, analysis, and interpretation of data; in the writing of
   the report or in the decision to submit the report for publication.
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NR 20
TC 13
Z9 14
U1 0
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1879-4068
EI 1879-4076
J9 J GERIATR ONCOL
JI J. Geriatr. Oncol.
PD MAY
PY 2016
VL 7
IS 3
BP 187
EP 194
DI 10.1016/j.jgo.2016.03.004
PG 8
WC Oncology; Geriatrics & Gerontology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Geriatrics & Gerontology
GA DM7PO
UT WOS:000376552700007
PM 27085302
DA 2025-01-04
ER

PT J
AU Yao, J
   Zhang, P
   Li, J
   Xu, W
AF Yao, Jian
   Zhang, Ping
   Li, Jin
   Xu, Wei
TI MicroRNA-215 acts as a tumor suppressor in breast cancer by targeting
   AKT serine/threonine kinase 1
SO ONCOLOGY LETTERS
LA English
DT Article
DE breast cancer; microRNA-215; tumor suppressor; AKT serine/threonine
   kinase; targeted therapy
ID GASTRIC-CANCER; CELL-PROLIFERATION; METASTASIS; INVASION; MIR-215;
   PROGRESSION; EXPRESSION; GROWTH
AB There are accumulating reports that microRNAs are dysregulated in a number of human cancer types, and that they may function as tumor suppressors or oncogenes in tumorigenesis and tumor development. microRNA-215 (miR-215) has been identified as a tumor suppressor in epithelial ovarian, pancreatic, non-small cell lung and colon cancer, whereas it may act as an oncogene in gastric and cervical cancer. The role of miR-215 in breast cancer carcinogenesis and progression has yet to be elucidated. In the present study, the expression level of miR-215 was determined in breast cancer tissues and cell lines using the reverse transcription-quantitative polymerase chain reaction. The effects of miR-215 overexpression on proliferation and the invasive capacity of breast cancer cells were assessed using MTT and cell invasion assays. The results revealed that miR-215 was significantly downregulated in breast cancer tissues and cell lines. Restoration of miR-215 expression inhibited the proliferation and invasion of breast cancer cells. The underlying molecular mechanism for the suppression of proliferation and invasion by miR-215 was investigated. AKT serine/threonine kinase 1 (AKT1) was validated as a novel direct target of miR-215, and the effect of AKT1 small interfering RNA mimicked the effect of miR-215 overexpression in breast cancer cells. These results indicated that miR-215 acted as a tumor suppressor, and that its downregulation in tumor tissues may contribute to the carcinogenesis and progression of breast cancer, indicating that miR-215 may be a novel therapeutic target for the treatment of breast cancer.
C1 [Yao, Jian; Zhang, Ping; Li, Jin; Xu, Wei] Harbin Med Univ, Affiliated Hosp 1, Dept Integrated Tradit Chinese & Western Med, 23 You Zheng St, Harbin 150001, Heilongjiang, Peoples R China.
C3 Harbin Medical University
RP Xu, W (corresponding author), Harbin Med Univ, Affiliated Hosp 1, Dept Integrated Tradit Chinese & Western Med, 23 You Zheng St, Harbin 150001, Heilongjiang, Peoples R China.
EM xw2015great@163.com
RI , YAO JIAN/JMQ-3831-2023
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NR 40
TC 39
Z9 43
U1 0
U2 2
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 JUL
PY 2017
VL 14
IS 1
BP 1097
EP 1104
DI 10.3892/ol.2017.6200
PN B
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FA7RY
UT WOS:000405645800084
PM 28693279
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wang, JW
   Huang, YH
   Zhang, J
   Xing, BY
   Xuan, W
   Wang, HH
   Huang, H
   Yang, JY
   Tang, JW
AF Wang, Jingwen
   Huang, Yuhong
   Zhang, Jun
   Xing, Boyi
   Xuan, Wei
   Wang, Honghai
   Huang, He
   Yang, Jiayu
   Tang, Jianwu
TI NRP-2 in tumor lymphangiogenesis and lymphatic metastasis
SO CANCER LETTERS
LA English
DT Review
DE Neuropilin-2 (NRP-2); Lymphangiogenesis; Lymphatic metastasis;
   VEGF-C/D-NRP-2 axis tumor
ID VEGF-C; NEUROPILIN-2 EXPRESSION; COLORECTAL-CARCINOMA; POOR-PROGNOSIS;
   CELL CARCINOMA; IN-VITRO; CANCER; GROWTH; ANGIOGENESIS; INTEGRIN
AB Neuropilin-2 (NRP-2) not only functions as a receptor for semaphorins, a family of neural axon guidance factors, but also interacts with VEGFs, a family of vascular endothelial growth factors. As an independent receptor or a co-receptor, NRP-2 binds to ligands VEGF-C/D, activates the VEGF-C/D-NRP-2 signaling axis, and further regulates lymphangiogenesis-associated factors in both lymphatic endothelial cells (LECs) and some tumor cells during tumor progression. Via VEGF-C/D-NRP-2 axis, NRP-2 induces LEC proliferation, reconstruction and lymphangiogenesis and subsequently promotes tumor cell migration, invasion and lymphatic metastasis. There are similarities and differences among NRP-1, NRP-2 and VEGFR-3 in chemical structure, ligand specificity, chromosomal location, soluble protein forms, cellular functions and expression profiles. High expression of NRP-2 in LECs and tumor cells has been observed in different anatomic sites, histological patterns and progression stages of various tumors, especially during tumor lymphangiogenesis and lymphatic metastasis, and therefore the NRP-2 and VEGF-C/D-NRP-2 axis are closely related to tumor development, progression, invasion, and metastasis. In addition, it is important for prognosis of tumor. The studies on NRP-2 targeted therapy have recently achieved some successes, utilizing NRP-2 blocking antibodies, NRP-2 inhibitory peptides, soluble NRP-2 antagonists, small molecule inhibitors and various NRP-2 gene therapeutic strategies. (C) 2018 Elsevier B.V. All rights reserved.
C1 [Wang, Jingwen; Huang, Yuhong; Zhang, Jun; Xing, Boyi; Xuan, Wei; Wang, Honghai; Huang, He; Yang, Jiayu; Tang, Jianwu] Dalian Med Univ, Key Lab Tumor Metastasis & Intervent Liaoning Pro, Dept Pathol, 9 West,Lvshun Southern Rd, Dalian 116044, Liaoning, Peoples R China.
   [Wang, Jingwen] Ningbo Coll Hlth Sci, Inst Med Technol, 51 XueFu Rd, Ningbo 315100, Zhejiang, Peoples R China.
C3 Dalian Medical University
RP Tang, JW (corresponding author), Dalian Med Univ, Key Lab Tumor Metastasis & Intervent Liaoning Pro, Dept Pathol, 9 West,Lvshun Southern Rd, Dalian 116044, Liaoning, Peoples R China.
EM jianwutang@163.com
RI zhang, yuhan/HLH-1222-2023
FU National Natural Science Foundation of China [81071725]; Financial
   Department of Liaoning Province, PRC [20121203]
FX This work was funded by the National Natural Science Foundation of China
   (No.81071725) and the Financial Department of Liaoning Province, PRC.
   (No. 20121203)
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NR 84
TC 56
Z9 63
U1 3
U2 25
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0304-3835
EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PD APR 1
PY 2018
VL 418
BP 176
EP 184
DI 10.1016/j.canlet.2018.01.040
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FX5SL
UT WOS:000426139800018
PM 29339213
DA 2025-01-04
ER

PT J
AU Kumar, A
   Pramanik, J
   Batta, K
   Bamal, P
   Gaur, M
   Rustagi, S
   Prajapati, BG
   Bhattacharya, S
AF Kumar, Akash
   Pramanik, Jhilam
   Batta, Kajol
   Bamal, Pooja
   Gaur, Mukesh
   Rustagi, Sarvesh
   Prajapati, Bhupendra G.
   Bhattacharya, Sankha
TI Impact of metallic nanoparticles on gut microbiota modulation in
   colorectal cancer: A review
SO CANCER INNOVATION
LA English
DT Review
DE apoptosis; carcinogenesis; dysbiosis; gastrointestinal microbiome;
   titanium dioxide
ID TITANIUM-DIOXIDE NANOPARTICLES; IRON-OXIDE NANOPARTICLES; SILVER
   NANOPARTICLES; GOLD NANOPARTICLES; COLON-CANCER; OXIDATIVE STRESS; GREEN
   SYNTHESIS; EXTRACT; FOOD; ANTIBACTERIAL
AB Colorectal cancer (CRC) is the third most prevalent cancer. Ongoing research aims to uncover the causes of CRC, with a growing focus on the role of gut microbiota (GM) in carcinogenesis. The GM influences CRC development, progression, treatment efficacy, and therapeutic toxicities. For example, Fusobacterium nucleatum and Escherichia coli can regulate microbial gene expression through the incorporation of human small noncode RNA and potentially contribute to cancer progression. Metallic nanoparticles (MNPs) have both negative and positive impacts on GM, depending on their type. Several studies state that titanium dioxide may increase the diversity, richness, and abundance of probiotics bacteria, whereas other studies demonstrate dose-dependent GM dysbiosis. The MNPs offer cytotoxicity through the modulation of MAPK signaling pathways, NF-kB signaling pathways, PI3K/Akt signaling pathways, extrinsic signaling pathways, intrinsic apoptosis, and cell cycle arrest at G1, G2, or M phase. MNPs enhance drug delivery, enable targeted therapy, and may restore GM. However, there is a need to conduct well-designed clinical trials to assess the toxicity, safety, and effectiveness of MNPs-based CRC therapies.
   Metallic nanoparticles have the potential to be a new and effective treatment for colorectal cancer. image
C1 [Kumar, Akash] SRM Univ, Dept Food Technol, Sonepat, India.
   [Kumar, Akash] Maharishi Markandeshwar, MMICT & BM Hotel Management, Mullana, India.
   [Pramanik, Jhilam] William Carey Univ, Dept Food Technol, Shillong, India.
   [Batta, Kajol] ITM Univ, Dept Food Technol, Gwalior, India.
   [Bamal, Pooja] Chaudhary Devi Lal Univ, Dept Food Sci & Technol, Sirsa, India.
   [Gaur, Mukesh] Guru Jambheshwar Univ Sci & Technol, Dept Food Technol, Hisar, India.
   [Rustagi, Sarvesh] Uttaranchal Univ, Sch Appl & Life Sci, Dehra Dun, India.
   [Prajapati, Bhupendra G.] Ganpat Univ, Shree SK Patel Coll Pharmaceut Educ & Res, Mehsana 384012, India.
   [Bhattacharya, Sankha] SVKMS NMIMS, Sch Pharm & Technol Management, Dept Pharmaceut, Shirpur 425405, Maharashtra, India.
C3 SRM University Haryana; ITM University, Gwalior; Chaudhary Devi Lal
   University; Guru Jambheshwar University of Science & Technology;
   Uttaranchal University; Ganpat University; SVKM's NMIMS (Deemed to be
   University)
RP Prajapati, BG (corresponding author), Ganpat Univ, Shree SK Patel Coll Pharmaceut Educ & Res, Mehsana 384012, India.; Bhattacharya, S (corresponding author), SVKMS NMIMS, Sch Pharm & Technol Management, Dept Pharmaceut, Shirpur 425405, Maharashtra, India.
EM bhupen27@gmail.com; sankhabhatt@gmail.com
RI Kumar, Akash/LLN-1054-2024; Rustagi, Sarvesh/AEC-1996-2022; Prajapati,
   Dr. Bhupendra/A-3088-2015
OI Prajapati, Dr. Bhupendra/0000-0001-8242-4541
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NR 151
TC 0
Z9 0
U1 3
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2770-9191
EI 2770-9183
J9 CANCER INNOV
JI Cancer Innov.
PD DEC
PY 2024
VL 3
IS 6
AR e150
DI 10.1002/cai2.150
PG 18
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA I4G9Y
UT WOS:001329870000001
PM 39398260
OA gold
DA 2025-01-04
ER

PT J
AU Khan, S
   Madni, A
   Shah, HS
   Jan, NSL
   Shafiq, A
   Basit, A
   Rai, N
   Ali, A
   Khan, MM
AF Khan, Safiullah
   Madni, Asadullah
   Shah, Hassan
   Jan, Nasrullah
   Shafiq, Afifa
   Basit, Abdul
   Rai, Nadia
   Ali, Ahsan
   Khan, Muhammad Muzamil
TI Folate decorated lipid chitosan hybrid nanoparticles of 5-fluorouracil
   for enhanced anticancer efficacy against colon cancer
SO INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
LA English
DT Article
DE Chitosan; Folic acid; Colorectal cancer; Nanomedicine; 5-Fluorouracil
ID TARGETED DELIVERY; DRUG-DELIVERY; IN-VITRO; ORAL DELIVERY; CISPLATIN;
   CURCUMIN; THERAPY; CYTOTOXICITY; PACLITAXEL; SYSTEMS
AB The study aimed to develop folate decorated lipid chitosan hybrid nanoparticles for targeted delivery of 5-fluo-rouracil in colon cancer by utilizing the overexpressed folate receptors on the surface of HT-29 and HCT 116 cancer cell lines. The developed formulations were prepared by the ionic gelation method with slight modifi-cations. The developed formulations exhibited spherical morphology, smaller particle size (158 to 225 nm), zeta potential (32.24 to 35.95 mV), PDI (0.19 to 0.35), and high encapsulation efficiency (85.3 % to 94.2 %) with optimal physicochemical characteristics. The in vitro release showed a biphasic release pattern with an initial burst release followed by a sustained release for 48 h. Moreover, the in vitro cell line study revealed that FA-CLPN-2 exhibited an enhanced cellular uptake and greater cytotoxic effect in HT-29 and HCT 116 cell lines compared to non-targeted CLPN-2 and free drug solution due to the folate receptor facilitated endocytosis process. The in vivo toxicity study revealed the safety and biocompatibility of the developed formulations in biological systems. The stability study demonstrates the stability of the developed formulations. Overall, these results suggest that the folate decorated lipid chitosan hybrid nanoparticles could be used as a potential delivery system for tumor-targeted therapy with reduced side effects.
C1 [Khan, Safiullah; Madni, Asadullah; Shah, Hassan; Shafiq, Afifa; Rai, Nadia; Ali, Ahsan; Khan, Muhammad Muzamil] Islamia Univ Bahawalpur, Fac Pharm, Dept Pharmaceut, Bahawalpur 63100, Pakistan.
   [Jan, Nasrullah] Mirpur Univ Sci & Technol MUST, Akson Coll Pharm, Mirpur 10250, AJ &K, Pakistan.
   [Basit, Abdul] Islamia Univ Bahawalpur, Fac Pharm, Dept Pharmaceut Chem, Bahawalpur 63100, Pakistan.
   [Shah, Hassan; Ali, Ahsan] Northeastern Univ, Ctr Pharmaceut Biotechnol & Nanomed, Boston, MA 02115 USA.
C3 Islamia University of Bahawalpur; Islamia University of Bahawalpur;
   Northeastern University
RP Madni, A (corresponding author), Islamia Univ Bahawalpur, Fac Pharm, Dept Pharmaceut, Bahawalpur 63100, Pakistan.
EM asadpharmacist@hotmail.com
RI Basit, Abdul/GLS-9036-2022; Khan, Safiullah/JRF-7690-2023; Jan,
   Nasrullah/GPP-6186-2022; Madni, Prof. Dr. M. Asadullah/ABD-4544-2022;
   Shafiq, Dr Afifa/KUK-5402-2024; Madni, Prof. Dr. M.
   Asadullah/ABE-0757-2022; Khan, Muhammad Muzamil/ACP-3363-2022
OI Basit, Abdul/0000-0002-0012-8931; Shafiq, Dr. Afifa/0000-0002-1325-6158;
   Madni, Prof. Dr. M. Asadullah/0000-0002-0388-9867; Jan,
   Nasrullah/0000-0002-1279-2397; Ali, Ahsan/0000-0003-4346-0667; Khan,
   Muhammad Muzamil/0000-0002-5380-0533
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NR 57
TC 21
Z9 21
U1 3
U2 20
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0141-8130
EI 1879-0003
J9 INT J BIOL MACROMOL
JI Int. J. Biol. Macromol.
PD DEC 1
PY 2022
VL 222
BP 497
EP 508
DI 10.1016/j.ijbiomac.2022.09.196
EA SEP 2022
PN A
PG 12
WC Biochemistry & Molecular Biology; Chemistry, Applied; Polymer Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry; Polymer Science
GA 5U1ZR
UT WOS:000876352600001
PM 36174854
DA 2025-01-04
ER

PT J
AU Zhou, XR
   Li, CC
   Zhang, Z
   Li, DY
   Du, JW
   Ding, P
   Meng, HY
   Xu, H
   Li, RL
   Ho, E
   Zhang, AG
   Okunieff, P
   Lu, JW
   Sha, MY
AF Zhou, Xiaorong
   Li, Chenchen
   Zhang, Zhao
   Li, Daniel Y.
   Du, Jinwei
   Ding, Ping
   Meng, Haiyan
   Xu, Hui
   Li, Ronglei
   Ho, Effie
   Zhang, Aiguo
   Okunieff, Paul
   Lu, Jianwei
   Sha, Michael Y.
TI Kinetics of plasma cfDNA predicts clinical response in non-small cell
   lung cancer patients
SO SCIENTIFIC REPORTS
LA English
DT Article
ID CIRCULATING TUMOR DNA; COLORECTAL-CANCER; PROGNOSTIC BIOMARKER;
   ACQUIRED-RESISTANCE; TARGETED THERAPY; EGFR MUTATIONS; SERUM;
   CHEMOTHERAPY; SURVIVAL; NSCLC
AB Tyrosine kinase inhibitors (TKIs), VEGF/VEGF receptor inhibitors (VEGFIs) and immune checkpoint inhibitors (ICIs) have revolutionized the treatment of advanced cancers including non-small-cell lung cancer (NSCLC). This study aims to evaluate the utility of plasma cell-free DNA (cfDNA) as a prognostic biomarker and efficacy predictor of chemotherapy (CT) with or without these precision therapies in NSCLC patients. Peripheral cfDNA levels in 154 NSCLC patients were quantified before and after the first target cycle of chemotherapy. The correlations of cfDNA with tumor burden, clinical characteristics, progression-free survival (PFS)/disease-free survival (DFS), objective response ratio (ORR), and therapy regimens were analyzed respectively. Baseline cfDNA, but not post-chemotherapeutic cfDNA, positively correlates with tumor burden. Notably, cfDNA kinetics (cfDNA Ratio, the ratio of post-chemotherapeutic cfDNA to baseline cfDNA) well distinguished responsive individuals (CR/PR) from the non-responsive (PD/SD). Additionally, cfDNA Ratio was found negatively correlated with PFS in lung adenocarcinoma (LUAD), but not lung squamous-cell carcinoma (LUSC) which may be due to a limited number of LUSC patients in this cohort. LUAD patients with low cfDNA Ratio have prolonged PFS and improved ORR, compared to those with high cfDNA Ratio. When stratified by therapy regimen, the predictive value of cfDNA Ratio is significant in patients with chemotherapy plus VEGFIs, while more patients need be included to validate the value of cfDNA Ratio in other regimens. Thus, the kinetics of plasma cfDNA during chemotherapy may function as a prognostic biomarker and efficacy predictor for NSCLC patients.
C1 [Zhou, Xiaorong; Li, Chenchen; Lu, Jianwei] Nanjing Med Univ, Jiangsu Canc Hosp, Inst Canc Res, Affiliated Canc Hosp, Nanjing 210009, Jiangsu, Peoples R China.
   [Zhang, Zhao; Li, Daniel Y.; Du, Jinwei; Ding, Ping; Meng, Haiyan; Xu, Hui; Ho, Effie; Zhang, Aiguo; Sha, Michael Y.] DiaCarta Inc, 2600 Hilltop Dr, Richmond, CA 94806 USA.
   [Li, Ronglei] Genesmile Inc, Nanjing, Jiangsu, Peoples R China.
   [Okunieff, Paul] Univ Florida, Dept Radiat Oncol, Gainesville, FL USA.
C3 Nanjing Medical University; State University System of Florida;
   University of Florida
RP Lu, JW (corresponding author), Nanjing Med Univ, Jiangsu Canc Hosp, Inst Canc Res, Affiliated Canc Hosp, Nanjing 210009, Jiangsu, Peoples R China.; Sha, MY (corresponding author), DiaCarta Inc, 2600 Hilltop Dr, Richmond, CA 94806 USA.
EM lujw@medmail.com; msha@diacarta.com
RI Du, Jinwei/L-2175-2013
OI Zhao, Zhang/0000-0001-7910-2568; Sha, Michael/0000-0002-4552-6079
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PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD APR 7
PY 2021
VL 11
IS 1
AR 7633
DI 10.1038/s41598-021-85797-z
PG 12
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA RN5LX
UT WOS:000640393700006
PM 33828112
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Katsuta, E
   Rashid, OM
   Takabe, K
AF Katsuta, Eriko
   Rashid, Omar M.
   Takabe, Kazuaki
TI Clinical relevance of tumor microenvironment: immune cells, vessels, and
   mouse models
SO HUMAN CELL
LA English
DT Review
DE Tumor; Microenvironment; Cancer; Immune; Vessel
ID REGULATORY T-CELLS; BREAST-CANCER; COLORECTAL-CANCER; LUNG-CANCER;
   EXPRESSION; SPHINGOSINE-1-PHOSPHATE; ANGIOGENESIS; BEVACIZUMAB;
   LYMPHANGIOGENESIS; MACROPHAGES
AB The tumor microenvironment (TME) plays a crucial role in tumor progression, therapeutic response, and patient outcomes. TME includes immune cells, blood and lymphatic vessels, and so on. There are anti-cancer and pro-cancer immune cells. In general, infiltration of anti-cancer immune cells, such as cytotoxic T cells (CTLs), is associated with a favorable patient prognosis. In contrast, infiltration of pro-cancer immune cells, such as regulatory T cells (Tregs), tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs), is associated with a worse prognosis. However, some immune cells, which play an ambivalent role in cancer immunity, have demonstrated contradictory impacts on patient prognosis. Blood and lymphatic vessels play crucial roles in TME not only as delivery and draining systems of fluid and molecules, but also allowing cancer cells access to systematic circulation to metastasize. Angiogenesis promotes cancer aggressiveness and is associated with a worse prognosis. Its targeted therapy shows a benefit in some cancers, however, because the target can vary by caner type, a benefit of anti-angiogenesis therapy is limited in the current standard of care. Lymphangiogenesis plays a role in lymph node metastasis, thus, it is associated with a poor prognosis in some cancers. To study TME, the mouse model is one of the most commonly used tools. The choice of appropriate mouse model depends on the hypothesis being tested and the scientific question being asked. Here, we review recent studies that investigated the clinical relevance of TME components and introduce mouse models to study TME.
C1 [Katsuta, Eriko; Takabe, Kazuaki] Roswell Pk Comprehens Canc Ctr, Breast Surg, Dept Surg Oncol, Elm & Carlton St, Buffalo, NY 14263 USA.
   [Rashid, Omar M.] Holy Cross Hosp, Michael & Dianne Bienes Comprehens Canc Ctr, Ft Lauderdale, FL USA.
   [Rashid, Omar M.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
   [Rashid, Omar M.] Univ Miami, Miller Sch Med, Dept Surg, Miami, FL 33136 USA.
   [Rashid, Omar M.] Nova Southeastern Univ, Dept Surg, Sch Med, Ft Lauderdale, FL 33314 USA.
   [Takabe, Kazuaki] SUNY Buffalo, Dept Surg, Jacobs Sch Med & Biomed Sci, Buffalo, NY 14260 USA.
   [Takabe, Kazuaki] Tokyo Med Univ, Dept Breast Surg & Oncol, Tokyo, Japan.
   [Takabe, Kazuaki] Yokohama City Univ, Dept Surg, Yokohama, Kanagawa, Japan.
   [Takabe, Kazuaki] Niigata Univ, Dept Surg, Grad Sch Med & Dent Sci, Niigata, Japan.
   [Takabe, Kazuaki] Fukushima Med Univ, Dept Breast Surg, Fukushima, Japan.
C3 Roswell Park Comprehensive Cancer Center; Harvard University;
   Massachusetts General Hospital; University of Miami; Nova Southeastern
   University; State University of New York (SUNY) System; University at
   Buffalo, SUNY; Tokyo Medical University; Yokohama City University;
   Niigata University; Fukushima Medical University
RP Takabe, K (corresponding author), Roswell Pk Comprehens Canc Ctr, Breast Surg, Dept Surg Oncol, Elm & Carlton St, Buffalo, NY 14263 USA.; Takabe, K (corresponding author), SUNY Buffalo, Dept Surg, Jacobs Sch Med & Biomed Sci, Buffalo, NY 14260 USA.; Takabe, K (corresponding author), Tokyo Med Univ, Dept Breast Surg & Oncol, Tokyo, Japan.; Takabe, K (corresponding author), Yokohama City Univ, Dept Surg, Yokohama, Kanagawa, Japan.; Takabe, K (corresponding author), Niigata Univ, Dept Surg, Grad Sch Med & Dent Sci, Niigata, Japan.; Takabe, K (corresponding author), Fukushima Med Univ, Dept Breast Surg, Fukushima, Japan.
EM kazuaki.takabe@roswellpark.org
RI Katsuta, Eriko/IQU-9184-2023
OI Katsuta, Eriko/0000-0001-5862-2919
FU NIH [R01CA160688]; National Cancer Institute (NCI) [P30CA016056]
FX This work was supported by NIH Grant R01CA160688 to K.T, and National
   Cancer Institute (NCI) Grant and P30CA016056 to Roswell Park Cancer
   Comprehensive Cancer Center. KT is the Alfiero Foundation Chair of
   Breast Oncology at Roswell Park Comprehensive Cancer Center.
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NR 71
TC 49
Z9 52
U1 1
U2 17
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
   JAPAN
SN 0914-7470
EI 1749-0774
J9 HUM CELL
JI Hum. Cell
PD OCT
PY 2020
VL 33
IS 4
BP 930
EP 937
DI 10.1007/s13577-020-00380-4
EA JUN 2020
PG 8
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA NS0UM
UT WOS:000539327100001
PM 32507979
DA 2025-01-04
ER

PT J
AU Milano, G
   Innocenti, F
   Lacarelle, B
   Ciccolini, J
AF Milano, G.
   Innocenti, F.
   Lacarelle, B.
   Ciccolini, J.
TI "No pain, No gain" still true with immunotherapy: When the finger shows
   the moon, look at the moon!
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE Toxicity; Efficacy; Pharmacokinetics; Pharmacogenetics; Modeling;
   Immunotherapy; Adherence
ID RENAL-CELL CARCINOMA; GROWTH-FACTOR RECEPTOR; METASTATIC
   COLORECTAL-CANCER; IMMUNE CHECKPOINT BLOCKADE; HAND-FOOT SYNDROME;
   ADVERSE EVENTS; BREAST-CANCER; LUNG-CANCER; METRONOMIC CHEMOTHERAPY;
   PRECISION MEDICINE
AB There is a rising evidence that the proverbial statement "No pain, No gain" first coined at the light of pioneering clinical experiences with canonical chemotherapy still holds true in the era of modern treatments of cancer. This close relationship between the occurrence of specific drug-related toxicity and treatment outcome has been confirmed since then with a large variety of treatments, ranging from cytotoxics, hormonotherapy, targeted therapy and much interestingly even with the latest immune checkpoint inhibitors. In the current context of precision medicine, and along with the constant quest for identifying predictive biomarkers, close monitoring of treatment-related toxicities could therefore be convenient to help predicting therapeutic response, but presents several caveats. The purpose of this review is to briefly describe these relationships across the different treatments, to comment on possible underlying mechanisms and to comment on possible strategies aiming at exploiting this relationship while keeping the maximal safety ensured in patients with cancer. In particular, this review will investigate on how drug exposure along with germinal and somatic genetic issues does impact on the "No Pain, No Gain" aphorism, and why the temptation to use treatment-related toxicities as a cheap and convenient way to predict clinical outcome or to adapt dosing should be resisted. We do advocate instead for developing comprehensive genomic support along with extensive biomathematical modeling to better customize dosing and shift towards a new "No Pain, Maximal Gain" paradigm.
C1 [Milano, G.] Ctr Antoine Lacassagne, UNS EA3836, Oncopharrnacol Unit, 33 Ave Valombrose, F-06100 Nice, France.
   [Innocenti, F.] Univ N Carolina, Eshelman Sch Pharm, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27515 USA.
   [Lacarelle, B.; Ciccolini, J.] La Timone Univ Hosp Marseille, SMARTc Unit, Inserm S 911, Marseille, France.
C3 UNICANCER; Centre Antoine Lacassagne; University of North Carolina;
   University of North Carolina Chapel Hill; Aix-Marseille Universite;
   Assistance Publique-Hopitaux de Marseille; Institut National de la Sante
   et de la Recherche Medicale (Inserm)
RP Milano, G (corresponding author), Ctr Antoine Lacassagne, UNS EA3836, Oncopharrnacol Unit, 33 Ave Valombrose, F-06100 Nice, France.
EM gerard.milano@nice.unicancer.fr; innocent@email.unc.edu;
   bruno.lacarelle@ap-hm.fr; joseph.ciccolini@univ-amu.fr
RI Innocenti, Federico/G-3206-2018; Ciccolini, Joseph/AAP-7193-2021
OI Ciccolini, Joseph/0000-0003-1733-3410; Milano,
   Gerard/0000-0003-2478-0040
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NR 60
TC 4
Z9 4
U1 0
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1040-8428
EI 1879-0461
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD JUL
PY 2018
VL 127
BP 1
EP 5
DI 10.1016/j.critrevonc.2018.04.003
PG 5
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA GL3NT
UT WOS:000437044500001
PM 29891106
DA 2025-01-04
ER

PT J
AU Ozturk, BT
   Yildirim, MS
   Zamani, A
   Bozkurt, B
AF Ozturk, B. T.
   Yildirim, M. S.
   Zamani, A.
   Bozkurt, B.
TI <i>K-ras</i> oncogene mutation in pterygium
SO EYE
LA English
DT Article
ID COLORECTAL-CANCER; SKIN TUMORS; MICROSATELLITE INSTABILITY;
   ULTRAVIOLET-RADIATION; RECURRENT PTERYGIA; NORMAL CONJUNCTIVA;
   PYRIMIDINE DIMERS; UV PHOTOPRODUCTS; KRAS MUTATIONS; P53
AB Purpose Pterygium is claimed to be a benign proliferation triggered by prolonged exposure to ultraviolet radiation. The frequency of K-ras oncogene mutation, which is among the initial mutations in tumorigenesis, is evaluated in this study. Patients and methods In this prospective randomized clinical, trial pterygium tissues and normal conjunctiva tissue specimens are obtained from the superotemporal quadrant of patients who underwent primary pterygium excision with autograft transplantation. DNA extraction from tissues was performed using the QIAamp DNA FFPE tissue kit. A PCR reaction was performed to amplify sequences containing codons 12, 13, and 61 of the K-ras gene in DNA. These PCR products then underwent the ` pyrosequencing' procedure for mutations at these codons.
   Results Pterygium and normal conjunctival tissue samples of 25 patients (10 females, 15 males) were evaluated in the study. The mean age of the patients was 54.54 +/- 13.13 years. Genetic analysis revealed no K-ras mutations in normal conjunctival tissues, whereas pterygium tissues of the same cases demonstrated mutation at codon 12 in one case and mutations at codon 61 in seven cases, which was statistically significant (P<0.05). The point missense mutations at codon 61 were glutamine to arginine (Glu61Arg CAA>CGA) in four cases and glutamine to leucine (Glu61Leu CAA>CTA) in three cases.
   Conclusion The significantly higher frequency of codon 61 mutation of the ras oncogene in primary and bilateral pterygium specimens compared with normal conjunctiva supports the tumoral origin of pterygium, and thus set the stage for research into a targeted therapy for pterygium with better outcomes than surgical excision.
C1 [Ozturk, B. T.; Bozkurt, B.] Selcuk Univ, Dept Ophthalmol, Fac Med, TR-42075 Konya, Turkey.
   [Yildirim, M. S.; Zamani, A.] Konya Necmettin Erbakan Univ, Dept Med Genet, Fac Med, Konya, Turkey.
C3 Selcuk University; Necmettin Erbakan University
RP Ozturk, BT (corresponding author), Selcuk Univ, Dept Ophthalmol, Fac Med, TR-42075 Konya, Turkey.
EM ozturkbanuturgut@yahoo.com
RI YILDIRIM, Mahmut/AAR-7483-2021; Zamani, Ayse Gul/A-6567-2016; Bozkurt,
   Banu/ACI-1564-2022
OI YILDIRIM, MAHMUT SELMAN/0000-0002-3986-5517; Zamani, Ayse
   Gul/0000-0003-0329-9047; Turgut Ozturk, Banu/0000-0003-0702-6951;
   Bozkurt, Banu/0000-0002-9847-3521
FU Konya Necmettin Erbakan University Scientific Research Project
   Coordinatory [131318009]
FX This study was granted by the Konya Necmettin Erbakan University
   Scientific Research Project Coordinatory (project number: 131318009).
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NR 52
TC 9
Z9 9
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-222X
EI 1476-5454
J9 EYE
JI Eye
PD MAR
PY 2017
VL 31
IS 3
BP 491
EP 498
DI 10.1038/eye.2016.254
PG 8
WC Ophthalmology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Ophthalmology
GA EN4QG
UT WOS:000395991400024
PM 27834959
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Viter, R
   Jekabsons, K
   Kalnina, Z
   Poletaev, N
   Hsu, SH
   Riekstina, U
AF Viter, R.
   Jekabsons, K.
   Kalnina, Z.
   Poletaev, N.
   Hsu, S. H.
   Riekstina, U.
TI Bioanalytical system for detection of cancer cells with photoluminescent
   ZnO nanorods
SO NANOTECHNOLOGY
LA English
DT Article
DE ZnO nanorods; cancer detection; carbohydrate marker; SSEA-4;
   photoluminescence
ID STEM-CELLS; SSEA-4; IMMUNOSENSOR; EXPRESSION; BIOSENSOR; BINDING;
   PROTEIN; TARGET
AB Using photoluminescent ZnO nanorods and carbohydrate marker SSEA-4,. a novel cancer cell recognition system was developed. Immobilization of SSEA-4 antibodies (alpha SSEA-4) on ZnO nanorods was performed in buffer solution (pH = 7.1) over. 2 h. The cancer cell line probes were fixed on the glass slide. One hundred microliters of ZnO-alpha SSEA-4 conjugates were deposited on the cell probe and exposed for 30 min. After washing photoluminescence spectra were recorded. Based on the developed methodology, ZnO-aSSEA-4 probes were tested on patient-derived breast and colorectal carcinoma cells. Our data clearly show that the. carbohydrate SSEA-4 molecule is expressed on cancer cell lines and patient-derived cancer cells. Moreover, SSEA-4 targeted ZnO nanorods bind to the patient-derived cancer cells with high selectivity and the photoluminescence signal. increased tremendously compared to the signal from the control samples. Furthermore, the photoluminescence intensity increase correlated with the extent of malignancy in the target cell population. A novel portable bioanalytical system, based on optical ZnO nanorods and fiber optic detection system was developed. We propose that carbohydrate SSEA-4 specific ZnO nanorods could be used for the development of cancer diagnostic biosensors and for. targeted therapy.
C1 [Viter, R.] Univ Latvia, Inst Atom Phys & Spect, Riga, Latvia.
   [Jekabsons, K.; Riekstina, U.] Univ Latvia, Fac Med, Riga, Latvia.
   [Kalnina, Z.] Latvian Biomed Res & Study Ctr, Riga, Latvia.
   [Poletaev, N.] Odessa II Mechnikov Univ, Fac Phys, Odessa, Ukraine.
   [Hsu, S. H.] Natl Taiwan Univ, Inst Polymer Sci & Engn, Taipei, Taiwan.
C3 University of Latvia; University of Latvia; Latvian Biomedical Research
   & Study Centre; Ministry of Education & Science of Ukraine; Odesa I. I.
   Mechnikov National University; National Taiwan University
RP Riekstina, U (corresponding author), Univ Latvia, Fac Med, Riga, Latvia.
EM una.riekstina@lu.lv
RI Viter, Roman/R-9982-2019; Kalnina, Zane/AAH-9884-2021; Poletaev,
   Nicolay/I-5136-2015; Viter, Roman/G-2319-2012
OI Kalnina, Zane/0000-0001-9002-3131; Poletaev,
   Nicolay/0000-0002-1340-582X; Riekstina, Una/0000-0003-2217-7053; Viter,
   Roman/0000-0002-9996-041X
FU Taiwan-Latvia-Lithuania [TW-LT-LV/2015/7]; Latvia Science Council
   [625/2014]; BIOSENSORS-AGRICULT (FP7-PEOPLE-IRSES) project [318520]
FX This work was supported by the Taiwan-Latvia-Lithuania research grant
   (No. TW-LT-LV/2015/7), Latvia Science Council grant (No. 625/2014) and
   BIOSENSORS-AGRICULT (FP7-PEOPLE-2012-IRSES, contract no. 318520)
   project. We thank Ms. Elina Zandberga for technical help on cancer cell
   propagation.
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NR 36
TC 18
Z9 18
U1 0
U2 28
PU IOP PUBLISHING LTD
PI BRISTOL
PA TEMPLE CIRCUS, TEMPLE WAY, BRISTOL BS1 6BE, ENGLAND
SN 0957-4484
EI 1361-6528
J9 NANOTECHNOLOGY
JI Nanotechnology
PD NOV 18
PY 2016
VL 27
IS 46
AR 465101
DI 10.1088/0957-4484/27/46/465101
PG 11
WC Nanoscience & Nanotechnology; Materials Science, Multidisciplinary;
   Physics, Applied
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Materials Science; Physics
GA EV2TJ
UT WOS:000401607700001
PM 27731308
DA 2025-01-04
ER

PT J
AU Bäumer, N
   Rehkämper, J
   Appel, N
   Terheyden, L
   Hartmann, W
   Wardelmann, E
   Buchholz, F
   Müller-Tidow, C
   Berdel, WE
   Bäumer, S
AF Baeumer, Nicole
   Rehkaemper, Jan
   Appel, Neele
   Terheyden, Lisa
   Hartmann, Wolfgang
   Wardelmann, Eva
   Buchholz, Frank
   Mueller-Tidow, Carsten
   Berdel, Wolfgang E.
   Baeumer, Sebastian
TI Downregulation of PIK3CA via antibody-esiRNA-complexes suppresses human
   xenograft tumor growth
SO PLOS ONE
LA English
DT Article
ID COLORECTAL-CANCER; PROGNOSTIC ROLE; KRAS; RESISTANCE; CETUXIMAB;
   MUTATION; THERAPY; PATHWAY; SIRNA; PI3K
AB Precision cancer therapy requires on the one hand detailed knowledge about a tumor's driver oncogenes and on the other hand an effective targeted therapy that specifically inhibits these oncogenes. While the determination of genomic landscape of a tumor has reached a very precise level, the respective therapy options are scarce. The application of small inhibitory (si) RNAs is a promising field of investigation. Here, we present the effective in vivo-treatment of colorectal cancer (CRC) xenograft tumors with antibody-complexed, endoribonuclease-prepared small inhibitory (esi)RNAs. We chose heterogeneous endoribonuclease-prepared siRNA pools (esiRNAs) against the frequently mutated genes PIK3CA and KRAS and coupled them to the anti-EGFR antibody cetuximab, which was internalized specifically into the tumor cells. esiRNA pools have been shown to exhibit superior specificity in target gene knockdown compared to classic siRNAs. We identified a significant decrease in tumor growth upon this treatment due to decreased tumor cell proliferation. The ex vivo-analysis of the xenograft CRC tumors revealed the expected downregulation of the intended direct targets PIK3CA and KRAS on protein level. Moreover, known downstream targets for EGFR signaling such as p-ERK, p-AKT, and c-MYC were decreased as well. We therefore propose the use of antibody-esiRNA complexes as a novel experimental treatment option against key components of the EGFR signaling cascade.
C1 [Baeumer, Nicole; Appel, Neele; Terheyden, Lisa; Mueller-Tidow, Carsten; Berdel, Wolfgang E.; Baeumer, Sebastian] Univ Munster, Dept Med A, Hematol Oncol, Munster, Germany.
   [Rehkaemper, Jan; Hartmann, Wolfgang; Wardelmann, Eva] Univ Munster, Gerhard Domagk Inst Pathol, Munster, Germany.
   [Buchholz, Frank] Tech Univ Dresden, Univ KrebsCtr UCC, Med Fac, Med Syst Biol, Dresden, Germany.
   [Buchholz, Frank] German Canc Res Ctr, Heidelberg, Germany.
   [Buchholz, Frank] German Canc Consortium DKTK Partner Site, Dresden, Germany.
   [Buchholz, Frank] Max Planck Inst Mol Cell Biol & Genet, Dresden, Germany.
   [Buchholz, Frank] Tech Univ Dresden, Univ Hosp Carl Gustav Carus, Natl Ctr Tumor Dis NCT, Dresden, Germany.
   [Mueller-Tidow, Carsten] Heidelberg Univ, Dept Med 5, Heidelberg, Germany.
C3 University of Munster; University of Munster; Technische Universitat
   Dresden; Helmholtz Association; German Cancer Research Center (DKFZ);
   Max Planck Society; Technische Universitat Dresden; Carl Gustav Carus
   University Hospital; Helmholtz Association; German Cancer Research
   Center (DKFZ); Ruprecht Karls University Heidelberg; Ruprecht Karls
   University Heidelberg
RP Bäumer, S (corresponding author), Univ Munster, Dept Med A, Hematol Oncol, Munster, Germany.
RI Baeumer, Sebastian/GYU-0544-2022; Buchholz, Frank/B-4700-2017;
   Muller-Tidow, Carsten/O-7207-2018; Hartmann, Wolfgang/G-1893-2017
OI Buchholz, Frank/0000-0002-4577-3344; Baumer, Nicole/0000-0002-7530-467X;
   Muller-Tidow, Carsten/0000-0002-7166-5232; Hartmann,
   Wolfgang/0000-0002-7609-5021
FU Wilhelm Sander-Stiftung [2014.054.1, 2009.041.2, 2017.071.1]; Deutsche
   Forschungsgemeinschaft-DFG [EXC 1003]; Deutsche Krebshilfe [70112282];
   innovative medical research (IMF) University of Muenster [111418,
   111501]; Innovative Medical Research (IMF) University of
   Muenster-Sebastian Baumer Innovative Medical Research (IMF) of the
   University of Muenster [121314, 211502]
FX This study was funded by Wilhelm Sander-Stiftung-2009.041.2-Carsten
   MuEller-Tidow, Sebastian Baumer; Wilhelm
   Sander-Stiftung-2014.054.1-Wolfgang E. Berdel, Sebastian Baumer;
   Deutsche Forschungsgemeinschaft-DFG EXC 1003-Wolfgang E. Berdel;
   Deutsche Krebshilfe 70112282-Nicole BaEumer, Sebastian BaEumer;
   innovative medical research (IMF) University of
   Muenster-111418-Sebastian Baumer; Innovative Medical Research (IMF)
   University of Muenster-211502-Sebastian Baumer Innovative Medical
   Research (IMF) of the University of Muenster-121314-Nicole BaEumer;
   Innovative Medical Research (IMF) of the University of Muenster-111501-
   Nicole BaEumer, Sebastian BaEumer; Wilhelm
   Sander-Stiftung-2017.071.1-Wolfgang E. Berdel, Sebastian BaEumer. 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 56
TC 5
Z9 7
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 JUL 12
PY 2018
VL 13
IS 7
AR e0200163
DI 10.1371/journal.pone.0200163
PG 22
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA GM8FT
UT WOS:000438457400031
PM 30001368
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Yang, QR
   Xu, J
   Gu, JM
   Shi, H
   Zhang, JY
   Zhang, JY
   Chen, ZS
   Fang, XJ
   Zhu, TF
   Zhang, X
AF Yang, Qiurong
   Xu, Jing
   Gu, Jianmei
   Shi, Hui
   Zhang, Jiayin
   Zhang, Jianye
   Chen, Zhe-Sheng
   Fang, Xinjian
   Zhu, Taofeng
   Zhang, Xu
TI Extracellular Vesicles in Cancer Drug Resistance: Roles, Mechanisms, and
   Implications
SO ADVANCED SCIENCE
LA English
DT Review
DE cancer therapy; drug delivery; drug resistance; extracellular vesicles;
   nanomedicine
ID CELL LUNG-CANCER; MESENCHYMAL STEM-CELLS; PROMOTES CISPLATIN RESISTANCE;
   EXOSOME-MEDIATED TRANSFER; BREAST-CANCER; P-GLYCOPROTEIN;
   PANCREATIC-CANCER; TEMOZOLOMIDE RESISTANCE; MULTIDRUG-RESISTANCE;
   COLORECTAL-CANCER
AB Extracellular vesicles (EVs) are cell-derived nanosized vesicles that mediate cell-to-cell communication via transporting bioactive molecules and thus are critically involved in various physiological and pathological conditions. EVs contribute to different aspects of cancer progression, such as cancer growth, angiogenesis, metastasis, immune evasion, and drug resistance. EVs induce the resistance of cancer cells to chemotherapy, radiotherapy, targeted therapy, antiangiogenesis therapy, and immunotherapy by transferring specific cargos that affect drug efflux and regulate signaling pathways associated with epithelial-mesenchymal transition, autophagy, metabolism, and cancer stemness. In addition, EVs modulate the reciprocal interaction between cancer cells and noncancer cells in the tumor microenvironment (TME) to develop therapy resistance. EVs are detectable in many biofluids of cancer patients, and thus are regarded as novel biomarkers for monitoring therapy response and predicting prognosis. Moreover, EVs are suggested as promising targets and engineered as nanovehicles to deliver drugs for overcoming drug resistance in cancer therapy. In this review, the biological roles of EVs and their mechanisms of action in cancer drug resistance are summarized. The preclinical studies on using EVs in monitoring and overcoming cancer drug resistance are also discussed.
C1 [Yang, Qiurong; Xu, Jing; Shi, Hui; Zhang, Jiayin; Zhang, Xu] Jiangsu Univ, Sch Med, Jiangsu Key Lab Med Sci & Lab Med, Zhenjiang 212013, Jiangsu, Peoples R China.
   [Gu, Jianmei] Nantong Tumor Hosp, Dept Clin Lab Med, Nantong 226361, Jiangsu, Peoples R China.
   [Zhang, Jianye] Guangzhou Med Univ, Sch Pharmaceut Sci, Guangdong Prov Key Lab Mol Target & Clin Pharmaco, Guangzhou 511436, Guangdong, Peoples R China.
   [Zhang, Jianye] Guangzhou Med Univ, Affiliated Hosp 5, Guangzhou 511436, Guangdong, Peoples R China.
   [Chen, Zhe-Sheng] St Johns Univ, Coll Pharm & Hlth Sci, Queens, NY 11439 USA.
   [Fang, Xinjian] Jiangsu Univ, Dept Oncol, Lianyungang Hosp, Lianyungang 222000, Jiangsu, Peoples R China.
   [Zhu, Taofeng] Jiangsu Univ, Dept Pulm & Crit Care Med, Yixing Hosp, Yixing 214200, Jiangsu, Peoples R China.
C3 Jiangsu University; Guangzhou Medical University; Guangzhou Medical
   University; Saint John's University; Jiangsu University; Jiangsu
   University
RP Zhang, X (corresponding author), Jiangsu Univ, Sch Med, Jiangsu Key Lab Med Sci & Lab Med, Zhenjiang 212013, Jiangsu, Peoples R China.; Chen, ZS (corresponding author), St Johns Univ, Coll Pharm & Hlth Sci, Queens, NY 11439 USA.; Fang, XJ (corresponding author), Jiangsu Univ, Dept Oncol, Lianyungang Hosp, Lianyungang 222000, Jiangsu, Peoples R China.; Zhu, TF (corresponding author), Jiangsu Univ, Dept Pulm & Crit Care Med, Yixing Hosp, Yixing 214200, Jiangsu, Peoples R China.
EM chenz@stjohns.edu; lygfxj@126.com; staff1639@yxph.com;
   xuzhang@ujs.edu.cn
RI Chen, Zhe-Sheng/AAI-7465-2020; SHI, HUI/KXQ-4873-2024
FU National Natural Science Foundation of China [81972310, 81872901];
   Distinguished Young Scholar Project of Jiangsu Province [BK20200043];
   Key Laboratory of Molecular Diagnostics and Precision Medicine for
   Surgical Oncology in Gansu Province [2019GSZDSYS01, 2019GSZDSYS02];
   Priority Academic Program Development of Jiangsu Higher Education
   Institutions (PAPD); Top Talent Support Program of Yixing Health
   Committee [BJ2020107]
FX Q.Y., J.X., J.G., and H.S. contributed equally to this work. This work
   was supported by the National Natural Science Foundation of China
   (81972310 and 81872901), the Distinguished Young Scholar Project of
   Jiangsu Province (BK20200043), the Key Laboratory of Molecular
   Diagnostics and Precision Medicine for Surgical Oncology in Gansu
   Province (2019GSZDSYS01 and 2019GSZDSYS02), the Priority Academic
   Program Development of Jiangsu Higher Education Institutions (PAPD), and
   the Top Talent Support Program of Yixing Health Committee (BJ2020107).
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NR 324
TC 54
Z9 54
U1 6
U2 91
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2198-3844
J9 ADV SCI
JI Adv. Sci.
PD DEC
PY 2022
VL 9
IS 34
DI 10.1002/advs.202201609
EA OCT 2022
PG 33
WC Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials
   Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA 6W1YL
UT WOS:000869313500001
PM 36253096
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Venturini, J
   Massaro, G
   Lavacchi, D
   Rossini, D
   Pillozzi, S
   Caliman, E
   Pellegrini, E
   Antonuzzo, L
AF Venturini, Jacopo
   Massaro, Giulia
   Lavacchi, Daniele
   Rossini, Daniele
   Pillozzi, Serena
   Caliman, Enrico
   Pellegrini, Elisa
   Antonuzzo, Lorenzo
TI The emerging HER2 landscape in colorectal cancer: the key to unveil the
   future treatment algorithm?
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE Metastatic colorectal cancer; HER2 amplifications; HER2 mutations;
   Negative predictive biomarker; Resistance mechanism; ctDNA
ID EGFR MONOCLONAL-ANTIBODIES; TRASTUZUMAB EMTANSINE; TARGETED THERAPY;
   PATIENTS PTS; OPEN-LABEL; GUIDELINES; MANAGEMENT; RESISTANCE; MUTATIONS;
   EFFICACY
AB Colorectal cancer (CRC) represents a global health threat, standing as the second leading cause of cancer-related death worldwide. Targeted therapies brought new hope for the metastatic stage, which historically bore a very poor prognosis. Human epidermal growth receptor 2 (HER2) overexpression concerns about 5 % of the metastatic CRC (mCRC) patients, including both gene amplifications and point mutations. Albeit its controversial prognostic role, preclinical and clinical data indicate HER2 as a negative predictive biomarker of response to anti-EGFR therapies. Tissue and plasma-based NGS testing, could permit a precise identification of this resistance mechanism both at baseline and during treatment, thus guiding decision-making. Furthermore, promising results come from completed and ongoing randomized trials, testing HER2 as an actionable target. In this review, we discuss the available evidence on HER2 targeting in advanced CRC, analyzing its possible future role in the treatment algorithm.
C1 [Venturini, Jacopo; Massaro, Giulia; Lavacchi, Daniele; Caliman, Enrico; Antonuzzo, Lorenzo] Careggi Univ Hosp, Clin Oncol Unit, I-50134 Florence, Italy.
   [Rossini, Daniele; Pillozzi, Serena; Antonuzzo, Lorenzo] Univ Florence, Dept Expt & Clin Med, I-50134 Florence, Italy.
   [Rossini, Daniele] Univ Florence, Dept Hlth Sci, I-50139 Florence, Italy.
   [Pillozzi, Serena; Pellegrini, Elisa; Antonuzzo, Lorenzo] Careggi Univ Hosp, Med Oncol Unit, I-50134 Florence, Italy.
C3 University of Florence; Azienda Ospedaliero Universitaria Careggi;
   University of Florence; University of Florence; University of Florence;
   Azienda Ospedaliero Universitaria Careggi
RP Antonuzzo, L (corresponding author), Careggi Univ Hosp, Clin Oncol Unit, I-50134 Florence, Italy.
EM lorenzo.antonuzzo@unifi.it
RI Caliman, Enrico/AAC-3749-2022; Lavacchi, Daniele/AAC-3109-2022;
   pillozzi, serena/K-5876-2016
FX agencies in the public, commercial, or not-for-profit sectors.
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NR 140
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1040-8428
EI 1879-0461
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD DEC
PY 2024
VL 204
AR 104515
DI 10.1016/j.critrevonc.2024.104515
EA SEP 2024
PG 13
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA H3C3S
UT WOS:001322245100001
PM 39304034
OA hybrid
DA 2025-01-04
ER

PT J
AU Wang, XX
   Lin, JY
   Wang, Z
   Li, Z
   Wang, MH
AF Wang, Xixi
   Lin, Junyi
   Wang, Zhe
   Li, Zhi
   Wang, Minghua
TI Possible therapeutic targets for NLRP3 inflammasome-induced breast
   cancer
SO DISCOVER ONCOLOGY
LA English
DT Review
DE Inflammasome; NLRP3; Breast cancer; Nanoparticles; Gene therapy
ID SIGNALING PATHWAY; NONCODING RNAS; ACTIVATION; MITOCHONDRIA; INHIBITOR;
   CELLS; IL-1-BETA; MONOCYTES; PROTEIN; SUSCEPTIBILITY
AB Inflammation plays a major role in the development and progression of breast cancer(BC). Proliferation, invasion, angiogenesis, and metastasis are all linked to inflammation and tumorigenesis. Furthermore, tumor microenvironment (TME) inflammation-mediated cytokine releases play a critical role in these processes. By recruiting caspase-1 through an adaptor apoptosis-related spot protein, inflammatory caspases are activated by the triggering of pattern recognition receptors on the surface of immune cells. Toll-like receptors, NOD-like receptors, and melanoma-like receptors are not triggered. It activates the proinflammatory cytokines interleukin (IL)-1 beta and IL-18 and is involved in different biological processes that exert their effects. The Nod-Like Receptor Protein 3 (NLRP3) inflammasome regulates inflammation by mediating the secretion of proinflammatory cytokines and interacting with other cellular compartments through the inflammasome's central role in innate immunity. NLRP3 inflammasome activation mechanisms have received much attention in recent years. Inflammatory diseases including enteritis, tumors, gout, neurodegenerative diseases, diabetes, and obesity are associated with abnormal activation of the NLRP3 inflammasome. Different cancer diseases have been linked to NLRP3 and its role in tumorigenesis may be the opposite. Tumors can be suppressed by it, as has been seen primarily in the context of colorectal cancer associated with colitis. However, cancers such as gastric and skin can also be promoted by it. The inflammasome NLRP3 is associated with breast cancer, but there are few specific reviews. This review focuses on the structure, biological characteristics and mechanism of inflammasome, the relationship between NLRP3 in breast cancer Non-Coding RNAs, MicroRNAs and breast cancer microenvironment, especially the role of NLRP3 in triple-negative breast cancer (TNBC). And the potential strategies of using NLRP3 inflammasome to target breast cancer, such as NLRP3-based nanoparticle technology and gene target therapy, are reviewed.
C1 [Wang, Xixi; Wang, Zhe; Li, Zhi; Wang, Minghua] Hubei Univ Med, Taihe Hosp, Dept Gen Surg, Shiyan 442000, Peoples R China.
   [Lin, Junyi] Hubei Univ Med, Sinopharm Dongfeng Gen Hosp, Shiyan 442000, Peoples R China.
   [Lin, Junyi] Hubei Univ Med, Hubei Key Lab Wudang Local Chinese Med Res, Shiyan, Peoples R China.
   [Li, Zhi] Shanghai Univ Tradit Chinese Med, Putuo Hosp, Intervent Canc Inst Chinese Integrat Med, Shanghai 200333, Peoples R China.
   [Li, Zhi] Hubei Univ Med, Taihe Hosp, Hubei Clin Res Ctr Precise Diag & Treatment Liver, Shiyan, Peoples R China.
C3 Hubei University of Medicine; Hubei University of Medicine; Hubei
   University of Medicine; Shanghai University of Traditional Chinese
   Medicine; Hubei University of Medicine
RP Li, Z; Wang, MH (corresponding author), Hubei Univ Med, Taihe Hosp, Dept Gen Surg, Shiyan 442000, Peoples R China.; Li, Z (corresponding author), Shanghai Univ Tradit Chinese Med, Putuo Hosp, Intervent Canc Inst Chinese Integrat Med, Shanghai 200333, Peoples R China.; Li, Z (corresponding author), Hubei Univ Med, Taihe Hosp, Hubei Clin Res Ctr Precise Diag & Treatment Liver, Shiyan, Peoples R China.
EM lizhi2019@taihehospital.com; taihewmh@126.com
RI Li, Zhi/JFA-0464-2023
OI Li, Zhi/0000-0001-6555-7107; Lin, Junyi/0009-0004-4962-0814
FU Foundation Project of Taihe Hospital, Hubei University of Medicine
   [2022JJXM023]
FX This work was supported by the Foundation Project of Taihe Hospital,
   Hubei University of Medicine (2022JJXM023).
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NR 137
TC 9
Z9 9
U1 0
U2 7
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 JUN 10
PY 2023
VL 14
IS 1
AR 93
DI 10.1007/s12672-023-00701-7
PG 15
WC Oncology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Endocrinology & Metabolism
GA I4PQ0
UT WOS:001002619600001
PM 37300757
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Alqahtani, A
   Choucair, K
   Ashraf, M
   Hammouda, DM
   Alloghbi, A
   Khan, T
   Senzer, N
   Nemunaitis, J
AF Alqahtani, Ali
   Choucair, Khalil
   Ashraf, Mushtaq
   Hammouda, Danae M.
   Alloghbi, Abduraham
   Khan, Talal
   Senzer, Neil
   Nemunaitis, John
TI Bromodomain and extra-terminal motif inhibitors: a review of preclinical
   and clinical advances in cancer therapy
SO FUTURE SCIENCE OA
LA English
DT Review
DE BET inhibitors; BET protein; cancer; clinical trials; combination
   therapy; hematological malignancies; solid tumors; targeted therapy
ID 1ST-IN-HUMAN PHASE-I; C-MYC; BET PROTEINS; BREAST-CANCER; HISTONE
   DEACETYLASES; SELECTIVE-INHIBITION; ANTITUMOR-ACTIVITY;
   COLORECTAL-CANCER; LEUKEMIA-CELLS; PATIENTS PTS
AB Histone lysine acetylation is critical in regulating transcription. Dysregulation of this process results in aberrant gene expression in various diseases, including cancer. The bromodomain, present in several proteins, recognizes promotor lysine acetylation and recruits other transcription factors. The bromodomain extra-terminal (BET) family of proteins consists of four conserved mammalian members that regulate transcription of oncogenes such as MYC and the NUT fusion oncoprotein. Targeting the acetyl-lysine-binding property of BET proteins is a potential therapeutic approach of cancer. Consequently, following the demonstration that thienotriazolodiazepine small molecules effectively inhibit BET, clinical trials were initiated. We thus discuss the mechanisms of action of various BET inhibitors and the prospects for their clinical use as cancer therapeutics.
   Lay abstract: Addition of acetyl groups to histone proteins that are present in DNA is critical for proper copying of genetic information into producing proteins. This process is dysregulated in various diseases including cancer, resulting in continuous production of oncogenes - genes responsible for promoting cancer - such as NUT and MYC. Bromodomain extra-terminal (BET) proteins mediate acetyl addition, and as a result, transcription. BET inhibitors are small molecules that block the action of BET proteins and the transcription of oncogenes. In this review, we discuss the different available BET inhibitors, the way they act, and their potential use in clinical settings for cancer treatment.
C1 [Alqahtani, Ali; Alloghbi, Abduraham] Univ Toledo, Dept Internal Med, Coll Med & Life Sci, Toledo, OH 43614 USA.
   [Choucair, Khalil; Ashraf, Mushtaq; Hammouda, Danae M.; Khan, Talal; Senzer, Neil; Nemunaitis, John] Univ Toledo, Coll Med & Life Sci, Div Hematol & Med Oncol, Dept Med, Toledo, OH 43614 USA.
   [Nemunaitis, John] ProMed Hlth Syst, Toledo, OH 43606 USA.
C3 University System of Ohio; University of Toledo; University System of
   Ohio; University of Toledo
RP Nemunaitis, J (corresponding author), Univ Toledo, Coll Med & Life Sci, Div Hematol & Med Oncol, Dept Med, Toledo, OH 43614 USA.; Nemunaitis, J (corresponding author), ProMed Hlth Syst, Toledo, OH 43606 USA.
EM john.nemunaitis@utoledo.edu
RI Alloghbi, Abdurahman/AAF-5169-2020
OI Nemunaitis, John/0000-0002-2234-2381; Alloghbi,
   Abdurahman/0000-0002-1620-7853
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NR 115
TC 199
Z9 224
U1 0
U2 30
PU FUTURE SCI LTD
PI LONDON
PA UNITED HOUSE, 2 ALBERT PL, LONDON, N3 1QB, ENGLAND
SN 2056-5623
J9 FUTUR SCI OA
JI Futur. Sci. OA
PD MAR
PY 2019
VL 5
IS 3
AR FSO372
DI 10.4155/fsoa-2018-0115
PG 20
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA HQ8GM
UT WOS:000462662300005
PM 30906568
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Zheng, Q
   Chen, CY
   Guan, HY
   Kang, WBA
   Yu, CJ
AF Zheng, Qiang
   Chen, Changyu
   Guan, Haiyang
   Kang, Weibiao
   Yu, Changjun
TI Prognostic role of microRNAs in human gastrointestinal cancer: A
   systematic review and meta-analysis
SO ONCOTARGET
LA English
DT Review
DE microRNAs; prognosis; gastrointestinal cancer; target; meta-analysis
ID SQUAMOUS-CELL CARCINOMA; KAPPA-B ACTIVATION; GASTRIC-CANCER;
   DOWN-REGULATION; POOR-PROGNOSIS; REDUCED EXPRESSION; TUMOR PROGRESSION;
   MESSENGER-RNA; SERUM MIR-21; COLON-CANCER
AB Background: Gastrointestinal cancers (GICs) mainly including esophageal, gastric and colorectal cancer, are the most common cause of cancer-related death and lead into high mortality worldwide. We performed this systematic review and meta-analysis to elucidate relationship between multiple microRNAs (miRs) expression and survival of GIC patients.
   Methods: We searched a wide range of database. Fixed-effects and randomeffects models were used to calculate the pooled hazard ratio values of overall survival and disease free survival. In addition, funnel plots were used to qualitatively analyze the publication bias and verified by Begg's test while it seems asymmetry.
   Results: 60 studies involving a total of 6225 patients (1271 with esophageal cancer, 3467 with gastric cancer and 1517 with colorectal cancer) were included in our meta-analysis. The pooled hazard ratio values of overall survival related to different miRs expression in esophageal, gastric, colorectal and gastrointestinal cancer were 2.10 (1.78-2.49), 2.02 (1.83-2.23), 2.54 (2.14-3.02) and 2.15 (1.992.31), respectively. We have identified a total of 59 miRs including 23 significantly up-regulated expression miRs (miR-214, miR-17, miR-20a, miR-200c, miR-107, miR27a, etc.) and 36 significantly down-regulated expression miRs (miR-433, let-7g, miR-125a-5p, miR-760, miR-206, miR-26a, miR-200b, miR-185, etc.) correlated with poor prognosis in GIC patients. Moreover, 35 of them revealed mechanisms.
   Conclusion: Overall, specific miRs are significantly associated with the prognosis of GIC patients and potentially eligible for the prediction of patients survival. It also provides a potential value for clinical decision-making development and may serve as a promising miR-based target therapy waiting for further elucidation.
C1 [Zheng, Qiang; Kang, Weibiao; Yu, Changjun] Anhui Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Hefei, Peoples R China.
   [Chen, Changyu] Anhui Tradit Med Univ, Affiliated Hosp 1, Dept Gen Surg, Hefei, Peoples R China.
   [Guan, Haiyang] Univ Sci & Technol China, Hefei Natl Lab Phys Sci Microscale, Hefei, Peoples R China.
   [Guan, Haiyang] Univ Sci & Technol China, Sch Life Sci, Hefei, 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
RP Yu, CJ (corresponding author), Anhui Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Hefei, Peoples R China.
EM changjuyu212@163.com
FU Science and Technology Project of Anhui [3101005002598]
FX This work was granted from Science and Technology Project of Anhui
   (3101005002598).
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NR 78
TC 64
Z9 69
U1 1
U2 14
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 JUL 11
PY 2017
VL 8
IS 28
BP 46611
EP 46623
DI 10.18632/oncotarget.16679
PG 13
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FA5SS
UT WOS:000405504600139
PM 28402940
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Pant, S
   Hubbard, J
   Martinelli, E
   Bekaii-Saab, T
AF Pant, Shubham
   Hubbard, Joleen
   Martinelli, Erika
   Bekaii-Saab, Tanios
TI Clinical update on K-Ras targeted therapy in gastrointestinal cancers
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE K-Ras inhibitor; Gastrointestinal cancer; Colorectal cancer; Pancreatic
   cancer
ID ORAL MEK INHIBITOR; KRAS-MUTANT LUNG; METASTATIC COLORECTAL-CANCER;
   SMALL-MOLECULE INHIBITORS; REFRACTORY SOLID TUMORS; INTEGRIN-LINKED
   KINASE; 1ST-IN-HUMAN PHASE-I; PANCREATIC-CANCER; ANTITUMOR-ACTIVITY;
   DOSE-ESCALATION
AB KRAS mutations are common in pancreatic and colorectal cancers and are associated with lack of response to anti-epidermal growth factor receptor therapy. Ras is an established therapeutic target that has long eluded efforts to develop specific inhibitors, while targeting downstream signaling pathways has proven largely ineffective, highlighting a need for rational combination strategies to overcome resistance. Recently, renewed interest in directly targeting Ras has led to the development of several small-molecule inhibitors that bind directly to K-Ras or its effector proteins, downregulation of K-Ras expression using therapeutic antisense oligonucleotides or siRNAs, and targeting scaffold proteins such as kinase suppressor of Ras. Indirect approaches to inhibiting K-Ras include combining inhibitors of the mitogen-activated protein kinase pathway with novel targeted agents. Immunotherapy in early studies has also shown clinical promise. This review summarizes the current evidence for each of these approaches.
C1 [Pant, Shubham] Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapeut, POB 301402, Houston, TX 77230 USA.
   [Pant, Shubham] Univ Texas MD Anderson Canc Ctr, GI Med Oncol, POB 301402, Houston, TX 77230 USA.
   [Hubbard, Joleen] Mayo Clin, Rochester, MN USA.
   [Martinelli, Erika] Univ Campania L Vanvitelli, Dept Precis Med, Naples, Italy.
   [Bekaii-Saab, Tanios] Mayo Clin, Canc Ctr, Phoenix, AZ USA.
C3 University of Texas System; UTMD Anderson Cancer Center; University of
   Texas System; UTMD Anderson Cancer Center; Mayo Clinic; Universita della
   Campania Vanvitelli; Mayo Clinic; Mayo Clinic Phoenix
RP Pant, S (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapeut, POB 301402, Houston, TX 77230 USA.; Pant, S (corresponding author), Univ Texas MD Anderson Canc Ctr, GI Med Oncol, POB 301402, Houston, TX 77230 USA.
EM SPant@mdanderson.org
RI Bekaii-Saab, Tanios/AGD-6851-2022
OI Bekaii-Saab, Tanios/0000-0001-7721-1699
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NR 174
TC 16
Z9 18
U1 0
U2 19
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1040-8428
EI 1879-0461
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD OCT
PY 2018
VL 130
BP 78
EP 91
DI 10.1016/j.critrevonc.2018.07.011
PG 14
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA GV3GR
UT WOS:000445982900009
PM 30196915
DA 2025-01-04
ER

PT J
AU Liu, YS
   Li, JZ
   Zhang, YQ
   Wang, YY
   Chen, JN
   Bian, YT
   Xia, YZ
   Yang, MH
   Zheng, KW
   Wang, KB
   Kong, LY
AF Liu, Yushuang
   Li, Jinzhu
   Zhang, Yongqiang
   Wang, Yingying
   Chen, Juannan
   Bian, Yuting
   Xia, Yuanzheng
   Yang, Ming-Hua
   Zheng, Kewei
   Wang, Kai-Bo
   Kong, Ling-Yi
TI Structure of the Major G-Quadruplex in the Human <i>EGFR</i> Oncogene
   Promoter Adopts a Unique Folding Topology with a Distinctive Snap-Back
   Loop
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID DNA G-QUADRUPLEX; SMALL-MOLECULE; HUMAN GENOME; CANCER; REGION;
   ACTIVATION; POTASSIUM; DYNAMICS; INSIGHTS; MOTIFS
AB EGFR tyrosine kinase inhibitors have made remarkablesuccess intargeted cancer therapy. However, therapeutic resistance inevitablyoccurred and EGFR-targeting therapy has been demonstrated to havelimited efficacy or utility in glioblastoma, colorectal cancer, andhepatocellular carcinoma. Therefore, there is a high demand for thedevelopment of new targets to inhibit EGFR signaling.Herein, we found that the EGFR oncogene proximalpromoter sequence forms a unique type of snap-back loop containingG-quadruplex (G4), which can be targeted by small molecules. For thefirst time, we determined the NMR solution structure of this snap-back EGFR-G4, a three-tetrad-core, parallel-stranded G4 withnaturally occurring flanking residues at both the 5 & PRIME;-end and3 & PRIME;-end. The snap-back loop located at the 3 & PRIME;-end regionforms a stable capping structure through two stacked G-triads connectedby multiple potential hydrogen bonds. Notably, the flanking residuesare consistently absent in reported snap-back G4s, raising the questionof whether such structures truly exist under in vivo conditions. Theresolved EGFR-G4 structure has eliminated the doubtand showed distinct structural features that distinguish it from thepreviously reported snap-back G4s, which lack the flanking residues.Furthermore, we found that the snap-back EGFR-G4structure is highly stable and can form on an elongated DNA templateto inhibit DNA polymerase. The unprecedented high-resolution EGFR-G4 structure has thus contributed a promising moleculartarget for developing alternative EGFR signalinginhibitors in cancer therapeutics. Meanwhile, the two stacked triadsmay provide an attractive site for specific small-molecule targeting.
C1 [Liu, Yushuang; Li, Jinzhu; Zhang, Yongqiang; Wang, Yingying; Bian, Yuting; Xia, Yuanzheng; Yang, Ming-Hua; Wang, Kai-Bo; Kong, Ling-Yi] China Pharmaceut Univ, Jiangsu Key Lab Bioact Nat Prod Res, Nanjing 210009, Jiangsu, Peoples R China.
   [Liu, Yushuang; Li, Jinzhu; Zhang, Yongqiang; Wang, Yingying; Bian, Yuting; Xia, Yuanzheng; Yang, Ming-Hua; Wang, Kai-Bo; Kong, Ling-Yi] China Pharmaceut Univ, State Key Lab Nat Med, Nanjing 210009, Jiangsu, Peoples R China.
   [Chen, Juannan; Zheng, Kewei] Hunan Univ, Sch Biomed Sci, Changsha 410082, Hunan, Peoples R China.
C3 China Pharmaceutical University; China Pharmaceutical University; Hunan
   University
RP Wang, KB; Kong, LY (corresponding author), China Pharmaceut Univ, Jiangsu Key Lab Bioact Nat Prod Res, Nanjing 210009, Jiangsu, Peoples R China.; Wang, KB; Kong, LY (corresponding author), China Pharmaceut Univ, State Key Lab Nat Med, Nanjing 210009, Jiangsu, Peoples R China.
EM kbwang@cpu.edu.cn; cpu_lykong@126.com
RI Li, Jinzhu/F-8687-2010; Wang, Yingying/HPF-9431-2023; Wang,
   Xiaobing/H-5927-2019; wang, kaibo/I-8670-2014
OI Zheng, Kewei/0000-0002-4110-4776; Liu, Yushuang/0000-0002-2706-3066
FU National Natural Science Foundation of China [82173707, 81773886,
   82204241]; Program for Jiangsu Province Innovative Research Scholar
   [JSSCRC2021512]; "Double First-Class" University Project [CPUQNJC22_08];
   Natural Science Foundation of Jiangsu Province [BK20210420, BK20221039];
   Scientific Research Foundation of Nanjing for Returned Chinese Scholar
   [1412100026]; Scientific Research Foundation for High-Level Faculty,
   China Pharmaceutical University, Nanjing, China [3150020065]
FX This research was supported by the National Natural Science Foundation
   of China (K.-B.W., 82173707, L.-Y.K., 81773886, and Y.L., 82204241), the
   Program for Jiangsu Province Innovative Research Scholar (K.-B.W.,
   JSSCRC2021512), the "Double First-Class" University Project (K.-B.W.,
   CPUQNJC22_08), the Natural Science Foundation of Jiangsu Province
   (K.-B.W., BK20210420, and Y.L., BK20221039), the Scientific Research
   Foundation of Nanjing for Returned Chinese Scholar (K.-B.W.,
   1412100026), and the Scientific Research Foundation for High-Level
   Faculty, China Pharmaceutical University, Nanjing, China (K.-B.W.,
   3150020065).
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NR 73
TC 7
Z9 8
U1 11
U2 52
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
EI 1520-5126
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD JUL 17
PY 2023
VL 145
IS 29
BP 16228
EP 16237
DI 10.1021/jacs.3c05214
EA JUL 2023
PG 10
WC Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA M8IP5
UT WOS:001031271000001
PM 37460135
DA 2025-01-04
ER

PT J
AU Tapeh, BEG
   Mosayyebi, B
   Mansoori, B
   Gravand, ZA
   Sarvnaz, H
   Mohammadi, A
AF Tapeh, Behnam Emamgolizadeh Gurt
   Mosayyebi, Bashir
   Mansoori, Behzad
   Gravand, Zahra Alipoor
   Sarvnaz, Hamzeh
   Mohammadi, Ali
TI Emerging Molecular Functions of MicroRNA-9: Cancer Pathology and
   Thera-peutic Implications
SO ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
LA English
DT Review
DE Angiogenesis; cancer; drug resistance; miR-9; signaling pathway;
   proliferation
ID EPITHELIAL-MESENCHYMAL TRANSITION; CELL-PROLIFERATION; TUMOR-SUPPRESSOR;
   HEPATOCELLULAR-CARCINOMA; PROMOTES APOPTOSIS; NONCODING RNA;
   DNA-BINDING; COLORECTAL-CANCER; MIR-9; INVASION
AB MiRNAs that are characterized by small non-coding RNAs orchestrate the expression of important genes involved in cancer cell development processes, including apoptosis, proliferation, angiogenesis, metasta-sis, and drug resistance at the post-transcriptional level. Dysregulation of miR-9 in various cancers has been re-ported. Recently, miR-9 has been considered as a key miRNA in various malignancies. However, its impor-tance in the pathogenesis of different neoplasms is not yet well defined. Accordingly, this study was conducted in order to clarify the potential roles of miR-9 in the development of various cancers, prognosis, and treatment approaches. We have shown that a large number of miR-9 targets play fundamental roles in carcinogenesis, and that is dysregulated in various cancer cells. Our findings werefound aberrant miR-9 expression in a majority of cancers. This review article generally emphasizesthe critical roles of miR-9 in cancer cell progression. Addition-ally, we intended to investigate the effects of down-regulation or up-regulation of miR-9 in different types of cancers. It is hoped that a good understanding of the regulatory roles of miR-9 in various cancers ishelpful for using miR-9 in clinical settings, including prognosis, diagnosis, and miRNA-based target therapy.
C1 [Tapeh, Behnam Emamgolizadeh Gurt; Mansoori, Behzad; Mohammadi, Ali] Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran.
   [Tapeh, Behnam Emamgolizadeh Gurt] Tabriz Univ Med Sci, Dept Hematol & Oncol, Res Ctr, Tabriz, Iran.
   [Tapeh, Behnam Emamgolizadeh Gurt] Tabriz Univ Med Sci, Student Res Comm, Tabriz, Iran.
   [Sarvnaz, Hamzeh] Univ Tehran Med Sci, Sch Publ Hlth, Dept Immunol, Tehran, Iran.
   [Mosayyebi, Bashir] Tabriz Univ Med Sci, Dept Med Biotechnol, Tabriz, Iran.
   [Gravand, Zahra Alipoor] Lorestan Univ Med Sci, Dept Lab Sci, Lorestan, Iran.
   [Mohammadi, Ali] Univ Southern Denmark, Inst Mol Med, Dept Canc & Inflammat Res, Odense, Denmark.
C3 Tabriz University of Medical Science; Tabriz University of Medical
   Science; Tabriz University of Medical Science; Tehran University of
   Medical Sciences; Tabriz University of Medical Science; Lorestan
   University of Medical Sciences; University of Southern Denmark
RP Mohammadi, A (corresponding author), Univ Southern Denmark, Inst Mol Med, Dept Canc & Inflammat Res, Odense, Denmark.
EM ali_mohammadi6868@yahoo.com
RI Mansoori, Behzad/T-2720-2017
OI Mosayyebi, Bashir/0000-0001-6661-0504
FU Tabriz University of medical sciences, Tabriz, Iran
FX This study was supported by Tabriz University of medical sci-ences,
   Tabriz, Iran.
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NR 114
TC 3
Z9 4
U1 1
U2 6
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 17
BP 2304
EP 2314
DI 10.2174/1871520621666210217094839
PG 11
WC Oncology; Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA WV9LM
UT WOS:000717550700003
PM 33596811
DA 2025-01-04
ER

PT J
AU Di Francia, R
   De Monaco, A
   Saggese, M
   Iaccarino, G
   Crisci, S
   Frigeri, F
   De Filippi, R
   Berretta, M
   Pinto, A
AF Di Francia, Raffaele
   De Monaco, Angela
   Saggese, Mariangela
   Iaccarino, Giancarla
   Crisci, Stefania
   Frigeri, Ferdinando
   De Filippi, Rosaria
   Berretta, Massimiliano
   Pinto, Antonio
TI Pharmacological Profile and Pharmacogenomics of Anti-Cancer Drugs Used
   for Targeted Therapy
SO CURRENT CANCER DRUG TARGETS
LA English
DT Review
DE Anticancer mAbs; personalized medicine; pharmacogenomics; tailored
   therapy; tyrosine kinase inhibitors; cancer cell
ID GROWTH-FACTOR RECEPTOR; COMBINED CANCER-THERAPY; COLORECTAL-CANCER;
   CHEMOTHERAPY; BEVACIZUMAB; INHIBITORS; THERAPEUTICS; ANGIOGENESIS;
   RESISTANCE; STRATEGIES
AB AAbstract: Background: Drugs for targeted therapies are primarily Small Molecules Inhibitors (SMIs), monoclonal antibodies (mAbs), interfering RNA molecules and microRNA. The use of these new agents generates a multifaceted step in the pharmacokinetics (PK) of these drugs. Individual PK variability is often large, and unpredictability observed in the response to the pharmacogenetic profile of the patient (e.g. cytochome P450 enzyme), patient characteristics such as adherence to treatment and environmental factors.
   Objective: This review aims to overview the latest anticancer drugs eligible for targeted therapies and the most recent finding in pharmacogenomics related to toxicity/resistance of either individual gene polymorphisms or acquired mutation in a cancer cell. In addition, an early outline evaluation of the genotyping costs and methods has been taken into consideration.
   Future Outlook: To date, therapeutic drug monitoring (TDM) of mAbs and SMIs is not yet supported by heavy scientific evidence. Extensive effort should be made for targeted therapies to better define concentration-effect relationships and to perform comparative randomized trials of classic dosing versus PK-guided adaptive dosing. The detection of individual pharmacogenomics profile could be the key for the oncologists that will have new resources to make treatment decisions for their patients in order to maximize the benefit and minimize the toxicity. Based on this purpose, the clinician should evaluate advantages and limitations, in terms of costs and applicability, of the most appropriate pharmacological approach to performing a tailored therapy.
C1 [Di Francia, Raffaele; De Monaco, Angela; Saggese, Mariangela; Iaccarino, Giancarla; Crisci, Stefania; Frigeri, Ferdinando; Pinto, Antonio] Natl Canc Inst, Hematol Oncol & Stem Cell Transplantat Unit, Fdn G Pascale IRCCS, Naples, Italy.
   [De Filippi, Rosaria] Univ Naples Federico II, Dept Clin Med & Surg, Naples, Italy.
   [Berretta, Massimiliano] CRO Natl Canc Inst, Dept Med Oncol, Aviano, PN, Italy.
C3 IRCCS Fondazione Pascale; University of Naples Federico II; IRCCS Aviano
   (CRO)
RP Di Francia, R (corresponding author), Natl Canc Inst, Hematol Oncol & Stem Cell Transplantat Unit, Fdn G Pascale IRCCS, Naples, Italy.
EM raffaele.difrancia@istitutotumori.na.it
RI Crisci, Stefania/AAA-4049-2021; Saggese, Mariangela/AAA-7589-2020;
   Giancarla, Iaccarino/AAA-6264-2021; Pinto, Antonio/A-5579-2016; FRIGERI,
   FERDINANDO/KBR-1629-2024; Berretta, Massimiliano/S-5853-2019
OI DE FILIPPI, Rosaria/0000-0001-7899-3071; FRIGERI,
   FERDINANDO/0000-0002-9818-3073; Pinto, Antonio/0000-0002-9425-9026;
   Berretta, Massimiliano/0000-0002-9837-9148
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NR 61
TC 12
Z9 12
U1 0
U2 12
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1568-0096
EI 1873-5576
J9 CURR CANCER DRUG TAR
JI Curr. Cancer Drug Targets
PY 2018
VL 18
IS 5
BP 499
EP 511
DI 10.2174/1568009617666170208162841
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GH0KY
UT WOS:000433092100010
PM 28183252
DA 2025-01-04
ER

PT J
AU Duan, QY
   Xu, M
   Wu, M
   Zhang, X
   Gan, M
   Jiang, HB
AF Duan, Qingyun
   Xu, Mei
   Wu, Meng
   Zhang, Xiong
   Gan, Min
   Jiang, Hongbing
TI Long noncoding RNA <i>UCA1</i> promotes cell growth, migration, and
   invasion by targeting miR-143-3p in oral squamous cell carcinoma
SO CANCER MEDICINE
LA English
DT Article
DE miR-143-3p; MYO6; oral squamous cell carcinoma; UCA1
ID INHIBITS PROLIFERATION; COLORECTAL-CANCER; MESENCHYMAL-TRANSITION;
   PROGRESSION; KNOCKDOWN; SUPPRESSES; NETWORKS
AB Background The long noncoding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) is dysregulated in many types of tumors; however, its role in oral squamous cell carcinoma (OSCC) remains unclear. This study aims to determine the effect of lncRNA UCA1 on OSCC.
   Methods Fifty-six paired OSCC and adjacent nontumorous tissues were collected and the levels of UCA1, miR-143-3p, and MYO6 in the tissues were evaluated by qRT-PCR. In in vitro experiments, cell viability, migration, and invasion were measured by, respectively, performing CCK-8, wound healing, and transwell assays. The target relationships among UCA1, miR-143-3p, and MYO6 were verified by dual-luciferase assay. Western blot and immunohistochemistry were carried out to determine the protein levels. Xenograft mouse model was established to explore the effects of UCA1 in vivo.
   Results Levels of UCA1 and MYO6 were increased significantly in OSCC, while the level of miR-143-3p was decreased compared with the adjacent nontumorous tissues. UCA1 promoted OSCC cell growth, migration, and invasion both in vitro and in vivo, while miR-143-3p reversed the progression. MYO6 was validated as a target for miR-143-3p, and MYO6 overexpression reversed the effects of miR-143-3p mimic on OSCC cells.
   Conclusion LncRNA UCA1 contributes to the proliferation and metastasis of OSCC cells by targeting miR-143-3p and upregulating its downstream gene MYO6. UCA1 could serve as a promising novel target therapy for treatment of OSCC.
C1 [Duan, Qingyun; Jiang, Hongbing] Nanjing Med Univ, Jiangsu Key Lab Oral Dis, Nanjing, Jiangsu, Peoples R China.
   [Duan, Qingyun; Zhang, Xiong; Gan, Min] Zhejiang Univ, Coll Med, Dept Oral & Maxillofacial Surg, Affiliated Hangzhou Peoples Hosp 1, Hangzhou, Zhejiang, Peoples R China.
   [Xu, Mei] Hangzhou Jianggan Dist Peoples Hosp, Dept Ophtalmol, Hangzhou, Zhejiang, Peoples R China.
   [Wu, Meng] Nanjing Med Univ, Affiliated Huaian 1 Peoples Hosp, Dept Oral & Maxillofacial Surg, Huaian, Jiangsu, Peoples R China.
   [Jiang, Hongbing] Nanjing Med Univ, Affiliated Stomatol Hosp, Dept Oral & Maxillofacial Surg, 136 Hanzhong Rd, Nanjing 210029, Jiangsu, Peoples R China.
C3 Nanjing Medical University; Zhejiang University; Nanjing Medical
   University; Nanjing Medical University
RP Jiang, HB (corresponding author), Nanjing Med Univ, Jiangsu Key Lab Oral Dis, Nanjing, Jiangsu, Peoples R China.; Jiang, HB (corresponding author), Nanjing Med Univ, Affiliated Stomatol Hosp, Dept Oral & Maxillofacial Surg, 136 Hanzhong Rd, Nanjing 210029, Jiangsu, Peoples R China.
EM jianghb_hongbing@163.com
RI Wu, Meng/GRS-6281-2022; Jiang, Hongbing/AAQ-6331-2021
CR [Anonymous], J CLIN CELL IMMUNOL
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NR 52
TC 22
Z9 24
U1 0
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD MAY
PY 2020
VL 9
IS 9
BP 3115
EP 3129
DI 10.1002/cam4.2808
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LI8UX
UT WOS:000529754600018
PM 32130788
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Salla, M
   Karaki, N
   El Kaderi, B
   Ayoub, AJ
   Younes, S
   Abou Chahla, MN
   Baksh, S
   El Khatib, S
AF Salla, Mohamed
   Karaki, Nadine
   El Kaderi, Belal
   Ayoub, Abeer J.
   Younes, Samar
   Abou Chahla, Maya N.
   Baksh, Shairaz
   El Khatib, Sami
TI Enhancing the Bioavailability of Resveratrol: Combine It, Derivatize It,
   or Encapsulate It?
SO PHARMACEUTICS
LA English
DT Review
DE resveratrol; bioavailability; nanoparticle; derivatization; tumor;
   inflammation
ID SOLID LIPID NANOPARTICLES; INDUCED OXIDATIVE STRESS; DELIVERY-SYSTEMS;
   BREAST-CANCER; IN-VITRO; MOLECULAR-MECHANISMS; ANTIOXIDANT ACTIVITY;
   ANTIFUNGAL ACTIVITY; CONTROLLED-RELEASE; TRANS-RESVERATROL
AB Overcoming the limited bioavailability and extensive metabolism of effective in vitro drugs remains a challenge that limits the translation of promising drugs into clinical trials. Resveratrol, despite its well-reported therapeutic benefits, is not metabolically stable and thus has not been utilized as an effective clinical drug. This is because it needs to be consumed in large amounts to overcome the burdens of bioavailability and conversion into less effective metabolites. Herein, we summarize the more relevant approaches to modify resveratrol, aiming to increase its biological and therapeutic efficacy. We discuss combination therapies, derivatization, and the use of resveratrol nanoparticles. Interestingly, the combination of resveratrol with established chemotherapeutic drugs has shown promising therapeutic effects on colon cancer (with oxaliplatin), liver cancer (with cisplatin, 5-FU), and gastric cancer (with doxorubicin). On the other hand, derivatizing resveratrol, including hydroxylation, amination, amidation, imidation, methoxylation, prenylation, halogenation, glycosylation, and oligomerization, differentially modifies its bioavailability and could be used for preferential therapeutic outcomes. Moreover, the encapsulation of resveratrol allows its trapping within different forms of shells for targeted therapy. Depending on the nanoparticle used, it can enhance its solubility and absorption, increasing its bioavailability and efficacy. These include polymers, metals, solid lipids, and other nanoparticles that have shown promising preclinical results, adding more "hype" to the research on resveratrol. This review provides a platform to compare the different approaches to allow directed research into better treatment options with resveratrol.
C1 [Salla, Mohamed; Karaki, Nadine; El Kaderi, Belal; Ayoub, Abeer J.; Abou Chahla, Maya N.; El Khatib, Sami] Lebanese Int Univ, Sch Arts & Sci, Dept Biol & Chem Sci, POB 146404, Bayrut, Lebanon.
   [Salla, Mohamed] Univ Alberta, Fac Med & Dent, Dept Biochem, 113 St 87 Ave, Edmonton, AB T6G 2E1, Canada.
   [Karaki, Nadine] Lebanese Univ, Fac Arts & Sci, Dept Chem & Biochem, Zahle 1801, Lebanon.
   [Younes, Samar] Lebanese Int Univ, Sch Pharm, Dept Biomed Sci, POB 146404, Bayrut, Lebanon.
   [Younes, Samar] Natl Inst Publ Hlth, INSPECT LB, Clin Epidemiol & Toxicol Lebanon INSPECT LB, Beirut 1103, Lebanon.
   [Baksh, Shairaz] BioImmuno Designs, 4747 154 Ave, Edmonton, AB T5Y 0C2, Canada.
   [Baksh, Shairaz] Biostream Diagnost, 2011 94 St, Edmonton, AB T6H 1N1, Canada.
   [El Khatib, Sami] Lebanese Int Univ, Sch Arts & Sci, Dept Biomed Sci, POB 146404, Bayrut, Lebanon.
   [El Khatib, Sami] Gulf Univ Sci & Technol, Ctr Appl Math & Bioinformat CAMB, Mubarak Al Abdullah 32093, Kuwait.
C3 University of Alberta; Lebanese University
RP Salla, M (corresponding author), Lebanese Int Univ, Sch Arts & Sci, Dept Biol & Chem Sci, POB 146404, Bayrut, Lebanon.; Salla, M (corresponding author), Univ Alberta, Fac Med & Dent, Dept Biochem, 113 St 87 Ave, Edmonton, AB T6G 2E1, Canada.
EM mohammad.salla@liu.edu.lb; nadine.karaki@liu.edu.lb;
   belal.kadri@liu.edu.lb; abeer.ayoub@liu.edu.lb; samar.younes@liu.edu.lb;
   maya.aboushahla@liu.edu.lb; sbakshbid@gmail.com; sami.khatib@liu.edu.lb
RI Baksh, Shairaz/GRX-2106-2022; Salla, Mohamed/ABA-5843-2021; El Khatib,
   Dr. Sami/ABI-7100-2020
OI Baksh, Shairaz/0000-0003-3822-6286; El Khatib, Dr.
   Sami/0000-0003-3611-3288; Salla, Mohamed/0000-0003-4744-0954; Younes,
   Samar/0000-0003-0443-0326; Abou Chahla, Maya/0000-0002-6352-4122
FU Lebanese International University (LIU)
FX The authors would like to thank Fatima El Khatib for drawing the
   chemical structure of RSV and the different derivatives.
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NR 246
TC 13
Z9 13
U1 9
U2 15
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1999-4923
J9 PHARMACEUTICS
JI Pharmaceutics
PD APR
PY 2024
VL 16
IS 4
AR 569
DI 10.3390/pharmaceutics16040569
PG 34
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA OV6C0
UT WOS:001210083200001
PM 38675230
OA gold
DA 2025-01-04
ER

PT J
AU Evangelisti, C
   Chiarini, F
   Cappellini, A
   Paganelli, F
   Fini, M
   Santi, S
   Martelli, AM
   Neri, LM
   Evangelisti, C
AF Evangelisti, Cecilia
   Chiarini, Francesca
   Cappellini, Alessandra
   Paganelli, Francesca
   Fini, Milena
   Santi, Spartaco
   Martelli, Alberto M.
   Neri, Luca M.
   Evangelisti, Camilla
TI Targeting Wnt/β-catenin and PI3K/Akt/mTOR pathways in T-cell acute
   lymphoblastic leukemia
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Article
DE combination therapy; hypoxia; PI3K; Akt; mTOR; T-ALL; targeted therapy;
   Wnt; beta-catenin
ID BETA-CATENIN; STEM-CELLS; COLON-CANCER; PHOSPHATIDYLINOSITOL 3-KINASE;
   PTEN LOSS; INHIBITION; MYC; ACTIVATION; PROLIFERATION; MECHANISMS
AB T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological disorder that results from the clonal transformation of T-cell precursors. Phosphatidylinositol 3-kinase (PI3K)/Akt/mechanistic target of rapamycin (mTOR) and canonical Wnt/beta-catenin signaling pathways play a crucial role in T-cell development and in self-renewal of healthy and leukemic stem cells. Notably, beta-catenin is a transcriptional regulator of several genes involved in cancer cell proliferation and survival. In this way, aberrations of components belonging to the aforementioned networks contribute to T-ALL pathogenesis. For this reason, inhibition of both pathways could represent an innovative strategy in this hematological malignancy. Here, we show that combined targeting of Wnt/beta-catenin pathway through ICG-001, a CBP/beta-catenin transcription inhibitor, and of the PI3K/Akt/mTOR axis through ZSTK-474, a PI3K inhibitor, downregulated proliferation, survival, and clonogenic activity of T-ALL cells. ICG-001 and ZSTK-474 displayed cytotoxic effects, and, when combined together, induced a significant increase in apoptotic cells. This induction of apoptosis was associated with the downregulation of Wnt/beta-catenin and PI3K/Akt/mTOR pathways. All these findings were confirmed under hypoxic conditions that mimic the bone marrow niche where leukemic stem cells are believed to reside. Taken together, our findings highlight potentially promising treatment consisting of cotargeting Wnt/beta-catenin and PI3K/Akt/mTOR pathways in T-ALL settings.
C1 [Evangelisti, Cecilia; Cappellini, Alessandra; Paganelli, Francesca; Martelli, Alberto M.] Univ Bologna, Dept Biomed & Neuromotor Sci, Bologna, Italy.
   [Chiarini, Francesca; Santi, Spartaco; Evangelisti, Camilla] CNR, Inst Mol Genet Luigi Luca Cavalli Sforza, Bologna, Italy.
   [Chiarini, Francesca; Fini, Milena; Santi, Spartaco; Evangelisti, Camilla] IRCCS, Ist Ortoped Rizzoli, Bologna, Italy.
   [Neri, Luca M.] Univ Ferrara, Dept Morphol Surg & Expt Med, Via Fossato Mortara 64-b, I-44121 Ferrara, Italy.
   [Neri, Luca M.] Univ Ferrara, LTTA Electron Microscopy Ctr, Ferrara, Italy.
C3 University of Bologna; Consiglio Nazionale delle Ricerche (CNR); IRCCS
   Istituto Ortopedico Rizzoli; University of Ferrara; University of
   Ferrara
RP Neri, LM (corresponding author), Univ Ferrara, Dept Morphol Surg & Expt Med, Via Fossato Mortara 64-b, I-44121 Ferrara, Italy.; Evangelisti, C (corresponding author), IRCCS, CNR, Inst Mol Genet Luigi Luca Cavalli Sforza, Ist Ortoped Rizzoli, Via Barbiano 1-10, I-40136 Bologna, Italy.
EM luca.neri@unife.it; camilla.evangelisti@cnr.it
RI Neri, Luca/AAU-1772-2021; Fini, Milena/J-4808-2016; Evangelisti,
   Camilla/C-6977-2019; Evangelisti, Cecilia/JJE-0478-2023; Santi,
   Spartaco/Q-7587-2016
OI Santi, Spartaco/0000-0001-9856-7053; Paganelli,
   Francesca/0000-0002-8694-2140; EVANGELISTI, CECILIA/0000-0002-0877-7696;
   Fini, Milena/0000-0002-3732-3570
FU Fondo di Ateneo per la Ricerca Scientifica (FAR); Fondo per
   l'Incentivazione alla Ricerca (FIR), Lega Italiana Lotta contro i Tumori
   (LILT) Sezione provinciale di Ferrara
FX This work was partly supported by current research funds Fondo di Ateneo
   per la Ricerca Scientifica (FAR) and Fondo per l'Incentivazione alla
   Ricerca (FIR), Lega Italiana Lotta contro i Tumori (LILT) Sezione
   provinciale di Ferrara (to L.M.N.).
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NR 93
TC 47
Z9 50
U1 1
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 JUN
PY 2020
VL 235
IS 6
BP 5413
EP 5428
DI 10.1002/jcp.29429
EA JAN 2020
PG 16
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA KR5BZ
UT WOS:000505603900001
PM 31904116
DA 2025-01-04
ER

PT J
AU Cicenas, J
   Cicenas, E
AF Cicenas, Jonas
   Cicenas, Erikas
TI Multi-kinase inhibitors, AURKs and cancer
SO MEDICAL ONCOLOGY
LA English
DT Review
DE Protein kinases; Aurora kinases; Multi-kinase inhibitors; Cancer; Cell
   cycle
ID SMALL-MOLECULE INHIBITOR; ACUTE LYMPHOBLASTIC-LEUKEMIA; CYCLIN-DEPENDENT
   KINASES; HUMAN COLORECTAL-CANCER; POTENT AURORA KINASE; I
   DOSE-ESCALATION; CELL LUNG-CANCER; TYROSINE KINASE; PHASE-I;
   TUMOR-GROWTH
AB Inhibitors that impact function of kinases are valuable both for the biological research as well as therapy of kinase-associated diseases, such as different cancers. There are quite a number of inhibitors, which are quite specific for certain kinases and several of them are either already approved for the cancer therapy or are in clinical studies of various phases. However, that does not mean that each single kinase inhibitor is suitable for targeted therapy. Some of them are not effective others might be toxic or fail some other criteria for the use in vivo. On the other hand, even in case of successful therapy, many responders eventually develop resistance to the inhibitors. The limitations of various single kinase inhibitors can be fought using compounds which target multiple kinases. This tactics can increase effectiveness of the inhibitors by the synergistic effect or help to diminish the likelihood of drug resistance. To date, several families of kinases are quite popular targets of the inhibition in cancers, such as tyrosine kinases, cycle-dependent kinases, mitogen-activated protein kinases, phosphoinositide 3-kinases as well as their pathway "players" and aurora kinases. Aurora kinases play an important role in the control of the mitosis and are often altered in diverse human cancers. Here, we will describe the most interesting multi-kinase inhibitors which inhibit aurora kinases among other targets and their use in preclinical and clinical cancer studies.
C1 [Cicenas, Jonas] Univ Bern, Vetsuisse Fac, Inst Anim Pathol, CH-3012 Bern, Switzerland.
   [Cicenas, Jonas] MAP Kinase Resource, Melchiorstr 9, CH-3027 Bern, Switzerland.
   [Cicenas, Jonas] Vilnius Univ, Prote Ctr, Inst Biochem, LT-08662 Vilnius, Lithuania.
   [Cicenas, Jonas] CMU1, Swiss Inst Bioinformat, CALIPHO, Ru Michael Servet, CH-1211 Geneva, Switzerland.
   [Cicenas, Erikas] Bethlehemacker Secondary Sch, CH-3027 Bern, Switzerland.
C3 University of Bern; Vilnius University; Swiss Institute of
   Bioinformatics
RP Cicenas, J (corresponding author), Univ Bern, Vetsuisse Fac, Inst Anim Pathol, CH-3012 Bern, Switzerland.; Cicenas, J (corresponding author), MAP Kinase Resource, Melchiorstr 9, CH-3027 Bern, Switzerland.; Cicenas, J (corresponding author), Vilnius Univ, Prote Ctr, Inst Biochem, LT-08662 Vilnius, Lithuania.; Cicenas, J (corresponding author), CMU1, Swiss Inst Bioinformat, CALIPHO, Ru Michael Servet, CH-1211 Geneva, Switzerland.
EM j.cicenas@mapkinases.eu
RI Cicenas, Jonas/B-4347-2017
OI Cicenas, Jonas/0000-0002-9365-1843
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NR 89
TC 38
Z9 41
U1 2
U2 29
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 MAY
PY 2016
VL 33
IS 5
AR 43
DI 10.1007/s12032-016-0758-4
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DK7BT
UT WOS:000375080500006
PM 27038473
DA 2025-01-04
ER

PT J
AU Tikhonov, D
   Kulikova, L
   Kopylov, A
   Malsagova, K
   Stepanov, A
   Rudnev, V
   Kaysheva, A
AF Tikhonov, Dmitry
   Kulikova, Liudmila
   Kopylov, Arthur
   Malsagova, Kristina
   Stepanov, Alexander
   Rudnev, Vladimir
   Kaysheva, Anna
TI Super Secondary Structures of Proteins with Post-Translational
   Modifications in Colon Cancer
SO MOLECULES
LA English
DT Article
DE colorectal cancer; ultrahigh-resolution mass spectrometry;
   post-translational modifications; helical pair; protein structural
   motifs; supersecondary structure
ID PHOSPHORYLATION; ALBUMIN
AB New advances in protein post-translational modifications (PTMs) have revealed a complex layer of regulatory mechanisms through which PTMs control cell signaling and metabolic pathways, contributing to the diverse metabolic phenotypes found in cancer. Using conformational templates and the three-dimensional (3D) environment investigation of proteins in patients with colorectal cancer, it was demonstrated that most PTMs (phosphorylation, acetylation, and ubiquitination) are localized in the supersecondary structures (helical pairs). We showed that such helical pairs are represented on the outer surface of protein molecules and characterized by a largely accessible area for the surrounding solvent. Most promising and meaningful modifications were observed on the surface of vitamin D-binding protein (VDBP), complement C4-A (CO4A), X-ray repair cross-complementing protein 6 (XRCC6), Plasma protease C1 inhibitor (IC1), and albumin (ALBU), which are related to colorectal cancer developing. Based on the presented data, we propose the impact of the observed modifications in immune response, inflammatory reaction, regulation of cell migration, and promotion of tumor growth. Here, we suggest a computational approach in which high-throughput analysis for identification and characterization of PTM signature, associated with cancer metabolic reprograming, can be improved to prognostic value and bring a new strategy to the targeted therapy.
C1 [Tikhonov, Dmitry; Kulikova, Liudmila] Russian Acad Sci, Branch Keldysh Inst Appl Math, Inst Math Problems Biol RAS, Pushchino 142290, Moscow Region, Russia.
   [Tikhonov, Dmitry; Rudnev, Vladimir] Russian Acad Sci, Inst Theoret & Expt Biophys, Pushchino 142290, Moscow Region, Russia.
   [Kopylov, Arthur; Malsagova, Kristina; Stepanov, Alexander; Kaysheva, Anna] VN Orekhovich Inst Biomed Chem, Moscow 119121, Russia.
C3 Russian Academy of Sciences; Russian Academy of Sciences; Pushchino
   Scientific Center for Biological Research (PSCBI) of the Russian Academy
   of Sciences; Institute of Theoretical & Experimental Biophysics; Russian
   Academy of Medical Sciences; Institute of Biomedical Chemistry
RP Kaysheva, A (corresponding author), VN Orekhovich Inst Biomed Chem, Moscow 119121, Russia.
EM dmitry.tikhonov@gmail.com; likulikova@mail.ru; a.t.kopylov@gmail.com;
   kristina.malsagova86@gmail.com; aleks.a.stepanov@gmail.com;
   volodyarv@mail.ru; kaysheva1@gmail.com
RI Malsagova, Kristina/F-5580-2017; Kulikova, Liudmila/AAH-1463-2021;
   Kaysheva, Anna/K-1279-2015; Kopylov, Arthur/E-3288-2012; Stepanov,
   Alexander/V-8781-2018; Tikhonov, Dmitry/O-2214-2013
OI Kaysheva, Anna/0000-0003-4472-2016; Kopylov, Arthur/0000-0002-7199-372X;
   Stepanov, Alexander/0000-0002-9113-9440; Malsagova,
   Kristina/0000-0001-9404-1660; Tikhonov, Dmitry/0000-0002-1779-464X
FU Russian Science Foundation [19-14-00298]; Russian Science Foundation
   [19-14-00298] Funding Source: Russian Science Foundation
FX The research was carried out with financial support from the Russian
   Science Foundation, grant no. 19-14-00298.
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NR 43
TC 10
Z9 11
U1 0
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD JUL
PY 2020
VL 25
IS 14
AR 3144
DI 10.3390/molecules25143144
PG 17
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA MS4GH
UT WOS:000554236200001
PM 32660089
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Sun, W
   Zhou, HD
   Han, XT
   Hou, LB
   Xue, XY
AF Sun, Wei
   Zhou, Huandi
   Han, Xuetao
   Hou, Liubing
   Xue, Xiaoying
TI Circular RNA: A novel type of biomarker for glioma
SO MOLECULAR MEDICINE REPORTS
LA English
DT Review
DE circRNAs; glioma; miRNA sponges; biomarker; targeted therapy
ID LONG NONCODING RNAS; CELL PROLIFERATION; MESSENGER-RNA; COLON-CANCER;
   PROMOTES; PROGRESSION; CIRCRNAS; ANGIOGENESIS; LANDSCAPE; ACTS
AB With the rapid development of sequencing technologies, the characteristics and functions of circular RNAs (circRNAs) in different tissues, and their underlying pathophysiological mechanisms, have been identified. circRNAs are significantly enriched in the brain and are continually expressed from the embryonic stage to the adult stage in rats. Previous studies have reported that certain circRNAs are differentially expressed in glioma and regulate a number of biological processes, such as cell proliferation, metastasis and oncogenesis of glioma. Furthermore, certain circRNAs have been associated with tumor size, World Health Organization tumor grade and poor prognosis in patients with glioma. It has been hypothesized that circRNAs may be involved in the onset and progression of glioma through transcriptional regulation, protein translation and binding to microRNAs. These properties and functions suggest the potential of circRNAs as prognostic biomarkers and therapeutic targets for glioma. For the present review, published studies were examined from PubMed, Embase, Cochrane Central and the reference lists of the retrieved articles. The aim of the present review was to summarize the progress of circRNA research in glioma, discuss the potential diagnostic and prognostic values, and the roles of circRNAs in glioma, and provide a novel theoretical basis and research concepts for the prediction, diagnosis and treatment of glioma.
C1 [Sun, Wei; Xue, Xiaoying] Hebei Med Univ, Second Hosp, Dept Radiotherapy, 215 West Heping Rd, Shijiazhuang 050000, Hebei, Peoples R China.
   [Zhou, Huandi; Hou, Liubing] Hebei Med Univ, Second Hosp, Cent Lab, Shijiazhuang 050000, Hebei, Peoples R China.
   [Xue, Xiaoying] Hebei Med Univ, Ctr Metab Dis & Canc Res, Shijiazhuang 050017, Hebei, Peoples R China.
C3 Hebei Medical University; Hebei Medical University; Hebei Medical
   University
RP Xue, XY (corresponding author), Hebei Med Univ, Second Hosp, Dept Radiotherapy, 215 West Heping Rd, Shijiazhuang 050000, Hebei, Peoples R China.
EM xxy0636@163.com
OI Xue, Xiaoying/0000-0002-4934-2904
FU Hebei Province Key research and development projects of China
   [19277737D]
FX The present study was supported by The Hebei Province Key research and
   development projects of China (grant no. 19277737D).
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NR 124
TC 9
Z9 11
U1 0
U2 23
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1791-2997
EI 1791-3004
J9 MOL MED REP
JI Mol. Med. Rep.
PD AUG
PY 2021
VL 24
IS 2
AR 602
DI 10.3892/mmr.2021.12240
PG 12
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA TB6LC
UT WOS:000668056100001
PM 34165178
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Daglioglu, C
   Kaci, FN
AF Daglioglu, Cenk
   Kaci, Fatma Necmiye
TI Cascade therapy with doxorubicin and survivin-targeted tailored
   nanoparticles: An effective alternative for sensitization of cancer
   cells to chemotherapy
SO INTERNATIONAL JOURNAL OF PHARMACEUTICS
LA English
DT Article
DE Nanoparticles; Chemoresistance; Doxorubicin; Survivin; Colon cancer;
   Pancreatic cancer; Leukemia
ID CONJUGATED MULTIFUNCTIONAL NANOPARTICLES; APOPTOSIS; NANOMEDICINE;
   COMBINATION; RESISTANCE; AICAR; GENE
AB Chemotherapy frequently involves combination treatment protocols to maximize tumor cell killing. Unfortunately these intensive chemotherapeutic regimes, often show disappointing results due to the development of drug resistance and higher nonspecific toxicity on normal tissues. In cancer treatment, it is critically important to minimize toxicity while preserving efficacy. We have previously addressed this issue and proposed a nanoparticle-based combination therapy involving both a molecularly targeted therapy and chemotherapeutic agent for neutralizing antiapoptotic survivin (BIRC5) to potentiate the efficacy of doxorubicin (DOX). Although the particles exhibited strong anticancer effect on the lung carcinoma A549 and the cervical carcinoma HeLa cells, there were lower-level therapeutic outcomes on the colon carcinoma HCT-116, the leukemia Jurkat and the pancreatic carcinoma MIA PaCa-2 cells. Since targeted therapies are one of the key approaches for overcoming drug resistance, tailoring the treatment of cancer cells with distinct characteristics is necessary to improve the therapeutic outcome of cancer therapy and to minimize potential pharmacokinetic interactions of drugs. In the light of this issue, this study examined whether a cascade therapy with low-dose DOX and survivin-targeted tailored nanoparticles is more effective at sensitizing HCT-116, Jurkat and MIA PaCa-2 cancer cells to DOX-chemotherapy than simultaneous combination therapy. The results demonstrated that the sequential therapy with the protocol comprising addition of the nanoparticles after incubation of cells with DOX clearly advanced the therapeutic outcome of related cancer cells, whereas the reverse protocol resulted in a reduction or delay in apoptosis, emphasizing the critical importance of formulating synergistic drug combinations in cancer therapy.
C1 [Daglioglu, Cenk] Izmir Inst Technol, Fac Sci, Dept Mol Biol & Genet, TR-35430 Urla Izmir, Turkey.
   [Kaci, Fatma Necmiye] Erzurum Tech Univ, Fac Sci, Dept Mol Biol & Genet, TR-25050 Yakutiye Erzurum, Turkey.
C3 Izmir Institute of Technology; Erzurum Technical University
RP Daglioglu, C (corresponding author), Izmir Inst Technol, Fac Sci, Dept Mol Biol & Genet, TR-35430 Urla Izmir, Turkey.
EM cenkdaglioglu@iyte.edu.tr
RI Daglioglu, Cenk/S-5857-2019; Kaci, Fatma Necmiye/AAA-6418-2022
OI daglioglu, cenk/0000-0002-3857-2317; Kaci, Fatma
   Necmiye/0000-0003-3745-8173
FU TUBITAK (The Scientific and Technological Research Council of Turkey)
   Incentive Program for International Scientific Publications [355155,
   371332]
FX The authors would like to thank TUBITAK (The Scientific and
   Technological Research Council of Turkey) Incentive Program for
   International Scientific Publications for financial assistance (355155,
   371332), Professor Alper Arslanoglu at the Izmir Institute of Technology
   for providing the opportunity to work in his laboratory, all members of
   Department of Molecular Biology and Genetics and High Technology
   Research and Application Center of Erzurum Technical University for
   their technical support, and Dr. Mark Thompson for proofreading the
   manuscript.
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NR 24
TC 9
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U1 11
U2 54
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-5173
EI 1873-3476
J9 INT J PHARMACEUT
JI Int. J. Pharm.
PD APR 20
PY 2019
VL 561
BP 74
EP 81
DI 10.1016/j.ijpharm.2019.02.036
PG 8
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA HQ5QW
UT WOS:000462468700008
PM 30825555
OA Green Published
DA 2025-01-04
ER

PT J
AU Aredia, F
   Czaplinski, S
   Fulda, S
   Scovassi, AI
AF Aredia, Francesca
   Czaplinski, Sebastian
   Fulda, Simone
   Scovassi, A. Ivana
TI Molecular features of the cytotoxicity of an NHE inhibitor: Evidence of
   mitochondrial alterations, ROS overproduction and DNA damage
SO BMC CANCER
LA English
DT Article
DE Apoptosis; Autophagy; HMA; Mitochondria; NHE; PAR; RIPK3; ROS
ID CELL-DEATH; CANCER; NECROPTOSIS; APOPTOSIS; STRESS; POLY(ADP-RIBOSE);
   MECHANISMS; AMILORIDE; WARBURG; PATHWAY
AB Background: NH exchangers (NHEs) play a crucial role in regulating intra/extracellular pH, which is altered in cancer cells, and are therefore suitable targets to alter cancer cell metabolism in order to inhibit cell survival and proliferation. Among NHE inhibitors, amiloride family members are commonly used in clinical practice as diuretics; we focused on the amiloride HMA, reporting a net cytotoxic effect on a panel of human cancer cell lines; now we aim to provide new insights into the molecular events leading to cell death by HMA.
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   Results: HMA affects cellular morphology, alters mitochondrial structure and function, causes an increase in ROS, which is detrimental to DNA integrity, stimulates poly(ADP-ribose) synthesis, activates RIPK3-dependent death and triggers autophagy, which is unable to rescue cell survival. These features are hot points of an intricate network of processes, including necroptosis and autophagy, regulating the homeostasis between survival and death.
   Conclusion: Our results allow the identification of multiple events leading to cell death in cancer cells treated with HMA. The here-defined intricate network activated by HMA could be instrumental to selectively target the key players of each pathway in the attempt to improve the global response to HMA. Our data could be the starting point for developing a newly designed targeted therapy.
C1 [Aredia, Francesca; Scovassi, A. Ivana] CNR, Ist Genet Mol, Via Abbiategrasso 207, I-27100 Pavia, Italy.
   [Aredia, Francesca] Univ Pavia, Dipartimento Biol & Biotecnol L Spallanzani, Via Ferrata 9, I-27100 Pavia, Italy.
   [Czaplinski, Sebastian; Fulda, Simone] Goethe Univ, Inst Expt Canc Res Pediat, Komturstr 3A, D-60528 Frankfurt, Germany.
C3 Consiglio Nazionale delle Ricerche (CNR); Istituto di Genetica
   Molecolare (IGM-CNR); University of Pavia; Goethe University Frankfurt
RP Scovassi, AI (corresponding author), CNR, Ist Genet Mol, Via Abbiategrasso 207, I-27100 Pavia, Italy.
EM scovassi@igm.cnr.it
RI Fulda, Simone/D-5864-2011
OI Fulda, Simone/0000-0002-0459-6417
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NR 49
TC 18
Z9 20
U1 0
U2 5
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD NOV 5
PY 2016
VL 16
AR 851
DI 10.1186/s12885-016-2878-9
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EB8KL
UT WOS:000387639800001
PM 27816051
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zhu, MJ
   Molina, JR
   Dy, GK
   Croghan, GA
   Qi, YW
   Glockner, J
   Hanson, LJ
   Roos, MM
   Tan, AD
   Adjei, AA
AF Zhu, Mojun
   Molina, Julian R.
   Dy, Grace K.
   Croghan, Gary A.
   Qi, Yingwei
   Glockner, James
   Hanson, Lorelei J.
   Roos, Michelle M.
   Tan, Angelina D.
   Adjei, Alex A.
TI A phase I study of the VEGFR kinase inhibitor vatalanib in combination
   with the mTOR inhibitor, everolimus, in patients with advanced solid
   tumors
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE Phase I; Targeted therapy; Vatalanib; Everolimus
ID ADVANCED COLORECTAL-CANCER; RECEPTOR TYROSINE KINASES; PTK787/ZK 222584;
   GROWTH; BEVACIZUMAB; TRIAL; OXALIPLATIN; LUNG
AB Purpose Combining small-molecule inhibitors of different targets was shown to be synergistic in preclinical studies. Testing this concept in clinical trials is, however, daunting due to challenges in toxicity management and efficacy assessment. This study attempted to evaluate the safety and efficacy of vatalanib plus everolimus in patients with advanced solid tumors and explore the utility of dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) studies as a predictive biomarker. Patients and Methods This single-center, phase I trial containing 70 evaluable patients consisted of a dose escalation proportion based on the traditional "3 + 3" design (cohort IA and IB) and a dose expansion proportion (cohort IIA and IIB). Toxicity was evaluated using the Common Terminology Criteria of Adverse Events. Antitumor activity was assessed using the Modified Response Evaluation Criteria in Solid Tumors. Results The maximum tolerated doses were determined to be vatalanib 1250 mg once daily or 750 mg twice daily in combination with everolimus 10 mg once daily. No treatment-related death occurred. The most common toxicities were hypertriglyceridemia, hypercholesterolemia, fatigue, vomiting, nausea and diarrhea. There was no complete response. Nine patients (12.9%) had partial response (PR) and 41 (58.6%) had stable disease (SD). Significant antitumor activity was observed in neuroendocrine tumors with a disease-control rate (PR + SD) of 66.7% and other tumor types including renal cancer, melanoma, and non-small-cell lung cancer. Conclusions The combination of vatalanib and everolimus demonstrated reasonable toxicity and clinical activity. Future studies combining targeted therapies and incorporating biomarker analysis are warranted based on this phase I trial.
C1 [Zhu, Mojun; Molina, Julian R.; Croghan, Gary A.; Glockner, James; Hanson, Lorelei J.; Roos, Michelle M.; Tan, Angelina D.; Adjei, Alex A.] Mayo Clin, 200 First St SW, Rochester, MN 55905 USA.
   [Dy, Grace K.] Roswell Park Canc Inst, Buffalo, NY 14263 USA.
   [Qi, Yingwei] Dign Hlth Med Fdn, San Francisco, CA 94107 USA.
C3 Mayo Clinic; Roswell Park Comprehensive Cancer Center
RP Adjei, AA (corresponding author), Mayo Clin, 200 First St SW, Rochester, MN 55905 USA.
EM adjei.alex@mayo.edu
FU National Cancer Institute [P30CA015083, U01CA069912]
FX This study was funded by the National Cancer Institute P30CA015083 and
   U01CA069912 grants.
CR [Anonymous], 2019, EVEROLIMUS
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NR 20
TC 10
Z9 10
U1 0
U2 2
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 DEC
PY 2020
VL 38
IS 6
BP 1755
EP 1762
DI 10.1007/s10637-020-00936-z
EA APR 2020
PG 8
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA OF8YE
UT WOS:000528297100001
PM 32328844
DA 2025-01-04
ER

PT J
AU Kim, BJ
   Kim, JH
   Jang, HJ
   Kim, HS
AF Kim, Bum Jun
   Kim, Jung Han
   Jang, Hyun Joo
   Kim, Hyeong Su
TI The role of anti-EGFR agents in the first-line treatment of advanced
   esophago-gastric adenocarcinoma: a meta-analysis
SO ONCOTARGET
LA English
DT Article
DE esophageal cancer; gastric cancer; anti-EGFR agent; meta-analysis
ID METASTATIC COLORECTAL-CANCER; ADVANCED GASTRIC-CANCER; GROWTH-FACTOR
   RECEPTOR; RANDOMIZED PHASE-II; TARGETED THERAPY; PLUS IRINOTECAN;
   CETUXIMAB; OXALIPLATIN; CAPECITABINE; CHEMOTHERAPY
AB The role of anti-epidermal growth factor receptor (EGFR) therapy is controversial in patients with esophago-gastric adenocarcinoma. We performed this meta-analysis to evaluate whether the addition of an anti-EGFR agent to chemotherapy can produce survival benefits in patients with advanced esophageal adenocarcinoma, gastric adenocarcinoma, or gastroesophageal junction adenocarcinoma. Electronic databases were searched for eligible randomized studies. From six studies, 1,817 patients were included in the meta-analysis of hazard ratios (HRs) for progression-free survival (PFS) and overall survival (OS). Compared with chemotherapy alone, anti-EGFR agents in combination with chemotherapy were significantly associated with shorter PFS (HR = 1.14 [95% confidence interval {CI}, 1.01-1.28], P = 0.03). In terms of OS, the addition of an anti-EGFR agent to chemotherapy showed no advantage (HR = 1.10 [95% CI, 0.98-1.23], P = 0.11). In addition, the combination of an anti-EGFR agent with chemotherapy significantly increased some grade 3/4 toxicities including diarrhea (risk ratio {RR} = 1.42, [95% CI, 1.03-1.94], P = 0.03), mucositis (RR = 3.30 [95% CI, 1.54-7.07], P = 0.002), and skin rash (RR = 6.82 [95% CI, 3.15-14.78], P < 0.00001). In conclusion, this meta-analysis indicates that the addition of an antiEGFR agent to chemotherapy conveys no additional benefit for patients with advanced esophago-gastric adenocarcinoma. As of now, anti-EGFR agents should not be used in the first-line treatment of adenocarcinoma of the upper gastrointestinal tract.
C1 [Kim, Bum Jun; Kim, Jung Han; Kim, Hyeong Su] Hallym Univ, Med Ctr, Kangnam Sacred Heart Hosp, Div Hematooncol,Coll Med,Dept Internal Med, Seoul 07441, South Korea.
   [Kim, Bum Jun] Armed Forces Med Command, Natl Army Capital Hosp, Dept Internal Med, Seongnam 13574, South Korea.
   [Jang, Hyun Joo] Hallym Univ, Coll Med, Dongtan Sacred Heart Hosp, Div Gastroenterol,Dept Internal Med,Med Ctr, Hwasung 18450, South Korea.
C3 Hallym University; Hallym University
RP Kim, JH (corresponding author), Hallym Univ, Med Ctr, Kangnam Sacred Heart Hosp, Div Hematooncol,Coll Med,Dept Internal Med, Seoul 07441, South Korea.; Jang, HJ (corresponding author), Hallym Univ, Coll Med, Dongtan Sacred Heart Hosp, Div Gastroenterol,Dept Internal Med,Med Ctr, Hwasung 18450, South Korea.
EM harricil@hotmail.com; jhj1229@hallym.or.kr
OI kim, bum jun/0000-0003-2360-5160
FU Hallym University Research Fund [HURF-2015-38]
FX This work was supported by Hallym University Research Fund 2015
   (HURF-2015-38).
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NR 34
TC 5
Z9 5
U1 0
U2 0
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 2017
VL 8
IS 58
BP 99033
EP 99040
DI 10.18632/oncotarget.20958
PG 8
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FR9KJ
UT WOS:000419392300105
PM 29228748
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Shrestha, G
   MacNeil, SM
   McQuerry, JA
   Jenkins, DF
   Sharma, S
   Bild, AH
AF Shrestha, Gajendra
   MacNeil, Shelley M.
   McQuerry, Jasmine A.
   Jenkins, David F.
   Sharma, Sunil
   Bild, Andrea H.
TI The value of genomics in dissecting the RAS-network and in guiding
   therapeutics for RAS-driven cancers
SO SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE RAS; Genomics Gene expression signature; Targeted therapy; Cancer
ID GENE-EXPRESSION SIGNATURES; RECEPTOR TYROSINE KINASES; K-RAS;
   COLORECTAL-CANCER; TRANSFERASE INHIBITORS; SELUMETINIB AZD6244; PATHWAY
   SIGNATURES; SIGNALING PATHWAYS; ONCOGENIC PATHWAYS; DRUG-RESISTANCE
AB The rise in genomic knowledge over the past decade has revealed the molecular etiology of many diseases, and has identified intricate signaling network activity in human cancers. Genomics provides the opportunity to determine genome structure and capture the activity of thousands of molecular events concurrently, which is important for deciphering highly complex genetic diseases such as cancer. In this review, we focus on genomic efforts directed towards one of cancer's most frequently mutated networks, the RAS pathway. Genomic tools such as gene expression signatures and assessment of mutations across the RAS network enable the capture of RAS signaling complexity. Due to this high level of interaction and cross-talk within the network, efforts to target RAS signaling in the clinic have generally failed, and we currently lack the ability to directly inhibit the RAS protein with high efficacy. We propose that the use of gene expression data can identify effective treatments that broadly inhibit the RAS network as this approach measures pathway activity independent of mutation status or any single mechanism of activation. Here, we review the genomic studies that map the complexity of the RAS network in cancer, and that show how genomic measurements of RAS pathway activation can identify effective RAS inhibition strategies. We also address the challenges and future directions for treating RAS-driven tumors. In summary, genomic assessment of RAS signaling provides a level of complexity necessary to accurately map the network that matches the intricacy of RAS pathway interactions in cancer. (C) 2016 The Authors. Published by Elsevier Ltd.
C1 [Shrestha, Gajendra; MacNeil, Shelley M.; McQuerry, Jasmine A.; Bild, Andrea H.] Univ Utah, Dept Pharmacol & Toxicol, 30 S 2000 E, Salt Lake City, UT 84112 USA.
   [MacNeil, Shelley M.; McQuerry, Jasmine A.; Bild, Andrea H.] Univ Utah, Dept Oncol Sci, Salt Lake City, UT USA.
   [Sharma, Sunil] Univ Utah, Sch Med, Dept Med, Salt Lake City, UT USA.
   [Sharma, Sunil] Huntsman Canc Inst, Ctr Invest Therapeut, Salt Lake City, UT USA.
   [Jenkins, David F.] Boston Univ, Sch Med, Div Computat Biomed, Boston, MA 02118 USA.
C3 Utah System of Higher Education; University of Utah; Utah System of
   Higher Education; University of Utah; Utah System of Higher Education;
   University of Utah; Utah System of Higher Education; University of Utah;
   Huntsman Cancer Institute; Boston University
RP Bild, AH (corresponding author), Univ Utah, Dept Pharmacol & Toxicol, 30 S 2000 E, Salt Lake City, UT 84112 USA.
EM andreab@genetics.utah.edu
OI Jenkins, David/0000-0002-7451-4288; Johnson, W. Evan/0000-0002-6247-6595
FU NIH grant [5U01CA164720]
FX AHB, SMM, GS, and JAM are funded by the NIH grant 5U01CA164720.
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NR 101
TC 9
Z9 12
U1 2
U2 9
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1084-9521
J9 SEMIN CELL DEV BIOL
JI Semin. Cell Dev. Biol.
PD OCT
PY 2016
VL 58
BP 108
EP 117
DI 10.1016/j.semcdb.2016.06.012
PG 10
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA DV9TD
UT WOS:000383284000013
PM 27338857
OA hybrid, Green Accepted
DA 2025-01-04
ER

PT J
AU Choi, S
   Yoo, S
   Jeon, M
   Park, S
   Choi, Y
   An, J
   Jeon, S
   Lee, M
   Yun, JH
   Park, JW
   Kim, I
AF Choi, Sanga
   Yoo, Seongkyeong
   Jeon, Miyeon
   Park, Soohyun
   Choi, Yunsup
   An, Jiyeon
   Jeon, Sungmi
   Lee, Mingyu
   Yun, Jang-Hyuk
   Park, Jong-Wan
   Kim, Iljin
TI SPATA20 deficiency enhances the metastatic and angiogenic potential of
   cancer cells by promoting HIF-1α synthesis
SO AMERICAN JOURNAL OF CANCER RESEARCH
LA English
DT Article
DE SPATA20; HIF-1 alpha; hypoxia; cancer
ID HYPOXIA-INDUCIBLE FACTOR-1; THIOREDOXIN; EXPRESSION; MECHANISMS;
   PROTEIN; HIF-1; GENE; OVEREXPRESSION; ACTIVATION; THERAPY
AB Hypoxia-inducible factors (HIFs) regulates cellular oxygen balance and play a central role in cancer metastasis and angiogenesis. Despite extensive research on HIFs, successful therapeutic strategies remain limited due to the intricate nature of their regulation. In this study, we identified SPATA20, a relatively understudied protein with a thioredoxin-like domain, as an upstream regulator of HIF-1 alpha. Depleting SPATA20 induced HIF-1 alpha expression, suggesting a tumor-suppressive role for SPATA20 in cancer cells. SPATA20 depletion increased HIF-1 alpha protein levels and transcriptional activity without affecting its degradation. It appears that SPATA20 inhibits the de novo synthesis of HIF-1 alpha, possibly by repressing the cap-dependent translation process involving AKT phosphorylation. Additionally, depletion of SPATA20 promoted cancer cell migration and invasion, which can be reversed by pharmacological inhibition of HIF-1 alpha. Clinical data analysis revealed an inverse correlation between SPATA20 expression and colorectal cancer progression, providing evidence of its role as a potential biomarker. Utilizing SPATA20 as an indicator for HIF1 alpha-targeting therapy may be an attractive strategy for treating patients with hypoxia-driven cancers. In conclusion, this study demonstrates that SPATA20 deficiency promotes cancer progression by activating the HIF-1 alpha signaling pathway.
C1 [Choi, Sanga; Yoo, Seongkyeong; Jeon, Miyeon; Park, Soohyun; Choi, Yunsup; An, Jiyeon; Kim, Iljin] Inha Univ, Dept Pharmacol, Coll Med, 100 Inha Ro, Incheon 22212, South Korea.
   [Choi, Sanga; Yoo, Seongkyeong; Jeon, Miyeon; Park, Soohyun; Choi, Yunsup; An, Jiyeon; Kim, Iljin] Inha Univ, Coll Med, Program Biomed Sci & Engn, 100 Inha Ro, Incheon 22212, South Korea.
   [Choi, Sanga; Yoo, Seongkyeong; Jeon, Miyeon; Park, Soohyun; Choi, Yunsup; An, Jiyeon] Inha Univ, Coll Med, Res Ctr Controlling Intercellular Commun, Incheon 22212, South Korea.
   [Jeon, Sungmi] Seoul Natl Univ, Dept Plast & Reconstruct Surg, Coll Med, Seoul Natl Univ Hosp, Seoul 03080, South Korea.
   [Lee, Mingyu] Harvard Med Sch, Div Allergy & Clin Immunol, Brigham & Womens Hosp, Boston, MA 02115 USA.
   [Lee, Mingyu] Harvard Med Sch, Dept Med, Boston, MA 02115 USA.
   [Yun, Jang-Hyuk] Kangwon Natl Univ, Coll Vet Med, Chunchon 24341, South Korea.
   [Yun, Jang-Hyuk] Kangwon Natl Univ, Inst Vet Sci, Chunchon 24341, South Korea.
   [Park, Jong-Wan] Seoul Natl Univ, Coll Med, Dept Pharmacol, Seoul 03080, South Korea.
C3 Inha University; Inha University; Inha University; Seoul National
   University (SNU); Seoul National University Hospital; Harvard
   University; Harvard Medical School; Brigham & Women's Hospital; Harvard
   University; Harvard Medical School; Kangwon National University; Kangwon
   National University; Seoul National University (SNU)
RP Kim, I (corresponding author), Inha Univ, Dept Pharmacol, Coll Med, 100 Inha Ro, Incheon 22212, South Korea.; Kim, I (corresponding author), Inha Univ, Coll Med, Program Biomed Sci & Engn, 100 Inha Ro, Incheon 22212, South Korea.
EM ijk@inha.ac.kr
FU National Research Foundation of Korea [NRF-2021R1C-1C2004561,
   NRF-2021R1A5A2031612]
FX This research was funded by the National Research Foundation of Korea
   (NRF-2021R1C-1C2004561 and NRF-2021R1A5A2031612).
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NR 45
TC 0
Z9 0
U1 0
U2 0
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 2024
VL 14
IS 2
PG 24
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KI3K1
UT WOS:001179289200008
DA 2025-01-04
ER

PT J
AU Tae, IH
   Lee, J
   Kang, Y
   Lee, JM
   Park, K
   Yang, H
   Kim, HW
   Ko, JH
   Park, DS
   Kim, DS
   Son, MY
   Cho, HS
AF Tae, In Hwan
   Lee, Jinkwon
   Kang, Yunsang
   Lee, Jeong Min
   Park, Kunhyang
   Yang, Haneol
   Kim, Hee-Won
   Ko, Jeong Heon
   Park, Doo-Sang
   Kim, Dae-Soo
   Son, Mi-Young
   Cho, Hyun-Soo
TI Induction of Cell Death by<i> Bifidobacterium</i><i> infantis</i> DS1685
   in Colorectal and Breast Cancers via SMAD4/TGF-Beta Activation
SO JOURNAL OF MICROBIOLOGY AND BIOTECHNOLOGY
LA English
DT Article
DE B. infantis DS1685 supernatant; SMAD4; TGF-beta; colorectal cancer;
   breast cancer
AB Therapeutic advancements in treatments for cancer, a leading cause of mortality worldwide, have lagged behind the increasing incidence of this disease. There is a growing interest in multifaceted approaches for cancer treatment, such as chemotherapy, targeted therapy, and immunotherapy, but due to their low efficacy and severe side effects, there is a need for the development of new cancer therapies. Recently, the human microbiome, which is comprised of various microorganisms, has emerged as an important research field due to its potential impact on cancer treatment. Among these microorganisms, Bifidobacterium infantis has been shown to significantly improve the efficacy of various anticancer drugs. However, research on the role of B. infantis in cancer treatment remains insufficient. Thus, in this study, we explored the anticancer effect of treatment with B. infantis DS1685 supernatant (BI sup) in colorectal and breast cancer cell lines. Treatment with BI sup induced SMAD4 expression to suppress cell growth in colon and breast cancer cells. Furthermore, a decrease in tumor cohesion was observed through the disruption of the regulation of EMT-related genes by BI sup in 3D spheroid models. Based on these findings, we anticipate that BI sup could play an adjunctive role in cancer therapy, and future cotreatment of BI sup with various anticancer drugs may lead to synergistic effects in cancer treatment.
C1 [Tae, In Hwan; Lee, Jinkwon; Kang, Yunsang; Lee, Jeong Min; Park, Kunhyang; Yang, Haneol; Kim, Hee-Won; Ko, Jeong Heon; Park, Doo-Sang; Kim, Dae-Soo; Son, Mi-Young; Cho, Hyun-Soo] Korea Res Inst Biosci & Biotechnol, Daejeon 34141, South Korea.
   [Lee, Jinkwon; Kang, Yunsang; Lee, Jeong Min; Kim, Hee-Won; Ko, Jeong Heon; Park, Doo-Sang; Kim, Dae-Soo; Son, Mi-Young; Cho, Hyun-Soo] Korea Univ Sci & Technol, Daejeon 34316, South Korea.
   [Son, Mi-Young; Cho, Hyun-Soo] Sungkyunkwan Univ, Dept Biol Sci, Suwon 16419, South Korea.
C3 Korea Research Institute of Bioscience & Biotechnology (KRIBB);
   Sungkyunkwan University (SKKU)
RP Kim, DS; Son, MY; Cho, HS (corresponding author), Korea Res Inst Biosci & Biotechnol, Daejeon 34141, South Korea.; Kim, DS; Son, MY; Cho, HS (corresponding author), Korea Univ Sci & Technol, Daejeon 34316, South Korea.; Son, MY; Cho, HS (corresponding author), Sungkyunkwan Univ, Dept Biol Sci, Suwon 16419, South Korea.
EM kds2465@kribb.re.kr; myson@kribb.re.kr; chohs@kribb.re.kr
FU Technology Innovation Program - Ministry of Trade, Industry & Energy
   (MOTIE, Korea) [20008777]; National Research Foundation (NRF) of Korea -
   Ministry of Science, ICT and Future Planning
   [NRF-2018M3A9H3023077/NRF-2021M3A9H3016046, RS-2023-00225239,
   RS-2024-00336620, 2022R1A2C1003118]; Korean Fund for Regenerative
   Medicine (KFRM) grant - Korean government (Ministry of Science and ICT);
   Korean Fund for Regenerative Medicine (KFRM) grant - Korean government
   (Ministry of Health Welfare) [21A0404L1]; KRIBB Research Initiative
   Program
FX This work was supported by a grant from the Technology Innovation
   Program (No. 20008777) funded by the Ministry of Trade, Industry &
   Energy (MOTIE, Korea) , a National Research Foundation (NRF) of Korea
   grant funded by the Ministry of Science, ICT and Future Planning
   (NRF-2018M3A9H3023077/NRF-2021M3A9H3016046, RS-2023-00225239,
   RS-2024-00336620, 2022R1A2C1003118) , a Korean Fund for Regenerative
   Medicine (KFRM) grant funded by the Korean government (the Ministry of
   Science and ICT, the Ministry of Health & Welfare, 21A0404L1) , and the
   KRIBB Research Initiative Program. The funders had no role in the study
   design, data collection or analysis, decision to publish, or preparation
   of the manuscript.
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NR 34
TC 0
Z9 0
U1 4
U2 4
PU KOREAN SOC MICROBIOLOGY & BIOTECHNOLOGY
PI SEOUL
PA KOREA SCI TECHNOL CENTER #402,  635-4 YEOGSAM-DONG, KANGNAM-GU, SEOUL,
   SOUTH KOREA
SN 1017-7825
EI 1738-8872
J9 J MICROBIOL BIOTECHN
JI J. Microbiol. Biotechnol.
PD AUG
PY 2024
VL 34
IS 8
BP 1698
EP 1704
DI 10.4014/jmb.2404.04055
PG 7
WC Biotechnology & Applied Microbiology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Microbiology
GA E2J1H
UT WOS:001301306600016
PM 39113194
OA Green Published
DA 2025-01-04
ER

PT J
AU Chelariu-Raicu, A
   Mahdi, H
   Slomovitz, BM
AF Chelariu-Raicu, Anca
   Mahdi, Haider
   Slomovitz, Brian M.
TI Changing treatments paradigms and role of immunotherapy in recurrent
   endometrial cancer
SO CURRENT OPINION IN OBSTETRICS & GYNECOLOGY
LA English
DT Review
DE endometrial cancer; immunotherapy; mismatch repair system; molecular
   biomarkers
ID MISMATCH REPAIR DEFICIENCY; MICROSATELLITE INSTABILITY;
   COLORECTAL-CANCER; LYNCH-SYNDROME; CARCINOMA; THERAPY; TUMORS; WOMEN;
   RISK
AB Purpose of review Over the past decade, the treatment of patients diagnosed with endometrial cancer (EC) shifted away from the use of chemotherapy to more novel targeted therapy and immunotherapy approaches. Recent findings The Cancer Genome Atlas data demonstrated different subgroups within ECs, more specifically, it facilitated the identification of predictive biomarkers. In particular, immunotherapies (immuno-oncology (IO)) are active either as monotherapy or in combination with other agents, depending on the biomarker profile of the tumor. In May 2017, pembrolizumab was approved for patients with microsatellite instability high (MSI-H) EC. More recently, this approval was extended for patients harvesting tumors with a high tumor mutational burden status. Furthermore, in July 2021, the combination of pembrolizumab and lenvatinib was approved for patients who do not exhibit MSI-H disease. Given the wealth of targets in EC and different targetable mutations, the challenge will be to choose the proper treatment and the proper sequencing to derive the best outcome in the first-line setting and improve outcomes in subsequent settings. This review summarizes the current indications of immunotherapy for the treatment of advanced and recurrent EC. We outline the role of testing for uterine cancer and its implication in therapy management. Finally, we address new concepts for immunotherapy combinations with other therapies.
C1 [Chelariu-Raicu, Anca] LMU Univ Hosp, Breast Canc, Gynecol Oncol Ctr, Dept Obstet & Gynecol, Munich, Germany.
   [Chelariu-Raicu, Anca] LMU Univ Hosp, CCC Munich, Munich, Germany.
   [Mahdi, Haider] Univ Pittsburgh, Med Ctr, Div Gynecol Oncol, Pittsburgh, PA USA.
   [Slomovitz, Brian M.] Mt Sinai Med Ctr, Div Gynecol Oncol, Miami Beach, FL 33140 USA.
C3 University of Munich; University of Munich; Pennsylvania Commonwealth
   System of Higher Education (PCSHE); University of Pittsburgh; Mount
   Sinai Medical Center
RP Slomovitz, BM (corresponding author), Mt Sinai Med Ctr, Div Gynecol Oncol, Miami Beach, FL 33140 USA.
EM bslomovitz@gog.org
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NR 42
TC 0
Z9 1
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1040-872X
EI 1473-656X
J9 CURR OPIN OBSTET GYN
JI Curr. Opin. Obstet. Gynecol.
PD FEB
PY 2022
VL 34
IS 1
BP 28
EP 35
DI 10.1097/GCO.0000000000000768
PG 8
WC Obstetrics & Gynecology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Obstetrics & Gynecology
GA XX2QB
UT WOS:000736146000007
PM 34967812
DA 2025-01-04
ER

PT J
AU Shah, AS
   Patel, C
   Parmar, G
   Patel, A
   Jain, M
AF Shah, Ashish
   Patel, Chhagan
   Parmar, Ghanshaym
   Patel, Ashish
   Jain, Manav
TI A Concise Review on Tyrosine Kinase Targeted Cancer Therapy
SO CURRENT DRUG THERAPY
LA English
DT Review
DE Tyrosine kinase; types of receptors; tyrosine kinase inhibitors; cancer;
   small molecules; targeted therapy
ID CELL LUNG-CANCER; GROWTH-FACTOR RECEPTOR; METASTATIC COLORECTAL-CANCER;
   SRC FAMILY KINASES; OPEN-LABEL; BREAST-CANCER; DOUBLE-BLIND; 1ST-LINE
   TREATMENT; MOLECULAR TARGETS; THYROID-CANCER
AB Tyrosine Kinase (TK) is considered one of the important family members of the kinase family due to its important role in various cellular processes like cell growth, cell differentiation, apoptosis, etc. Mutation, overexpression, and dysfunction of tyrosine kinase receptors lead to the development of malignancy; thus, they are considered one of the important targets for the development of anti-cancer molecules. The tyrosine kinase family is majorly divided into two classes; receptor and non-receptor tyrosine kinase. Both of the classes have an important role in the development of tumour cells. Currently, more than 40 FDA-approved tyrosine kinase inhibitors are used to treat various types of cancers. Tyrosine kinase inhibitors mainly block the phosphorylation of tyrosine residue of the corresponding kinase substrate, so activation of downstream signalling pathways can be inhibited. The promising results of tyrosine kinase inhibitors in solid tumours have revolutionized oncology research. In this article, we summarized the role of some important members of the tyrosine kinase family in the development and progression of tumour cells and the significance of tyrosine kinase inhibitors in the treatment of various types of cancer.
C1 [Shah, Ashish; Parmar, Ghanshaym] Sumandeep Vidyapeeth, Dept Pharm, Vadodara, Gujarat, India.
   [Patel, Chhagan] Shree Sarvajaink Pharm Coll, Mehsana, Gujarat, India.
   [Patel, Ashish] CHARUSAT, Ramanbhai Patel Coll Pharm, Anand, Gujarat, India.
   [Jain, Manav] Postgrad Inst Med Educ & Res, Dept Pharmacol, Chandigarh, Punjab, India.
C3 Sumandeep Vidyapeeth; Charotar University of Science & Technology -
   Charusat; Post Graduate Institute of Medical Education & Research
   (PGIMER), Chandigarh
RP Shah, AS (corresponding author), Sumandeep Vidyapeeth, Dept Pharm, Vadodara, Gujarat, India.
EM shah_ashishpharmacy@yahoo.co.in
RI Jain, Manav/KIH-0333-2024; Shah, Ashish/AAC-5501-2020; Patel,
   Ashish/Y-3630-2019; Parmar, Ghanshyam/F-6611-2013
OI Patel, Ashish/0000-0001-5773-3756; Jain, Dr Manav/0000-0002-6365-8411;
   Shah, Ashish/0000-0003-0817-5940; Parmar, Ghanshyam/0000-0002-4614-9797
FU Sumandeep Vidyapeeth University
FX The authors would like to thank Sumandeep Vidyapeeth University for
   supporting this work.
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NR 118
TC 0
Z9 0
U1 3
U2 31
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1574-8855
EI 2212-3903
J9 CURR DRUG THER
JI Curr. Drug Ther.
PY 2022
VL 17
IS 2
BP 96
EP 107
DI 10.2174/1574885517666220331104025
PG 12
WC Pharmacology & Pharmacy
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA 3M5XE
UT WOS:000835533300005
DA 2025-01-04
ER

PT J
AU Rahman, S
   Pavelic, SK
   Markova-Car, E
AF Rahman, Sadia
   Pavelic, Sandra Kraljevic
   Markova-Car, Elitza
TI Circadian (De)regulation in Head and Neck Squamous Cell Carcinoma
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE head and neck squamous cell carcinoma (HNSCC); circadian rhythm;
   circadian clock genes; cancer
ID CLOCK GENE BMAL1; RECEPTOR-TARGETED THERAPY; ROTATING NIGHT SHIFTS;
   BREAST-CANCER; DNA-DAMAGE; ALTERED EXPRESSION; COLORECTAL-CANCER; TUMOR
   PROGRESSION; DOWN-REGULATION; ORAL-CANCER
AB Head and neck cancer encompass different malignancies that develop in and around the throat, larynx, nose, sinuses and mouth. Most head and neck cancers are squamous cell carcinomas (HNSCC) that arise in the flat squamous cells that makeup the thin layer of tissue on the surface of anatomical structures in the head and neck. Each year, HNSCC is diagnosed in more than 600,000 people worldwide, with about 50,000 new cases. HNSCC is considered extremely curable if detected early. But the problem remains in treatment of inoperable cases, residues or late stages. Circadian rhythm regulation has a big role in developing various carcinomas, and head and neck tumors are no exception. A number of studies have reported that alteration in clock gene expression is associated with several cancers, including HNSCC. Analyses on circadian clock genes and their association with HNSCC have shown that expression of PER1, PER2, PER3, CRY1, CRY2, CKI epsilon, TIM, and BMAL1 are deregulated in HNSCC tissues. This review paper comprehensively presents data on deregulation of circadian genes in HNSCC and critically evaluates their potential diagnostics and prognostics role in this type of pathology.
C1 [Rahman, Sadia; Pavelic, Sandra Kraljevic; Markova-Car, Elitza] Univ Rijeka, Dept Biotechnol, Ctr High Throughput Technol, Rijeka 51000, Croatia.
C3 University of Rijeka
RP Markova-Car, E (corresponding author), Univ Rijeka, Dept Biotechnol, Ctr High Throughput Technol, Rijeka 51000, Croatia.
EM sadiahusen@gmail.com; sandrakp@biotech.uniri.hr; elitza@biotech.uniri.hr
RI Kraljevic Pavelic, Sandra/J-3864-2012; Markova-Car, Elitza/R-6810-2018
OI Kraljevic Pavelic, Sandra/0000-0003-0491-673X; Markova-Car,
   Elitza/0000-0001-6979-0731
FU University of Rijeka [uniri-biomed-18-257, uniri-biomed-18-133]
FX This research was funded by the University of Rijeka under the project
   number uniri-biomed-18-257 and uniri-biomed-18-133.
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NR 113
TC 24
Z9 26
U1 2
U2 12
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 JUN 1
PY 2019
VL 20
IS 11
AR 2662
DI 10.3390/ijms20112662
PG 16
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA IE8OX
UT WOS:000472634100056
PM 31151182
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Li, XY
   Zhao, LN
   Chen, CS
   Nie, JY
   Jiao, BW
AF Li, Xiyin
   Zhao, Lina
   Chen, Ceshi
   Nie, Jianyun
   Jiao, Baowei
TI Can EGFR be a therapeutic target in breast cancer?
SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
LA English
DT Review
DE EGFR Breast cancer; Protein degradation; Targeted therapy
ID GROWTH-FACTOR-RECEPTOR; TYROSINE KINASE INHIBITOR; SQUAMOUS-CELL
   CARCINOMA; PHASE-II TRIAL; WILD-TYPE EGFR; ONCOGENIC MUTATIONS;
   LUNG-CANCER; EXON 19; MOLECULAR PORTRAITS; PROGNOSTIC VALUE
AB Epidermal growth factor receptor (EGFR) is highly expressed in certain cancer types and is involved in regulating the biological characteristics of cancer progression, including proliferation, metastasis, and drug resistance. Various medicines targeting EGFR have been developed and approved for several cancer types, such as lung and colon cancer. To date, however, EGFR inhibitors have not achieved satisfactory clinical results in breast cancer, which continues to be the most serious malignant tumor type in females. Therefore, clarifying the underlying mechanisms related to the ineffectiveness of EGFR inhibitors in breast cancer and developing new EGFR-targeted strategies (e.g., combination therapy) remain critical challenges. Various studies have demonstrated aberrant expression and maintenance of EGFR levels in breast cancer. In this review, we summarize the regulatory mechanisms underlying EGFR protein expression in breast cancer cells, including EGFR mutations, amplification, endocytic dysfunction, recycling acceleration, and degradation disorders. We also discuss potential therapeutic strategies that act directly or indirectly on EGFR, including reducing EGFR protein expression, treating the target protein to mediate precise clearance, and inhibiting non-EGFR signaling pathways. This review should provide new therapeutic perspectives for breast cancer patients with high EGFR expression.
C1 [Li, Xiyin; Nie, Jianyun] Kunming Med Univ, Affiliated Hosp 3, Dept Breast Canc 3, 519 Kunzhou Rd, Kunming 650118, Yunnan, Peoples R China.
   [Li, Xiyin; Zhao, Lina; Jiao, Baowei] Chinese Acad Sci, Kunming Inst Zool, State Key Lab Genet Resources & Evolut, Kunming 650201, Yunnan, Peoples R China.
   [Chen, Ceshi] Chinese Acad Sci, Chinese Acad Sci & Yunnan Prov, Kunming Inst Zool, Key Lab Anim Models & Human Dis Mech, Kunming 650201, Yunnan, Peoples R China.
   [Chen, Ceshi; Jiao, Baowei] Chinese Acad Sci, Kunming Inst Zool, KIZ CUHK Joint Lab Bioresources & Mol Res Common, Kunming 650201, Yunnan, Peoples R China.
C3 Kunming Medical University; Chinese Academy of Sciences; Kunming
   Institute of Zoology, CAS; Chinese Academy of Sciences; Kunming
   Institute of Zoology, CAS; Chinese Academy of Sciences; Kunming
   Institute of Zoology, CAS
RP Nie, JY (corresponding author), Kunming Med Univ, Affiliated Hosp 3, Dept Breast Canc 3, 519 Kunzhou Rd, Kunming 650118, Yunnan, Peoples R China.; Jiao, BW (corresponding author), Chinese Acad Sci, Kunming Inst Zool, State Key Lab Genet Resources & Evolut, Kunming 650201, Yunnan, Peoples R China.; Chen, CS (corresponding author), Chinese Acad Sci, Chinese Acad Sci & Yunnan Prov, Kunming Inst Zool, Key Lab Anim Models & Human Dis Mech, Kunming 650201, Yunnan, Peoples R China.; Chen, CS; Jiao, BW (corresponding author), Chinese Acad Sci, Kunming Inst Zool, KIZ CUHK Joint Lab Bioresources & Mol Res Common, Kunming 650201, Yunnan, Peoples R China.
EM chenc@mail.kiz.ac.cn; njyvip@sina.com; jiaobaowei@mail.kiz.ac.cn
RI Chen, Ceshi/C-1720-2008
OI JIAO, BAOWEI/0000-0001-8559-9160
FU National Key Research and Development Program of China [2020YFA0112300];
   National Natural Science Foundation of China [U1802285, 31970612,
   82103191, 81902714]; Yunnan Applied Basic Research Key Projects
   [2019FB047, 202101AT070284, 2019FA040]; CAS "Light of West China"
   Program [xbzg-zdsys-201913]
FX This work was supported by the National Key Research and Development
   Program of China (2020YFA0112300), National Natural Science Foundation
   of China (U1802285, 31970612, 82103191 and 81902714), Yunnan Applied
   Basic Research Key Projects (2019FB047, 202101AT070284, 2019FA040), and
   CAS "Light of West China" Program (xbzg-zdsys-201913).
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NR 207
TC 35
Z9 39
U1 5
U2 34
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0304-419X
EI 1879-2561
J9 BBA-REV CANCER
JI Biochim. Biophys. Acta-Rev. Cancer
PD SEP
PY 2022
VL 1877
IS 5
DI 10.1016/j.bbcan.2022.188789
PG 13
WC Biochemistry & Molecular Biology; Biophysics; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Oncology
GA 7Q9SN
UT WOS:000909722000004
PM 36064121
DA 2025-01-04
ER

PT J
AU Yun, M
   You, SH
   Nguyen, VH
   Prakash, J
   Glasl, S
   Gujrati, V
   Choy, HE
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   Min, JJ
   Ntziachristos, V
AF Yun, Misun
   You, Sung-Hwan
   Vu Hong Nguyen
   Prakash, Jaya
   Glasl, Sarah
   Gujrati, Vipul
   Choy, Hyon E.
   Stiel, Andre C.
   Min, Jung-Joon
   Ntziachristos, Vasilis
TI Reporter gene-based optoacoustic imaging of <i>E. coli</i> targeted
   colon cancer in vivo
SO SCIENTIFIC REPORTS
LA English
DT Article
ID ESCHERICHIA-COLI; MELANIN PRODUCTION; SPECTROSCOPY; TYROSINASE; PROBES
AB Bacteria-mediated cancer-targeted therapy is a novel experimental strategy for the treatment of cancers. Bacteria can be engineered to overcome a major challenge of existing therapeutics by differentiating between malignant and healthy tissue. A prerequisite for further development and study of engineered bacteria is a suitable imaging concept which allows bacterial visualization in tissue and monitoring bacterial targeting and proliferation. Optoacoustics (OA) is an evolving technology allowing whole-tumor imaging and thereby direct observation of bacterial colonization in tumor regions. However, bacterial detection using OA is currently hampered by the lack of endogenous contrast or suitable transgene fluorescent labels. Here, we demonstrate improved visualization of cancer-targeting bacteria using OA imaging and E. coli engineered to express tyrosinase, which uses L-tyrosine as the substrate to produce the strong optoacoustic probe melanin in the tumor microenvironment. Tumors of animals injected with tyrosinase-expressing E. coli showed strong melanin signals, allowing to resolve bacterial growth in the tumor over time using multispectral OA tomography (MSOT). MSOT imaging of melanin accumulation in tumors was confirmed by melanin and E. coli staining. Our results demonstrate that using tyrosinase-expressing E. coli enables non-invasive, longitudinal monitoring of bacterial targeting and proliferation in cancer using MSOT.
C1 [Yun, Misun; Prakash, Jaya; Glasl, Sarah; Gujrati, Vipul; Stiel, Andre C.; Ntziachristos, Vasilis] Helmholtz Zentrum Munchen GmbH, Inst Biol & Med Imaging, D-85764 Neuherberg, Germany.
   [You, Sung-Hwan; Min, Jung-Joon] Chonnam Natl Univ, Dept Nucl Med, Med Sch, Gwangju, South Korea.
   [Vu Hong Nguyen] City Hope Natl Med Ctr, Dept Expt Therapeut, Beckman Res Inst, Duarte, CA USA.
   [Prakash, Jaya] Indian Inst Sci, Dept Instrumentat & Appl Phys, CV Raman Ave, Bengaluru 560012, India.
   [Choy, Hyon E.] Chonnam Natl Univ, Dept Microbiol, Med Sch, Gwangju, South Korea.
   [Gujrati, Vipul; Ntziachristos, Vasilis] Tech Univ Munich, Chair Biol Imaging, Sch Med, Ctr Translat Canc Res TranslaTUM, D-81675 Munich, Germany.
C3 Helmholtz Association; Helmholtz-Center Munich - German Research Center
   for Environmental Health; Chonnam National University; City of Hope;
   Beckman Research Institute of City of Hope; Indian Institute of Science
   (IISC) - Bangalore; Chonnam National University; Technical University of
   Munich
RP Ntziachristos, V (corresponding author), Helmholtz Zentrum Munchen GmbH, Inst Biol & Med Imaging, D-85764 Neuherberg, Germany.; Min, JJ (corresponding author), Chonnam Natl Univ, Dept Nucl Med, Med Sch, Gwangju, South Korea.; Ntziachristos, V (corresponding author), Tech Univ Munich, Chair Biol Imaging, Sch Med, Ctr Translat Canc Res TranslaTUM, D-81675 Munich, Germany.
EM jjmin@jnu.ac.kr; bioimaging.translatum@tum.de
RI Stiel, Andre/B-1644-2014; Gujrati, Vipul/AAI-4675-2021; Nguyen,
   Vu/HGV-1806-2022; Prakash, Jaya/K-2479-2012
OI Prakash, Jaya/0000-0002-2375-154X; Ntziachristos,
   Vasilis/0000-0002-9988-0233; Choy, Hyon E/0000-0002-2791-1416; Stiel,
   Andre/0000-0001-8675-6797
FU European Research Council (ERC) under the European Union [694968];
   Deutsche Forschungsgemeinschaft (DFG), Germany [NT 3/10-1]; DFG [CRC
   1123]; National Research Foundation - Ministry of Science and ICT, South
   Korea [NRF-2017R1A2B3012157]; Alexander von Humboldt Postdoctoral
   Fellowship program
FX This project has received funding from the European Research Council
   (ERC) under the European Union's Horizon 2020 research and innovation
   programme under grant agreement no. 694968 (PREMSOT). The research
   leading to these results was supported by the Deutsche
   Forschungsgemeinschaft (DFG), Germany (Gottfried Wilhelm Leibniz Prize
   2013, NT 3/10-1) as well as by the DFG as part of the CRC 1123 (Z1).
   J.J.M. was supported by the National Research Foundation grant
   (NRF-2017R1A2B3012157) funded by the Ministry of Science and ICT, South
   Korea. JP acknowledges the Alexander von Humboldt Postdoctoral
   Fellowship program. We wish to thank Dr. Doris Bengel, Uwe Klemm and Pia
   Anzenhofer for assisting with experimental procedures. We also wish to
   thank Dr. A. Chapin Rodriguez and Dr. Sergey Sulima for helpful
   suggestions on the manuscript.
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NR 33
TC 11
Z9 11
U1 0
U2 26
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD DEC 24
PY 2021
VL 11
IS 1
AR 24430
DI 10.1038/s41598-021-04047-4
PG 9
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA XU1LQ
UT WOS:000734036000001
PM 34952915
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Dai, PH
   Wang, WY
   Yang, N
   Serna-Tamayo, C
   Ricca, JM
   Zamarin, D
   Shuman, S
   Merghoub, T
   Wolchok, JD
   Deng, L
AF Dai, Peihong
   Wang, Weiyi
   Yang, Ning
   Serna-Tamayo, Cristian
   Ricca, Jacob M.
   Zamarin, Dmitriy
   Shuman, Stewart
   Merghoub, Taha
   Wolchok, Jedd D.
   Deng, Liang
TI Intratumoral delivery of inactivated modified vaccinia virus Ankara
   (iMVA) induces systemic antitumor immunity via STING and Batf3-dependent
   dendritic cells
SO SCIENCE IMMUNOLOGY
LA English
DT Article
ID CYCLIC GMP-AMP; ARMED ONCOLYTIC POXVIRUSES; I INTERFERON; DNA; CANCER;
   ACTIVATION; RESPONSES; IMMUNOGENICITY; IMMUNOTHERAPY; CANDIDATE
AB Advanced cancers remain a therapeutic challenge despite recent progress in targeted therapy and immunotherapy. Novel approaches are needed to alter the tumor immunosuppressive microenvironment and to facilitate the recognition of tumor antigens that leads to antitumor immunity. Poxviruses, such as modified vaccinia virus Ankara (MVA), have potential as immunotherapeutic agents. We show that infection of conventional dendritic cells (DCs) with heat- or ultraviolet-inactivated MVA leads to higher levels of interferon induction than MVA alone through the cGAS (cyclic guanosine monophosphate-adenosine monophosphate synthase)-STING cytosolic DNA-sensing pathway. Intratumoral injection of inactivated MVA (iMVA) was effective and generated adaptive antitumor immunity in murine melanoma and colon cancer models. iMVA-induced antitumor therapy was less effective in STING- or Batf3-deficient mice than in wild-type mice, indicating that both cytosolic DNA sensing and Batf3-dependent CD103(+)/CD8 alpha(+) DCs are essential for iMVA immunotherapy. The combination of intratumoral delivery of iMVA and systemic delivery of immune checkpoint blockade generated synergistic antitumor effects in bilateral tumor implantation models as well as in a unilateral large established tumor model. Our results suggest that inactivated vaccinia virus could be used as an immunotherapeutic agent for human cancers.
C1 [Dai, Peihong; Wang, Weiyi; Yang, Ning; Serna-Tamayo, Cristian; Deng, Liang] Mem Sloan Kettering Canc Ctr, Dept Med, Dermatol Serv, New York, NY 10065 USA.
   [Dai, Peihong; Shuman, Stewart] Mem Sloan Kettering Canc Ctr, Program Mol Biol, New York, NY 10065 USA.
   [Ricca, Jacob M.; Zamarin, Dmitriy; Merghoub, Taha; Wolchok, Jedd D.] Mem Sloan Kettering Canc Ctr, Parker Inst Canc Immunotherapy, New York, NY 10065 USA.
   [Zamarin, Dmitriy; Merghoub, Taha; Wolchok, Jedd D.] Mem Sloan Kettering Canc Ctr, Ludwig Ctr Canc Immunotherapy, New York, NY 10065 USA.
   [Zamarin, Dmitriy; Merghoub, Taha; Wolchok, Jedd D.] Mem Sloan Kettering Canc Ctr, Dept Med, Melanoma & Immunotherapeut Serv, New York, NY 10065 USA.
   [Zamarin, Dmitriy; Wolchok, Jedd D.; Deng, Liang] Weill Cornell Med & Grad Coll, New York, NY 10065 USA.
C3 Memorial Sloan Kettering Cancer Center; Memorial Sloan Kettering Cancer
   Center; Memorial Sloan Kettering Cancer Center; Memorial Sloan Kettering
   Cancer Center; Memorial Sloan Kettering Cancer Center; Cornell
   University; Weill Cornell Medicine
RP Deng, L (corresponding author), Mem Sloan Kettering Canc Ctr, Dept Med, Dermatol Serv, New York, NY 10065 USA.; Deng, L (corresponding author), Weill Cornell Med & Grad Coll, New York, NY 10065 USA.
EM dengl@mskcc.org
RI Wolchok, Jedd/ACT-4947-2022; Yang, Ning/KAL-6559-2024; Merghoub,
   Taha/ABD-8362-2021; Deng, Liang/GXH-6710-2022; Wang,
   Weiyi/GZN-0408-2022; Zamarin, Dmitriy/L-9774-2019
OI Merghoub, Taha/0000-0002-1518-5111; Wolchok, Jedd/0000-0001-6718-2222;
   Zamarin, Dmitriy/0000-0002-0094-0161
FU NIH [K-08 AI073736, R56AI095692]; Lucille Castori Center for Microbes,
   Inflammation and Cancer seed grant; Society of Memorial Sloan Kettering
   (MSK) research grant; MSK Technology Development Fund;
   Physician-Scientist Career Development Award from the Dermatology
   Foundation; Carolyn L. Kuckein Student Research Fellowship; Swim Across
   America; Ludwig Institute for Cancer Research; National Cancer Institute
   [R01 CA56821]; NIH/National Cancer Institute Cancer Center Support Grant
   [P30 CA008748]
FX This work was supported by NIH grants K-08 AI073736 (L.D.) and
   R56AI095692 (L.D.); Lucille Castori Center for Microbes, Inflammation
   and Cancer seed grant (L.D.); the Society of Memorial Sloan Kettering
   (MSK) research grant (L.D.); and MSK Technology Development Fund (L.D.).
   L.D. is the recipient of a Physician-Scientist Career Development Award
   from the Dermatology Foundation and a research scholar from American
   Skin Association. S.S. is an American Cancer Society Research professor.
   C.S.-T. was supported by the 2014 Carolyn L. Kuckein Student Research
   Fellowship. D.Z. is a Bart A. Kamen Fellow of the Damon Runyon Cancer
   Research Foundation. This work was supported, in part, by Swim Across
   America (J.D.W. and T.M.), Ludwig Institute for Cancer Research (J.D.W.
   and T.M.), and National Cancer Institute grant R01 CA56821 (J.D.W.).
   This research was also funded, in part, through the NIH/National Cancer
   Institute Cancer Center Support Grant P30 CA008748.
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NR 45
TC 92
Z9 106
U1 1
U2 19
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 2470-9468
J9 SCI IMMUNOL
JI Sci. Immunol.
PD MAY
PY 2017
VL 2
IS 11
AR eaal1713
DI 10.1126/sciimmunol.aal1713
PG 15
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA GI4BD
UT WOS:000434315000004
PM 28763795
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Iskit, S
   Lieftink, C
   Halonen, P
   Shahrabi, A
   Possik, PA
   Beijersbergen, RL
   Peeper, DS
AF Iskit, Sedef
   Lieftink, Cor
   Halonen, Pasi
   Shahrabi, Aida
   Possik, Patricia A.
   Beijersbergen, Roderick L.
   Peeper, Daniel S.
TI Integrated <i>in</i> <i>vivo</i> genetic and pharmacologic screening
   identifies co-inhibition of EGRF and ROCK as a potential treatment
   regimen for triple-negative breast cancer
SO ONCOTARGET
LA English
DT Article
DE in vivo screen; targeted therapy; TNBC; EGFR; ROCK
ID COLON-CANCER; THERAPEUTIC TARGET; RHO-KINASE/ROCK; RNAI SCREEN;
   THERAPIES; ACTIVATION; PATHWAY; FASUDIL; AKT; PHOSPHATASES
AB Breast cancer is the second most common cause of cancer-related deaths worldwide among women. Despite several therapeutic options, 15% of breast cancer patients succumb to the disease owing to tumor relapse and acquired therapy resistance. Particularly in triple-negative breast cancer (TNBC), developing effective treatments remains challenging owing to the lack of a common vulnerability that can be exploited by targeted approaches. We have previously shown that tumor cells have different requirements for growth in vivo than in vitro. Therefore, to discover novel drug targets for TNBC, we performed parallel in vivo and in vitro genetic shRNA dropout screens. We identified several potential drug targets that were required for tumor growth in vivo to a greater extent than in vitro. By combining pharmacologic inhibitors acting on a subset of these candidates, we identified a synergistic interaction between EGFR and ROCK inhibitors. This combination effectively reduced TNBC cell growth by inducing cell cycle arrest. These results illustrate the power of in vivo genetic screens and warrant further validation of EGFR and ROCK as combined pharmacologic targets for breast cancer.
C1 [Iskit, Sedef; Shahrabi, Aida; Peeper, Daniel S.] Netherlands Canc Inst, Dept Mol Oncol, Plesmanlaan, Amsterdam, Netherlands.
   [Lieftink, Cor; Beijersbergen, Roderick L.] Netherlands Canc Inst, Dept Mol Carcinogenesis, Plesmanlaan, Amsterdam, Netherlands.
   [Halonen, Pasi] BioFocus, Drug Discovery Res & Screening Serv, Darwinweg, Leiden, Netherlands.
   [Possik, Patricia A.] Brazilian Natl Canc Inst, Rua Andre Cavalcanti, Rio De Janeiro, Brazil.
C3 Netherlands Cancer Institute; Netherlands Cancer Institute; National
   Cancer Institute (Inca)
RP Peeper, DS (corresponding author), Netherlands Canc Inst, Dept Mol Oncol, Plesmanlaan, Amsterdam, Netherlands.
EM d.peeper@nki.nl
RI Peeper, Daniel/AAA-2430-2020; Possik, Patricia/K-3949-2014
OI Abrao Possik, Patricia/0000-0003-2899-0969; Beijersbergen,
   Roderick/0000-0003-0116-4130
FU Dutch Cancer Society [2009-4552]
FX The authors would like to thank Prof. Sabine Linn for advice and all the
   members of the Peeper Laboratory for their valuable input. We would also
   like to acknowledge the Sequencing Core Facility and Animal Caretakers
   for their assistance. This work was financially supported by a grant
   from the Dutch Cancer Society (2009-4552) to SI and DP. DP is also the
   recipient of a Queen Wilhelmina Award by the Dutch Cancer Society.
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NR 60
TC 11
Z9 14
U1 0
U2 1
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 JUL 12
PY 2016
VL 7
IS 28
BP 42859
EP 42872
DI 10.18632/oncotarget.10230
PG 14
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DY8QU
UT WOS:000385395700002
PM 27374095
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Nian, ZK
   Deng, M
   Ye, LL
   Tong, XY
   Xu, YX
   Xu, YL
   Chen, RY
   Wang, YL
   Mao, FY
   Xu, CY
   Lu, RA
   Mao, YC
   Xu, HL
   Shen, X
   Xue, XY
   Guo, GQ
AF Nian, Zekai
   Deng, Ming
   Ye, Lele
   Tong, Xinya
   Xu, Yixi
   Xu, Yiliu
   Chen, Ruoyao
   Wang, Yulin
   Mao, Feiyang
   Xu, Chenyv
   Lu, Ruonan
   Mao, Yicheng
   Xu, Hanlu
   Shen, Xian
   Xue, Xiangyang
   Guo, Gangqiang
TI RNA epigenetic modifications in digestive tract cancers: Friends or foes
SO PHARMACOLOGICAL RESEARCH
LA English
DT Article
DE RNA modifications; Crosstalk; Clinical perspectives; Digestive tract
   cancers; Targeted therapy
ID COLORECTAL-CANCER; HEPATOCELLULAR-CARCINOMA; M(6)A MODIFICATION;
   NONCODING RNAS; PROMOTES; METTL3; CELLS; N-6-METHYLADENOSINE;
   METASTASIS; INHIBITORS
AB Digestive tract cancers are among the most common malignancies worldwide and have high incidence and mortality rates. Thus, the discovery of more effective diagnostic and therapeutic targets is urgently required. The development of technologies to accurately detect RNA modification has led to the identification of numerous RNA chemical modifications in humans (epitranscriptomics) that are involved in the occurrence and development of digestive tract cancers. RNA modifications can cooperatively regulate gene expression to facilitate normal physiological functions of the digestive system. However, the dysfunction of relevant RNA-modifying enzymes ("writers," "erasers," and "readers") can lead to the development of digestive tract cancers. Consequently, targeting dysregulated enzyme activity could represent a potent therapeutic strategy for the treatment of digestive tract cancers. In this review, we summarize the most widely studied roles and mechanisms of RNA modifications (m6A, m1A, m5C, m7G, A-to-I editing, pseudouridine ['P]) in relation to digestive tract cancers, highlight the crosstalk between RNA modifications, and discuss their roles in the interactions between the digestive system and microbiota during carcinogenesis. The clinical significance of novel therapeutic methods based on RNA-modifying enzymes is also discussed. This review will help guide future research into digestive tract cancers that are resistant to current therapeutics.
C1 [Nian, Zekai; Chen, Ruoyao; Mao, Feiyang] Wenzhou Med Univ, Clin Coll 2, Wenzhou, Peoples R China.
   [Deng, Ming; Wang, Yulin] Wenzhou Med Univ, Sch Publ Hlth, Wenzhou, Peoples R China.
   [Ye, Lele; Tong, Xinya; Xu, Chenyv; Xue, Xiangyang; Guo, Gangqiang] Wenzhou Med Univ, Dept Microbiol & Immunol, Sch Basic Med Sci,Inst Mol Virol & Immunol,Inst Tr, Wenzhou Key Lab Canc Related Pathogens & Immun,Wen, Wenzhou, Peoples R China.
   [Xu, Yixi] Hangzhou Normal Univ, Sch Publ Adm, Hangzhou, Peoples R China.
   [Xu, Yiliu] Jiangsu Univ, Res Ctr Fluid Machinery Engn & Technol, Zhenjiang, Peoples R China.
   [Lu, Ruonan] Wenzhou Med Univ, Clin Coll 1, Wenzhou, Peoples R China.
   [Mao, Yicheng; Xu, Hanlu] Wenzhou Med Univ, Ophthalmol Coll, Wenzhou, Peoples R China.
   [Shen, Xian] Wenzhou Med Univ, Affiliated Hosp 1, Dept Gen Surg, Wenzhou, Peoples R China.
C3 Wenzhou Medical University; Wenzhou Medical University; Wenzhou Medical
   University; Hangzhou Normal University; Jiangsu University; Wenzhou
   Medical University; Wenzhou Medical University; Wenzhou Medical
   University
RP Xue, XY; Guo, GQ (corresponding author), Wenzhou Med Univ, Dept Microbiol & Immunol, Sch Basic Med Sci,Inst Mol Virol & Immunol,Inst Tr, Wenzhou Key Lab Canc Related Pathogens & Immun,Wen, Wenzhou, Peoples R China.; Shen, X (corresponding author), Wenzhou Med Univ, Affiliated Hosp 1, Dept Gen Surg, Wenzhou, Peoples R China.
EM shenxian@wmu.edu.cn; wzxxy001@163.com; gangqiangg@wmu.edu.cn
RI xu, hanlu/KBQ-0603-2024; ye, lele/HLW-0156-2023
OI zhan, ze kai/0009-0003-0016-7580
FU National Natural Science Foundation of China [32200476]; Zhejiang
   Provincial Natural Science Foundation of China [LQ23C060002]; Wenzhou
   Municipal Science and Technology Bureau [Y20220044]; National Innovation
   and Entrepreneurship Training Program for College Students
   [202210343023]; College Students' Science and Technology Innovation
   Project of Zhejiang Province [2022R413B071]; Key Incubation College
   Students Team for Innovation and Entrepreneurship of the Second Clinical
   College of Wenzhou Medical University [WMLEFH2022004]
FX This work was supported by the National Natural Science Foundation of
   China (grant number 32200476) , Zhejiang Provincial Natural Science
   Foundation of China (grant number LQ23C060002) , Wenzhou Munic- ipal
   Science and Technology Bureau (grant number Y20220044) , National
   Innovation and Entrepreneurship Training Program for College Students
   (grant number 202210343023) , College Students' Science and Technology
   Innovation Project of Zhejiang Province (grant number 2022R413B071) ,
   and Key Incubation College Students Team for Inno- vation and
   Entrepreneurship of the Second Clinical College of Wenzhou Medical
   University (grant number WMLEFH2022004) .
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NR 181
TC 1
Z9 1
U1 7
U2 7
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
EI 1096-1186
J9 PHARMACOL RES
JI Pharmacol. Res.
PD AUG
PY 2024
VL 206
AR 107280
DI 10.1016/j.phrs.2024.107280
EA JUN 2024
PG 14
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA XI1T1
UT WOS:001260968100001
PM 38914382
OA hybrid
DA 2025-01-04
ER

PT J
AU Ando, T
   Sakumura, M
   Mihara, H
   Fujinami, H
   Yasuda, I
AF Ando, Takayuki
   Sakumura, Miho
   Mihara, Hiroshi
   Fujinami, Haruka
   Yasuda, Ichiro
TI A Review of Potential Role of Capsule Endoscopy in the Work-Up for
   Chemotherapy-Induced Diarrhea
SO HEALTHCARE
LA English
DT Article
DE chemotherapy-induced diarrhea; fluoropyrimidine; capsule endoscopy;
   small intestinal mucosal injury; gastrointestinal cancer
ID METASTATIC COLORECTAL-CANCER; PHASE-III TRIAL; INTESTINAL MUCOSAL
   INJURY; FOLFIRI PLUS BEVACIZUMAB; OPEN-LABEL; 1ST-LINE TREATMENT;
   DOUBLE-BLIND; GASTROESOPHAGEAL JUNCTION; RANDOMIZED-TRIAL;
   HEPATOCELLULAR-CARCINOMA
AB Chemotherapy-induced diarrhea (CID) is a common, severe side effect of chemotherapy, immunotherapy, and targeted therapy. Because patients are more prone to continuing chemotherapy if they do not suffer from CID, appropriate diagnosis and monitoring of this disease are essential. However, suitable monitoring methods are yet to be developed. To date, several studies have shown that small-bowel capsule endoscopy (SBCE) is useful in visualizing the entire small intestinal mucosa and detecting small intestinal abnormalities, including bleeding, malignant tumors, and mucosal injury, associated with the use of nonsteroidal anti-inflammatory drugs and low-dose aspirin. Currently, limited studies have evaluated the small intestinal mucosa using SBCE in patients receiving fluoropyrimidine-based chemotherapy or immune checkpoint inhibitors. These studies have reported that small intestinal mucosal injury is common in patients with severe fluoropyrimidine-induced diarrhea. SBCE might be a useful screening method for the early detection of enterocolitis induced by immune checkpoint inhibitors. SBCE may be a powerful tool for the diagnosis and monitoring of CID, and understanding its indication, contraindication, and capsule-retention risk for each patient is important for clinicians.
C1 [Ando, Takayuki; Sakumura, Miho; Mihara, Hiroshi; Fujinami, Haruka; Yasuda, Ichiro] Univ Toyama, Fac Med, Dept Internal Med 3, Toyama 9300194, Japan.
C3 University of Toyama
RP Ando, T (corresponding author), Univ Toyama, Fac Med, Dept Internal Med 3, Toyama 9300194, Japan.
EM taando33@gmail.com; princess_and_pea_78@yahoo.co.jp; m164.tym@gmail.com;
   haruka52@med.u-toyama.ac.jp; yasudaich@gmail.com
RI Mihara, Hiroshi/ISU-2768-2023; Fujinami, Haruka/HJA-1887-2022; Yasuda,
   Ichiro/IUP-0131-2023
OI Yasuda, Ichiro/0000-0002-6888-0310; Fujinami, Haruka/0000-0003-4410-6272
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NR 118
TC 2
Z9 3
U1 0
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9032
J9 HEALTHCARE-BASEL
JI Healthcare
PD FEB
PY 2022
VL 10
IS 2
AR 218
DI 10.3390/healthcare10020218
PG 15
WC Health Care Sciences & Services; Health Policy & Services
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Health Care Sciences & Services
GA ZI1SA
UT WOS:000761407000001
PM 35206833
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU El-Nakeep, S
   Rashad, N
   Oweira, H
   Schmidt, J
   Helbling, D
   Giryes, A
   Petrausch, U
   Mehrabi, A
   Decker, M
   Abdel-Rahman, O
AF El-Nakeep, Sarah
   Rashad, Noha
   Oweira, Hani
   Schmidt, Jan
   Helbling, Daniel
   Giryes, Anwar
   Petrausch, Ulf
   Mehrabi, Arianeb
   Decker, Michael
   Abdel-Rahman, Omar
TI Intraperitoneal chemotherapy and cytoreductive surgery for peritoneal
   metastases coupled with curative treatment of colorectal liver
   metastases: an updated systematic review
SO EXPERT REVIEW OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
DE HIPEC; hepatic resection; cytoreduction; colorectal cancer; peritoneal
   carcinomatosis; combined modality
ID HIGH-RISK; CARCINOMATOSIS; CANCER; MANAGEMENT; ORIGIN; HIPEC;
   DISSEMINATION; BEVACIZUMAB; RESECTION; DISEASE
AB Introduction: We aimed to assess the efficacy and safety of delivering intraperitoneal chemotherapy and cytoreductive surgery for peritoneal metastases coupled with curative treatment of colorectal liver metastases.Areas covered: A comprehensive literature search using PubMed was conducted to screen for eligible records. Studies evaluating colorectal surgery and intraperitoneal chemotherapy combined with curative treatment of liver metastases were included. We excluded duplicate publications. Sixty-seven full-text papers were assessed and six papers were finally included. The overall survival in the included studies ranged from 6-49months. Five-year survival ranged from 18%-28%, three-year survival ranged from 22%-42% and two-year survival ranged from 34%-78%. Survival was lower in patients with liver metastases and peritoneal carcinomatosis (PC) than those with PC alone in the majority of studies.Expert commentary: This review poses questions rather than presenting answers. The heterogeneity of survival data suggests the possible benefit of this aggressive treatment approach in selected patients. Standardization of the technique used for intraperitoneal chemotherapy instillation, agent used as well as the systemic chemotherapy and targeted therapy type and duration through prospective controlled trials is required to provide an evidence of a higher strength to support or prohibit this treatment strategy.
C1 [El-Nakeep, Sarah] Ain Shams Univ, Div Gastroenterol & Hepatol, Dept Internal Med, Fac Med, Cairo, Egypt.
   [Rashad, Noha] Maadi Mil Hosp, Dept Med Oncol, Cairo, Egypt.
   [Oweira, Hani; Giryes, Anwar; Decker, Michael; Abdel-Rahman, Omar] Swiss Canc Inst, Dept Surg, Zurich, Switzerland.
   [Oweira, Hani; Schmidt, Jan; Mehrabi, Arianeb] Heidelberg Univ, Dept Gen Visceral & Transplant Surg, Heidelberg, Germany.
   [Helbling, Daniel; Petrausch, Ulf] Gastrointestinal Tumor Ctr Zurich GITZ, Dept Surg, OncoCtr Zurich, Zurich, Switzerland.
   [Abdel-Rahman, Omar] Ain Shams Univ, Dept Clin Oncol, Fac Med, Cairo, Egypt.
C3 Egyptian Knowledge Bank (EKB); Ain Shams University; Ruprecht Karls
   University Heidelberg; Egyptian Knowledge Bank (EKB); Ain Shams
   University
RP Rashad, N (corresponding author), Mil Med Acad, Maadi Armed Forces Med Compound, Dept Med Oncol, Cairo, Egypt.
EM omar.abdelrhman@med.asu.edu.eg
RI El-Nakeep, Sarah/AAY-8687-2020; Oweira, Hani/AAQ-4102-2020; Rashad,
   Noha/JGD-9104-2023; Schmidt, Jan/JOZ-2184-2023
OI Rashad, Noha/0000-0002-3684-9271; El-Nakeep, Sarah/0000-0003-2830-5052
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NR 50
TC 20
Z9 21
U1 1
U2 9
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1747-4124
EI 1747-4132
J9 EXPERT REV GASTROENT
JI Expert Rev. Gastroenterol. Hepatol.
PD MAR
PY 2017
VL 11
IS 3
BP 249
EP 258
DI 10.1080/17474124.2017.1284586
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA EM1OY
UT WOS:000395088100007
PM 28099818
DA 2025-01-04
ER

PT J
AU Wang, Q
AF Wang, Qing
TI Cancer predisposition genes: molecular mechanisms and clinical impact on
   personalized cancer care: examples of Lynch and HBOC syndromes
SO ACTA PHARMACOLOGICA SINICA
LA English
DT Review
DE hereditary cancers; cancer predisposition genes; cancer susceptibility;
   Lynch syndrome; breast and ovary cancer syndrome; biomarkers
ID DNA MISMATCH REPAIR; MICROSATELLITE INSTABILITY; COLORECTAL-CANCER;
   POLY(ADP-RIBOSE) POLYMERASE; HOMOLOGOUS RECOMBINATION; HEREDITARY
   CANCER; EARLY-ONSET; MUTATIONS; OVARIAN; MLH1
AB Up to 10% of cancers occur through the inherited mutation of a group of genes called cancer predisposition genes. Individuals who carry a mutant allele of these genes have an increased susceptibility to cancer. A growing number of cancer susceptibility genes are being identified, and the physiopathology of germline mutation-based cancer development is also being elucidated with accumulating clinical and molecular data. More importantly, the identification of familial mutations has become routine practice, which is a perfect example of bench-to-bed translational medicine. Recently, other clinical applications of predisposition genes have been exploited, especially as efficient biomarkers predicting prognosis or response to treatment. Thus, it appears interesting to give an overview of the advances and impacts of predisposition genes in personalized cancer care by taking representative and common cancer syndromes as examples: Lynch syndrome for the first example, which is related to cancer susceptibility, and breast and ovary cancer syndrome for the second example, which involves BRCA deficiency-related targeted therapy.
C1 [Wang, Qing] Leon Berard Comprehens Canc Ctr, Lab Constitut Genet Frequent Canc HCL CLB, Mol Biol Platform, Lyon, France.
C3 UNICANCER; Centre Leon Berard
RP Wang, Q (corresponding author), Leon Berard Comprehens Canc Ctr, Lab Constitut Genet Frequent Canc HCL CLB, Mol Biol Platform, Lyon, France.
EM qing.wang@lyon.unicancer.fr
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NR 51
TC 32
Z9 37
U1 1
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1671-4083
EI 1745-7254
J9 ACTA PHARMACOL SIN
JI Acta Pharmacol. Sin.
PD FEB
PY 2016
VL 37
IS 2
BP 143
EP 149
DI 10.1038/aps.2015.89
PG 7
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA DE5NG
UT WOS:000370677100001
PM 26616728
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Zanzonico, P
   Carrasquillo, JA
   Pandit-Taskar, N
   O'Donoghue, JA
   Humm, JL
   Smith-Jones, P
   Ruan, S
   Divgi, C
   Scott, AM
   Kemeny, NE
   Fong, YM
   Wong, D
   Scheinberg, D
   Ritter, G
   Jungbluth, A
   Old, LJ
   Larson, SM
AF Zanzonico, Pat
   Carrasquillo, Jorge A.
   Pandit-Taskar, Neeta
   O'Donoghue, Joseph A.
   Humm, John L.
   Smith-Jones, Peter
   Ruan, Shutian
   Divgi, Chaitanya
   Scott, Andrew M.
   Kemeny, Nancy E.
   Fong, Yuman
   Wong, Douglas
   Scheinberg, David
   Ritter, Gerd
   Jungbluth, Achem
   Old, Lloyd J.
   Larson, Steven M.
TI PET-based compartmental modeling of <SUP>124</SUP>I-A33 antibody:
   quantitative characterization of patient-specific tumor targeting in
   colorectal cancer
SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
LA English
DT Article
DE A33; Iodine-124; Modeling; PET
ID PHASE-I; A33 ANTIGEN; COLON-CANCER; SAAM II; BINDING; XENOGRAFT;
   SOFTWARE; TRIAL; I/II
AB Purpose The molecular specificity of monoclonal antibodies (mAbs) directed against tumor antigens has proven effective for targeted therapy of human cancers, as shown by a growing list of successful antibody-based drug products. We describe a novel, nonlinear compartmental model using PET-derived data to determine the "best-fit" parameters and model-derived quantities for optimizing biodistribution of intravenously injected I-124-labeled antitumor antibodies.
   Methods As an example of this paradigm, quantitative image and kinetic analyses of anti-A33 humanizedmAb (also known as "A33") were performed in 11 colorectal cancer patients. Serial whole-body PET scans of I-124-labeled A33 and blood samples were acquired and the resulting tissue time-activity data for each patient were fit to a nonlinear compartmental model using the SAAM II computer code.
   Results Excellent agreement was observed between fitted and measured parameters of tumor uptake, "off-target" uptake in bowel mucosa, blood clearance, tumor antigen levels, and percent antigen occupancy.
   Conclusion This approach should be generally applicable to antibody-antigen systems in human tumors for which the masses of antigen-expressing tumor and of normal tissues can be estimated and for which antibody kinetics can be measured with PET. Ultimately, based on each patient's resulting "best-fit" nonlinear model, a patient-specific optimum mAb dose (in micromoles, for example) may be derived.
C1 [Zanzonico, Pat; O'Donoghue, Joseph A.; Humm, John L.] Mem Sloan Kettering Canc Ctr, Dept Med Phys, New York, NY 10021 USA.
   [Carrasquillo, Jorge A.; Pandit-Taskar, Neeta; Smith-Jones, Peter; Ruan, Shutian; Larson, Steven M.] Mem Sloan Kettering Canc Ctr, Dept Radiol, New York, NY 10021 USA.
   [Divgi, Chaitanya] Columbia Univ, Med Ctr, New York, NY USA.
   [Scott, Andrew M.] La Trobe Univ, Olivia Newton John Canc Res Inst, Melbourne, Vic, Australia.
   [Kemeny, Nancy E.; Wong, Douglas; Scheinberg, David] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10021 USA.
   [Fong, Yuman] Mem Sloan Kettering Canc Ctr, Dept Surg, New York, NY 10021 USA.
   [Ritter, Gerd; Jungbluth, Achem; Old, Lloyd J.] Mem Sloan Kettering Canc Ctr, Ludwig Inst Canc Res, New York, NY 10021 USA.
C3 Memorial Sloan Kettering Cancer Center; Memorial Sloan Kettering Cancer
   Center; Columbia University; La Trobe University; Olivia Newton-John
   Cancer Research Institute; Memorial Sloan Kettering Cancer Center;
   Memorial Sloan Kettering Cancer Center; Ludwig Institute for Cancer
   Research; Memorial Sloan Kettering Cancer Center
RP Zanzonico, P (corresponding author), Mem Sloan Kettering Canc Ctr, Dept Med Phys, 1275 York Ave, New York, NY 10021 USA.
EM zanzonip@mskcc.org
RI Carrasquillo, Jorge/E-7120-2010
OI Scott, Andrew/0000-0002-6656-295X; Carrasquillo,
   Jorge/0000-0002-8513-5734; O'Donoghue, Joseph A/0000-0002-2761-0015
FU Ludwig Center for Cancer Immunotherapy; National Institutes of Health
   (NIH) [P50 CA 86438-11, PO1 CA 33049]
FX This study was supported by the Ludwig Center for Cancer Immunotherapy
   and National Institutes of Health (NIH) grant numbers P50 CA 86438-11
   and PO1 CA 33049.
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NR 26
TC 11
Z9 12
U1 1
U2 14
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 OCT
PY 2015
VL 42
IS 11
BP 1700
EP 1706
DI 10.1007/s00259-015-3061-2
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA CS3SV
UT WOS:000361996100011
PM 26194713
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Alburquerque-González, B
   Bernabé-García, M
   Montoro-García, S
   Bernabé-García, A
   Rodrigues, PC
   Sanz, JR
   López-Calderón, FF
   Luque, I
   Nicolas, FJ
   Cayuela, ML
   Salo, T
   Pérez-Sánchez, H
   Conesa-Zamora, P
AF Alburquerque-Gonzalez, Begona
   Bernabe-Garcia, Manuel
   Montoro-Garcia, Silvia
   Bernabe-Garcia, Angel
   Rodrigues, Priscila Campioni
   Ruiz Sanz, Javier
   Lopez-Calderon, Fernando F.
   Luque, Irene
   Nicolas, Francisco Jose
   Cayuela, Maria Luisa
   Salo, Tuula
   Perez-Sanchez, Horacio
   Conesa-Zamora, Pablo
TI New role of the antidepressant imipramine as a Fascin1 inhibitor in
   colorectal cancer cells
SO EXPERIMENTAL AND MOLECULAR MEDICINE
LA English
DT Article
ID BASAL-LIKE PHENOTYPE; EXPRESSION; MIGRATION; ADENOCARCINOMA; METASTASIS;
   MUTATIONS; INVASION; PROFILE; MARKER; SHOWS
AB Colorectal cancer: Antitumor antidepressant The antidepressant drug imipramine can block the activity of a protein that contributes to the progression of certain aggressive tumors. Serrated adenocarcinoma (SAC) is a form of colorectal cancer with a poor prognosis. A key factor in SAC development is the overexpression of the protein fascin1, which promotes the formation of structures that help cancer cells move around, thereby leading to metastasis. Pablo Conesa-Zamora at Santa Lucia University Hospital in Cartagena, Horacio Perez-Sanchez at the Universidad Catolica de Murcia in Guadalupe, Spain, and coworkers demonstrated that imipramine shows promise in binding to fascin1 and blocking its activity. The team analyzed over 9500 compounds as potential fascin1 blockers, identifying imipramine as a possible option. In tests on human tissues and in vivo studies using zebrafish, the drug reduced cancer invasion and metastasis.
   Serrated adenocarcinoma (SAC) is more invasive, has worse outcomes than conventional colorectal carcinoma (CRC), and is characterized by frequent resistance to anti-epidermal growth factor receptor (EGFR) and overexpression of fascin1, a key protein in actin bundling that plays a causative role in tumor invasion and is overexpressed in different cancer types with poor prognosis. In silico screening of 9591 compounds, including 2037 approved by the Food and Drug Administration (FDA), was performed, and selected compounds were analyzed for their fascin1 binding affinity by differential scanning fluorescence. The results were compared with migrastatin as a typical fascin1 inhibitor. In silico screening and differential scanning fluorescence yielded the FDA-approved antidepressant imipramine as the most evident potential fascin1 blocker. Biophysical and different in vitro actin-bundling assays confirm this activity. Subsequent assays investigating lamellipodia formation and migration and invasion of colorectal cancer cells in vitro using 3D human tissue demonstrated anti-fascin1 and anti-invasive activities of imipramine. Furthermore, expression profiling suggests the activity of imipramine on the actin cytoskeleton. Moreover, in vivo studies using a zebrafish invasion model showed that imipramine is tolerated, its anti-invasive and antimetastatic activities are dose-dependent, and it is associated with both constitutive and induced fascin1 expression. This is the first study that demonstrates an antitumoral role of imipramine as a fascin1 inhibitor and constitutes a foundation for a molecular targeted therapy for SAC and other fascin1-overexpressing tumors.
C1 [Alburquerque-Gonzalez, Begona; Lopez-Calderon, Fernando F.; Conesa-Zamora, Pablo] UCAM Univ Catolica San Antonio Murcia, Pathol & Histol Dept, Fac Ciencias Salud, Campus Jeronimos S-N, Murcia 30107, Spain.
   [Bernabe-Garcia, Manuel] Hosp Clin Univ Virgen Arrixaca, Res Grp Telomerasa Envejecimiento & Canc, CIBERehd, Murcia, Spain.
   [Montoro-Garcia, Silvia; Nicolas, Francisco Jose] UCAM Univ Catolica San Antonio Murcia, Fac Ciencias Salud, Cell Culture Lab, Campus Jeronimos S-N, Murcia 30107, Spain.
   [Bernabe-Garcia, Angel; Cayuela, Maria Luisa] Hosp Clin Univ Virgen Arrixaca Carretera Madrid C, Res Grp Regenerac Oncol Mol & TGF, Inst Biohlth Res Murcia IMIB, El Palmar, Spain.
   [Rodrigues, Priscila Campioni; Salo, Tuula] Univ Oulu, Canc Res & Translat Med Res Unit, Aapistie 5A, FI-90220 Oulu, Finland.
   [Rodrigues, Priscila Campioni; Salo, Tuula] Univ Oulu, Oulu Univ Hosp, Med Res Ctr Oulu, Oulu, Finland.
   [Ruiz Sanz, Javier; Luque, Irene] Univ Granada, Dept Phys Chem, Campus Fuentenueva S-N, E-18071 Granada, Spain.
   [Ruiz Sanz, Javier; Luque, Irene] Univ Granada, Inst Biotechnol, Campus Fuentenueva S-N, E-18071 Granada, Spain.
   [Salo, Tuula] Univ Helsinki, Inst Oral & Maxillofacial Dis, Helsinki, Finland.
   [Salo, Tuula] Helsinki Univ Hosp, Dept Pathol, HUSLAB, Helsinki, Finland.
   [Perez-Sanchez, Horacio] Univ Catolica Murcia UCAM, Struct Bioinformat & High Performance Comp BIO HP, Guadalupe, Spain.
   [Conesa-Zamora, Pablo] Hosp Univ Santa Lucia, Clin Anal Dept, Grp Mol Pathol & Pharmacogenet, Inst Biohlth Res Murcia IMIB, C Mezquita Sn, Cartagena 30202, Spain.
   [Conesa-Zamora, Pablo] C Mezquita S-N CP, Murcia 30202, Spain.
C3 Universidad Catolica de Murcia; Hospital Clinico Universitario Virgen de
   la Arrixaca; CIBER - Centro de Investigacion Biomedica en Red; CIBEREHD;
   Universidad Catolica de Murcia; University of Oulu; University of Oulu;
   University of Granada; University of Granada; University of Helsinki;
   University of Helsinki; Helsinki University Central Hospital;
   Universidad Catolica de Murcia
RP Conesa-Zamora, P (corresponding author), UCAM Univ Catolica San Antonio Murcia, Pathol & Histol Dept, Fac Ciencias Salud, Campus Jeronimos S-N, Murcia 30107, Spain.; Pérez-Sánchez, H (corresponding author), Univ Catolica Murcia UCAM, Struct Bioinformat & High Performance Comp BIO HP, Guadalupe, Spain.; Conesa-Zamora, P (corresponding author), Hosp Univ Santa Lucia, Clin Anal Dept, Grp Mol Pathol & Pharmacogenet, Inst Biohlth Res Murcia IMIB, C Mezquita Sn, Cartagena 30202, Spain.; Conesa-Zamora, P (corresponding author), C Mezquita S-N CP, Murcia 30202, Spain.
EM hperez@ucam.edu; pablo.conesa@carm.es
RI , tuula/ABG-2051-2021; cayuela, maria/S-1148-2019; Montoro-García,
   Silvia/K-8101-2014; Nicolás, Francisco/H-9422-2019; Bernabé-García,
   Ángel/AAB-2934-2020; Pérez-Sánchez, Horacio/O-5017-2016; Alburquerque
   González, Begoña/HKW-3633-2023; Luque, Irene/K-4758-2012
OI Conesa-Zamora, Pablo/0000-0003-0190-3044; Ruiz Sanz,
   Javier/0000-0002-4336-1274; Luque, Irene/0000-0003-2757-4779;
   Bernabe-Garcia, Angel/0000-0002-2266-5949; Salo,
   Tuula/0000-0001-6039-0088; Alburquerque Gonzalez,
   Begona/0000-0003-3413-5889; Nicolas, Francisco Jose/0000-0002-3969-1430;
   Bernabe Garcia, Manuel/0000-0003-4334-0059
FU Instituto de Salud Carlos III (Spanish Ministry of Health); FEDER funds
   [PI15/00626]; UCAM; Fundacion Seneca; Sigrid Juselius Foundation;
   Finnish Cultural Foundation
FX We are grateful to Dr. Milind Valdya from the Advanced Centre for
   Treatment Research and Education in Cancer (Maharashtra, India) for
   kindly providing us with the vectors used in the transfection assay; to
   Dr. Steven Almo from Albert Einstein College of Medicine (New York, USA)
   for kindly providing purified fascin1 protein; to Dr. Antonio Parrado
   from Genomic Platform, Institute for Biohealth Research from Murcia
   Region (IMIB), for bioinformatic support; and to Dr. Diego Arcas for
   revising the English version of the manuscript. This work is supported
   by the Instituto de Salud Carlos III (Spanish Ministry of Health) and
   FEDER funds (ref: PI15/00626). B.A.-G. belongs to the "Programa de
   Doctorado en ciencias de la Salud" from the Catholic University of
   Murcia (UCAM) and holds a predoctoral grant from UCAM. S.M.-G. was
   supported by the Fundacion Seneca and PCR by the Finnish Cultural and
   Sigrid Juselius Foundations (2017-2018 and 2018-2019 grants).
CR [Anonymous], BIOMED J SCI TECH RE, DOI DOI 10.26717/BJSTR.2018.04.001118
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NR 30
TC 39
Z9 43
U1 0
U2 12
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 1226-3613
EI 2092-6413
J9 EXP MOL MED
JI Exp. Mol. Med.
PD FEB
PY 2020
VL 52
IS 2
BP 281
EP 292
DI 10.1038/s12276-020-0389-x
EA FEB 2020
PG 12
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine
GA KU3LJ
UT WOS:000514763500001
PM 32080340
OA gold, Green Published
DA 2025-01-04
ER

PT S
AU Moore, PC
   Henderson, KW
   Classon, M
AF Moore, Paul C.
   Henderson, Kurt W.
   Classon, Marie
BE Landry, JW
   Das, SK
   Fisher, PB
TI The epigenome and the many facets of cancer drug tolerance
SO EPIGENETIC REGULATION OF CANCER IN RESPONSE TO CHEMOTHERAPY
SE Advances in Cancer Research
LA English
DT Article; Book Chapter
ID CELL LUNG-CANCER; STEM-CELLS; TARGETED THERAPY; PROSTATE-CANCER;
   BREAST-CANCER; COLON-CANCER; MESENCHYMAL TRANSITION;
   ACQUIRED-RESISTANCE; INTRATUMORAL HETEROGENEITY; BRAF(V600E) INHIBITION
AB The use of chemotherapeutic agents and the development of new cancer therapies over the past few decades has consequently led to the emergence of myriad therapeutic resistance mechanisms. Once thought to be explicitly driven by genetics, the coupling of reversible sensitivity and absence of pre-existing mutations in some tumors opened the way for discovery of drug-tolerant persisters (DTPs): slow-cycling subpopulations of tumor cells that exhibit reversible sensitivity to therapy. These cells confer multi-drug tolerance, to targeted and chemotherapies alike, until the residual disease can establish a stable, drug-resistant state. The DTP state can exploit a multitude of distinct, yet interlaced, mechanisms to survive otherwise lethal drug exposures. Here, we categorize these multi-faceted defense mechanisms into unique Hallmarks of Cancer Drug Tolerance. At the highest level, these are comprised of heterogeneity, signaling plasticity, differentiation, proliferation/metabolism, stress management, genomic integrity, crosstalk with the tumor microenvironment, immune escape, and epigenetic regulatory mechanisms. Of these, epigenetics was both one of the first proposed means of non-genetic resistance and one of the first discovered. As we describe in this review, epigenetic regulatory factors are involved in most facets of DTP biology, positioning this hallmark as an overarching mediator of drug tolerance and a potential avenue to novel therapies.
C1 [Moore, Paul C.; Henderson, Kurt W.; Classon, Marie] Pfizer Ctr Therapeut Innovat, San Francisco, CA 94080 USA.
C3 Pfizer
RP Classon, M (corresponding author), Pfizer Ctr Therapeut Innovat, San Francisco, CA 94080 USA.
EM marie.classon@pfizer.com
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NR 229
TC 3
Z9 3
U1 0
U2 3
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0065-230X
EI 2162-5557
BN 978-0-443-19418-4
J9 ADV CANCER RES
JI Adv.Cancer Res.
PY 2023
VL 158
BP 1
EP 39
DI 10.1016/bs.acr.2022.12.002
PG 39
WC Oncology; Cell Biology
WE Book Citation Index – Science (BKCI-S)
SC Oncology; Cell Biology
GA BV8BW
UT WOS:001075275900002
PM 36990531
DA 2025-01-04
ER

PT J
AU Tolba, MF
AF Tolba, Mai F.
TI Revolutionizing the landscape of colorectal cancer treatment: The
   potential role of immune checkpoint inhibitors
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Review
DE clinical trials; colon cancer; immune checkpoint inhibitors;
   immunotherapy
ID TUBULIN POLYMERIZATION INHIBITOR; ADHESION MOLECULE ALCAM/CD166;
   PROMOTES CELL-PROLIFERATION; VASCULAR DISRUPTING AGENT; T-CELL; PHASE-I;
   ANTITUMOR-ACTIVITY; HEPATOCELLULAR-CARCINOMA; ACQUIRED-RESISTANCE;
   TARGETING AGENT
AB Colorectal cancer (CRC) represents the third cause of cancer-related mortalities worldwide. The progression of CRC to the metastatic phase significantly compromises the overall survival rates. Despite the advances in the therapeutic protocols, CRC treatment is still challenging. Cancer immunotherapy joined the ranks of surgery, chemotherapy, radiotherapy and targeted therapy as the fifth pillar in the foundation of cancer therapeutics. Interruption of the immunosuppressive signals within the tumor microenvironment and reactivation of antitumor immunity via targeting the molecular immune checkpoints generated promising therapeutic outcomes in several types of hard-to-treat cancers. The year 2017 witnessed the first US Food and Drug Administration (FDA) approval of immune checkpoint inhibitor (ICI) immunotherapy for the management of CRC. The approval was granted to pembrolizumab (anti-PD-1) for the treatment of patients with advanced/metastatic solid malignancies with mismatch-repair deficiency including CRCs. Such natively immunogenic tumors constitute only a minor percentage of all CRCs. Therefore, it is imperative to utilize novel combinatorial regimens to enhance the response of a wider range of CRC tumors to cancer immunotherapy and help in extending the survival rates in patients with advanced/metastatic disease. This review highlights the novel approaches under clinical development to overcome the resistance of CRCs to immunotherapy and improve the therapeutic outcomes.
C1 [Tolba, Mai F.] Ain Shams Univ, Dept Pharmacol & Toxicol, Fac Pharm, Cairo 11566, Egypt.
   [Tolba, Mai F.] Ain Shams Univ, Ctr Drug Discovery Res & Dev, Cairo, Egypt.
C3 Egyptian Knowledge Bank (EKB); Ain Shams University; Egyptian Knowledge
   Bank (EKB); Ain Shams University
RP Tolba, MF (corresponding author), Ain Shams Univ, Dept Pharmacol & Toxicol, Fac Pharm, Cairo 11566, Egypt.
EM tolba.mf@pharma.asu.edu.eg
RI Tolba, Mai/R-8192-2019
OI Tolba, Mai/0000-0002-2559-6299
FU African Academy of Sciences (AAS) through the AAS affiliates' program
   (FY2019-2023)
FX Gratitude is extended to the African Academy of Sciences (AAS) for the
   support provided through the AAS affiliates' program (FY2019-2023).
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NR 107
TC 42
Z9 48
U1 0
U2 11
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 1
PY 2020
VL 147
IS 11
BP 2996
EP 3006
DI 10.1002/ijc.33056
EA JUN 2020
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA NY2JJ
UT WOS:000536717100001
PM 32415713
OA Bronze
DA 2025-01-04
ER

PT J
AU Horikirizono, H
   Ishigaki, K
   Iizuka, K
   Tamura, K
   Sakurai, N
   Terai, K
   Heishima, T
   Yoshida, O
   Asano, K
AF Horikirizono, Hiro
   Ishigaki, Kumiko
   Iizuka, Keigo
   Tamura, Kei
   Sakurai, Naoki
   Terai, Kazuyuki
   Heishima, Tatsuya
   Yoshida, Orie
   Asano, Kazushi
TI Serum vascular endothelial growth factor in dogs with various
   proliferative diseases
SO JOURNAL OF VETERINARY MEDICAL SCIENCE
LA English
DT Article
DE angiogenesis; dog; molecular-targeted therapy; tumor; vascular
   endothelial growth factor
ID METASTATIC COLORECTAL-CANCER; FACTOR VEGF; BREAST-CANCER; TUMOR-MARKER;
   BEVACIZUMAB; EXPRESSION; ANGIOGENESIS; PLASMA; FEATURES; THERAPY
AB Angiogenesis plays an important role in the proliferation and metastasis mechanisms of malignant tumors. Vascular endothelial growth factor (VEGF), a group of cytokines that contribute to angiogenesis and vasculogenesis. This study aimed to investigate the serum VEGF-A concentrations in dogs with various proliferative diseases. A total of 202 dogs that were histopathologically diagnosed with proliferative diseases were included in the study. Serum VEGF-A concentrations were measured using enzyme-linked immunosorbent assay. Median serum VEGF-A concentrations in dogs were as follows: healthy dogs, 4 pg/ml [0???21 pg/ml]; hepatocellular carcinoma, 30 pg/ml [0???158 pg/ml, P=<0.001]; hepatocellular adenoma, 32 pg/ml [0???49 pg/ml, P=0.003]; hepatic nodular hyperplasia, 18 pg/ml [0???51 pg/ml, P=0.595]; adrenal pheochromocytoma, 32 pg/ml [0???187 pg/ml, P=<0.001]; adrenocortical carcinoma, 32 pg/ml [3???161 pg/ml, P=0.002]; adrenocortical adenoma, 27 pg/ml [0???106 pg/ml, P=0.005]; colorectal adenocarcinoma, 36 pg/ml [0???75 pg/ml, P=0.002]; colorectal adenoma, 43 pg/ml [0???48 pg/ml, P=0.144]; inflammatory colorectal polyps, 37 pg/ml [0???111 pg/ml, P=<0.001]; pulmonary adenocarcinoma, 35 pg/ml [4???107 pg/ml, P=0.002]; pulmonary histiocytic sarcoma, 35 pg/ml [0???131 pg/ml, P=0.016]; and follicular thyroid carcinoma, 35 pg/ml [0???106 pg/ml, P=0.009]. The serum VEGF-A concentrations were significantly higher in dogs with neoplastic lesions compared to healthy dogs, except for colorectal adenoma. High serum VEGF-A concentrations were observed in dogs with proliferative diseases. The present study suggests that angiogenesis-inhibiting therapy, which targets VEGF-A, may be useful for canine neoplastic diseases.
C1 [Horikirizono, Hiro; Ishigaki, Kumiko; Iizuka, Keigo; Tamura, Kei; Sakurai, Naoki; Terai, Kazuyuki; Heishima, Tatsuya; Yoshida, Orie; Asano, Kazushi] Nihon Univ, Coll Bioresource Sci, Dept Vet Med, Lab Vet Surg, 1866 Ka Meino, Fujisawa, Kanagawa 2520880, Japan.
   [Horikirizono, Hiro] Yamaguchi Univ, Joint Fac Vet Med, Dept Vet Radiol, Yamaguchi, Japan.
C3 Nihon University; Yamaguchi University
RP Asano, K (corresponding author), Nihon Univ, Coll Bioresource Sci, Dept Vet Med, Lab Vet Surg, 1866 Ka Meino, Fujisawa, Kanagawa 2520880, Japan.
EM asano.kazushi@nihon-u.ac.jp
RI Horikirizono, Hiro/ISA-5254-2023; Tamura, Kei/JRX-0933-2023
OI Sakurai, Naoki/0000-0002-7600-5380; Asano, Kazushi/0000-0003-0099-7974;
   Ishigaki, Kumiko/0000-0002-7491-2315
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U1 0
U2 4
PU JAPAN SOC VET SCI
PI TOKYO
PA UNIV TOKYO, 1-1-1 YAYOI, BUNKYO-KU, TOKYO, 103, JAPAN
SN 0916-7250
EI 1347-7439
J9 J VET MED SCI
JI J. Vet. Med. Sci.
PD MAY
PY 2022
VL 84
IS 5
BP 720
EP 725
DI 10.1292/jvms.21-0509
PG 6
WC Veterinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Veterinary Sciences
GA 2X4ES
UT WOS:000825159500017
PM 35370210
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Russo, M
   Siravegna, G
   Blaszkowsky, LS
   Corti, G
   Crisafulli, G
   Ahronian, LG
   Mussolin, B
   Kwak, EL
   Buscarino, M
   Lazzari, L
   Valtorta, E
   Truini, M
   Jessop, NA
   Robinson, HE
   Hong, TS
   Mino-Kenudson, M
   Di Nicolantonio, F
   Thabet, A
   Sartore-Bianchi, A
   Siena, S
   Iafrate, AJ
   Bardelli, A
   Corcoran, RB
AF Russo, Mariangela
   Siravegna, Giulia
   Blaszkowsky, Lawrence S.
   Corti, Giorgio
   Crisafulli, Giovanni
   Ahronian, Leanne G.
   Mussolin, Benedetta
   Kwak, Eunice L.
   Buscarino, Michela
   Lazzari, Luca
   Valtorta, Emanuele
   Truini, Mauro
   Jessop, Nicholas A.
   Robinson, Hayley E.
   Hong, Theodore S.
   Mino-Kenudson, Mari
   Di Nicolantonio, Federica
   Thabet, Ashraf
   Sartore-Bianchi, Andrea
   Siena, Salvatore
   Iafrate, A. John
   Bardelli, Alberto
   Corcoran, Ryan B.
TI Tumor Heterogeneity and Lesion-Specific Response to Targeted Therapy in
   Colorectal Cancer
SO CANCER DISCOVERY
LA English
DT Article
ID ACQUIRED-RESISTANCE; EGFR BLOCKADE; INTRATUMOR HETEROGENEITY;
   COLON-CANCER; MUTATIONS; EVOLUTION; EMERGENCE; CETUXIMAB
AB How genomic heterogeneity associated with acquired resistance to targeted agents affects response to subsequent therapy is unknown. We studied EGFR blockade in colorectal cancer to assess whether tissue and liquid biopsies can be integrated with radiologic imaging to monitor the impact of individual oncogenic alterations on lesion-specific responses. Biopsy of a patient's progressing liver metastasis following prolonged response to cetuximab revealed a MEK1(K57T) mutation as a novel mechanism of acquired resistance. This lesion regressed upon treatment with panitumumab and the MEK inhibitor trametinib. In circulating tumor DNA (ctDNA), mutant MEK1 levels declined with treatment, but a previously unrecognized KRAS(Q61H) mutation was also identified that increased despite therapy. This same KRAS mutation was later found in a separate nonresponding metastasis. In summary, parallel analyses of tumor biopsies and serial ctDNA monitoring show that lesion-specific radiographic responses to subsequent targeted therapies can be driven by distinct resistance mechanisms arising within separate tumor lesions in the same patient.
   SIGNIFICANCE: Molecular heterogeneity ensuing from acquired resistance drives lesion-specific responses to subsequent targeted therapies. Analysis of a single-lesion biopsy is inadequate to guide selection of subsequent targeted therapies. ctDNA profiles allow the detection of concomitant resistance mechanisms residing in separate metastases and assessment of the effect of therapies designed to overcome resistance. (C) 2015 AACR.
C1 [Russo, Mariangela; Siravegna, Giulia; Corti, Giorgio; Crisafulli, Giovanni; Mussolin, Benedetta; Buscarino, Michela; Lazzari, Luca; Di Nicolantonio, Federica; Bardelli, Alberto] IRCCS, Candiolo Canc Inst FPO, Turin, Italy.
   [Russo, Mariangela; Siravegna, Giulia; Di Nicolantonio, Federica; Bardelli, Alberto] Univ Turin, Dept Oncol, Turin, Italy.
   [Russo, Mariangela] IFOM, Milan, Italy.
   [Blaszkowsky, Lawrence S.; Ahronian, Leanne G.; Kwak, Eunice L.; Hong, Theodore S.; Corcoran, Ryan B.] Massachusetts Gen Hosp, Ctr Canc, 149 13th St,7th Floor, Boston, MA 02129 USA.
   [Blaszkowsky, Lawrence S.; Ahronian, Leanne G.; Kwak, Eunice L.; Corcoran, Ryan B.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
   [Valtorta, Emanuele; Truini, Mauro; Sartore-Bianchi, Andrea; Siena, Salvatore] Osped Maggiore Niguarda, Niguarda Canc Ctr, Milan, Italy.
   [Jessop, Nicholas A.; Robinson, Hayley E.; Mino-Kenudson, Mari; Iafrate, A. John] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02129 USA.
   [Hong, Theodore S.] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02129 USA.
   [Thabet, Ashraf] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02129 USA.
C3 IRCCS Fondazione del Piemonte per l'Oncologia; University of Turin; IFOM
   - FIRC Institute of Molecular Oncology; Harvard University;
   Massachusetts General Hospital; Harvard University; Harvard Medical
   School; Harvard University; Massachusetts General Hospital; Harvard
   University; Massachusetts General Hospital; Harvard University;
   Massachusetts General Hospital
RP Corcoran, RB (corresponding author), Massachusetts Gen Hosp, Ctr Canc, 149 13th St,7th Floor, Boston, MA 02129 USA.; Bardelli, A (corresponding author), Univ Turin, Dept Oncol, FPO, IRCCS, SP 142,Km 3-95, I-10060 Candiolo, TO, Italy.
EM alberto.bardelli@unito.it; rbcorcoran@partners.org
RI Siravegna, Giulia/Z-2826-2019; Lazzari, Luca/HGA-5930-2022;
   Sartore-Bianchi, Andrea/AAB-9848-2019; Mino-Kenudson, Mari/C-2029-2009;
   SIENA, SALVATORE/AAC-5806-2019; BARDELLI, Alberto/J-9721-2018;
   Crisafulli, Giovanni/AAB-6256-2019; Russo, Mariangela/K-1900-2018; Di
   Nicolantonio, Federica/A-2503-2011
OI Corti, Giorgio/0000-0001-6379-4117; VALTORTA,
   EMANUELE/0000-0002-5087-6233; Sartore-Bianchi,
   Andrea/0000-0003-0780-0409; Lazzari, Luca/0000-0001-6841-4240;
   Siravegna, Giulia/0000-0002-7132-6484; BARDELLI,
   Alberto/0000-0003-1647-5070; Crisafulli, Giovanni/0000-0002-5511-1555;
   SIENA, SALVATORE/0000-0002-2681-2846; Russo,
   Mariangela/0000-0003-4625-1449; MUSSOLIN, BENEDETTA/0000-0001-5723-5685;
   Di Nicolantonio, Federica/0000-0001-9618-2010
FU NIH/NCI Gastrointestinal Cancer SPORE [P50 CA127003]; Damon Runyon
   Clinical Investigator Award; NIH/NCI [1K08CA166510]; European Community
   [602901]; IMI [115749]; AIRC [9970]; AIRC IG [12812]; Fondazione
   Piemontese per la Ricerca sul Cancro-ONLUS; Ministero dell'Istruzione,
   dell'Universita e della Ricerca, progetto PRIN
FX This study was supported by grants from the NIH/NCI Gastrointestinal
   Cancer SPORE P50 CA127003, a Damon Runyon Clinical Investigator Award,
   and NIH/NCI 1K08CA166510 (all to R.B. Corcoran); by the European
   Community's Seventh Framework Programme under grant agreement no. 602901
   MErCuRIC (A. Bardelli); IMI contract no. 115749 CANCER-ID (A. Bardelli);
   AIRC 2010 Special Program Molecular Clinical Oncology 5 per mille,
   Project no. 9970 (A. Bardelli, S. Siena); AIRC IG no. 12812 (A.
   Bardelli); Fondazione Piemontese per la Ricerca sul Cancro-ONLUS 5 per
   mille 2010 e 2011 Ministero della Salute (A. Bardelli); and Ministero
   dell'Istruzione, dell'Universita e della Ricerca, progetto PRIN
   2010-2011 (A. Bardelli).
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EI 2159-8290
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IS 2
BP 147
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PG 7
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SC Oncology
GA DG8HF
UT WOS:000372323000023
PM 26644315
OA Green Submitted, Green Accepted, Bronze
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Lv, LM
   Zhou, XX
AF Lv, Liemei
   Zhou, Xiangxiang
TI Targeting Hippo signaling in cancer: novel perspectives and therapeutic
   potential
SO MEDCOMM
LA English
DT Review
DE drug resistance; epigenetic; hippo signaling; metabolism; target
   therapy; tumorigenesis
ID PROMOTES CHEMOTHERAPEUTIC RESISTANCE; TRANSCRIPTION FACTOR TEAD;
   AMPK-MEDIATED REGULATION; YAP INHIBITION RESTORES; YES-ASSOCIATED
   PROTEIN; PATHWAY EFFECTORS YAP; CELL LUNG-CANCER; TUMOR-SUPPRESSOR;
   COLORECTAL-CANCER; BREAST-CANCER
AB As highly conserved among diverse species, Hippo signaling pathway regulates various biological processes, including development, cell proliferation, stem cell function, tissue regeneration, homeostasis, and organ size. Studies in the last two decades have provided a good framework for how these fundamental functions of Hippo signaling are tightly regulated by a network with numerous intracellular and extracellular factors. The Hippo signaling pathway, when dysregulated, may lead to a wide variety of diseases, especially cancer. There is growing evidence demonstrating that dysregulated Hippo signaling is closely associated with tumorigenesis, cancer cell invasion, and migration, as well as drug resistance. Therefore, the Hippo pathway is considered an appealing therapeutic target for the treatment of cancer. Promising novel agents targeting the Hippo signaling pathway for cancers have recently emerged. These novel agents have shown antitumor activity in multiple cancer models and demonstrated therapeutic potential for cancer treatment. However, the detailed molecular basis of the Hippo signaling-driven tumor biology remains undefined. Our review summarizes current advances in understanding the mechanisms by which Hippo signaling drives tumorigenesis and confers drug resistance. We also propose strategies for future preclinical and clinical development to target this pathway.
   Hippo signaling consists of conserved kinases tightly regulated by intracellular and extracellular signals. Abnormalities in the Hippo pathway are implicated in a wide range of pathological processes, including tumorigenesis and cancer drug resistance. This review highlights novel strategies to target this pathway and its therapeutic implications, as well as the mechanisms underlying its function in tumorigenesis and cancer drug resistance.image
C1 [Lv, Liemei; Zhou, Xiangxiang] Shandong Univ, Shandong Prov Hosp, Dept Hematol, 324 Jingwu Rd, Jinan 250021, Shandong, Peoples R China.
   [Zhou, Xiangxiang] Shandong First Med Univ, Shandong Prov Hosp, Dept Hematol, Jinan, Shandong, Peoples R China.
   [Zhou, Xiangxiang] Branch Natl Clin Res Ctr Hematol Dis, Jinan, Shandong, Peoples R China.
   [Zhou, Xiangxiang] Soochow Univ, Affiliated Hosp 1, Natl Clin Res Ctr Hematol Dis, Suzhou, Peoples R China.
C3 Shandong First Medical University & Shandong Academy of Medical
   Sciences; Shandong University; Shandong First Medical University &
   Shandong Academy of Medical Sciences; Soochow University - China
RP Zhou, XX (corresponding author), Shandong Univ, Shandong Prov Hosp, Dept Hematol, 324 Jingwu Rd, Jinan 250021, Shandong, Peoples R China.
EM xiangxiangzhou@sdu.edu.cn
FU The authors have nothing to report.
FX The authors have nothing to report.
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NR 262
TC 12
Z9 12
U1 2
U2 18
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2688-2663
J9 MEDCOMM
JI MedComm
PD OCT
PY 2023
VL 4
IS 5
AR e375
DI 10.1002/mco2.375
PG 23
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA T1EY2
UT WOS:001075499900001
PM 37799806
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Wijewantha, N
   Eikanger, MM
   Antony, RM
   Potts, RA
   Rezvani, K
   Sereda, G
AF Wijewantha, Nisitha
   Eikanger, Morgan M.
   Antony, Ryan M.
   Potts, Rashaun A.
   Rezvani, Khosrow
   Sereda, Grigoriy
TI Targeting Colon Cancer Cells with Enzyme-Triggered Casein-Gated Release
   of Cargo from Mesoporous Silica-Based Nanoparticles
SO BIOCONJUGATE CHEMISTRY
LA English
DT Article
ID MATRIX METALLOPROTEINASE-7; MATRILYSIN MMP-7; EXPRESSION; MEMBRANE;
   VERATRIDINE; ACTIVATION; PH
AB Colorectal cancer (CRC) is one of the most widely diagnosed cancers worldwide. Despite notable improvements in therapeutic strategies available to CRC patients, late stages of CRC have a higher incidence rate of drug resistance, which is associated with a higher mortality rate. The development of therapeutic strategies that use nanoparticles as a drug delivery system has become one of the most promising potential approaches for cancer therapy. Previous studies have shown that a natural plant alkaloid, veratridine (VTD), suppresses colon cancer cell migration and invasion, two essential factors in tumor metastasis, through activation of the gene that encodes the tumor-suppressor protein UBXN2A. The goal of this study is to develop a nanoassembly to selectively deliver VTD to cancer cells and release it on demand while leaving normal cells intact. We packaged the targeted therapy anticancer molecule VTD inside mesoporous silica nanoparticles (MSNs) impermeable to the blood-brain barrier (BBB) and with selective affinity to CRC cells and sealed the VTD-loaded nanoparticles with an enzymatically cleavable protein. The particles will deliver and release VTD only at the targeted colorectal tumor sites. Since the enzyme MMP-7 protease is dominantly secreted by CRC cells, the release triggered by the enzymes will increase VTD concentration at tumor cells, enhancing the efficiency of the new therapy. We have proven the selective affinity of two types of VTD-carrying particles to CRC cells and enzyme- or acid-triggered VTD release. Negatively surface-charged MSNs showed significant affinity toward positively charged cancer cells but not negatively charged normal fibroblast colon cells, making VTD-MSNs a promising anticancer drug with minimal side effects.
C1 [Wijewantha, Nisitha; Sereda, Grigoriy] Univ South Dakota, Dept Chem, Vermillion, SD 57069 USA.
   [Eikanger, Morgan M.; Antony, Ryan M.; Potts, Rashaun A.; Rezvani, Khosrow] Univ South Dakota, Sanford Sch Med, Div Basic Biomed Sci, Vermillion, SD 57069 USA.
C3 University of South Dakota; University of South Dakota
RP Sereda, G (corresponding author), Univ South Dakota, Dept Chem, Vermillion, SD 57069 USA.
EM gsereda@usd.edu
RI Antony, Ryan/HQD-2088-2023
OI Wijewantha, Nisitha/0000-0001-7539-6853; Eikanger,
   Morgan/0000-0002-6435-6175; Sereda, Grigoriy/0000-0002-1121-8211;
   Antony, Ryan/0000-0002-1286-7731
FU National Institute of General Medical Sciences of the National
   Institutes of Health [U54GM128729]; NSF-MRI [CHE-1337707]; Department of
   Chemistry of the University of South Dakota; National Cancer Institute
   of the National Institutes of Health [1R03CA22393501]; National Science
   Foundation [DGE-1633213, ECCS: 1542182]; Nebraska Research Initiative
FX The authors thank the National Institute of General Medical Sciences of
   the National Institutes of Health under award U54GM128729 for financial
   support of this work, NSF-MRI CHE-1337707 for the purchase of the
   SEM/EDX instrument, and the Department of Chemistry of the University of
   South Dakota. K.R. is supported by the National Cancer Institute of the
   National Institutes of Health under award 1R03CA22393501 and supported
   by the National Institute of General Medical Sciences of the National
   Institutes of Health under award U54GM128729. This research was
   supported, in part, by a grant from the National Science Foundation
   (DGE-1633213) to N.W. The research was performed in part at the Nebraska
   Nanoscale and NanoEngineering Research Core Facilities: National
   Nano-technology Coordinated Infrastructure and the Nebraska Center for
   Materials and Nanoscience, which are supported by the National Science
   Foundation under Award ECCS: 1542182, and the Nebraska Research
   Initiative. We want to thank Dr. Tim Ridgway (Dean of the USD Sanford
   School of Medicine) for his clinical insights during the execution of
   this study.
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NR 40
TC 8
Z9 9
U1 1
U2 15
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1043-1802
EI 1520-4812
J9 BIOCONJUGATE CHEM
JI Bioconjugate Chem.
PD NOV 17
PY 2021
VL 32
IS 11
BP 2353
EP 2365
DI 10.1021/acs.bioconjchem.1c00416
EA OCT 2021
PG 13
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
   Chemistry, Multidisciplinary; Chemistry, Organic
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA XB5CK
UT WOS:000721347100008
PM 34672618
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Li, DY
   Zhang, Z
   Wang, L
AF Li, Dongyu
   Zhang, Zhe
   Wang, Lei
TI Emerging role of tumor microenvironmental nutrients and metabolic
   molecules in ferroptosis: Mechanisms and clinical implications
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE Ferroptosis; Lactate; TME; Hypoxia; Drug resistance
ID AMINO-ACID-METABOLISM; CELL-DEATH; ARGININOSUCCINATE SYNTHETASE;
   LIPID-PEROXIDATION; COLORECTAL-CANCER; SIGNALING PATHWAY; OLD DRUGS;
   MITOCHONDRIAL; SENSITIVITY; EXPRESSION
AB In recent years, ferroptosis has gradually attracted increasing attention because of its important role in tumors. Ferroptosis resistance is an important cause of tumor metastasis, recurrence and drug resistance. Exploring the initiating factors and specific mechanisms of ferroptosis has become a key strategy to block tumor progression and improve drug sensitivity. As the external space in direct contact with tumor cells, the tumor microenvironment has a great impact on the biological function of tumor cells. The relationships between abnormal environmental characteristics (hypoxia, lactic acid accumulation, etc.) in the microenvironment and ferroptosis of tumor cells has not been fully characterized. This review focuses on the characteristics of the tumor micro- environment and summarizes the mechanisms of ferroptosis under different environmental factors, aiming to provide new insights for subsequent targeted therapy. Moreover, considering the presence of anticancer drugs in the microenvironment, we further summarize the mechanisms of ferroptosis to provide new strategies for the sensitization of tumor cells to drugs.
C1 [Li, Dongyu] China Med Univ, Hosp 1, Dept VIP Inpatient Ward, Shenyang 110001, Liaoning, Peoples R China.
   [Zhang, Zhe] China Med Univ, Hosp 1, Dept Hepatobiliary & Pancreat Surg, Shenyang 110001, Liaoning, Peoples R China.
   [Wang, Lei] China Med Univ, Hosp 1, Dept Vasc & Thyroid Surg, Shenyang 110001, Liaoning, Peoples R China.
C3 China Medical University; China Medical University; China Medical
   University
RP Wang, L (corresponding author), China Med Univ, Hosp 1, Dept Vasc & Thyroid Surg, Shenyang 110001, Liaoning, Peoples R China.
EM wanglei@cmu.edu.cn
RI Li, Dongyu/LOU-0061-2024
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NR 201
TC 0
Z9 0
U1 12
U2 12
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 OCT
PY 2024
VL 179
AR 117406
DI 10.1016/j.biopha.2024.117406
EA SEP 2024
PG 13
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA I9Q9A
UT WOS:001333535600001
PM 39255738
OA gold
DA 2025-01-04
ER

PT J
AU Khan, SA
   Zeng, ZS
   Shia, JR
   Paty, PB
AF Khan, Sajid A.
   Zeng, Zhaoshi
   Shia, Jinru
   Paty, Philip B.
TI <i>EGFR</i> Gene Amplification and <i>KRAS</i> Mutation Predict Response
   to Combination Targeted Therapy in Metastatic Colorectal Cancer
SO PATHOLOGY & ONCOLOGY RESEARCH
LA English
DT Article
DE Colorectal cancer; Cetuximab; Bevacizumab; Metastasis; EGFR; KRAS
ID GROWTH-FACTOR RECEPTOR; PHASE-II TRIAL; ADJUVANT THERAPY; COPY NUMBER;
   CETUXIMAB; IRINOTECAN; BEVACIZUMAB; OXALIPLATIN; EXPRESSION; CARCINOMA
AB Genetic variability in KRAS and EGFR predicts response to cetuximab in irinotecan refractory colorectal cancer. Whether these markers or others remain predictive in combination biologic therapies including bevacizumab is unknown. We identified predictive biomarkers from patients with irinotecan refractory metastatic colorectal cancer treated with cetuximab plus bevacizumab. Patients who received cetuximab plus bevacizumab for irinotecan refractory colorectal cancer in either of two Phase II trials conducted were identified. Tumor tissue was available for 33 patients. Genomic DNA was extracted and used for mutational analysis of KRAS, BRAF, and p53 genes. Fluorescence in situ hybridization was performed to assess EGFR copy number. The status of single genes and various combinations were tested for association with response. Seven of 33 patients responded to treatment. KRAS mutations were found in 14/33 cases, and 0 responded to treatment (p = 0.01). EGFR gene amplification was seen in 3/33 of tumors and in every case was associated with response to treatment (p < 0.001). TP53 and BRAF mutations were found in 18/33 and 0/33 tumors, respectively, and there were no associations with response to either gene. EGFR gene amplification and KRAS mutations are predictive markers for patients receiving combination biologic therapy of cetuximab plus bevacizumab for metastatic colorectal cancer. One marker or the other is present in the tumor of half of all patients allowing treatment response to be predicted with a high degree of certainty. The role for molecular markers in combination biologic therapy seems promising.
C1 [Khan, Sajid A.] Yale Univ, Sch Med, Dept Surg, Sect Surg Oncol, 310 Cedar St,FMB 130, New Haven, CT 06520 USA.
   [Zeng, Zhaoshi; Paty, Philip B.] Mem Sloan Kettering Canc Ctr, Dept Surg, Colorectal Serv, New York, NY 10021 USA.
   [Shia, Jinru] Mem Sloan Kettering Canc Ctr, Dept Pathol, Colorectal Serv, 1275 York Ave, New York, NY 10021 USA.
C3 Yale University; Memorial Sloan Kettering Cancer Center; Memorial Sloan
   Kettering Cancer Center
RP Khan, SA (corresponding author), Yale Univ, Sch Med, Dept Surg, Sect Surg Oncol, 310 Cedar St,FMB 130, New Haven, CT 06520 USA.
EM sajid.khan@yale.edu
RI khan, sajid/HGE-2406-2022
FU National Cancer Institute [PO1-CA65930, CA 09501]
FX This work was supported by the Program Project Grant PO1-CA65930 and T32
   surgical oncology training grant CA 09501 of the National Cancer
   Institute.
CR [Anonymous], ASIA PAC J CLIN ONCO
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NR 33
TC 24
Z9 25
U1 1
U2 6
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 JUL
PY 2017
VL 23
IS 3
BP 673
EP 677
DI 10.1007/s12253-016-0166-2
PG 5
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA EW5TU
UT WOS:000402570200026
PM 28025786
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Zhang, YC
   Zhu, LN
   Wang, X
AF Zhang, Yuchen
   Zhu, Lina
   Wang, Xin
TI NEM-Tar: A Probabilistic Graphical Model for Cancer Regulatory Network
   Inference and Prioritization of Potential Therapeutic Targets From
   Multi-Omics Data
SO FRONTIERS IN GENETICS
LA English
DT Article
DE nested effects model; molecular subtype; regulatory network; drug
   targets; combination therapy; cancer
ID BETA-CATENIN; SIGNALING NETWORKS; PATHWAY; EXPRESSION; SUBTYPES;
   SCREENS; GROWTH; EMT
AB Targeted therapy has been widely adopted as an effective treatment strategy to battle against cancer. However, cancers are not single disease entities, but comprising multiple molecularly distinct subtypes, and the heterogeneity nature prevents precise selection of patients for optimized therapy. Dissecting cancer subtype-specific signaling pathways is crucial to pinpointing dysregulated genes for the prioritization of novel therapeutic targets. Nested effects models (NEMs) are a group of graphical models that encode subset relations between observed downstream effects under perturbations to upstream signaling genes, providing a prototype for mapping the inner workings of the cell. In this study, we developed NEM-Tar, which extends the original NEMs to predict drug targets by incorporating causal information of (epi)genetic aberrations for signaling pathway inference. An information theory-based score, weighted information gain (WIG), was proposed to assess the impact of signaling genes on a specific downstream biological process of interest. Subsequently, we conducted simulation studies to compare three inference methods and found that the greedy hill-climbing algorithm demonstrated the highest accuracy and robustness to noise. Furthermore, two case studies were conducted using multi-omics data for colorectal cancer (CRC) and gastric cancer (GC) in the TCGA database. Using NEM-Tar, we inferred signaling networks driving the poor-prognosis subtypes of CRC and GC, respectively. Our model prioritized not only potential individual drug targets such as HER2, for which FDA-approved inhibitors are available but also the combinations of multiple targets potentially useful for the design of combination therapies.
C1 [Zhang, Yuchen; Zhu, Lina; Wang, Xin] City Univ Hong Kong, Dept Biomed Sci, Hong Kong, Peoples R China.
   [Wang, Xin] City Univ Hong Kong, Shenzhen Res Inst, Key Lab Biochip Technol, Biotech & Hlth Ctr, Shenzhen, Peoples R China.
C3 City University of Hong Kong; Shenzhen Research Institute, City
   University of Hong Kong; City University of Hong Kong
RP Wang, X (corresponding author), City Univ Hong Kong, Dept Biomed Sci, Hong Kong, Peoples R China.; Wang, X (corresponding author), City Univ Hong Kong, Shenzhen Res Inst, Key Lab Biochip Technol, Biotech & Hlth Ctr, Shenzhen, Peoples R China.
EM xin.wang@cityu.edu.hk
RI Wang, Xin/A-1130-2012
OI ZHU, Lina/0000-0002-8558-2120; Wang, Xin/0000-0002-5122-2418
FU Guangdong Basic and Applied Basic Research Foundation [2019B030302012];
   Young Scientists Fund of the National Natural Science Foundation of
   China [81802384]; Science Technology and Innovation Commission of
   Shenzhen Municipality [JCYJ20200109120425045]; Research Grants Council
   of the Hong Kong Special Administrative Region, China [21101115,
   11102317, 11103718, 11103619, R4017-18, C4041-17GF]
FX This work was supported by a grant from Guangdong Basic and Applied
   Basic Research Foundation (Project No. 2019B030302012), a grant
   supported by the Young Scientists Fund of the National Natural Science
   Foundation of China (81802384), a grant by the Science Technology and
   Innovation Commission of Shenzhen Municipality (Project No.
   JCYJ20200109120425045), and grants from the Research Grants Council of
   the Hong Kong Special Administrative Region, China (Project No. CityU
   21101115, 11102317, 11103718, 11103619, R4017-18, C4041-17GF) awarded to
   XW.
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NR 61
TC 1
Z9 1
U1 3
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 APR 22
PY 2021
VL 12
AR 608042
DI 10.3389/fgene.2021.608042
PG 14
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA RX8KT
UT WOS:000647468300001
PM 33968127
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Yuan, B
   Miao, LL
   Mei, DS
   Li, LZ
   Zhou, QY
   Dong, D
   Wang, ST
   Zhu, XX
   Xu, SL
AF Yuan, Bo
   Miao, Linlin
   Mei, Disen
   Li, Lingzhi
   Zhou, Qiongyan
   Dong, Dong
   Wang, Songting
   Zhu, Xiaoxia
   Xu, Suling
TI RETRACTED: Value of a Signature of Immune-Related Genes in Predicting
   the Prognosis of Melanoma and Its Responses to Immune Checkpoint Blocker
   Therapies (Retracted Article)
SO COMPUTATIONAL AND MATHEMATICAL METHODS IN MEDICINE
LA English
DT Article; Retracted Publication
ID SPONTANEOUS REGRESSION; MALIGNANT-MELANOMA; COLORECTAL-CANCER;
   EXPRESSION; PARAMETERS; BIOLOGY; CTLA-4; LFA-1; PD-1
AB Melanoma is becoming increasingly common worldwide, with high rates of transformation into malignancy compared to other skin lesions. The prognosis of patients with melanoma at an advanced stage is highly unsatisfying despite the development of immunotherapy, target therapy, or combinative therapy. The major barrier to exploiting immune checkpoint therapies and achieving the best benefits clinically is resistance that can easily develop if regimens are not selected appropriately. In this study, we investigated the possibility of using immune-related genes to predict patient survival and their responses to immune checkpoint blocker therapies with the expression profiles available at The Cancer Genome Atlas (TCGA) Program plus expression data from the Gene Expression Omnibus (GEO) for validation. A five gene signature that is highly correlated with the local infiltration of cytotoxic lymphocytes in the tumor microenvironment was identified, and a scoring model was developed with stepwise regression after multivariate Cox analyses. The score calculated strongly correlates with Breslow depth, and this model effectively predicts the prognosis of patients with melanoma, whether primary or metastasized. It also depicts the heterogenous immune-related nature of melanoma by revealing different predicted responses to immune checkpoint blocker therapies through its correlation to tumor immune dysfunction and exclusion (TIDE) score.
C1 [Yuan, Bo; Li, Lingzhi; Zhou, Qiongyan; Wang, Songting; Zhu, Xiaoxia; Xu, Suling] Ningbo Univ, Affiliated Hosp, Dermatol Dept, Med Sch, 247 Renmin Rd, Ningbo 315020, Peoples R China.
   [Miao, Linlin] Ningbo Univ, Sch Med, Surg Dept, 818, Fenghua Rd, Ningbo 315210, Peoples R China.
   [Mei, Disen] Ningbo Univ, Basic Med Expt Ctr, Sch Med, 818 Fenghua Rd, Ningbo 315211, Peoples R China.
   [Dong, Dong] Ningbo Univ, Affiliated Hosp, Plast & Reconstruct Surg Dept, Med Sch, 247 Renmin Rd, Ningbo 315020, Peoples R China.
C3 Ningbo University; Ningbo University; Ningbo University; Ningbo
   University
RP Yuan, B (corresponding author), Ningbo Univ, Affiliated Hosp, Dermatol Dept, Med Sch, 247 Renmin Rd, Ningbo 315020, Peoples R China.
EM fyyuanbo@nbu.edu.cn; miaolinlin9988@163.com; meidisen@nbu.edu.cn;
   lilingzhi912@163.com; zhou.qiongyan@163.com; ddaisyf@163.com;
   wstnbdx@sina.com; nb_zhuxiaoxia@126.com; xusuling@nbu.edu.cn
RI zhu, xiaoxia/B-5018-2011; dong, dong/JQV-8909-2023; 苗, 琳琳/HZM-3391-2023
OI Xu, Suling/0000-0002-2472-0403; Yuan, Bo/0000-0002-5315-7007
FU Ningbo Science and Technology Bureau, research on the construction and
   application of an intelligent image analysis system;  [202002N3190]
FX This work was supported by Ningbo Science and Technology Bureau,
   research on the construction and application of an intelligent image
   analysis system for early screening of skin cancer, approval numbers:
   202002N3190.
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NR 53
TC 3
Z9 3
U1 0
U2 10
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1748-670X
EI 1748-6718
J9 COMPUT MATH METHOD M
JI Comput. Math. Method Med.
PD JUN 20
PY 2022
VL 2022
AR 9633416
DI 10.1155/2022/9633416
PG 13
WC Mathematical & Computational Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Mathematical & Computational Biology
GA 5A9EP
UT WOS:000863182600001
PM 35770115
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Feria, A
   Times, M
AF Feria, Alejandro
   Times, Melissa
TI Effectiveness of Standard Treatment for Stage 4 Colorectal Cancer:
   Traditional Management with Surgery, Radiation, and Chemotherapy
SO CLINICS IN COLON AND RECTAL SURGERY
LA English
DT Article
DE colorectal cancer treatment; stage 4 colon cancer
ID PERITONEAL METASTASES; 1ST-LINE TREATMENT; LIVER METASTASES; PULMONARY
   METASTASECTOMY; SIMULTANEOUS RESECTIONS; CYTOREDUCTIVE SURGERY; HEPATIC
   RESECTION; SUBGROUP ANALYSES; OPEN-LABEL; SURVIVAL
AB Colorectal cancer (CRC) is the second most common cause of cancer-related death in the United States comprising 7.9% of all new cancer diagnoses and 8.6% of all cancer deaths. The combined 5-year relative survival rate for all stages is 65.1% but in its most aggressive form, stage 4 CRC has a 5-year relative survival rate of just 15.1%. For most with stage 4 CRC, treatment is palliative not curative, with the goal to prolong overall survival and maintain an acceptable quality of life.The identification of unique cancer genomic and biologic markers allows patient-specific treatment options. Treatment of stage 4 CRC consists of systemic therapy with chemotherapeutic agents, surgical resection if feasible, potentially including resection of metastasis, palliative radiation in select settings, and targeted therapy toward growth factors. Despite advances in surgical and medical management, metastatic CRC remains a challenging clinical problem associated with poor prognosis and low overall survival.
C1 [Feria, Alejandro] MetroHlth Syst, Dept Surg, Cleveland, OH USA.
   [Times, Melissa] MetroHlth Syst, Dept Surg, Div Colon & Rectal Surg, Cleveland, OH USA.
   [Times, Melissa] MetroHlth Med Ctr, Dept Surg, Cleveland, OH 44109 USA.
C3 MetroHealth System; MetroHealth System; MetroHealth System
RP Times, M (corresponding author), MetroHlth Med Ctr, Dept Surg, Cleveland, OH 44109 USA.
EM mtimes@metrohealth.org
OI Feria, Alejandro/0000-0003-0419-6488
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NR 44
TC 5
Z9 5
U1 0
U2 3
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 1531-0043
EI 1530-9681
J9 CLIN COLON RECT SURG
JI Clin. Colon Rectal Surg.
PD MAR
PY 2024
VL 37
IS 02
BP 62
EP 65
DI 10.1055/s-0043-1761420
EA MAR 2023
PG 4
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA GS3A6
UT WOS:000952399800002
PM 38322607
OA Green Published
DA 2025-01-04
ER

PT J
AU Shi, LP
   Su, YB
   Zheng, ZH
   Qi, JY
   Wang, WD
   Wang, CC
AF Shi, Liangpan
   Su, Yibin
   Zheng, Zhihua
   Qi, Jinyu
   Wang, Weidong
   Wang, Cunchuan
TI miR-146b-5p promotes colorectal cancer progression by targeting TRAF6
SO EXPERIMENTAL AND THERAPEUTIC MEDICINE
LA English
DT Article
DE colorectal cancer; microRNA-146b-5p; tumor necrosis factor
   receptor-associated factor 6; tumorigenesis
ID COLON-CANCER; DOWN-REGULATION; EXPRESSION; CELLS; IDENTIFICATION;
   PROGNOSIS; SUPPRESSOR; MICRORNAS; RECEPTOR; PATHWAY
AB Increasing evidence highlights the multiple roles of microRNAs (miRs) in the tumorigenesis of colorectal cancer (CRC); however, the molecular mechanism, particularly the target of miR-146b-5p in CRC has not been fully elucidated. The present study aimed to elucidate the influence of miR-146b-5p via regulating tumor necrosis factor receptor-associated factor 6 (TRAF6) in CRC. The expression levels of miR-146b-5p and TRAF6 in CRC tissue and cells were determined by reverse transcription quantitative PCR and western blotting. Binding between miR-146b-5p and TRAF6 was examined using a dual luciferase reporter gene assay. The impact of miR-146b-5p and TRAF6 on proliferation and migration of CRC cells was determined using Cell Counting Kit-8 and Transwell assays, respectively. An animal model of CRC was established to determine the carcinogenic effect of the miR-146b-5p-TRAF6 axis. The results demonstrated that miR-146b-5p was highly expressed in CRC tissue samples compared with in normal adjacent tissue samples and in CRC cells compared with in the normal NCM460 cell line, whereas TRAF6 was expressed at low levels. Overexpression of miR-146b-5p decreased TRAF6 expression in CRC HT29 and SW620 cells. miR-146b-5p targeted and inhibited TRAF6 expression in CRC cells. Furthermore, transfection with a miR-146b-5p mimic promoted the proliferation, migration and invasion of CRC cells and tumor growth; however, these effects were abolished by TRAF6 overexpression. Transfection with a miR-146b-5p inhibitor suppressed the proliferation of CRC cells. Taken together, the results from the present study demonstrated that miR-146b-5p could enhance the initiation and tumorigenesis of CRC by targeting TRAF6. These results will help elucidate the mechanisms underlying CRC development and will facilitate the development of targeted therapy for CRC.
C1 [Shi, Liangpan; Wang, Cunchuan] Jinan Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, 613 Huangpu Ave West, Guangzhou 510630, Guangdong, Peoples R China.
   [Shi, Liangpan; Su, Yibin; Zheng, Zhihua; Qi, Jinyu; Wang, Weidong] Fujian Med Univ, Hosp Quanzhou 1, Dept Gastrointestinal Surg, Quanzhou 362000, Fujian, Peoples R China.
C3 Jinan University; Fujian Medical University
RP Wang, CC (corresponding author), Jinan Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, 613 Huangpu Ave West, Guangzhou 510630, Guangdong, Peoples R China.
EM wcc8069@126.com
OI Su, Yi-bin/0000-0002-9307-8311
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NR 56
TC 9
Z9 10
U1 0
U2 7
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-0981
EI 1792-1015
J9 EXP THER MED
JI Exp. Ther. Med.
PD MAR
PY 2022
VL 23
IS 3
AR 231
DI 10.3892/etm.2022.11155
PG 12
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA YV0CJ
UT WOS:000752400800001
PM 35222708
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Hong, KS
   Jeon, EY
   Chung, SS
   Kim, KH
   Lee, RA
AF Hong, Kyung Sook
   Jeon, Eun-Young
   Chung, Soon Sup
   Kim, Kwang Ho
   Lee, Ryung-Ah
TI Epidermal growth factor-mediated Rab25 pathway regulates integrin β1
   trafficking in colon cancer
SO CANCER CELL INTERNATIONAL
LA English
DT Article
DE Colonic neoplasms; Receptor trafficking; Endocytosis; Shedding;
   Integrins; Epidermal growth factor; Epidermal growth factor receptor;
   Rab25; Target therapy
ID TUMOR-CELLS; BETA-1-INTEGRIN; RECEPTORS; COOPERATION; GTPASES
AB Background: Integrins play a critical role in carcinogenesis. Integrin beta 1 localization is regulated by the guanosine5'- triphosphate hydrolase Rab25 and integrin beta 1 levels are elevated in the serum of colon cancer patients; thus, the present study examined the effects of epidermal growth factor (EGF) and Rab25 on integrin beta 1 localization in colon cancer cells.
   Methods: HCT116 human colon cancer cells were treated with increasing concentrations of EGF, and cell proliferation and protein expression were monitored by MTT and western blot analyses, respectively. Cell fractionation was performed to determine integrin beta 1 localization in the membrane and cytosol. Integrin beta 1 extracellular shedding was monitored by enzyme-linked immunosorbent assays (ELISAs) with culture supernatants from stimulated cells. HCT116 cells were transfected with Rab25-specific siRNA to determine the significance of Rab25 in integrin beta 1 trafficking in the presence of EGF.
   Results: Total integrin beta 1 expression increased in response to EGF and subsequently decreased at 24 h post-stimulation. A similar decrease was observed in purified membrane fractions, whereas no changes were observed in cytosolic levels. ELISAs using media from stimulated cell cultures demonstrated increased integrin beta 1 levels corresponding to the decrease observed in membrane fractions, suggesting that EGF induces integrin receptor shedding. EGF stimulation in Rab25-knockdown cells resulted in integrin beta 1 accumulation in the membrane, suggesting that Rab25 promotes integrin endocytosis.
   Conclusions: Integrin beta 1 is shed from colon cancer cells in response to EGF stimulation in a Rab25-dependent manner. These results further the present understanding of the role of integrin beta 1 in colon cancer progression.
C1 [Hong, Kyung Sook] Ewha Womans Univ, Dept Surg & Crit Care Med, Coll Med, Seoul, South Korea.
   [Jeon, Eun-Young] Ewha Womans Univ, Ewha Med Res Inst, Coll Med, Seoul, South Korea.
   [Chung, Soon Sup; Kim, Kwang Ho; Lee, Ryung-Ah] Ewha Womans Univ, Dept Surg, Coll Med, Seoul, South Korea.
C3 Ewha Womans University; Ewha Womans University; Ewha Womans University
RP Lee, RA (corresponding author), Ewha Womans Univ, Dept Surg, Coll Med, Seoul, South Korea.
EM ralee@ewha.ac.kr
RI Hong, Kyung Sook/AAX-7067-2021
OI Hong, Kyung Sook/0000-0002-8022-5693
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NR 37
TC 8
Z9 9
U1 0
U2 4
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1475-2867
J9 CANCER CELL INT
JI Cancer Cell Int.
PD MAR 5
PY 2018
VL 18
AR 32
DI 10.1186/s12935-018-0526-y
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FY2HE
UT WOS:000426635300002
PM 29515334
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Abdallah, FM
   Helmy, MW
   Katary, MA
   Ghoneim, AI
AF Abdallah, Fatma M.
   Helmy, Maged W.
   Katary, Mohamed A.
   Ghoneim, Asser I.
TI Synergistic antiproliferative effects of curcumin and celecoxib in
   hepatocellular carcinoma HepG2 cells
SO NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
LA English
DT Article
DE Curcumin; Celecoxib; HepG2; Proliferation; Apoptosis
ID NF-KAPPA-B; PROSTATE-CANCER CELLS; GROWTH IN-VITRO; CYCLOOXYGENASE-2
   COX-2; LIVER-CANCER; COLON-CANCER; 5-FLUOROURACIL-INDUCED APOPTOSIS;
   ANTICANCER DRUGS; CYCLIN D1; HIGH-RISK
AB Hepatocellular carcinoma (HCC) is still a leading cancer killer in the community. Molecular targeted therapy with celecoxib (CXB) has shown promising antitumor effects; however, its use may be limited due to serious side effects. Curcumin (CUR) has also shown beneficial effects against HCC. Then, it was aimed to investigate the effects of adding CUR to CXB on HCC HepG2 cells. HepG2 cells were treated with CXB and/or CUR at increasing concentrations to investigate synergistic drug interactions, as calculated combination index (CI). Combination treatment effects on cell viability and caspase-3 activation were assessed. The levels of Akt, nuclear factor-kappa B (NF-B), prostaglandin E-2 (PGE(2)), malondialdehyde (MDA), cyclin D1 (CD1), and vascular endothelial growth factor (VEGF) were also evaluated. CXB (3.13-100M) and/or CUR (1.25-40M) reduced HepG2 cell viability dose-dependently. Nevertheless, lower combined concentrations showed higher synergism (CI<1) and higher CXB dose reduction index (DRI>1). Also, the addition of CUR to CXB resulted in increased cytotoxicity and caspase-3 activation, as compared to CXB alone. In addition, the selected combination significantly reduced the levels of Akt, NF-B, PGE(2), MDA, CD1, and VEGF, as compared to either agent alone. In conclusion,CUR augmented the CXB-mediated antitumor effects in HepG2 cells through, at least in part, antiproliferative, antioxidant, and pro-apoptotic mechanisms. This may allow the further use of CXB at lower concentrations, combined with CUR, as a promising safer targeted strategy for HCC management.
C1 [Abdallah, Fatma M.; Helmy, Maged W.; Katary, Mohamed A.; Ghoneim, Asser I.] Damanhour Univ, Fac Pharm, Dept Pharmacol & Toxicol, Damanhour 22514, Egypt.
C3 Egyptian Knowledge Bank (EKB); Damanhour University
RP Ghoneim, AI (corresponding author), Damanhour Univ, Fac Pharm, Dept Pharmacol & Toxicol, Damanhour 22514, Egypt.
EM asser@damanhour.edu.eg
RI Abdallah, Fatma/LTE-6637-2024; Helmy, Maged/AFU-2420-2022; Ghoneim,
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OI Abdallah, Fatma/0009-0008-0934-8827
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NR 91
TC 32
Z9 32
U1 0
U2 21
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0028-1298
EI 1432-1912
J9 N-S ARCH PHARMACOL
JI Naunyn-Schmiedebergs Arch. Pharmacol.
PD DEC
PY 2018
VL 391
IS 12
BP 1399
EP 1410
DI 10.1007/s00210-018-1557-6
PG 12
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA GY8DG
UT WOS:000448849700009
PM 30155693
DA 2025-01-04
ER

PT J
AU Islam, F
   Gopalan, V
   Vider, J
   Wahab, R
   Ebrahimi, F
   Lu, CT
   Kasem, K
   Lam, AKY
AF Islam, Farhadul
   Gopalan, Vinod
   Vider, Jelena
   Wahab, Riajul
   Ebrahimi, Faeza
   Lu, Cu-tai
   Kasem, Kais
   Lam, Alfred K. Y.
TI MicroRNA-186-5p overexpression modulates colon cancer growth by
   repressing the expression of the <i>FAM134B</i> tumour inhibitor
SO EXPERIMENTAL CELL RESEARCH
LA English
DT Article
DE Colorectal cancer; miR-186-5p; FAM134B; Targeted therapy; Oncogenic
   micro-RNA
ID COLORECTAL-CANCER; TARGET PREDICTION; P16 EXPRESSION; BIOMARKERS;
   METASTASIS; JK1; ADENOCARCINOMA; MIGRATION; INVASION; MIR-126
AB Objectives: The role and underlying mechanism of miR-186-5p in colorectal cancer remain unknown. The present study aims to examine the various cellular effects of miR-186-5p in the carcinogenesis of colorectal cancer. Also, the interacting targets and association of clinicopathological factors with miR-186-5p expression in patients with colorectal cancer were analysed.
   Methods: The miR-186-5p expression levels in colorectal cancer tissues (n=126) and colon cancer cell lines (n=3) were analysed by real-time PCR. Matched non-neoplastic colorectal tissues and a non-neoplastic colonic epithelial cell line were used as controls. Various in vitro assays such as cell proliferation, wound healing and colony formation assays were performed to examine the miR-186-5p specific cellular effects. Western blots and immunohistochemistry analysis were performed to examine the modulation of FAM134B, PARP9 and KLF7 proteins expression.
   Results: Significant high expression of miR-186-5p was noted in cancer tissues (p < 0.001) and cell lines (p < 0.05) when compared to control tissues and cells. The majority of the patients with colorectal cancer (88/126) had shown overexpression of miR-186-5p. This miR-186-5p overexpression was predominantly noted with in cancer with distant metastasis (p=0.001), lymphovascular permeation (p=0.037), microsatellite instability (MSI) stable (p=0.015), in distal colorectum (p=0.043) and with associated adenomas (p=0.047). Overexpression of miR-186-5p resulted in increased cell proliferation, colony formation, wound healing capacities and induced alteration of cell cycle kinetics in colon cancer cells. On the other hand, inhibition of endogenous miR-186-5p reduced the cancer growth properties. miR-186-5p overexpression reduced FAM134B expression significantly in the cancer cells (p < 0.01). Also, FAM134B and miR-186-5p expressions are inversely correlated in colorectal cancer tissues and cells.
   Conclusion: The miR-186-5p expression promotes colorectal cancer pathogenesis by regulating tumour suppressor FAM134B. Reduced cancer cells growth followed by inhibition of miR-186-5p highlights the potential of miR-186-5p inhibitor as a novel strategy for targeting colorectal cancer initiation and progression.
C1 [Islam, Farhadul; Gopalan, Vinod; Wahab, Riajul; Ebrahimi, Faeza; Kasem, Kais; Lam, Alfred K. Y.] Griffith Univ, Canc Mol Pathol, Sch Med, Gold Coast, NSW, Australia.
   [Islam, Farhadul; Gopalan, Vinod; Vider, Jelena; Wahab, Riajul; Ebrahimi, Faeza; Kasem, Kais; Lam, Alfred K. Y.] Griffith Univ, Menzies Hlth Inst Queensland, Gold Coast, NSW, Australia.
   [Islam, Farhadul] Rajshahi Univ, Dept Biochem & Mol Biol, Rajshahi 6205, Bangladesh.
   [Vider, Jelena] Griffith Univ, Sch Med Sci, Gold Coast, Qld, Australia.
   [Lu, Cu-tai] Gold Coast Hosp, Dept Surg, Gold Coast, Qld, Australia.
C3 Griffith University; Griffith University - Gold Coast Campus; Griffith
   University; Griffith University - Gold Coast Campus; Menzies Health
   Institute Queensland; University of Rajshahi; Griffith University;
   Griffith University - Gold Coast Campus; 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 Vider, Jelena/AAW-8577-2020; Wahab, Riajul/AEC-9343-2022; Gopalan,
   Vinod/C-4269-2016; Islam, Farhadul/R-5643-2017; Lam, Alfred/C-1652-2008
OI Wahab, S M Riajul/0000-0002-5967-4419; Gopalan,
   Vinod/0000-0003-0366-9482; Islam, Farhadul/0000-0001-5262-4702; Lam,
   Alfred/0000-0003-2771-564X; Vider, Jelena/0000-0003-1696-9812; Lu, Cu
   Tai/0000-0001-9565-3749
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NR 44
TC 57
Z9 59
U1 0
U2 15
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 AUG 15
PY 2017
VL 357
IS 2
BP 260
EP 270
DI 10.1016/j.yexcr.2017.05.021
PG 11
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FC6XT
UT WOS:000406985700013
PM 28549913
OA Green Published
DA 2025-01-04
ER

PT J
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   Hoffmann, Jean Sebastien
   Saffi, Jenifer
TI Analyzing the Opportunities to Target DNA Double-Strand Breaks Repair
   and Replicative Stress Responses to Improve Therapeutic Index of
   Colorectal Cancer
SO CANCERS
LA English
DT Review
DE colorectal cancer; DNA double strand break repair; replication stress;
   target therapy
ID III COLON-CANCER; RECOMBINATION DEFICIENCY HRD; DEFECTIVE MISMATCH
   REPAIR; HOMOLOGOUS-RECOMBINATION; STAGE-II; DAMAGE RESPONSE;
   POLYMERASE-THETA; MICROSATELLITE-INSTABILITY; ATAXIA-TELANGIECTASIA;
   SYNTHETICALLY LETHAL
AB Simple Summary Colorectal cancer (CRC) is among the most common cancers and the third leading cause of cancer deaths worldwide. Despite the identification of alterations in DNA repair genes and the resulting genomic instability in sub-populations of CRC, therapies that exploit defects in DNA repair pathways or high level of replicative stress have been explored only in breast, ovarian, and other tumor types, but not yet systematically in CRC. Here, we discuss how targeting genes involved in the responses to replication stress and the repair of DNA double-strand breaks (DSBs) could provide new therapeutic opportunities to treat CRCs and have the potential to confer increased sensitivity to current chemotherapy regimens, thus, expanding the spectrum of therapy options, and potentially improving clinical outcomes for CRC patients. Despite the ample improvements of CRC molecular landscape, the therapeutic options still rely on conventional chemotherapy-based regimens for early disease, and few targeted agents are recommended for clinical use in the metastatic setting. Moreover, the impact of cytotoxic, targeted agents, and immunotherapy combinations in the metastatic scenario is not fully satisfactory, especially the outcomes for patients who develop resistance to these treatments need to be improved. Here, we examine the opportunity to consider therapeutic agents targeting DNA repair and DNA replication stress response as strategies to exploit genetic or functional defects in the DNA damage response (DDR) pathways through synthetic lethal mechanisms, still not explored in CRC. These include the multiple actors involved in the repair of DNA double-strand breaks (DSBs) through homologous recombination (HR), classical non-homologous end joining (NHEJ), and microhomology-mediated end-joining (MMEJ), inhibitors of the base excision repair (BER) protein poly (ADP-ribose) polymerase (PARP), as well as inhibitors of the DNA damage kinases ataxia-telangiectasia and Rad3 related (ATR), CHK1, WEE1, and ataxia-telangiectasia mutated (ATM). We also review the biomarkers that guide the use of these agents, and current clinical trials with targeted DDR therapies.
C1 [Tomasini, Paula Pellenz; Leguisamo, Natalia Motta; Saffi, Jenifer] Fed Univ Hlth Sci Porto Alegre, Lab Genet Toxicol, Ave Sarmento Leite 245, BR-90050170 Porto Alegre, RS, Brazil.
   [Tomasini, Paula Pellenz; Saffi, Jenifer] Univ Fed Rio Grande do Sul, Postgrad Program Cell & Mol Biol, Ave Bento Goncalves 9500, BR-91501970 Porto Alegre, RS, Brazil.
   [Guecheva, Temenouga Nikolova] Univ Fdn Cardiol IC FUC, Cardiol Inst Rio Grande do Sul, BR-90620000 Porto Alegre, RS, Brazil.
   [Pericart, Sarah; Brunac, Anne-Cecile; Hoffmann, Jean Sebastien] Inst Univ Canc Toulouse, Lab Excellence Toulouse Canc TOUCAN, Lab Pathol, Oncopole, 1 Ave Irene Joliot Curie, F-31059 Toulouse, France.
C3 Universidade Federal do Rio Grande do Sul
RP Saffi, J (corresponding author), Fed Univ Hlth Sci Porto Alegre, Lab Genet Toxicol, Ave Sarmento Leite 245, BR-90050170 Porto Alegre, RS, Brazil.; Saffi, J (corresponding author), Univ Fed Rio Grande do Sul, Postgrad Program Cell & Mol Biol, Ave Bento Goncalves 9500, BR-91501970 Porto Alegre, RS, Brazil.
EM paula-tomasini@hotmail.com; tgesheva@gmail.com; nmleguisamo@gmail.com;
   pericart.sarah@iuct-oncopole.fr; brunac.annececile@iuct-oncopole.fr;
   jean-sebastien.hoffmann@inserm.fr; jenifers@ufcspa.edu.br
RI Hoffmann, Jean-Sebastien/O-9183-2014; Guecheva, Temenouga/C-3495-2009;
   Saffi, Jenifer/G-4199-2018
OI Hoffmann, Jean-Sebastien/0000-0003-2222-354X; Guecheva,
   Temenouga/0000-0001-8671-7317; Saffi, Jenifer/0000-0002-5372-2934;
   Pellenz Tomasini, Paula/0000-0002-9621-688X
FU Brazilian agency Fundacao de Amparo a Pesquisa do Estado do Rio Grande
   do Sul (FAPERGS); Brazilian agency Conselho Nacional de Desenvolvimento
   Cientifico e Tecnologico, (CNPq) - PRONEX-FAPERS/CNPq
   [16/2551-0000473-0-1]
FX P.P.T and J.S were supported by the Brazilian agencies Fundacao de
   Amparo a Pesquisa do Estado do Rio Grande do Sul (FAPERGS) and Conselho
   Nacional de Desenvolvimento Cientifico e Tecnologico, (CNPq) -
   PRONEX-FAPERS/CNPq - Grant no. 16/2551-0000473-0-1.
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NR 278
TC 15
Z9 15
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 JUL
PY 2021
VL 13
IS 13
AR 3130
DI 10.3390/cancers13133130
PG 37
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TG1ST
UT WOS:000671191700001
PM 34201502
OA Green Published
DA 2025-01-04
ER

PT J
AU Sandhiya, V
   Senthilkumaran, K
   Ubaidulla, U
AF Sandhiya, V.
   Senthilkumaran, K.
   Ubaidulla, U.
TI Signal Passageway of Phenolic Acid in Opposition to Malignancy
   Management
SO CURRENT PHARMACOLOGY REPORTS
LA English
DT Review
DE Polyphenols; Anticancer agent; Herbal medicines
ID COLON-CANCER CELLS; COMPLEMENTARY THERAPY USE; BREAST-CANCER; GREEN TEA;
   ALTERNATIVE MEDICINE; PHASE-II; ANTICANCER ACTIVITY; HERBAL MEDICINE;
   INHIBIT GROWTH; APOPTOSIS
AB BackgroundOne of the main causes of concern for the worldwide public health system is cancer, which is a diverse disease. Here, the abundance of different chemicals and pharmacologically active substances found in nature serves as a source for anticancer medications. Some natural compounds and their synthetic analogues have been studied in the last 10 years as potential cancer treatments. Polyphenols are secondary metabolites of plants that are amongst the enormous phytochemicals engaged in the defence against many types of stress.BodyPolyphenols have demonstrated potential health advantages in a number of oxidative stress-related disorders, including cancer, as a result of their powerful antioxidant effects. Polyphenols have the ability to stop the growth, spread, and carcinogenesis of tumour cells. The development of successful anticancer medicines depends on a thorough understanding of tumour biology, the discovery of novel molecular targets, the creation of specialised antitumour agents, and increasing the susceptibility of tumour cells to standard/targeted therapy. The use of natural compounds, particularly polyphenols, as a source of anticancer medications is the main topic of this review paper. This briefly describes the molecular mechanisms that affect various cancer cell types.
C1 [Sandhiya, V.] CL Baid Metha Coll Pharm, Dept Pharmaceut, Chennai, India.
   [Senthilkumaran, K.] KK Coll Pharm, Dept Pharmaceut, Chennai, India.
   [Ubaidulla, U.] BS Abdur Rahman Crescent Inst Sci & Technol, Crescent Sch Pharm, Dept Pharmaceut, Chennai 600048, Tamilnadu, India.
C3 B. S. Abdur Rahman Crescent Institute of Science & Technology
RP Sandhiya, V (corresponding author), CL Baid Metha Coll Pharm, Dept Pharmaceut, Chennai, India.
EM sandhiyavaithi@gmail.com
RI Uthumansha, Ubaidulla/G-1533-2016
OI Uthumansha, Ubaidulla/0000-0001-5064-6676
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NR 96
TC 0
Z9 0
U1 0
U2 0
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2198-641X
J9 CURR PHARMACOL REP
JI Curr. Pharmacol. Rep.
PD AUG
PY 2023
VL 9
IS 4
BP 247
EP 259
DI 10.1007/s40495-023-00321-3
PG 13
WC Pharmacology & Pharmacy
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA A2W2H
UT WOS:001281176500006
DA 2025-01-04
ER

PT J
AU Naseer, QA
   Malik, A
   Zhang, FY
   Chen, SX
AF Naseer, Qais Ahmad
   Malik, Abdul
   Zhang, Fengyuan
   Chen, Shengxia
TI Exploring the enigma: history, present, and future of long non-coding
   RNAs in cancer
SO DISCOVER ONCOLOGY
LA English
DT Review
DE LncRNA; Gene expression; Biogenesis; Regulatory mechanisms; Genomic
   location
ID CELL LUNG-CANCER; ENHANCES RADIOSENSITIVITY; PROSTATE-CANCER;
   GASTRIC-CANCER; NASOPHARYNGEAL CARCINOMA; COLORECTAL-CANCER;
   BREAST-CANCER; XIST GENE; CHROMOSOMAL RNA; SATELLITE DNA
AB Long noncoding RNAs (lncRNAs), which are more than 200 nucleotides in length and do not encode proteins, play crucial roles in governing gene expression at both the transcriptional and posttranscriptional levels. These molecules demonstrate specific expression patterns in various tissues and developmental stages, suggesting their involvement in numerous developmental processes and diseases, notably cancer. Despite their widespread acknowledgment and the growing enthusiasm surrounding their potential as diagnostic and prognostic biomarkers, the precise mechanisms through which lncRNAs function remain inadequately understood. A few lncRNAs have been studied in depth, providing valuable insights into their biological activities and suggesting emerging functional themes and mechanistic models. However, the extent to which the mammalian genome is transcribed into functional noncoding transcripts is still a matter of debate. This review synthesizes our current understanding of lncRNA biogenesis, their genomic contexts, and their multifaceted roles in tumorigenesis, highlighting their potential in cancer-targeted therapy. By exploring historical perspectives alongside recent breakthroughs, we aim to illuminate the diverse roles of lncRNA and reflect on the broader implications of their study for understanding genome evolution and function, as well as for advancing clinical applications.
C1 [Naseer, Qais Ahmad; Malik, Abdul; Zhang, Fengyuan; Chen, Shengxia] Jiangsu Univ, Sch Med, Dept Lab Med, 301 Xuefu Rd, Zhenjiang 212013, Jiangsu, Peoples R China.
C3 Jiangsu University
RP Chen, SX (corresponding author), Jiangsu Univ, Sch Med, Dept Lab Med, 301 Xuefu Rd, Zhenjiang 212013, Jiangsu, Peoples R China.
EM chensxia@ujs.edu.cn
RI Malik, Abdul/GQP-0935-2022; Zhang, Fengyuan/ITT-9036-2023
FU Basic Platform Project of the Ministry of Science and Technology of
   China
FX No Statement Available
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NR 245
TC 4
Z9 4
U1 0
U2 1
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 JUN 7
PY 2024
VL 15
IS 1
AR 214
DI 10.1007/s12672-024-01077-y
PG 22
WC Oncology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Endocrinology & Metabolism
GA TV3T5
UT WOS:001244002600002
PM 38847897
OA gold, Green Accepted
DA 2025-01-04
ER

PT J
AU Bhattacharya, D
   Sakhare, K
   Narayan, KP
   Banerjee, R
AF Bhattacharya, Dwaipayan
   Sakhare, Kalyani
   Narayan, Kumar Pranav
   Banerjee, Rajkumar
TI The prospects of nanotherapeutic approaches for targeting
   tumor-associated macrophages in oral cancer
SO NANOMEDICINE-NANOTECHNOLOGY BIOLOGY AND MEDICINE
LA English
DT Article
DE Oral cancer; Targeted cancer therapy; Tumor Microenvironment; Metastasis
ID SQUAMOUS-CELL CARCINOMA; LYMPH-NODE METASTASIS; EPITHELIAL-MESENCHYMAL
   TRANSITION; MICROENVIRONMENTAL REGULATION; INFLAMMATORY CYTOKINES;
   CLINICAL-SIGNIFICANCE; COLORECTAL-CANCER; IMMUNE PRIVILEGE; MYELOID
   CELLS; IN-VITRO
AB OSCC (oral squamous cell carcinoma) is currently one of the most formidable cancers plagued by challenges like low overall survivability, lymph node associated metastasis, drug resistance, and poor diagnostics. The tumor microenvironment (TME) and its constituent stromal elements are crucial modulators of tumor growth and treatment response, more specifically so with regards to resident tumor associated macrophages (TAMs) and their liaison with the different stromal elements in the tumor niche (Figure 1). Interestingly, there isn't much information on TAM-targeted nanotherapy in OSCC where the first line of therapeutics for oral cancer is surgery with other therapeutics such as chemo-and radiotherapy acting only as adjuvant therapy for oral cancer. In the face of this real time situation, there have been some successful attempts at targeted therapy for OSCC cells and we believe they might elicit favorable responses against TAMs as well. Demanding our immediate attention, this review intends to provide a glimpse of the prevailing anti-TAM treatment strategies, which present great prospect for an uncharted territory like OSCC. (C) 2021 Elsevier Inc. All rights reserved.
C1 [Bhattacharya, Dwaipayan; Sakhare, Kalyani; Narayan, Kumar Pranav] Bits Pilani, Dept Biol Sci, Hyderabad Campus, Hyderabad, India.
   [Banerjee, Rajkumar] CSIR Indian Inst Chem Technol, Div Appl Biol, Uppal Rd, Hyderabad, Telangana, India.
C3 Birla Institute of Technology & Science Pilani (BITS Pilani); Council of
   Scientific & Industrial Research (CSIR) - India; CSIR - Indian Institute
   of Chemical Technology (IICT)
RP Narayan, KP (corresponding author), Bits Pilani, Dept Biol Sci, Hyderabad Campus, Hyderabad, India.; Banerjee, R (corresponding author), CSIR Indian Inst Chem Technol, Div Appl Biol, Uppal Rd, Hyderabad, Telangana, India.
EM pranav@hyderabad.bits-pilani.ac.in; banerjee@iict.res.in
RI Banerjee, Rajkumar/AAC-2699-2020
OI Narayan, Kumar Pranav/0000-0001-5198-2495; Banerjee,
   Rajkumar/0000-0003-2336-6294
FU IICT [IICT/Pubs./2020/277]
FX RB acknowledges Director IICT for help with the project [IICT
   Communication No.-IICT/Pubs./2020/277]. KPN acknowledges Director, BITS
   Pilani, Hyderabad Campus and Centre for Human Diseases Research for help
   with the project.
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NR 196
TC 5
Z9 5
U1 2
U2 19
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1549-9634
EI 1549-9642
J9 NANOMED-NANOTECHNOL
JI Nanomed.-Nanotechnol. Biol. Med.
PD JUN
PY 2021
VL 34
AR 102371
DI 10.1016/j.nano.2021.102371
EA MAR 2021
PG 23
WC Nanoscience & Nanotechnology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Research & Experimental Medicine
GA SS5AX
UT WOS:000661767200004
PM 33662592
DA 2025-01-04
ER

PT J
AU Kim, HJ
   Lee, DS
   Park, JH
   Hong, HE
   Choi, HJ
   Kim, OH
   Kim, SJ
AF Kim, Hyung-Jin
   Lee, Do Sang
   Park, Jung Hyun
   Hong, Ha-Eun
   Choi, Ho Joong
   Kim, Ok-Hee
   Kim, Say-June
TI Exosome-based strategy against colon cancer using small interfering
   RNA-loaded vesicles targeting soluble a proliferation-inducing ligand
SO WORLD JOURNAL OF STEM CELLS
LA English
DT Article
DE Colon cancer; Drug delivery system; Exosome; Soluble a
   proliferation-inducing ligand; Peptidyl-prolyl cis-trans isomerase
   NIMA-interacting 1; Targeted therapy
ID BETA-CATENIN; APRIL; PIN1; BLOCKING; BAFF
AB BACKGROUND Recent advancements in nanomedicine have highlighted the potential of exosome (Ex)-based therapies, utilizing naturally derived nanoparticles, as a novel approach to targeted cancer treatment. AIM To explore the targetability and anticancer effectiveness of small interfering peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 RNA (siPIN1)-loaded soluble a proliferation-inducing ligand (sAPRIL)-targeted Exs (designated as tEx[p]) in the treatment of colon cancer models. METHODS tEx was generated by harvesting conditioned media from adipose-derived stem cells that had undergone transformation using pDisplay vectors encoding sAPRIL-binding peptide sequences. Subsequently, tEx[p] were created by incorporating PIN1 siRNA into the tEx using the Exofect kit. The therapeutic efficacy of these Exs was evaluated using both in vitro and in vivo models of colon cancer. RESULTS The tEx[p] group exhibited superior anticancer effects in comparison to other groups, including tEx, Ex[p], and Ex, demonstrated by the smallest tumor size, the slowest tumor growth rate, and the lightest weight of the excised tumors observed in the tEx[p] group (P < 0.05). Moreover, analyses of the excised tumor tissues, using western blot analysis and immunohistochemical staining, revealed that tEx[p] treatment resulted in the highest increase in E-cadherin expression and the most significant reduction in the mesenchymal markers Vimentin and Snail (P < 0.05), suggesting a more effective inhibition of epithelial-mesenchymal transition tEx[p], likely due to the enhanced delivery of siPIN1. CONCLUSION The use of bioengineered Exs targeting sAPRIL and containing siPIN1 demonstrated superior efficacy in inhibiting tumor growth and epithelial-mesenchymal transition, highlighting their potential as a therapeutic strategy for colon cancer.
C1 [Kim, Hyung-Jin; Park, Jung Hyun; Kim, Say-June] Catholic Univ Korea, Seoul St Marys Hosp, Coll Med, Dept Surg, 222 Banpo Daero, Seoul 06591, South Korea.
   [Lee, Do Sang; Choi, Ho Joong; Kim, Say-June] Catholic Univ Korea, Seoul St Marys Hosp, Coll Med, Dept Surg, Seoul 06591, South Korea.
   [Lee, Do Sang; Park, Jung Hyun; Hong, Ha-Eun; Kim, Ok-Hee; Kim, Say-June] Catholic Univ Korea, Coll Med, Catholic Cent Lab Surg, Seoul 06591, South Korea.
   [Hong, Ha-Eun; Kim, Ok-Hee] Surginex Co Ltd, Translat Res Team, Seoul 06591, South Korea.
C3 Catholic University of Korea; Seoul St. Mary's Hospital; Seoul St.
   Mary's Hospital; Catholic University of Korea; Catholic University of
   Korea
RP Kim, SJ (corresponding author), Catholic Univ Korea, Seoul St Marys Hosp, Coll Med, Dept Surg, 222 Banpo Daero, Seoul 06591, South Korea.
EM sayjunekim@catholic.ac.kr
FU National Research Foundation of Korea [NRF-2018R1D1A1B07047144]
FX Supported by the National Research Foundation of Korea, No.
   NRF-2018R1D1A1B07047144.
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NR 39
TC 0
Z9 0
U1 0
U2 0
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-0210
J9 WORLD J STEM CELLS
JI World J. Stem Cells
PD NOV 26
PY 2024
VL 16
IS 11
DI 10.4252/wjsc.v16.i11.956
PG 19
WC Cell & Tissue Engineering; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA O1Z8J
UT WOS:001369202800005
PM 39619877
DA 2025-01-04
ER

PT J
AU Varli, M
   Ji, M
   Kim, E
   Kim, SJ
   Choi, B
   Ha, HH
   Kim, KK
   Paik, MJ
   Kim, H
AF Varli, Muecahit
   Ji, Moongi
   Kim, Eunae
   Kim, Sung Jin
   Choi, Byeongchan
   Ha, Hyung-Ho
   Kim, Kyung Keun
   Paik, Man-Jeong
   Kim, Hangun
TI Emodin disrupts the KITENIN oncogenic complex by binding ErbB4 and
   suppresses colorectal cancer progression in dual blockade with
   KSRP-binding compound
SO PHYTOMEDICINE
LA English
DT Article
DE Emodin; Metastasis; KITENIN (VANGL1); ErbB4; KSRP; Energy metabolism
ID HNRNP PROTEINS; CELL MOTILITY; IN-VITRO; C-MYC; APOPTOSIS; METASTASIS;
   EXPRESSION; INVASIVENESS; NANOPARTICLES; PROLIFERATION
AB Background: The KITENIN/ErbB4 complex has been reported to participate in metastasis, which is the principal reason of death in most colorectal cancer patients. Purpose: New therapeutics need to be developed to suppress the malignant effects of the KITENIN/ErbB4 complex, which is related to drug resistance. The present study aimed to evaluate changes in cancer cell invasion capacity, transcriptional regulators, and cellular bioenergetics after targeting the KITENIN/ErbB4 complex with emodin. Moreover, we aimed to reveal the mechanistic effects of emodin and observe the dual blockade effects of ErbB4-targeted therapy with KH-type splicing regulatory protein (KSRP) and search for new alternative blockade pathways. Methods: Using in vitro, in vivo, molecular-docking, and metabolomics studies, we evaluated the anticancer effect of emodin alone or in combination with DKC-C14S. Results: Emodin treatment decreased KITENIN and ErbB4 protein levels. The dysfunctional KITENIN/ErbB4 complex suppressed KITENIN-mediated cell invasion and downregulated AP-1 activity, aerobic glycolysis, and the levels of transcriptional regulators associated with cell metabolism. We conclude that emodin targets the KITENIN/ErbB4 complex and offering a novel mechanism by which it disrupts KITENIN-mediated signaling. Furthermore, we were demonstrated that the dual blocking effect of emodin and DKC-C14S on the KITENIN complex showed synergistic effects in suppressing colorectal cancer progression under in cell-based and animal assay. Conclusion: The results suggest that co-treatment with ErbB4 and KSRP-binding compounds could constitute a potential strategy for controlling colorectal cancer progression by disrupting the KITENIN complex.
C1 [Varli, Muecahit; Ji, Moongi; Choi, Byeongchan; Ha, Hyung-Ho; Paik, Man-Jeong; Kim, Hangun] Sunchon Natl Univ, Coll Pharm, Sunchon 57922, South Korea.
   [Kim, Eunae] Chosun Univ, Coll Pharm, 146 Chosundae Gil, Gwangju 61452, South Korea.
   [Kim, Sung Jin; Kim, Kyung Keun] Chonnam Natl Univ, Med Sch, Dept Pharmacol, 160 Baekseoro, Gwangju 61469, South Korea.
C3 Sunchon National University; Chosun University; Chonnam National
   University
RP Kim, H (corresponding author), Sunchon Natl Univ, Coll Pharm, Sunchon 57922, South Korea.
EM mucahitvarli@s.scnu.ac.kr; wlansrl@naver.com; eunaekim@chosun.ac.kr;
   ksz910@naver.com; chlqudcks456@naver.com; hhha@sunchon.ac.kr;
   kimkk@chonnam.ac.kr; paik815@sunchon.ac.kr; hangunkim@scnu.ac.kr
RI Kim, Dae/D-8864-2013
OI VARLI, MUCAHIT/0000-0001-6175-4015; Kim, Hangun/0000-0001-5889-8907
FU National Research Foundation of Korea - Korean Government (MSIP)
   [RS-2024-00413760]
FX This work was supported by the National Research Foundation of Korea
   grant (RS-2024-00413760) funded by the Korean Government (MSIP) .
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NR 99
TC 0
Z9 0
U1 5
U2 5
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0944-7113
EI 1618-095X
J9 PHYTOMEDICINE
JI Phytomedicine
PD JAN
PY 2025
VL 136
AR 156247
DI 10.1016/j.phymed.2024.156247
EA NOV 2024
PG 17
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 N8S0G
UT WOS:001366952600001
PM 39586126
DA 2025-01-04
ER

PT J
AU Shi, WD
   Song, JX
   Wang, WC
   Zhang, YJ
   Zheng, SY
AF Shi, Woda
   Song, Jianxiang
   Wang, Wencai
   Zhang, Yajun
   Zheng, Shiying
TI RETRACTED: MACC-1 antibody target therapy suppresses growth and
   migration of non-small cell lung cancer (Retracted Article)
SO MOLECULAR MEDICINE REPORTS
LA English
DT Article; Retracted Publication
DE metastasis-associated in colon cancer-1; non-small-cell lung cancer;
   chimeric antibody-metastasis-associated in colon cancer-1; migration;
   metastasis
ID GASTRIC-CANCER; METASTASIS; OVEREXPRESSION; SURVIVAL; NSCLC; EXPRESSION;
   INVASION; REGULATOR; PROTEIN; MARKER
AB Non-small-cell lung cancer (NSCLC) accounts for similar to 80% of human lung cancers that result in mortalities worldwide. Metastasis-associated in colon cancer-1 (MACC-1) has been demonstrated to be significantly expressed in cases of NSCLC and promotes tumor cell migration and metastasis through transactivation of the metastasis-inducing hepatocyte growth factor/MET proto-gene, receptor tyrosine kinase (HGF/MET) signaling pathway. The present study constructed a chimeric antibody (Chanti-MACC-1) targeting MACC-1 and investigated its potential as a molecular therapeutic target in the treatment of NSCLC therapy. The expression of MACC-1 was detected by reverse transcription-quantitative polymerase chain reaction and western blotting in lung cancer cell lines and tissues. MTT assay was used to detect proliferation of A549 cells treated by Chanti-MACC-1, whereas the functional and regulatory effects of Chanti-MACC-1 in the migration and metastasis of NSCLC cells was investigated by a cell invasion assay. The therapeutic effect and survival time was observed in animal models. The results demonstrated that MACC-1 expression was increased and overexpression of MACC-1 promoted the progression of the cell cycle, significantly promoted NSCLC cell growth and enhanced tumor migration and invasion through the HGF/MET signaling pathway. It was further demonstrated that Chanti-MACC-1 efficiently suppressed MACC-1 expression and significantly inhibited NSCLC cell proliferation, migration and invasion by blocking the HGF/MET signaling pathway. The data revealed that Chanti-MACC-1 was not only beneficial for tumor remission, however additionally contributed to the long-term survival of NSCLC-bearing mice. The findings of the present study indicated that MACC-1 was significantly upregulated and promoted tumor cell growth and migration in NSCLC cells and tissues via transactivation of the metastasis-inducing HGF/MET signaling pathway. However, Chanti-MACC-1significantly inhibited tumor growth and metastasis, which suggested that MACC-1 may be essential for tumor initiation and progression by negatively regulating tumor suppressors.
C1 [Shi, Woda; Zheng, Shiying] Soochow Univ, Affiliated Hosp 1, Dept Cardiothorac Surg, 188 Shizi St, Suzhou 215006, Jiangsu, Peoples R China.
   [Song, Jianxiang; Wang, Wencai; Zhang, Yajun] Third Peoples Hosp, Dept Cardiothorac Surg, Yancheng 224001, Jiangsu, Peoples R China.
C3 Soochow University - China
RP Zheng, SY (corresponding author), Soochow Univ, Affiliated Hosp 1, Dept Cardiothorac Surg, 188 Shizi St, Suzhou 215006, Jiangsu, Peoples R China.
EM zhengshiying163@163.com
RI Zheng, Shiyou/AAG-3154-2019; Zhang, Y J/HLG-1022-2023; wencai,
   wang/GSD-9950-2022
CR Arora S, 2011, INT J CANCER, V129, P2621, DOI 10.1002/ijc.25939
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NR 45
TC 3
Z9 4
U1 0
U2 6
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1791-2997
EI 1791-3004
J9 MOL MED REP
JI Mol. Med. Rep.
PD NOV
PY 2017
VL 16
IS 5
BP 7329
EP 7336
DI 10.3892/mmr.2017.7517
PG 8
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA FM0ZU
UT WOS:000414698900207
PM 28944826
OA Green Published, Green Submitted, hybrid
DA 2025-01-04
ER

PT J
AU Ha, SD
   Lewin, N
   Li, SSC
   Kim, SO
AF Ha, Soon-Duck
   Lewin, Naomi
   Li, Shawn S. C.
   Kim, Sung-Ouk
TI HDAC8 Activates AKT through Upregulating PLCB1 and Suppressing DESC1
   Expression in MEK1/2 Inhibition-Resistant Cells
SO CELLS
LA English
DT Article
DE lethal toxin; AKT; PLCB1; PI-PLC; DESC1; HT-29 cells; cancer; resistance
ID LETHAL-TOXIN; PHOSPHOLIPASE-C; COLORECTAL-CANCER; TUMOR-SUPPRESSOR;
   MELANOMA-CELLS; KINASE-KINASE; CYCLE ARREST; CARCINOMA; PROLIFERATION;
   MUTATIONS
AB Inhibition of the RAF-MEK1/2-ERK signaling pathway is an ideal strategy for treating cancers with NRAS or BRAF mutations. However, the development of resistance due to incomplete inhibition of the pathway and activation of compensatory cell proliferation pathways is a major impediment of the targeted therapy. The anthrax lethal toxin (LT), which cleaves and inactivates MEKs, is a modifiable biomolecule that can be delivered selectively to tumor cells and potently kills various tumor cells. However, resistance to LT and the mechanism involved are yet to be explored. Here, we show that LT, through inhibiting MEK1/2-ERK activation, inhibits the proliferation of cancer cells with NRAS/BRAF mutations. Among them, the human colorectal tumor HT-29 and murine melanoma B16-BL6 cells developed resistance to LT in 2 to 3 days of treatment. These resistant cells activated AKT through a histone deacetylase (HDAC) 8-dependent pathway. Using an Affymetrix microarray, followed by qPCR validation, we identified that the differential expression of the phospholipase C-beta 1 (PLCB1) and squamous cell carcinoma-1 (DESC1) played an important role in HDAC8-mediated AKT activation and resistance to MEK1/2-ERK inhibition. By using inhibitors, small interference RNAs and/or expression vectors, we found that the inhibition of HDAC8 suppressed PLCB1 expression and induced DESC1 expression in the resistant cells, which led to the inhibition of AKT and re-sensitization to LT and MEK1/2 inhibition. These results suggest that targeting PLCB1 and DESC1 is a novel strategy for inhibiting the resistance to MEK1/2 inhibition.
C1 [Ha, Soon-Duck; Lewin, Naomi; Kim, Sung-Ouk] Univ Western Ontario, Schulich Sch Med & Dent, Dept Microbiol & Immunol, London, ON N6G 2V4, Canada.
   [Ha, Soon-Duck; Li, Shawn S. C.] Univ Western Ontario, Schulich Sch Med & Dent, Dept Biochem, London, ON N6G 2V4, Canada.
C3 Western University (University of Western Ontario); Western University
   (University of Western Ontario)
RP Kim, SO (corresponding author), Univ Western Ontario, Schulich Sch Med & Dent, Dept Microbiol & Immunol, London, ON N6G 2V4, Canada.
EM sha3@uwo.ca; naomi.lewin@mail.utoronto.ca; sli@uwo.ca; skim283@uwo.ca
RI Li, Shawn/A-9007-2012; Kim, Sung Ouk/AAO-1795-2020
OI Kim, Sung Ouk/0000-0002-0282-6661; Li, Shawn/0000-0003-3610-9035
FU NSERC [RGPIN-2018-05514]
FX This work was supported by the NSERC Discovery Grant (RGPIN-2018-05514)
   to S.O.K.
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NR 56
TC 11
Z9 11
U1 0
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD MAY
PY 2021
VL 10
IS 5
AR 1101
DI 10.3390/cells10051101
PG 16
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA SI2GB
UT WOS:000654643200001
PM 34064422
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kalimutho, M
   Bain, AL
   Mukherjee, B
   Nag, P
   Nanayakkara, DM
   Harten, SK
   Harris, JL
   Subramanian, GN
   Sinha, D
   Shirasawa, S
   Srihari, S
   Burma, S
   Khanna, KK
AF Kalimutho, Murugan
   Bain, Amanda L.
   Mukherjee, Bipasha
   Nag, Purba
   Nanayakkara, Devathri M.
   Harten, Sarah K.
   Harris, Janelle L.
   Subramanian, Goutham N.
   Sinha, Debottam
   Shirasawa, Senji
   Srihari, Sriganesh
   Burma, Sandeep
   Khanna, Kum Kum
TI Enhanced dependency of KRAS-mutant colorectal cancer cells on
   RAD51-dependent homologous recombination repair identified from genetic
   interactions in <i>Saccharomyces</i> <i>cerevisiae</i>
SO MOLECULAR ONCOLOGY
LA English
DT Article
DE colorectal cancer; DNA damage response; homologous recombination repair;
   KRAS; RAD51; therapeutic vulnerability
ID SYNTHETIC LETHAL INTERACTIONS; STRAND BREAK REPAIR; PI3K/MTOR INHIBITOR
   NVP-BEZ235; GROWTH-FACTOR RECEPTOR; DNA-DAMAGE; C-MYC; POTENT INHIBITOR;
   MEK INHIBITORS; RAS; YEAST
AB Activating KRAS mutations drive colorectal cancer tumorigenesis and influence response to anti-EGFR-targeted therapy. Despite recent advances in understanding Ras signaling biology and the revolution in therapies for melanoma using BRAF inhibitors, no targeted agents have been effective in KRAS-mutant cancers, mainly due to activation of compensatory pathways. Here, by leveraging the largest synthetic lethal genetic interactome in yeast, we identify that KRAS-mutated colorectal cancer cells have augmented homologous recombination repair (HRR) signaling. We found that KRAS mutation resulted in slowing and stalling of the replication fork and accumulation of DNA damage. Moreover, we found that KRAS-mutant HCT116 cells have an increase in MYC-mediated RAD51 expression with a corresponding increase in RAD51 recruitment to irradiation-induced DNA double- strand breaks (DSBs) compared to genetically complemented isogenic cells. MYC depletion using RNA interference significantly reduced IR-induced RAD51 foci formation and HRR. On the contrary, overexpression of either HA-tagged wild-type (WT) MYC or phospho-mutant S62A increased RAD51 protein levels and hence IR-induced RAD51 foci. Likewise, depletion of RAD51 selectively induced apoptosis in HCT116-mutant cells by increasing DSBs. Pharmacological inhibition targeting HRR signaling combined with PARP inhibition selectivity killed KRAS-mutant cells. Interestingly, these differences were not seen in a second isogenic pair of KRAS WT and mutant cells (DLD-1), likely due to their nondependency on the KRAS mutation for survival. Our data thus highlight a possible mechanism by which KRAS-mutant-dependent cells drive HRR in vitro by upregulating MYC-RAD51 expression. These data may offer a promising therapeutic vulnerability in colorectal cancer cells harboring otherwise nondruggable KRAS mutations, which warrants further investigation in vivo.
C1 [Kalimutho, Murugan; Bain, Amanda L.; Nag, Purba; Nanayakkara, Devathri M.; Harten, Sarah K.; Harris, Janelle L.; Subramanian, Goutham N.; Sinha, Debottam; Khanna, Kum Kum] QIMR Berghofer Med Res Inst, Signal Transduct Lab, 300 Herston Rd, Brisbane, Qld 4006, Australia.
   [Kalimutho, Murugan; Nag, Purba; Sinha, Debottam] Griffith Univ, Sch Nat Sci, Nathan, Qld, Australia.
   [Mukherjee, Bipasha; Burma, Sandeep] Univ Texas Southwestern Med Ctr Dallas, Dept Radiat Oncol, Div Mol Radiat Biol, Dallas, TX 75390 USA.
   [Shirasawa, Senji] Fukuoka Univ, Dept Cell Biol, Fac Med, Fukuoka, Japan.
   [Srihari, Sriganesh] Univ Queensland, Inst Mol Biosci, St Lucia, Qld, Australia.
C3 QIMR Berghofer Medical Research Institute; Griffith University;
   University of Texas System; University of Texas Southwestern Medical
   Center Dallas; Fukuoka University; University of Queensland
RP Kalimutho, M; Khanna, KK (corresponding author), QIMR Berghofer Med Res Inst, Signal Transduct Lab, 300 Herston Rd, Brisbane, Qld 4006, Australia.
EM Murugan.Kalimutho@qimrberghofer.edu.au;
   KumKum.Khanna@qimrberghofer.edu.au
RI Khanna, Kum/I-1747-2013; Kalimutho, Murugan/AAD-1441-2019; Nag,
   Purba/AAD-8676-2020; Sinha, Debottam/J-5521-2019; Srihari,
   Sriganesh/H-1740-2013; Subramanian, Goutham Narayanan/X-8001-2018; Nag,
   Purba/K-3595-2016
OI Wilkinson, Sarah/0000-0002-1912-8384; Srihari,
   Sriganesh/0000-0002-0713-6723; Kalimutho, Murugan/0000-0002-0772-8673;
   Subramanian, Goutham Narayanan/0000-0002-2835-8464; Khanna, Kum
   Kum/0000-0001-8650-5381; Nag, Purba/0000-0002-6863-5438; Sinha,
   Debottam/0000-0001-7153-856X; Hancock, Janelle/0000-0001-6703-7228
FU Cancer Council Queensland (CCQ) Project Grant [1087363]; National Health
   & Medical Research Council (NH& MRC) Program Grant [1017028]; National
   Institutes of Health [RO1CA149461, RO1CA197796, R21CA202403]; National
   Aeronautics and Space Administration [NNX16AD78G]
FX We wish to thank Professor Wuhan Xiao for the HAMYC constructs and
   Stephen Miles as well as Dr. Wei Shi for technical assistance in this
   project. This work was supported by Cancer Council Queensland (CCQ)
   Project Grant to MK [ID 1087363] and National Health & Medical Research
   Council (NH& MRC) Program Grant to KKK [ID 1017028]. KKK is a NHMRC
   Senior Principal Research Fellow (ID 613638). SB is supported by grants
   from the National Institutes of Health [RO1CA149461, RO1CA197796, and
   R21CA202403] and the National Aeronautics and Space Administration
   [NNX16AD78G].
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NR 87
TC 27
Z9 31
U1 1
U2 6
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 MAY
PY 2017
VL 11
IS 5
BP 470
EP 490
DI 10.1002/1878-0261.12040
PG 21
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FA9AW
UT WOS:000405739200002
PM 28173629
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Lei, LL
   Nan, B
   Yang, FR
   Guan, GQ
   Xu, JT
   Xu, L
   Yue, RY
   Wang, YJ
   Huan, SY
   Yin, X
   Zhang, XB
   Song, GS
AF Lei, Lingling
   Nan, Bin
   Yang, Fengrui
   Guan, Guoqiang
   Xu, Juntao
   Xu, Li
   Yue, Renye
   Wang, Youjuan
   Huan, Shuangyan
   Yin, Xia
   Zhang, Xiao-Bing
   Song, Guosheng
TI Zinc-Carnosine Metallodrug Network as Dual Metabolism Inhibitor
   Overcoming Metabolic Reprogramming for Efficient Cancer Therapy
SO NANO LETTERS
LA English
DT Article
DE Metabolic reprogramming; Cu-depletion; oxidative phosphorylation;
   glycolysis; cancer therapy
ID CELLS; NANOPARTICLES; RELEASE; GLYCOLYSIS
AB The targeting of tumor metabolism as a novel strategy for cancer therapy has attracted tremendous attention. Herein, we develop a dual metabolism inhibitor, Zn-carnosine metallodrug network nanoparticles (Zn-Car MNs), which exhibits good Cu-depletion and Cu-responsive drug release, causing potent inhibition of both OXPHOS and glycolysis. Notably, Zn-Car MNs can decrease the activity of cytochrome c oxidase and the content of NAD+, so as to reduce ATP production in cancer cells. Thereby, energy deprivation, together with the depolarized mitochondrial membrane potential and increased oxidative stress, results in apoptosis of cancer cells. In result, Zn-Car MNs exerted more efficient metabolism-targeted therapy than the classic copper chelator, tetrathiomolybdate (TM), in both breast cancer (sensitive to copper depletion) and colon cancer (less sensitive to copper depletion) models. The efficacy and therapy of Zn-Car MNs suggest the possibility to overcome the drug resistance caused by metabolic reprogramming in tumors and has potential clinical relevance.
C1 [Lei, Lingling; Nan, Bin; Yang, Fengrui; Guan, Guoqiang; Xu, Juntao; Xu, Li; Yue, Renye; Wang, Youjuan; Huan, Shuangyan; Yin, Xia; Zhang, Xiao-Bing; Song, Guosheng] Hunan Univ, Coll Chem & Chem Engn, State Key Lab Chemo Biosensing & Chemometr, Changsha 410082, Peoples R China.
C3 Hunan University
RP Yin, X; Song, GS (corresponding author), Hunan Univ, Coll Chem & Chem Engn, State Key Lab Chemo Biosensing & Chemometr, Changsha 410082, Peoples R China.
EM yinxia@hnu.edu.cn; songgs@hnu.edu.cn
RI Renye, Yue/IVV-8238-2023; Yang, Fengrui/AHD-3992-2022; liu,
   junyang/IXD-1201-2023; 张, 晓兵/C-5659-2018; Song, Guosheng/AEQ-6162-2022;
   Guan, Guoqiang/A-6820-2013; Huan, Shuangyan/U-1340-2017
OI yang, feng rui/0009-0006-7132-4792; Yue, Renye/0000-0002-9750-7291;
   Song, Guosheng/0000-0001-5628-6245
FU National Key R&D Program of China [2019YFA0210100]; National Natural
   Science Foundation of China [21974039, U21A20287, 22234003, 21977027,
   21890744]; Science and Technology Project of Hunan Province [2020RC3022,
   2020SK2014]; Shenzhen Science and Technology Program
   [JCYJ20210324140205013]
FX ? ACKNOWLEDGMENTS This work was supported by the National Key R&D
   Program of China (2019YFA0210100) , the National Natural Science
   Foundation of China (Grants 21974039,U21A20287, 22234003, 21977027,
   21890744) , the Science and Technology Project of Hunan Province
   (2020RC3022, 2020SK2014) , and the Shenzhen Science and Technology
   Program (JCYJ20210324140205013) .
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TC 30
Z9 30
U1 15
U2 95
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 APR 12
PY 2023
VL 23
IS 7
BP 2659
EP 2668
DI 10.1021/acs.nanolett.2c05029
EA MAR 2023
PG 10
WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience &
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   Physics, Condensed Matter
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science;
   Physics
GA D4ZH5
UT WOS:000951554900001
PM 36940420
DA 2025-01-04
ER

PT J
AU Song, P
   Gao, ZR
   Bao, YG
   Chen, L
   Huang, YH
   Liu, YY
   Dong, Q
   Wei, XW
AF Song, Pan
   Gao, Zirui
   Bao, Yige
   Chen, Li
   Huang, Yuhe
   Liu, Yanyan
   Dong, Qiang
   Wei, Xiawei
TI Wnt/β-catenin signaling pathway in carcinogenesis and cancer therapy
SO JOURNAL OF HEMATOLOGY & ONCOLOGY
LA English
DT Review
ID SMALL-MOLECULE INHIBITORS; PROTEIN-PROTEIN INTERACTION; ELEMENT-BINDING
   PROTEIN; CELLS IN-VITRO; BETA-CATENIN; COLORECTAL-CANCER; STEM-CELLS;
   BREAST-CANCER; HEPATOCELLULAR CARCINOMAS; PROMOTER METHYLATION
AB The Wnt/beta-catenin signaling pathway plays a crucial role in various physiological processes, encompassing development, tissue homeostasis, and cell proliferation. Under normal physiological conditions, the Wnt/beta-catenin signaling pathway is meticulously regulated. However, aberrant activation of this pathway and downstream target genes can occur due to mutations in key components of the Wnt/beta-catenin pathway, epigenetic modifications, and crosstalk with other signaling pathways. Consequently, these dysregulations contribute significantly to tumor initiation and progression. Therapies targeting the Wnt/beta-catenin signaling transduction have exhibited promising prospects and potential for tumor treatment. An increasing number of medications targeting this pathway are continuously being developed and validated. This comprehensive review aims to summarize the latest advances in our understanding of the role played by the Wnt/beta-catenin signaling pathway in carcinogenesis and targeted therapy, providing valuable insights into acknowledging current opportunities and challenges associated with targeting this signaling pathway in cancer research and treatment.
C1 [Song, Pan; Bao, Yige; Dong, Qiang] Sichuan Univ, Inst Urol, Dept Urol, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.
   [Gao, Zirui; Chen, Li; Huang, Yuhe; Liu, Yanyan; Wei, Xiawei] Sichuan Univ, Natl Clin Res Ctr Geriatr, Lab Aging Res & Canc Drug Target, State Key Lab Biotherapy,West China Hosp,Canc Ctr, 17 Block 3,Southern Renmin Rd, Chengdu 610041, Sichuan, Peoples R China.
C3 Sichuan University; Sichuan University
RP Dong, Q (corresponding author), Sichuan Univ, Inst Urol, Dept Urol, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.; Wei, XW (corresponding author), Sichuan Univ, Natl Clin Res Ctr Geriatr, Lab Aging Res & Canc Drug Target, State Key Lab Biotherapy,West China Hosp,Canc Ctr, 17 Block 3,Southern Renmin Rd, Chengdu 610041, Sichuan, Peoples R China.
EM dongqiang@scu.edu.cn; xiaweiwei@scu.edu.cn
RI Gao, Zirui/AAL-5179-2020; Wei, Weiqi/LKK-3400-2024
OI Dong, Qiang/0009-0009-2730-0752; Song, Pan/0000-0001-8509-2351
FU National Science Foundation for Excellent Young Scholars
FX We express our gratitude to members of the State Key Laboratory of
   Biotherapy, Sichuan University.
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NR 353
TC 11
Z9 11
U1 19
U2 19
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1756-8722
J9 J HEMATOL ONCOL
JI J. Hematol. Oncol.
PD JUN 18
PY 2024
VL 17
IS 1
AR 46
DI 10.1186/s13045-024-01563-4
PG 30
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA UN6D1
UT WOS:001248768700002
PM 38886806
OA gold
DA 2025-01-04
ER

PT J
AU Fath, MK
   Benam, SP
   Esfahani, NK
   Shahkarami, N
   Shafa, S
   Bagheri, H
   Shafagh, SG
   Payandeh, Z
   Barati, G
AF Karami Fath, Mohsen
   Pourbagher Benam, Sasan
   Kouhi Esfahani, Niloofar
   Shahkarami, Negar
   Shafa, Shahriyar
   Bagheri, Hossein
   Shafagh, Seyyed-Ghavam
   Payandeh, Zahra
   Barati, Ghasem
TI The functional role of circular RNAs in the pathogenesis of
   retinoblastoma: a new potential biomarker and therapeutic target?
SO CLINICAL & TRANSLATIONAL ONCOLOGY
LA English
DT Review
DE Retinoblastoma; Non-coding RNA; Circular RNA; Biomarker; Cancer therapy
ID BREAST-CANCER CELL; COLORECTAL-CANCER; HEPATOCELLULAR-CARCINOMA;
   MESENCHYMAL TRANSITION; INHIBITS PROLIFERATION; TUMOR-SUPPRESSOR;
   MIR-138-5P ACTS; DOWN-REGULATION; PROGRESSION; PROTEIN
AB Retinoblastoma (RB) is a common cancer in infants and children. It is a curable disease; however, a delayed diagnosis or treatment makes the treatment difficult. Genetic mutations have a central role in the pathogenesis of RB. Genetic materials such as RNAs (coding and non-coding RNAs) are also involved in the progression of the tumor. Circular RNA (circRNA) is the most recently identified RNA and is involved in regulating gene expression mainly through "microRNA sponges". The dysregulation of circRNAs has been observed in several diseases and tumors. Also, various studies have shown that circRNAs expression is changed in RB tissues. Due to their role in the pathogenesis of the disease, circRNAs might be helpful as a diagnostic or prognostic biomarker in patients with RB. In addition, circRNAs could be a suitable therapeutic target to treat RB in a targeted therapy approach.
C1 [Karami Fath, Mohsen] Kharazmi Univ, Fac Biol Sci, Dept Cellular & Mol Biol, Tehran, Iran.
   [Pourbagher Benam, Sasan] Urmia Univ Med Sci, Fac Med, Orumiyeh, Iran.
   [Kouhi Esfahani, Niloofar] Rudn Univ Moscow, Fac Med, Moscow, Russia.
   [Shahkarami, Negar] Fasa Univ Med Sci, Sch Allied Med Sci, Fasa, Iran.
   [Shafa, Shahriyar] Kerman Univ Med Sci, Sch Med, Kerman, Iran.
   [Bagheri, Hossein] Islamic Azad Univ Tehran Branch, Fac Med, Tehran, Iran.
   [Shafagh, Seyyed-Ghavam] Iran Univ Med Sci, Fac Med, Tehran, Iran.
   [Payandeh, Zahra] Karolinska Inst, Dept Med Biochem & Biophys, Div Med Inflammat Res, Stockholm, Sweden.
   [Barati, Ghasem] Stem Cell Technol Res Ctr, Tehran, Iran.
C3 Kharazmi University; Urmia University of Medical Sciences; Kerman
   University of Medical Sciences; Iran University of Medical Sciences;
   Karolinska Institutet
RP Barati, G (corresponding author), Stem Cell Technol Res Ctr, Tehran, Iran.
EM m.gh.barati@gmail.com
RI payandeh, zahra/CAF-0179-2022; nabi afjadi, mohsen/HJA-1747-2022;
   Shahkarami, Negar/AHA-4006-2022; Shafagh, Sayedghavam/ADI-6460-2022
OI shafa, shahriyar/0000-0001-7161-2272; bagheri,
   hossein/0000-0003-4331-6358; Shafagh, Sayedghavam/0000-0002-0101-8363;
   Karami Fath, Mohsen/0000-0003-2499-7960; Pourbagher benam,
   Sasan/0000-0002-5558-4459
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NR 148
TC 0
Z9 0
U1 1
U2 6
PU SPRINGER INT PUBL AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 1699-048X
EI 1699-3055
J9 CLIN TRANSL ONCOL
JI Clin. Transl. Oncol.
PD AUG
PY 2023
VL 25
IS 8
BP 2350
EP 2364
DI 10.1007/s12094-023-03144-2
EA MAR 2023
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA J8XD4
UT WOS:000961225600001
PM 37000290
DA 2025-01-04
ER

PT J
AU Wang, L
   Wang, XY
   Guo, ER
   Mao, XH
   Miao, SS
AF Wang, Lei
   Wang, Xueying
   Guo, Erliang
   Mao, Xionghui
   Miao, Susheng
TI Emerging roles of platelets in cancer biology and their potential as
   therapeutic targets
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE platelet activation; platelet aggregation activity; immune escape;
   NETosis; tumor metastasis; liquid biopsy; tumor treatment
ID ACTIVATION RECEPTOR CLEC-2; CIRCULATING TUMOR-CELLS; COLORECTAL-CANCER;
   BREAST-CANCER; METASTASIS; PROMOTES; THROMBOSIS; RNA; THROMBOSPONDIN-1;
   THROMBOCYTOSIS
AB The main role of platelets is to control bleeding and repair vascular damage via thrombosis. They have also been implicated to promote tumor metastasis through platelet-tumor cell interactions. Platelet-tumor cell interactions promote tumor cell survival and dissemination in blood circulation. Tumor cells are known to induce platelet activation and alter platelet RNA profiles. Liquid biopsies based on tumor-educated platelet biomarkers can detect tumors and correlate with prognosis, personalized therapy, treatment monitoring, and recurrence prediction. Platelet-based strategies for cancer prevention and tumor-targeted therapy include developing drugs that target platelet receptors, interfere with the release of platelet particles, inhibit platelet-specific enzymes, and utilize platelet-derived "nano-platelets" as a targeted drug delivery platform for tumor therapy. This review elaborates on platelet-tumor cell interactions and the molecular mechanisms and discusses future research directions for platelet-based liquid biopsy techniques and platelet-targeted anti-tumor strategies.
C1 [Wang, Lei; Mao, Xionghui; Miao, Susheng] Harbin Med Univ, Canc Hosp, Dept Head & Neck Surg, Harbin, Peoples R China.
   [Wang, Xueying] Cent South Univ, Xiangya Hosp, Dept Otolaryngol Head & Neck Surg, Changsha, Peoples R China.
   [Guo, Erliang] Harbin Med Univ, Affiliated Hosp 2, Dept Surg, Harbin, Peoples R China.
C3 Harbin Medical University; Central South University; Harbin Medical
   University
RP Mao, XH; Miao, SS (corresponding author), Harbin Med Univ, Canc Hosp, Dept Head & Neck Surg, Harbin, Peoples R China.
EM xiaomao01900@163.com; drmiaosusheng@126.com
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NR 168
TC 23
Z9 24
U1 4
U2 43
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 JUL 22
PY 2022
VL 12
AR 939089
DI 10.3389/fonc.2022.939089
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3O9BV
UT WOS:000837129500001
PM 35936717
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Hwang, JC
   Sung, WW
   Tu, HP
   Hsieh, KC
   Yeh, CM
   Chen, CJ
   Tai, HC
   Hsu, CT
   Shieh, GS
   Chang, JG
   Yeh, KT
   Liu, TC
AF Hwang, Jau-Chung
   Sung, Wen-Wei
   Tu, Hung-Pin
   Hsieh, Kun-Chou
   Yeh, Chung-Min
   Chen, Chih-Jung
   Tai, Hui-Chun
   Hsu, Chao-Tien
   Shieh, Grace S.
   Chang, Jan-Gowth
   Yeh, Kun-Tu
   Liu, Ta-Chih
TI The Overexpression of FEN1 and RAD54B May Act as Independent Prognostic
   Factors of Lung Adenocarcinoma
SO PLOS ONE
LA English
DT Article
ID COLORECTAL-CANCER CELLS; SYNTHETIC LETHALITY; GENOMIC INSTABILITY; FLAP
   ENDONUCLEASE-1; TARGETED THERAPIES; REPAIR; INHIBITION; RISK;
   CHEMOPREVENTION; MUTATIONS
AB Synthetic lethality arises when a combination of mutations in two or more genes leads to cell death. However, the prognostic role of concordant overexpression of synthetic lethality genes in protein level rather than a combination of mutations is not clear. In this study, we explore the prognostic role of combined overexpression of paired genes in lung adenocarcinoma. We used immunohistochemical staining to investigate 24 paired genes in 93 lung adenocarcinoma patients and Kaplan-Meier analysis and Cox proportional hazards models to evaluate their prognostic roles. Among 24 paired genes, only FEN1 (Flap endonuclease 1) and RAD54B (RAD54 homolog B) were overexpressed in lung adenocarcinoma patients with poor prognosis. Patients with expression of both FEN1 and RAD54B were prone to have advanced nodal involvement and significantly poor prognosis (HR = 2.35, P = 0.0230). These results suggest that intensive follow up and targeted therapy might improve clinical outcome for patients who show expression of both FEN1 and RAD54B.
C1 [Hwang, Jau-Chung; Liu, Ta-Chih] Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, Kaohsiung, Taiwan.
   [Hwang, Jau-Chung] Lin Shin Hosp, Dept Pathol, Taichung, Taiwan.
   [Sung, Wen-Wei; Chen, Chih-Jung; Yeh, Kun-Tu] Chung Shan Med Univ, Sch Med, Taichung, Taiwan.
   [Sung, Wen-Wei] Chung Shan Med Univ Hosp, Dept Med Educ, Taichung, Taiwan.
   [Sung, Wen-Wei; Chen, Chih-Jung] Jen Teh Jr Coll Med Nurisng & Management, Dept Med Technol, Miaoli, Taiwan.
   [Tu, Hung-Pin] Kaohsiung Med Univ, Sch Med, Dept Publ Hlth & Environm Med, Coll Med, Kaohsiung, Taiwan.
   [Hsieh, Kun-Chou] E Da Hosp, Div Thorac Surg, Dept Surg, Kaohsiung, Taiwan.
   [Yeh, Chung-Min; Chen, Chih-Jung; Tai, Hui-Chun; Yeh, Kun-Tu] Changhua Christian Hosp, Dept Surg Pathol, Changhua, Taiwan.
   [Hsu, Chao-Tien] E Da Hosp, Dept Pathol, Kaohsiung, Taiwan.
   [Hsu, Chao-Tien] I Shou Univ, Kaohsiung, Taiwan.
   [Shieh, Grace S.] Acad Sinica, Inst Stat Sci, Taipei 11529, Taiwan.
   [Chang, Jan-Gowth] China Med Univ, Dept Lab Med, China Med Univ Hosp, Taichung, Taiwan.
   [Chang, Jan-Gowth] China Med Univ, Ctr RNA Biol & Clin Applicat, China Med Univ Hosp, Taichung, Taiwan.
   [Liu, Ta-Chih] Kaohsiung Med Univ Hosp, Div Hematol Oncol, Dept Internal Med, Kaohsiung, Taiwan.
C3 Kaohsiung Medical University; Chung Shan Medical University; Chung Shan
   Medical University; Chung Shan Medical University Hospital; Kaohsiung
   Medical University; E-Da Hospital; Changhua Christian Hospital; E-Da
   Hospital; I Shou University; Academia Sinica - Taiwan; China Medical
   University Taiwan; China Medical University Hospital - Taiwan; China
   Medical University Taiwan; China Medical University Hospital - Taiwan;
   Kaohsiung Medical University; Kaohsiung Medical University Hospital
RP Yeh, KT (corresponding author), Chung Shan Med Univ, Sch Med, Taichung, Taiwan.
EM 10159@cch.org.tw; d730093@kmu.edu.tw
RI Sung, Wen-Wei/P-5053-2019; Liu, Ta-Chih/A-1413-2010; Shieh,
   Grace/AAP-2912-2021
OI Sung, Wen-Wei/0000-0002-2375-0029; Tu, Hung-Pin/0000-0003-1044-2673
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NR 44
TC 17
Z9 22
U1 0
U2 11
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 2
PY 2015
VL 10
IS 10
AR e0139435
DI 10.1371/journal.pone.0139435
PG 12
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA CS6HH
UT WOS:000362178700058
PM 26431531
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Schatoff, EM
   Goswami, S
   Zafra, MP
   Foronda, M
   Shusterman, M
   Leach, BI
   Katti, A
   Diaz, BJ
   Dow, LE
AF Schatoff, Emma M.
   Goswami, Sukanya
   Zafra, Maria Paz
   Foronda, Miguel
   Shusterman, Michael
   Leach, Benjamin I.
   Katti, Alyna
   Diaz, Bianca J.
   Dow, Lukas E.
TI Distinct Colorectal Cancer-Associated APC Mutations Dictate Response to
   Tankyrase Inhibition
SO CANCER DISCOVERY
LA English
DT Article
ID FAMILIAL ADENOMATOUS POLYPOSIS; BETA-CATENIN; SOMATIC MUTATION; EGFR
   INHIBITION; MODELS; CELLS; DISRUPTION; ACTIVATION; GENERATION; GROWTH
AB The majority of colorectal cancers show hyperactivated WNT signaling due to inactivating mutations in the adenomatous polyposis coli (APC) tumor suppressor. Genetically restoring APC suppresses WNT and induces rapid and sustained tumor regression, implying that reengaging this endogenous tumor-suppressive mechanism may be an effective therapeutic strategy. Here, using new animal models, human cell lines, and ex vivo organoid cultures. we show that tankyrase (TNKS) inhibition can control WNT hyperactivation and provide long-term tumor control in vivo, but that effective responses are critically dependent on how APC is disrupted. Mutant APC proteins truncated within the mutation cluster region physically engage the destruction complex and suppress the WNT transcriptional program, while APC variants with early truncations (e.g., Apc(min)) show limited interaction with AXIN1 and beta-catenin, and do not respond to TNKS blockade. Together, this work shows that TNKS inhibition, like APC restoration, can reestablish endogenous control of WNT/beta-catenin signaling, but that APC genotype is a crucial determinant of this response.
   SIGNIFICANCE This study reveals how subtle changes to the mutations in a critical colorectal tumor suppressor, APC, influence the cellular response to a targeted therapy. It underscores how investigating the specific genetic alterations that occur in human cancer can identify important biological mechanisms of drug response and resistance.
C1 [Schatoff, Emma M.; Goswami, Sukanya; Zafra, Maria Paz; Foronda, Miguel; Shusterman, Michael; Leach, Benjamin I.; Katti, Alyna; Diaz, Bianca J.; Dow, Lukas E.] Weill Cornell Med, Dept Med, Sandra & Edward Meyer Canc Ctr, New York, NY USA.
   [Schatoff, Emma M.] Weill Cornell Rockefeller Sloan Kettering TriI MD, New York, NY USA.
   [Schatoff, Emma M.; Katti, Alyna; Diaz, Bianca J.; Dow, Lukas E.] Weill Cornell Med, Weill Cornell Grad Sch Med Sci, New York, NY USA.
   [Dow, Lukas E.] Weill Cornell Med, Dept Biochem, New York, NY USA.
C3 Cornell University; Weill Cornell Medicine; Cornell University; Weill
   Cornell Medicine; Cornell University; Weill Cornell Medicine
RP Dow, LE (corresponding author), Weill Cornell Med, Belfer Res Bldg,413 E 69th St,BB1318, New York, NY 10044 USA.
EM lud2005@med.cornell.edu
RI Zafra, Maria/ABH-4756-2020
OI Foronda, Miguel/0000-0001-9590-9281; Dow, Lukas/0000-0001-7048-1418;
   ZAFRA, MARIA PAZ/0000-0001-9303-0097
FU NIH/NCI [CA195787-01]; Stand Up To Cancer Colorectal Cancer Dream Team
   Translational Research Grant [SU2C-AACR-DT22-17]; U54 grant from the
   NIH/NCI [U54OD020355]; NIH [P30 CA0088748]; Medical Scientist Training
   Program grant from the National Institute of General Medical Sciences of
   the NIH [T32GM07739]; F31 Award from the NCI/NIH [1 F31 CA224800-01];
   NCI [NIH T32 CA203702]; K22 Career Development Award from the NCI/NIH
   [CA 181280-01]
FX This work was supported by a project grant from the NIH/NCI
   (CA195787-01) and a Stand Up To Cancer Colorectal Cancer Dream Team
   Translational Research Grant (SU2C-AACR-DT22-17). Stand Up To Cancer
   (SU2C) is a division of the Entertainment Industry Foundation. Research
   grants are administered by the American Association for Cancer Research,
   the scientific partner of SU2C. We thank Kevin Blighe for assistance
   with the Enhanced Volcano R package. We thank Shiaoching Gong and the
   MSKCC Mouse Transgenic Core Facility who performed zygote
   microinjections, supported in part by a U54 grant from the NIH/NCI
   (U54OD020355). We thank Katia Manova and Mesruh Turkekul from the
   Molecular Cytology Core Facility who performed ISH experiments,
   supported in part by a core grant from the NIH (P30 CA0088748). E.M.
   Schatoff was supported by a Medical Scientist Training Program grant
   from the National Institute of General Medical Sciences of the NIH under
   award number T32GM07739 to the Weill Cornell/Rockefeller/Sloan Kettering
   Tri-Institutional MD-PhD Program, and an F31 Award from the NCI/NIH
   under grant number 1 F31 CA224800-01. M.P. Zafra is supported in part by
   NCI grant NIH T32 CA203702. L.E. Dow was supported by a K22 Career
   Development Award from the NCI/NIH (CA 181280-01). The content is solely
   the responsibility of the authors and does not necessarily represent the
   official views of the NIH.
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NR 53
TC 55
Z9 62
U1 2
U2 12
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 OCT
PY 2019
VL 9
IS 10
BP 1358
EP 1371
DI 10.1158/2159-8290.CD-19-0289
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JC9VD
UT WOS:000489623800021
PM 31337618
OA Green Submitted, Bronze, Green Accepted
DA 2025-01-04
ER

PT J
AU Fan, R
   Tao, XF
   Zhai, XH
   Zhu, YN
   Li, YM
   Chen, YW
   Dong, DS
   Yang, SL
   Lv, LL
AF Fan, Rui
   Tao, Xufeng
   Zhai, Xiaohan
   Zhu, Yanna
   Li, Yunming
   Chen, Yanwei
   Dong, Deshi
   Yang, Shilei
   Lv, Linlin
TI Application of aptamer-drug delivery system in the therapy of breast
   cancer
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE Aptamer; Drug delivery system; Breast cancer; Targeted therapy
ID GOLD NANOPARTICLES; IN-VITRO; CHITOSAN NANOPARTICLES; PHOTODYNAMIC
   THERAPY; TARGETED THERAPIES; DNA NANOSTRUCTURE; MESSENGER-RNA;
   COLON-CANCER; CELLS; 5-FLUOROURACIL
AB Despite significant treatment advances, breast cancer remains the leading cause of cancer death in women. From the current treatment situation, in addition to developing chemoresistant tumours, distant organ metastasis, and recurrences, patients with breast cancer often have a poor prognosis. Aptamers as "chemical antibodies" may be a way to resolve this dilemma. Aptamers are single-stranded, non-coding oligonucleotides (DNA or RNA), resulting their many advantages, including stability for long-term storage, simplicity of synthesis and function, and low immunogenicity, a high degree of specificity and antidote. Aptamers have gained popularity as a method for diagnosing and treating specific tumors in recent years. This article introduces the application of ten different aptamer delivery systems in the treatment and diagnosis of breast cancer, and systematically reviews their latest research progress in breast cancer treatment and diagnosis. It provides a new direction for the clinical treatment of breast cancer.
C1 [Fan, Rui; Tao, Xufeng; Zhai, Xiaohan; Zhu, Yanna; Li, Yunming; Chen, Yanwei; Dong, Deshi; Yang, Shilei; Lv, Linlin] Dalian Med Univ, Dept Pharm, Affiliated Hosp 1, Dalian, Peoples R China.
   [Lv, Linlin] Dalian Med Univ, Dept Pharm, Affiliated Hosp 1, Dalian 116024, Peoples R China.
C3 Dalian Medical University; Dalian Medical University
RP Lv, LL (corresponding author), Dalian Med Univ, Dept Pharm, Affiliated Hosp 1, Dalian 116024, Peoples R China.
EM lvlinlinyu@163.com
RI fan, rui/IQS-7247-2023
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NR 147
TC 22
Z9 22
U1 11
U2 78
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 MAY
PY 2023
VL 161
AR 114444
DI 10.1016/j.biopha.2023.114444
EA FEB 2023
PG 13
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 9Y3AO
UT WOS:000950331700001
PM 36857912
OA gold
DA 2025-01-04
ER

PT J
AU Boustani, J
   Huguet, F
   Vendrely, V
AF Boustani, J.
   Huguet, F.
   Vendrely, V.
TI Practice-changing clinical trials in radiation oncology for
   gastrointestinal malignancies in 2021-2023 Les essais qui changent nos
   pratiques en radiotherapie pour les cancers digestifs en 2021-2023
SO CANCER RADIOTHERAPIE
LA English
DT Article
DE Practice-changing trials; Radiation; Oesophageal cancer; Pancreatic
   cancer; Hepatocarcinoma; Rectal cancer; Anal cancer; Organ preservation;
   Dose escalation; SMART; Chemoradiation
ID ADVANCED RECTAL-CANCER; TOTAL MESORECTAL EXCISION; PREOPERATIVE
   CHEMORADIOTHERAPY; NEOADJUVANT CHEMORADIOTHERAPY; ORGAN PRESERVATION;
   OPEN-LABEL; ADJUVANT CHEMOTHERAPY; DOSE ESCALATION; LOCAL EXCISION;
   MULTICENTER
AB Gastrointestinal cancers are one of the most frequent cancers and a leading cause of cancer deaths worldwide. We provide an overview of the most important practice-changing trials that were either published or presented at the international scientific meetings in 2021-2023. Highlights included reports on three phase III trials (CONCORDE/PRODIGE 26, ARTDECO, and a study by Xu et al.) that evaluated dose escalation in the definitive setting for locally advanced oesophageal cancers, as well as two phase III trials that evaluated the role of chemotherapy (neo-AEGIS) and targeted therapy (NRG/RTOG 1010) in the neoadjuvant setting for adenocarcinoma oesophageal cancers or gastroesophageal junction cancer. CheckMate 577 evaluated nivolumab in patients who had residual pathological disease after neoadjuvant chemoradiation followed by complete resection. The use of radiation therapy for borderline and locally advanced pancreatic cancer is also discussed (SMART and CONKO-007 trials). Stereotactic body radiation therapy followed by sorafenib was compared to sorafenib alone in patients with hepatocellular carcinoma in the NRG/RTOG 1112 study. New options in the management of rectal cancer are emerging such as total neoadjuvant treatment (PRODIGE 23, RAPIDO, PROSPECT), organ preservation (OPRA, OPERA), and the role of immunotherapy in patients with DNA mismatch-repair deficient/microsatellite instability. Finally, preliminary results of the ACT 4 trial that evaluated de-escalation in anal cancer are presented.(c) 2023 Societe franc, aise de radiotherapie oncologique (SFRO). Published by Elsevier Masson SAS. All rights reserved.
C1 [Boustani, J.] CHU Besancon, Dept Radiat Oncol, Besancon, France.
   [Boustani, J.] Univ Franche Comte, Inserm, EFS BFC, UMR 1098,RIGHT,Greffon Hote Tumeur Interact Ingn C, Besancon, France.
   [Huguet, F.] Sorbonne Univ, Hop Tenon, AP HP, Dept Radiat Oncol, Paris, France.
   [Vendrely, V.] CHU Bordeaux, Dept Radiat Oncol, Bordeaux, France.
   [Vendrely, V.] Univ Bordeaux, BoRdeaux Inst onCol BRIC, Inserm, UMR1312, F-33000 Bordeaux, France.
C3 Universite de Franche-Comte; CHU Besancon; Universite de Franche-Comte;
   Institut National de la Sante et de la Recherche Medicale (Inserm);
   Assistance Publique Hopitaux Paris (APHP); Sorbonne Universite; Hopital
   Universitaire Tenon - APHP; Universite de Bordeaux; CHU Bordeaux;
   Institut National de la Sante et de la Recherche Medicale (Inserm);
   Universite de Bordeaux
RP Boustani, J (corresponding author), CHU Besancon, Dept Radiat Oncol, Besancon, France.; Boustani, J (corresponding author), Univ Franche Comte, Inserm, EFS BFC, UMR 1098,RIGHT,Greffon Hote Tumeur Interact Ingn C, Besancon, France.
EM jboustani@chu-besancon.fr
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NR 36
TC 0
Z9 1
U1 0
U2 0
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 DEC
PY 2023
VL 27
IS 8
BP 768
EP 777
DI 10.1016/j.canrad.2023.08.001
EA NOV 2023
PG 10
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA CV2M8
UT WOS:001127946500001
PM 38415359
DA 2025-01-04
ER

PT J
AU To, KKW
   Tong, CWS
   Wu, MX
   Cho, WCS
AF To, Kenneth K. W.
   Tong, Christy W. S.
   Wu, Mingxia
   Cho, William C. S.
TI MicroRNAs in the prognosis and therapy of colorectal cancer: From bench
   to bedside
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE microRNA; colorectal cancer; multidrug resistance; prognosis;
   therapeutic target; apoptosis; metastasis; recurrence; risk
   stratification
ID HUMAN COLON-CANCER; LOCKED NUCLEIC-ACID; POTENTIAL TUMOR-SUPPRESSOR; KEY
   ONCOGENIC COMPONENT; ANTI-EGFR THERAPY; WILD-TYPE KRAS; DRUG-RESISTANCE;
   POOR-PROGNOSIS; CIRCULATING MICRORNAS; HIGH EXPRESSION
AB MicroRNAs (miRNAs) are small, single-stranded, noncoding RNAs that can post-transcriptionally regulate the expression of various oncogenes and tumor suppressor genes. Dysregulated expression of many miRNAs have been shown to mediate the signaling pathways critical in the multistep carcinogenesis of colorectal cancer (CRC). MiRNAs are stable and protected from RNase-mediated degradation, thereby enabling its detection in biological fluids and archival tissues for biomarker studies. This review focuses on the role and application of miRNAs in the prognosis and therapy of CRC. While stage II CRC is potentially curable by surgical resection, a significant percentage of stage II CRC patients do develop recurrence. MiRNA biomarkers may be used to stratify such high-risk population for adjuvant chemotherapy to provide better prognoses. Growing evidence also suggests that miRNAs are involved in the metastatic process of CRC. Certain of these miRNAs may thus be used as prognostic biomarkers to identify patients more likely to have micro-metastasis, who could be monitored more closely after surgery and/or given more aggressive adjuvant chemotherapy. Intrinsic and acquired resis-tance to chemotherapy severely hinders successful chemotherapy in CRC treatment. Predictive miRNA biomarkers for response to chemotherapy may identify patients who will benefit the most from a particular regimen and also spare the patients from unnecessary side effects. Selection of patients to receive the new targeted therapy is becoming possible with the use of predictive miRNA biomarkers. Lastly, forced expression of tumor suppressor miRNA or silencing of oncogenic miRNA in tumors by gene therapy can also be adopted to treat CRC alone or in combination with other chemotherapeutic drugs.
C1 [To, Kenneth K. W.; Tong, Christy W. S.; Wu, Mingxia] Chinese Univ Hong Kong, Sch Pharm, Fac Med, Room 801N,Lo Kwee Seong Integrated Biomed Sci Bld, Shatin, Hong Kong, Peoples R China.
   [Cho, William C. S.] Queen Elizabeth Hosp, Dept Clin Oncol, Hong Kong, Hong Kong, Peoples R China.
C3 Chinese University of Hong Kong
RP To, KKW (corresponding author), Chinese Univ Hong Kong, Sch Pharm, Fac Med, Room 801N,Lo Kwee Seong Integrated Biomed Sci Bld, Shatin, Hong Kong, Peoples R China.
EM kennethto@cuhk.edu.hk
RI Cho, William/H-7429-2019; To, Kenneth/M-4500-2013
OI Wu, Mingxia/0000-0002-6070-5569; To, Kenneth/0000-0003-2755-0283
FU Direct Grant for Research, Faculty of Medicine, the Chinese University
   of Hong Kong [4054371]
FX Supported by the Direct Grant for Research, Faculty of Medicine, the
   Chinese University of Hong Kong, No. 4054371.
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SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD JUL 21
PY 2018
VL 24
IS 27
BP 2949
EP 2973
DI 10.3748/wjg.v24.i27.2949
PG 25
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GN5UH
UT WOS:000439131900003
PM 30038463
OA Green Published, Green Submitted, hybrid
DA 2025-01-04
ER

PT J
AU Czajka-Francuz, P
   Prendes, MJ
   Mankan, A
   Quintana, A
   Pabla, S
   Ramkissoon, S
   Jensen, TJ
   Peiró, S
   Severson, EA
   Achyut, BR
   Vidal, L
   Poelman, M
   Saini, KS
AF Czajka-Francuz, Paulina
   Prendes, Maria J.
   Mankan, Arun
   Quintana, Angela
   Pabla, Sarabjot
   Ramkissoon, Shakti
   Jensen, Taylor J.
   Peiro, Sandra
   Severson, Eric A.
   Achyut, Bhagelu R.
   Vidal, Laura
   Poelman, Martine
   Saini, Kamal S.
TI Mechanisms of immune modulation in the tumor microenvironment and
   implications for targeted therapy
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE tumor microenvironment; immune escape mechanisms; immunotherapy; cancer;
   immunosuppression mechanisms
ID COLORECTAL-CANCER CELLS; HLA CLASS-I; T-CELL; MYELOID CELLS; CHECKPOINT
   INHIBITORS; ANTI-PD-L1 ANTIBODY; AEROBIC GLYCOLYSIS; ADOPTIVE TRANSFER;
   SUPPRESSOR-CELLS; DENDRITIC CELLS
AB The efficacy of cancer therapies is limited to a great extent by immunosuppressive mechanisms within the tumor microenvironment (TME). Numerous immune escape mechanisms have been identified. These include not only processes associated with tumor, immune or stromal cells, but also humoral, metabolic, genetic and epigenetic factors within the TME. The identification of immune escape mechanisms has enabled the development of small molecules, nanomedicines, immune checkpoint inhibitors, adoptive cell and epigenetic therapies that can reprogram the TME and shift the host immune response towards promoting an antitumor effect. These approaches have translated into series of breakthroughs in cancer therapies, some of which have already been implemented in clinical practice. In the present article the authors provide an overview of some of the most important mechanisms of immunosuppression within the TME and the implications for targeted therapies against different cancers.
C1 [Czajka-Francuz, Paulina; Mankan, Arun; Achyut, Bhagelu R.; Vidal, Laura; Poelman, Martine; Saini, Kamal S.] Fortrea Inc, Durham, NC 27709 USA.
   [Prendes, Maria J.; Pabla, Sarabjot; Ramkissoon, Shakti; Jensen, Taylor J.; Severson, Eric A.] Labcorp Oncol, Durham, NC USA.
   [Quintana, Angela; Peiro, Sandra] Vall Hebron Inst Oncol, Breast Canc Unit, Barcelona, Spain.
   [Saini, Kamal S.] Cambridge Univ Hosp Natl Hlth Serv NHS Fdn Trust, Addenbrookes Hosp, Cambridge, England.
C3 Vall d'Hebron Institut d'Oncologia (VHIO); University of Cambridge;
   Cambridge University Hospitals NHS Foundation Trust; Addenbrooke's
   Hospital
RP Saini, KS (corresponding author), Fortrea Inc, Durham, NC 27709 USA.; Saini, KS (corresponding author), Cambridge Univ Hosp Natl Hlth Serv NHS Fdn Trust, Addenbrookes Hosp, Cambridge, England.
EM Kamalveer.saini@fortrea.com
RI Saini, Kamal S./ABD-5499-2021
OI Saini, Kamal S./0000-0001-6301-3309; Quintana,
   Angela/0000-0002-6470-0802; Czajka-Francuz, Paulina/0000-0003-1486-5630
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NR 275
TC 11
Z9 12
U1 2
U2 10
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 JUN 22
PY 2023
VL 13
AR 1200646
DI 10.3389/fonc.2023.1200646
PG 23
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA L4NQ3
UT WOS:001023052800001
PM 37427115
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zulkifli, AA
   Tan, FH
   Putoczki, TL
   Stylli, SS
   Luwor, RB
AF Zulkifli, Ahmad A.
   Tan, Fiona H.
   Putoczki, Tracy L.
   Stylli, Stanley S.
   Luwor, Rodney B.
TI STAT3 signaling mediates tumour resistance to EGFR targeted therapeutics
SO MOLECULAR AND CELLULAR ENDOCRINOLOGY
LA English
DT Article
DE STAT3; EGFR; Therapeutics; Cancer
ID EPIDERMAL-GROWTH-FACTOR; CELL LUNG-CANCER; METASTATIC COLORECTAL-CANCER;
   EPITHELIAL-MESENCHYMAL TRANSITION; HUMAN BLADDER-CANCER; FACTOR
   RECEPTOR; ACQUIRED-RESISTANCE; IN-VIVO; BREAST-CANCER; GEFITINIB
   RESISTANCE
AB Several EGFR inhibitors are currently undergoing clinical assessment or are approved for the clinical management of patients with varying tumour types. However, treatment often results in a lack of response in many patients. The majority of patients that initially respond eventually present with tumours that display acquired resistance to the original therapy. A large number of receptor tyrosine and intracellular kinases have been implicated in driving signaling that mediates this tumour resistance to anti-EGFR targeted therapy, and in a few cases these discoveries have led to overall changes in prospective tumour screening and clinical practice (K-RAS in mCRC and EGFR T790M in NSCLC). In this mini review, we specifically focus on the role of the STAT3 signaling axis in providing both intrinsic and acquired resistance to inhibitors of the EGFR. We also focus on STAT3 pathway targeting in an attempt to overcome resistance to anti-EGFR therapeutics. (C) 2017 Elsevier B.V. All rights reserved.
C1 [Zulkifli, Ahmad A.; Tan, Fiona H.; Stylli, Stanley S.; Luwor, Rodney B.] Univ Melbourne, Royal Melbourne Hosp, Dept Surg, Level 5,Clin Sci Bldg, Parkville, Vic 3050, Australia.
   [Putoczki, Tracy L.] Walter & Eliza Hall Inst Med Res, Inflammat Div, Parkville, Vic 3052, Australia.
   [Putoczki, Tracy L.] Univ Melbourne, Dept Med Biol, Parkville, Vic 3050, Australia.
   [Stylli, Stanley S.] Royal Melbourne Hosp, Dept Neurosurg, Parkville, Vic 3050, Australia.
C3 University of Melbourne; Melbourne Health; Royal Melbourne Hospital;
   Walter & Eliza Hall Institute; University of Melbourne; Melbourne
   Health; Royal Melbourne Hospital
RP Luwor, RB (corresponding author), Univ Melbourne, Royal Melbourne Hosp, Dept Surg, Level 5,Clin Sci Bldg, Parkville, Vic 3050, Australia.
EM rluwor@unimelb.edu.au
RI stylli, stanley/R-7540-2019; Stylli, Stanley/N-5982-2016
OI Zulkifli, Ahmad Azri/0000-0003-0543-365X; Stylli,
   Stanley/0000-0002-3505-7387; Luwor, Rodney/0000-0002-3020-4245
FU Worldwide Cancer Research [14-1197] Funding Source: Medline
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NR 110
TC 49
Z9 52
U1 0
U2 20
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0303-7207
J9 MOL CELL ENDOCRINOL
JI Mol. Cell. Endocrinol.
PD AUG 15
PY 2017
VL 451
IS C
SI SI
BP 15
EP 23
DI 10.1016/j.mce.2017.01.010
PG 9
WC Cell Biology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Endocrinology & Metabolism
GA EZ9JB
UT WOS:000405045300002
PM 28088467
DA 2025-01-04
ER

PT J
AU Warner, AB
   McQuade, JL
AF Warner, Allison Betof
   McQuade, Jennifer L.
TI Modifiable Host Factors in Melanoma: Emerging Evidence for Obesity,
   Diet, Exercise, and the Microbiome
SO CURRENT ONCOLOGY REPORTS
LA English
DT Review
DE Melanoma; Immunotherapy; Obesity; Diet; Microbiome; Exercise
ID BODY-MASS INDEX; BREAST-CANCER; PHYSICAL-ACTIVITY; COLORECTAL-CANCER;
   POOLED ANALYSIS; TUMOR MICROENVIRONMENT; EUROPEAN ORGANIZATION; GUT
   MICROBIOTA; STAGE-III; SURVIVAL
AB Purpose of ReviewWe discuss how potentially modifiable factors including obesity, the microbiome, diet, and exercise may impact melanoma development, progression, and therapeutic response.Recent FindingsObesity is unexpectedly associated with improved outcomes with immune and targeted therapy in melanoma, with early mechanistic data suggesting leptin as one mediator. The gut microbiome is both a biomarker of response to immunotherapy and a potential target. As diet is a major determinant of the gut microbiome, ongoing studies are examining the interaction between diet, the gut microbiome, and immunity. Data are emerging for a potential role of exercise in reducing hypoxia and enhancing anti-tumor immunity, though this has not yet been well-studied in the context of contemporary therapies.SummaryRecent data suggests energy balance may play a role in the outcomes of metastatic melanoma. Further studies are needed to demonstrate mechanism and causality as well as the feasibility of targeting these factors.
C1 [Warner, Allison Betof] Mem Sloan Kettering Canc Ctr, Dept Med, Melanoma & Linmunotherapeut Serv, 1275 York Ave,Box 8, New York, NY 10065 USA.
   [McQuade, Jennifer L.] Univ Texas MD Anderson Canc Ctr, Dept Melanoma Med Oncol, 1515 Holcombe Blvd,Unit 430, Houston, TX 77030 USA.
C3 Memorial Sloan Kettering Cancer Center; University of Texas System; UTMD
   Anderson Cancer Center
RP McQuade, JL (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Melanoma Med Oncol, 1515 Holcombe Blvd,Unit 430, Houston, TX 77030 USA.
EM betofa@mskcc.org; jmcquade@mdandeison.org
RI Warner, Allison/AAC-4299-2019
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NR 103
TC 28
Z9 29
U1 0
U2 21
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1523-3790
EI 1534-6269
J9 CURR ONCOL REP
JI Curr. Oncol. Rep.
PD AUG
PY 2019
VL 21
IS 8
AR 72
DI 10.1007/s11912-019-0814-2
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IH3OL
UT WOS:000474402100001
PM 31263961
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Khot, MI
   Andrew, H
   Svavarsdottir, HS
   Armstrong, G
   Quyn, AJ
   Jayne, DG
AF Khot, M. Ibrahim
   Andrew, Helen
   Svavarsdottir, Hafdis S.
   Armstrong, Gemma
   Quyn, Aaron J.
   Jayne, David G.
TI A Review on the Scope of Photothermal Therapy-Based Nanomedicines in
   Preclinical Models of Colorectal Cancer
SO CLINICAL COLORECTAL CANCER
LA English
DT Review
DE Nanoparticles; Optical imaging; Photosensitive agent; Targeted therapy;
   Thermal ablation
ID IRON-OXIDE NANOPARTICLES; DRUG-DELIVERY; GOLD NANOPARTICLES; THERMAL
   ABLATION; PHOTODYNAMIC THERAPY; 1ST-LINE TREATMENT; CARBON NANOTUBES;
   GRAPHENE OXIDE; ANHYDRASE-IX; LEUCOVORIN
AB Oncologic thermal ablation involves the use of hyperthermic temperatures to damage and treat solid cancers. Thermal ablation is being investigated as a method of treatment in colorectal cancers and has the potential to complement conventional anticancer treatments in managing local recurrence and metastatic disease. Photothermal therapy utilizes photosensitive agents to generate local heat and induce thermal ablation. There is growing interest in developing nanotechnology platforms to deliver such photosensitive agents. An advantage of nanomedicines is their multi-functionality, with the capability to deliver combinations of chemotherapeutics and cancer-imaging agents. To date, there have been no clinical studies evaluating photothermal therapy-based nanomedicines in colorectal cancers. This review presents the current scope of preclinical studies, investigating nanomedicines that have been developed for delivering multimodal photothermal therapy to colorectal cancers, with an emphasis on potential clinical applications. (C) 2019 Elsevier Inc. All rights reserved.
C1 [Khot, M. Ibrahim; Andrew, Helen; Svavarsdottir, Hafdis S.; Armstrong, Gemma; Quyn, Aaron J.; Jayne, David G.] Univ Leeds, St Jamess Univ Hosp, Sch Med, Leeds, W Yorkshire, England.
C3 Saint James's University Hospital; University of Leeds
RP Khot, MI (corresponding author), St James Univ Hosp, Sect Translat Anaesthesia & Surg Sci, Level 9,Wellcome Trust Brenner Bldg,Beckett St, Leeds LS9 7TF, W Yorkshire, England.
EM M.I.Khot@leeds.ac.uk
RI Khot, Ibrahim/AAG-6910-2019
OI Khot, Ibrahim/0000-0002-5062-2284; Quyn, Aaron/0000-0002-4333-5658;
   Jayne, David/0000-0002-8725-3283
FU National Institute for Health Research (NIHR) infrastructure at Leeds;
   University of Leeds 110 Anniversary Research Scholarship
FX Supported by the National Institute for Health Research (NIHR)
   infrastructure at Leeds. The views expressed are those of the authors
   and not necessarily those of the National Health Service, the NIHR, or
   the Department of Health. This review was also supported by a University
   of Leeds 110 Anniversary Research Scholarship to M.I.K.
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Z9 65
U1 2
U2 68
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 2019
VL 18
IS 2
BP E200
EP E209
DI 10.1016/j.clcc.2019.02.001
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IB2RP
UT WOS:000470116700004
PM 30852125
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Wu, DJ
   Wang, DC
   Cheng, YF
   Qian, MJ
   Zhang, MM
   Shen, Q
   Wang, XD
AF Wu, Duojiao
   Wang, Diane C.
   Cheng, Yunfeng
   Qian, Mengjia
   Zhang, Miaomiao
   Shen, Qi
   Wang, Xiangdong
TI Roles of tumor heterogeneity in the development of drug resistance: A
   call for precision therapy
SO SEMINARS IN CANCER BIOLOGY
LA English
DT Review
DE Tumor heterogeneity; Precision medicine; Genetic variations; Cancer;
   Drug resistance; Biomarker
ID RENAL-CELL CARCINOMA; COLORECTAL-CANCER; GROWTH-FACTOR; LUNG-CANCER;
   MDR1 GENE; MUTATIONS; INHIBITORS; LANDSCAPE; OPPORTUNITIES; RESTORATION
AB The drug resistance limits the optimal efficacy of drugs during target therapies for lung cancer and requires the development of precision medicine to identify and develop new highly selective drugs and more precise tailoring of medicine to the target population. Lung cancer heterogeneity as a potential cause of drug resistance to targeted therapy may foster tumor evolution and adaptation and fade personalized-medicine strategies. The present review elucidates the influence of tumor heterogeneity on drug efficacy and resistance, and discusses potential strategies to combat heterogeneity for cancer treatment. There is an urgent need to discover and develop disease- and biology-specific biomarkers for monitoring the existence and occurrence of lung cancer heterogeneity, testing targeted drugs in clinical trials, and implementing precision medicine for patients. Better understanding of lung cancer heterogeneity will strengthen therapeutic strategies and apply precision medicine to cure the disease. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [Wu, Duojiao; Wang, Diane C.; Cheng, Yunfeng; Qian, Mengjia; Zhang, Miaomiao; Shen, Qi; Wang, Xiangdong] Fudan Univ, Inst Clin Sci, Shanghai Inst Clin Bioinformat, Zhongshan Hosp, Shanghai, Peoples R China.
C3 Fudan University
RP Wu, DJ (corresponding author), Fudan Univ, Inst Clin Sci, Shanghai Inst Clin Bioinformat, Zhongshan Hosp, Shanghai, Peoples R China.
EM wuduojiao@126.com
RI zhang, mm/IWV-4201-2023; Wang, Xiangdong/AAF-9148-2020; Cheng,
   Yunfeng/ISS-0527-2023
FU Shanghai Leading Academic Discipline Project [B115]; Zhongshan
   Distinguished Professor Grant (XDW); National Nature Science Foundation
   of China [91230204, 81270099, 81320108001, 81270131, 81400035, 81570075,
   81500058, 81500025]; Shanghai Committee of Science and Technology
   [12JC1402200, 12431900207, 11410708600]; Zhejiang Provincial Natural
   Science Foundation [Z15H010002]; Zhejiang Provincial Science Technology
   Department Foundation [WKJ-ZJ-1526]
FX The work was supported by Shanghai Leading Academic Discipline Project
   (B115), Zhongshan Distinguished Professor Grant (XDW), The National
   Nature Science Foundation of China (91230204, 81270099, 81320108001,
   81270131, 81400035, 81570075, 81500058, 81500025), The Shanghai
   Committee of Science and Technology (12JC1402200, 12431900207,
   11410708600), Zhejiang Provincial Natural Science Foundation
   (Z15H010002), Zhejiang Provincial Science Technology Department
   Foundation (WKJ-ZJ-1526).
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NR 60
TC 50
Z9 56
U1 4
U2 34
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1044-579X
J9 SEMIN CANCER BIOL
JI Semin. Cancer Biol.
PD FEB
PY 2017
VL 42
BP 13
EP 19
DI 10.1016/j.semcancer.2016.11.006
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EN2LC
UT WOS:000395840700003
PM 27840278
DA 2025-01-04
ER

PT J
AU Deshmukh, R
   Simran
   Harwansh, RK
   Misra, A
   Mishra, S
   Kumar, A
AF Deshmukh, Rohitas
   Simran
   Harwansh, Ranjit K.
   Misra, Akshat
   Mishra, Sakshi
   Kumar, Arun
TI Therapeutic approaches of nanostructure metallic materials in management
   of colorectal cancer: Recent advancement
SO JOURNAL OF DRUG DELIVERY SCIENCE AND TECHNOLOGY
LA English
DT Review
DE Colorectal cancer; Nanocarriers; Nanoparticles; Metallic nanoparticles;
   Cancer; Delivery systems
ID ZINC-OXIDE NANOPARTICLES; MESOPOROUS SILICA NANOPARTICLES; COLON-CANCER;
   SILVER NANOPARTICLES; GOLD NANOPARTICLES; DRUG-DELIVERY; ANTICANCER
   ACTIVITY; GREEN SYNTHESIS; SELENIUM; SYSTEM
AB Colorectal cancer, a severe and widespread malignancy, is the second most lethal and third most often diagnosed cancer worldwide. The number of colorectal cancer cases is spiking globally. The incidence and mortality rates will likely increase in the coming decades. Adenomatous polyps, which can form and enlarge, alter the normal colonic epithelium in ways that lead to the growth of colorectal cancer through long-lasting genetic and epigenetic changes. Surgical intervention, radiotherapy, chemotherapy, and targeted therapy are the most popular colorectal cancer treatments. Still, as clinical research has shown, chemotherapy is genuinely among the most essential therapeutic possibilities for treating colorectal cancer. Metallic nanoparticles are the newly trending field of nanomedicine implied in cancer therapy. Several Metal-Organic Frameworks (MOFs), Superparamagnetic Iron Oxide Nanoparticles (SPIONs), and Mesoporous Silica Nanoparticles (MSNs) have recently been studied for colorectal cancer treatment. Oxaliplatin is the only metallic-based drug presently used for colorectal cancer approved by the FDA and combined with other anticancer medications, such as Capecitabine or 5-Fluorouracil, and given intravenously. Unfortunately, most recently created metal-based complexes lack selectivity against cancer cells, have poor solubility and permeability, have a high dose-limiting toxic effect, and are beginning to develop resistance. The present review addresses the general characteristics and clinical supervision of colorectal cancer, particularly emphasizing preclinical studies and clinical research using metallic compounds such as gold, silver, silica, titanium, copper, selenium, zinc, iron, etc.
C1 [Deshmukh, Rohitas; Harwansh, Ranjit K.] GLA Univ, Inst Pharmaceut Res, Mathura 281406, India.
   [Misra, Akshat] Life Cell Int Pvt Ltd, New Delhi 110058, India.
   [Mishra, Sakshi] Ashoka Inst Technol & Management, Varanasi 221007, Uttar Pradesh, India.
   [Kumar, Arun] Sharda Univ, Sch Pharm, Greater Noida 201310, India.
C3 GLA University; Sharda University
RP Kumar, A (corresponding author), Sharda Univ, Sch Pharm, Greater Noida 201310, India.
EM rahi18rahi@gmail.com; harwanshranjeet@gmail.com;
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   jvsarun@gmail.com
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OI Deshmukh, Rohitas/0000-0002-8962-6821
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NR 188
TC 0
Z9 0
U1 4
U2 4
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 DEC
PY 2024
VL 102
AR 106338
DI 10.1016/j.jddst.2024.106338
EA NOV 2024
PN A
PG 21
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA L8D3V
UT WOS:001352969900001
DA 2025-01-04
ER

PT J
AU Araujo, LH
   Souza, BM
   Leite, LR
   Parma, SAF
   Lopes, NP
   Malta, FSV
   Freire, MCM
AF Araujo, Luiz Henrique
   Souza, Bianca Mendes
   Leite, Laura Rabelo
   Parma, Sabrina A. F.
   Lopes, Natalia P.
   Malta, Frederico S. V.
   Freire, Maira C. M.
TI Molecular profile of <i>KRAS</i> G12C-mutant colorectal and
   non-small-cell lung cancer
SO BMC CANCER
LA English
DT Article
DE Lung neoplasms; Colorectal neoplasms; KRAS; Molecular targeted therapy;
   Molecular diagnostics
AB BackgroundKRAS is the most frequently mutated oncogene in cancer, however efforts to develop targeted therapies have been largely unsuccessful. Recently, two small-molecule inhibitors, AMG 510 and MRTX849, have shown promising activity in KRAS G12C-mutant solid tumors. The current study aims to assess the molecular profile of KRAS G12C in colorectal (CRC) and non-small-cell lung cancer (NSCLC) tested in a clinical certified laboratory.MethodsCRC and NSCLC samples submitted for KRAS testing between 2017 and 2019 were reviewed. CRC samples were tested for KRAS and NRAS by pyrosequencing, while NSCLC samples were submitted to next generation sequencing of KRAS, NRAS, EGFR, and BRAF.ResultsThe dataset comprised 4897 CRC and 4686 NSCLC samples. Among CRC samples, KRAS was mutated in 2354 (48.1%). Most frequent codon 12 mutations were G12D in 731 samples (14.9%) and G12V in 522 (10.7%), followed by G12C in 167 (3.4%). KRAS mutations were more frequent in females than males (p=0.003), however this difference was exclusive of non-G12C mutants (p<0.001). KRAS mutation frequency was lower in the South and North regions (p=0.003), but again KRAS G12C did not differ significantly (p=0.80). In NSCLC, KRAS mutations were found in 1004 samples (21.4%). As opposed to CRC samples, G12C was the most common mutation in KRAS, in 346 cases (7.4%). The frequency of KRAS G12C was higher in the South and Southeast regions (p=0.012), and lower in patients younger than 50years (p<0.001). KRAS G12C mutations were largely mutually exclusive with other driver mutations; only 11 NSCLC (3.2%) and 1 CRC (0.6%) cases had relevant co-mutations.ConclusionsKRAS G12C presents in frequencies higher than several other driver mutations, and may represent a large volume of patients in absolute numbers. KRAS testing should be considered in all CRC and NSCLC patients, independently of clinical or demographic characteristics.
C1 [Araujo, Luiz Henrique; Souza, Bianca Mendes; Leite, Laura Rabelo; Parma, Sabrina A. F.; Lopes, Natalia P.; Freire, Maira C. M.] Grp Pardini, Progenet, Vespaziano, Brazil.
   [Araujo, Luiz Henrique; Malta, Frederico S. V.] Grp Pardini, Rese & Dev Sect, Vespaziano, Brazil.
   [Araujo, Luiz Henrique] Inst COI Educ & Pesquisa, Rio De Janeiro, Brazil.
   [Araujo, Luiz Henrique] Inst Nacl Canc, Rio De Janeiro, Brazil.
C3 National Cancer Institute (Inca)
RP Araujo, LH (corresponding author), Grp Pardini, Progenet, Vespaziano, Brazil.; Araujo, LH (corresponding author), Grp Pardini, Rese & Dev Sect, Vespaziano, Brazil.
EM luizaraujo.md@gmail.com
OI Malta, Frederico/0000-0001-9495-0987
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NR 33
TC 26
Z9 29
U1 1
U2 7
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD FEB 25
PY 2021
VL 21
IS 1
AR 193
DI 10.1186/s12885-021-07884-8
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QQ1VO
UT WOS:000624315000002
PM 33632153
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Wang, J
   Sahengbieke, S
   Xu, XP
   Zhang, L
   Xu, XM
   Sun, LF
   Deng, Q
   Wang, D
   Chen, D
   Pan, Y
   Liu, ZH
   Yu, SJ
AF Wang, Jian
   Sahengbieke, Sana
   Xu, Xiaoping
   Zhang, Lei
   Xu, Xiaoming
   Sun, Lifeng
   Deng, Qun
   Wang, Da
   Chen, Dong
   Pan, Yuan
   Liu, Zhaohui
   Yu, Shaojun
TI Gene expression analyses identify a relationship between stanniocalcin 2
   and he malignant behavior of colorectal cancer
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE stanniocalcin 2; colorectal cancer; TCGA; RNAseq
ID EPITHELIAL-MESENCHYMAL TRANSITION; CONSENSUS MOLECULAR SUBTYPES;
   CLINICAL-SIGNIFICANCE; BREAST-CANCER; PROMOTES; CELLS; COLON; STC2;
   LYMPHANGIOGENESIS; OVEREXPRESSION
AB Background: Colorectal cancer (CRC) is one of the main causes of cancer-related death worldwide. Stanniocalcin 2 (STC2), a secreted glycoprotein, has been suggested to exert various functions in progression of many cancers. However, the precise biological role in CRC is not fully understood. Therefore, this study based on several public datasets aims at investigating the roles of STC2 in CRC.
   Methods: We used The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases to evaluate the STC2 expression and its clinical significance in CRC. Cell migration and invasion by STC2 overexpression and knockdown were assessed using Transwell migration and Matrigel invasion assays. We next performed RNAseq analysis on SW480 cells with or without STC2 overexpression. Differentially expressed genes were selected by using fold-change >5 and P-value <0.05.
   Results: In this study, we found that STC2 level was significantly higher in CRC than that in adjacent noncancerous tissues from TCGA and GEO. Tumors with high mRNA levels of STC2 were more common in patients with rectal cancer, left-sided CRC, advanced T-stage (T3-T4), positive lymph node involvement and advanced AJCC-stage (III-IV) from TCGA. STC2 displayed the negative correlation with the expressions of epithelial cell markers, while it was positively correlated with the expressions of mesenchymal cell markers, MMPs and the epithelial-mesenchymal transition (EMT)-related transcriptional factors. Furthermore, we found that STC2 promoted cell migration and invasion in vitro. And a group of differentially expressed genes, which were modulated by STC2, were identified from RNAseq analyses.
   Conclusion: Our study demonstrates that STC2 is overexpressed in CRC compared with normal tissues, and promotes CRC cell migration and invasion. Our data suggest that STC2 may be used as a potential biomarker for clinical application and target therapy in future.
C1 [Wang, Jian; Sun, Lifeng; Deng, Qun; Wang, Da; Yu, Shaojun] Zhejiang Univ, Affiliated Hosp 2, Sch Med, Dept Surg Oncol, 88 Jiefang Rd, Hangzhou 310009, Zhejiang, Peoples R China.
   [Sahengbieke, Sana] Zhejiang Univ, Dept Pathol, Sch Med, Hangzhou, Zhejiang, Peoples R China.
   [Xu, Xiaoping; Zhang, Lei; Chen, Dong; Pan, Yuan; Liu, Zhaohui] Yuhang Dist First Peoples Hosp, Dept Anorectal Surg, Hangzhou, Zhejiang, Peoples R China.
   [Xu, Xiaoming] Zhejiang Univ, Affiliated Hosp 2, Sch Med, Dept Pathol, Hangzhou, Zhejiang, Peoples R China.
C3 Zhejiang University; Zhejiang University; Zhejiang University
RP Yu, SJ (corresponding author), Zhejiang Univ, Affiliated Hosp 2, Sch Med, Dept Surg Oncol, 88 Jiefang Rd, Hangzhou 310009, Zhejiang, Peoples R China.
EM jackdavid1982@zju.edu.cn
RI Sun, Lifeng/AAV-7416-2021; Chen, Dong/ISV-3402-2023; wang,
   jian-wei/ABE-3064-2020; Liu, Zhaohui/AAB-1937-2020
OI Xu, Xiao-ming/0000-0002-0602-7955
FU National Natural Science Foundation of China [81772527, 81672342,
   81472819, 81302073, 81302072]; Zhejiang Provincial Natural Science
   Foundation of China [LY17H160034]
FX This study was supported by project grants from the National Natural
   Science Foundation of China (81772527, 81672342, 81472819, 81302073, and
   81302072) and the Zhejiang Provincial Natural Science Foundation of
   China (LY17H160034).
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NR 48
TC 6
Z9 6
U1 0
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 2018
VL 11
BP 7155
EP 7168
DI 10.2147/OTT.S167780
PG 14
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA GX4CK
UT WOS:000447674400001
PM 30425508
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Peng, X
   Na, RS
   Zhou, WT
   Meng, XL
   Yang, YH
   Amini, S
   Song, LW
AF Peng, Xiao
   Na, Risi
   Zhou, Wenting
   Meng, Xiaole
   Yang, Yunhai
   Amini, Shohreh
   Song, Liwei
TI Nuclear translocation of Gasdermin D sensitizes colorectal cancer to
   chemotherapy in a pyroptosis-independent manner
SO ONCOGENE
LA English
DT Article
ID KI-67 LABELING INDEX; OLAPARIB MONOTHERAPY; TARGETED THERAPY;
   GASTRIC-CANCER; OVARIAN-CANCER; CELL-SURVIVAL; DNA; HETEROGENEITY;
   COMBINATION; EXPRESSION
AB Gasdermin D (GSDMD) has recently been identified as a cytoplasmic effector protein that plays a central role in pyroptosis of immune cells. However, GSDMD is a universally expressed protein, and its function beyond pyroptosis, especially in cancer cells, has not been well characterized. Here, we report that predominant localization of GSDMD in the nucleoplasm in vivo indicates favorable clinical outcomes in colorectal cancer, while a lack of nuclear localization of GSDMD is associated with poor outcomes. Nuclear GSDMD, rather than cytoplasmic GSDMD, inhibits cell growth and promotes apoptosis in colorectal cancer. Hypoxia in the tumor microenvironment accounts for mild or moderate nuclear translocation of GSDMD in vivo. Under the stimulation of chemotherapy drugs, nuclear GSDMD promotes apoptosis via regulation of its subcellular distribution rather than pyroptosis-related cleavage. After nuclear translocation, GSDMD interacts with PARP-1 to dramatically inhibit its DNA damage repair-related function by functioning like the PARP inhibitor olaparib, thus forming a "hypoxia/chemotherapy-GSDMD nuclear translocation-PARP-1 blockade-DNA damage and apoptosis" axis. This study redefines the pyroptosis-independent function of GSDMD and suggests that the subcellular localization of GSDMD may serve as a molecular indicator of clinical outcomes and a promising therapeutic target in colorectal cancer.
C1 [Peng, Xiao; Amini, Shohreh] Temple Univ, Dept Biol, BioLife Bldg,1900 North 12th St, Philadelphia, PA 19122 USA.
   [Na, Risi; Zhou, Wenting; Meng, Xiaole] Xiamen Univ, Xiangan Hosp, Sch Med, Dept Gen Surg, 2000 Xiangan East Rd, Xiamen 361102, Peoples R China.
   [Yang, Yunhai; Song, Liwei] Shanghai Jiao Tong Univ, Shanghai Chest Hosp, Dept Oncol Surg, Sch Med, 241 West Huaihai Rd, Shanghai 200030, Peoples R China.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); Temple
   University; Xiamen University; Shanghai Jiao Tong University
RP Amini, S (corresponding author), Temple Univ, Dept Biol, BioLife Bldg,1900 North 12th St, Philadelphia, PA 19122 USA.; Yang, YH; Song, LW (corresponding author), Shanghai Jiao Tong Univ, Shanghai Chest Hosp, Dept Oncol Surg, Sch Med, 241 West Huaihai Rd, Shanghai 200030, Peoples R China.
EM yangyunhai_oncobio@shchest.org; shohreh.amini@temple.edu;
   songliwei_chest@shchest.org
RI Liu, Xiaoling/HGD-3566-2022; Li, xiaofei/GXF-7187-2022
OI Zhang, Narisi/0009-0002-8340-2330; XL, Meng/0000-0002-6388-9084
FU National Natural Science Foundation of China [NSFC82002427, NSFC
   30801132]; Shanghai Chest Hospital Outstanding Talent Cultivation
   Project [2018YNZYB03]
FX We thank Professor Feng Shao (National Institute of Biological Science)
   for the kind gift of the PCS2-Flag-tagged GSDMD plasmid. This project
   was supported by the National Natural Science Foundation of China
   (NSFC82002427, NSFC 30801132) and the Shanghai Chest Hospital
   Outstanding Talent Cultivation Project (2018YNZYB03).
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NR 55
TC 15
Z9 16
U1 3
U2 24
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD NOV 18
PY 2022
VL 41
IS 47
BP 5092
EP 5106
DI 10.1038/s41388-022-02503-7
EA OCT 2022
PG 15
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 6H3BD
UT WOS:000868470400001
PM 36245058
DA 2025-01-04
ER

PT J
AU Song, ZC
   Yang, DC
   Song, H
   Dong, WP
   Wu, JG
   Yang, JJ
   Gu, Y
AF Song, Zhicheng
   Yang, Dongchao
   Song, Heng
   Dong, Wenpei
   Wu, Jugang
   Yang, Jianjun
   Gu, Yan
TI Surgical treatment strategy for locally advanced colorectal cancer with
   abdominal wall invasion
SO ANNALS OF TRANSLATIONAL MEDICINE
LA English
DT Article
DE Three dimensional visualization; complex abdominal wall defects; locally
   advanced colorectal cancer with abdominal wall invasion (locally
   advanced CRC with abdominal wall invasion); abdominal wall
   reconstruction
ID METASTASES; MANAGEMENT; SURGERY
AB Background: The incidence of abdominal wall metastasis from colorectal cancer (CRC) is very low, but it has a poor prognosis. Despite the advances in radiotherapy, chemotherapy, and targeted therapy, patient prognosis has not improved significantly. Through surgical treatment, some patients with locally advanced CRC with abdominal wall invasion can achieve tumor-free survival or an improved quality of life.
   Methods: The clinical data of 15 patients in our department from January 2015 to January 2020 were retrospectively analyzed. All patients underwent preoperative three-dimensional reconstruction of the tumor and abdominal wall after discussion with a multidisciplinary team (MDT). Patient information, including tumor size, defect size, operation time, intraoperative bleeding, hospital stay, and other factors, was collected.
   Results: All 15 patients underwent resection followed by reconstruction for locally advanced CRC with abdominal wall invasion. The average tumor area and abdominal wall defects were 98.13 +/- 71.70 and 270.07 +/- 101.95 cm2, respectively; and accurate abdominal wall classification and zoning were obtained for all patients. The average operation time was 431.7 +/- 189.2 min, and the average blood loss was 513.3 +/- 244.6 mL. The recurrence rates in the incisional hernia and abdominal wall were 6.0% and 13.3%, respectively. The patient survival rate was 87.7%.
   Conclusions: Surgical treatment of locally advanced CRC with abdominal wall invasion is feasible, but requires accurate and comprehensive preoperative evaluation.
C1 [Song, Zhicheng; Yang, Dongchao; Gu, Yan] Fudan Univ, Huadong Hosp, 221 West Yanan Rd, Shanghai, Peoples R China.
   [Song, Zhicheng; Yang, Dongchao; Song, Heng; Dong, Wenpei; Wu, Jugang; Yang, Jianjun; Gu, Yan] Shanghai Jiao Tong Univ, Sch Med, Shanghai Peoples Hosp 9, Shanghai, Peoples R China.
C3 Fudan University; Shanghai Jiao Tong University
RP Gu, Y (corresponding author), Fudan Univ, Huadong Hosp, 221 West Yanan Rd, Shanghai, Peoples R China.
EM yangu@shsmu.edu.cn
RI Yang, Jianjun/AAN-4960-2021; Gu, Yan/AFQ-1163-2022; Yang,
   Dongchao/Y-8059-2018
FU National Natural Science Foundation of China [81970455]; Shanghai
   Science and Technology Committee [20Y11909100]; Medical and Industrial
   Cross Research Fund of Shanghai Ninth Hospital [JYJC201914]
FX This work was supported by the National Natural Science Foundation of
   China (81970455), the Shanghai Science and Technology Committee
   (20Y11909100) and the Medical and Industrial Cross Research Fund of
   Shanghai Ninth Hospital (JYJC201914). The funders had no role in the
   study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
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Z9 2
U1 0
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PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
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SN 2305-5839
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PD MAY
PY 2021
VL 9
IS 10
AR 874
DI 10.21037/atm-21-2094
PG 9
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA SO9BS
UT WOS:000659269200013
PM 34164508
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Dai, MY
   Li, S
   Qin, X
AF Dai, Meiyu
   Li, Shan
   Qin, Xue
TI Colorectal neoplasia differentially expressed: a long noncoding RNA with
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SO ONCOTARGETS AND THERAPY
LA English
DT Review
DE long noncoding RNA; CRNDE; cancer; biological function
ID PROMOTES CELL-PROLIFERATION; THERAPEUTIC TARGET; SF3B1 MUTATIONS;
   TUMOR-GROWTH; CRNDE; GLIOMA; CARCINOMA; INVASION; PROGRESSION;
   STATISTICS
AB Colorectal neoplasia differentially expressed (CRNDE), as a long noncoding RNA (lncRNA), has attracted increasing attention in recent years and has been documented to be at abnormally high expression in various types of cancer, such as colorectal cancer, glioma, hepatocellular carcinoma, lung cancer, and breast cancer. It could not only be used as a clinical biomarker for the early diagnosis and prognosis evaluation in a variety of cancers but also promote the development and progress of various tumor cells. Moreover, it is involved in the targeting regulation of multiple microRNAs and the activation/inhibition of multiple signaling pathways. In this review, we presented a systematic summary of the potential carcinogenicity and clinical value of CRNDE in the current evidence, so as to provide reference for early diagnosis, prognosis evaluation, and targeted therapy of various clinical cancers.
C1 [Dai, Meiyu; Li, Shan; 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 73
TC 20
Z9 21
U1 0
U2 8
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 3755
EP 3763
DI 10.2147/OTT.S162754
PG 9
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA GL5GI
UT WOS:000437191900001
PM 29988699
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Islam, SMA
   Dey, A
   Patel, R
   Smalley, T
   Acevedo-Duncan, M
AF Islam, S. M. Anisul
   Dey, Avijit
   Patel, Rekha
   Smalley, Tracess
   Acevedo-Duncan, Mildred
TI Atypical Protein Kinase-C inhibitors exhibit a synergistic effect in
   facilitating DNA damaging effect of 5-fluorouracil in colorectal cancer
   cells
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE CRC; DNA damage; Atypical PKC; Apoptosis; 5-FU
ID CDK-ACTIVATING KINASE; XPD HELICASE; PKC-IOTA; APOPTOSIS; FLUOROURACIL;
   OXALIPLATIN; LEUCOVORIN; MODULATION; SUBUNIT; COMPLEX
AB Colorectal cancer (CRC) is the third most common malignancy and the fourth most common cause of cancer-related death worldwide. The treatment of metastatic CRC considered palliative for many years aiming for an improved life, with little hope of a cure, highlighting the need for developing novel targeted therapy for CRC. Human protein kinases constitute a complicated system with complex internal and external interactions, which stimulates various cellular processes such as cell growth, metabolism, survival, and apoptosis. This study investigated the effect of a combination of atypical Protein Kinase C (PKC) inhibitor (either ICA-I or zeta-Stat) and 5-FU (a thymidylate synthase inhibitor) on CRC cells viability concerning cellular DNA damage. In this study, we took multiple approaches such as colony formation assay, flow cytometry, DNA ladder assay, TUNEL assay, etc. to examine the CRC cell viability and apoptosis as a function of combination treatment. Our findings showed that the combination of atypical PKC inhibitor and 5-FU synergistically reduced the viability of CRC cells and induced apoptosis. Additionally, the DNA ladder and TUNEL assays indicated that there was a notable DNA damage and fragmentation because of lack of thymidylate synthase and due to the deactivation of atypical PKC dependent CDK7. These data suggest that the simultaneous knockdown of upstream atypical PKC protein and downstream DNA damage repairing mechanism would be a useful approach to combat CRC and to improve overall patients' survival rate.
C1 [Islam, S. M. Anisul; Dey, Avijit; Patel, Rekha; Smalley, Tracess; Acevedo-Duncan, Mildred] Univ S Florida, 4202 E Fowler Ave,CHE 205, Tampa, FL 33620 USA.
C3 State University System of Florida; University of South Florida
RP Acevedo-Duncan, M (corresponding author), Univ S Florida, 4202 E Fowler Ave,CHE 205, Tampa, FL 33620 USA.
EM macevedo@usf.edu
OI Smalley, Tracess/0000-0002-3295-7443
FU Frederick H. Leonhardt Foundation; H.O., West Foundation; Kyrias
   Foundation; Jin and Joo Lee Family Foundation; Miami Foundation for
   Cancer Research, Inc.; Yolanda and Salvatore Gigante Charitable
   Foundation Trust; Daniel Tanner Foundation
FX This research was supported by Frederick H. Leonhardt Foundation, H.O.,
   West Foundation, Kyrias Foundation, Jin and Joo Lee Family Foundation,
   Miami Foundation for Cancer Research, Inc., Yolanda and Salvatore
   Gigante Charitable Foundation Trust, and the Daniel Tanner Foundation.
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NR 41
TC 5
Z9 6
U1 0
U2 7
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 2020
VL 121
AR 109665
DI 10.1016/j.biopha.2019.109665
PG 12
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA JT1GJ
UT WOS:000500746200119
PM 31810137
OA gold
DA 2025-01-04
ER

PT J
AU Uhlitz, F
   Bischoff, P
   Peidli, S
   Sieber, A
   Trinks, A
   Lüthen, M
   Obermayer, B
   Blanc, E
   Ruchiy, Y
   Sell, T
   Mamlouk, S
   Arsie, R
   Wei, TT
   Klotz-Noack, K
   Schwarz, RF
   Sawitzki, B
   Kamphues, C
   Beule, D
   Landthaler, M
   Sers, C
   Horst, D
   Blüthgen, N
   Morkel, M
AF Uhlitz, Florian
   Bischoff, Philip
   Peidli, Stefan
   Sieber, Anja
   Trinks, Alexandra
   Luethen, Mareen
   Obermayer, Benedikt
   Blanc, Eric
   Ruchiy, Yana
   Sell, Thomas
   Mamlouk, Soulafa
   Arsie, Roberto
   Wei, Tzu-Ting
   Klotz-Noack, Kathleen
   Schwarz, Roland F.
   Sawitzki, Birgit
   Kamphues, Carsten
   Beule, Dieter
   Landthaler, Markus
   Sers, Christine
   Horst, David
   Bluethgen, Nils
   Morkel, Markus
TI Mitogen-activated protein kinase activity drives cell trajectories in
   colorectal cancer
SO EMBO MOLECULAR MEDICINE
LA English
DT Article
DE cancer profiling; ERK; RNA velocity; single-cell RNA sequencing;
   SLAM-Seq
ID HUMAN COLON; STEM-CELLS; SECRETORY PRECURSORS; EXPRESSION; RNA;
   DEDIFFERENTIATION; RESISTANCE; SIGNATURES; EVOLUTION; CETUXIMAB
AB In colorectal cancer, oncogenic mutations transform a hierarchically organized and homeostatic epithelium into invasive cancer tissue lacking visible organization. We sought to define transcriptional states of colorectal cancer cells and signals controlling their development by performing single-cell transcriptome analysis of tumors and matched non-cancerous tissues of twelve colorectal cancer patients. We defined patient-overarching colorectal cancer cell clusters characterized by differential activities of oncogenic signaling pathways such as mitogen-activated protein kinase and oncogenic traits such as replication stress. RNA metabolic labeling and assessment of RNA velocity in patient-derived organoids revealed developmental trajectories of colorectal cancer cells organized along a mitogen-activated protein kinase activity gradient. This was in contrast to normal colon organoid cells developing along graded Wnt activity. Experimental targeting of EGFR-BRAF-MEK in cancer organoids affected signaling and gene expression contingent on predictive KRAS/BRAF mutations and induced cell plasticity overriding default developmental trajectories. Our results highlight directional cancer cell development as a driver of non-genetic cancer cell heterogeneity and re-routing of trajectories as a response to targeted therapy.
C1 [Uhlitz, Florian; Bischoff, Philip; Peidli, Stefan; Sieber, Anja; Trinks, Alexandra; Luethen, Mareen; Ruchiy, Yana; Sell, Thomas; Mamlouk, Soulafa; Wei, Tzu-Ting; Klotz-Noack, Kathleen; Sers, Christine; Horst, David; Bluethgen, Nils; Morkel, Markus] Charite Univ Med Berlin, Inst Pathol, Berlin, Germany.
   [Uhlitz, Florian; Bischoff, Philip; Peidli, Stefan; Sieber, Anja; Trinks, Alexandra; Luethen, Mareen; Ruchiy, Yana; Sell, Thomas; Mamlouk, Soulafa; Wei, Tzu-Ting; Klotz-Noack, Kathleen; Sawitzki, Birgit; Kamphues, Carsten; Sers, Christine; Horst, David; Bluethgen, Nils; Morkel, Markus] Free Univ Berlin, Berlin, Germany.
   [Uhlitz, Florian; Bischoff, Philip; Peidli, Stefan; Sieber, Anja; Trinks, Alexandra; Luethen, Mareen; Ruchiy, Yana; Sell, Thomas; Mamlouk, Soulafa; Wei, Tzu-Ting; Klotz-Noack, Kathleen; Sawitzki, Birgit; Kamphues, Carsten; Sers, Christine; Horst, David; Bluethgen, Nils; Morkel, Markus] Humboldt Univ, Berlin, Germany.
   [Uhlitz, Florian; Peidli, Stefan; Sieber, Anja; Sell, Thomas; Bluethgen, Nils] Humboldt Univ, IRI Life Sci, Berlin, Germany.
   [Uhlitz, Florian; Luethen, Mareen; Mamlouk, Soulafa; Kamphues, Carsten; Sers, Christine; Horst, David; Bluethgen, Nils; Morkel, Markus] German Canc Res Ctr, German Canc Consortium DKTK, Partner Site Berlin, Heidelberg, Germany.
   [Trinks, Alexandra; Morkel, Markus] Charite Univ Med Berlin, Berlin Inst Hlth, BIH Bioportal Single Cells, Berlin, Germany.
   [Obermayer, Benedikt; Blanc, Eric; Beule, Dieter] Charite Univ Med Berlin, Berlin Inst Hlth, Core Unit Bioinformat CUBI, Berlin, Germany.
   [Arsie, Roberto; Wei, Tzu-Ting; Schwarz, Roland F.; Landthaler, Markus] Max Delbruck Ctr Mol Med, Berlin Inst Med Syst Biol BIMSB, Berlin, Germany.
   [Klotz-Noack, Kathleen; Sawitzki, Birgit] Charite Univ Med Berlin, Inst Med Immunol, Berlin, Germany.
   [Schwarz, Roland F.] BIFOLD Berlin Inst Foundat Learning & Data, Berlin, Germany.
   [Kamphues, Carsten] Charite Univ Med Berlin, Dept Surg, Berlin, 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; Humboldt University
   of Berlin; Helmholtz Association; German Cancer Research Center (DKFZ);
   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; Helmholtz Association; Max
   Delbruck Center for Molecular Medicine; 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 Blüthgen, N; Morkel, M (corresponding author), Charite Univ Med Berlin, Inst Pathol, Berlin, Germany.; Blüthgen, N; Morkel, M (corresponding author), Free Univ Berlin, Berlin, Germany.; Blüthgen, N; Morkel, M (corresponding author), Humboldt Univ, Berlin, Germany.; Blüthgen, N (corresponding author), Humboldt Univ, IRI Life Sci, Berlin, Germany.; Blüthgen, N; Morkel, M (corresponding author), German Canc Res Ctr, German Canc Consortium DKTK, Partner Site Berlin, Heidelberg, Germany.; Morkel, M (corresponding author), Charite Univ Med Berlin, Berlin Inst Hlth, BIH Bioportal Single Cells, Berlin, Germany.
EM nils.bluethgen@charite.de; markus.morkel@charite.de
RI Morkel, Markus/HLQ-0079-2023; Sawitzki, Birgit/S-2307-2016; Mamlouk,
   Soulafa/AGU-7570-2022; Kamphues, Carsten/AAG-1457-2021; Schwarz,
   Roland/B-6451-2009; Bischoff, Philip/HHC-2955-2022; Bluthgen,
   Nils/A-1711-2011; Peidli, Stefan/GPP-4494-2022; Sers,
   Christine/B-5438-2010; Landthaler, Markus/A-1427-2010
OI Morkel, Markus/0000-0002-2553-9999; Ruchiy, Yana/0000-0003-1119-7809;
   Schwarz, Roland/0000-0001-9155-4268; Trinks,
   Alexandra/0000-0001-9983-1506; Mamlouk, Soulafa/0000-0001-7285-1320;
   Wei, Tzu-Ting/0000-0001-5719-721X; Beule, Dieter/0000-0002-3284-0632;
   Sers, christine/0000-0002-6219-1514; Horst, David/0000-0003-4755-5743;
   Luthen, Mareen/0000-0001-5557-6419; Obermayer,
   Benedikt/0000-0002-9116-630X; Sell, Thomas/0000-0002-5138-3967;
   Landthaler, Markus/0000-0002-1075-8734; Peidli,
   Stefan/0000-0002-4257-8690; Sawitzki, Birgit/0000-0001-8166-8579;
   Bischoff, Philip/0000-0002-4442-7116
FU Berlin Institute of Health; German Cancer Consortium DKTK; Deutsche
   Forschungsgemeinschaft [MO2783/5]; DFG research training group
   [GRK2424/1]; BMBF [02NUK027E]; Stiftung Charite-Einstein BIH Visiting
   Fellow Program; Helmholtz Association; Projekt DEAL
FX The work was in part funded by Berlin Institute of Health (PB, NB, CS,
   DH and MM), German Cancer Consortium DKTK (NB, MM), Deutsche
   Forschungsgemeinschaft (MM, grant MO2783/5), DFG research training group
   (SP and TTW, grant GRK2424/1), BMBF (NB, grant 02NUK027E), Stiftung
   Charite-Einstein BIH Visiting Fellow Program (NB) and the Helmholtz
   Association (RFS). We acknowledge excellent services by the BIH
   Cytometry core facility and the BIH Sequencing core facility. Open
   Access funding enabled and organized by Projekt DEAL.
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NR 63
TC 58
Z9 63
U1 2
U2 37
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1757-4676
EI 1757-4684
J9 EMBO MOL MED
JI EMBO Mol. Med.
PD OCT 7
PY 2021
VL 13
IS 10
AR e14123
DI 10.15252/emmm.202114123
EA AUG 2021
PG 17
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA WC5DP
UT WOS:000686074000001
PM 34409732
OA Green Published
DA 2025-01-04
ER

PT J
AU Iranpour, S
   Bahrami, AR
   Nekooei, S
   Saljooghi, AS
   Matin, MM
AF Iranpour, Sonia
   Bahrami, Ahmad Reza
   Nekooei, Sirous
   Sh. Saljooghi, Amir
   Matin, Maryam M.
TI Improving anti-cancer drug delivery performance of magnetic mesoporous
   silica nanocarriers for more efficient colorectal cancer therapy
SO JOURNAL OF NANOBIOTECHNOLOGY
LA English
DT Article
DE Colorectal cancer; Drug delivery system; pH-sensitive gatekeeper;
   Targeted therapy; Theranostic; Magnetic mesoporous silica NPs
ID IRON-OXIDE NANOPARTICLES; CELL ADHESION MOLECULE; POLY(ETHYLENE GLYCOL);
   THERANOSTIC AGENTS; CONTROLLED-RELEASE; PARTICLE-SIZE; POLYOXOMETALATE;
   TOXICITY; GROWTH; DOXORUBICIN
AB Background: Improving anti-cancer drug delivery performance can be achieved through designing smart and targeted drug delivery systems (DDSs). For this aim, it is important to evaluate overexpressed biomarkers in the tumor microenvironment (TME) for optimizing DDSs.
   Materials and methods: Herein, we designed a novel DDS based on magnetic mesoporous silica core-shell nanoparticles (SPION@MSNs) in which release of doxorubicin (DOX) at the physiologic pH was blocked with gold gatekeepers. In this platform, we conjugated heterofunctional polyethylene glycol (PEG) onto the outer surface of nanocarriers to increase their biocompatibility. At the final stage, an epithelial cell adhesion molecule (EpCAM) aptamer as an active targeting moiety was covalently attached (Apt-PEG-Au@NPs-DOX) for selective drug delivery to colorectal cancer (CRC) cells. The physicochemical properties of non-targeted and targeted nanocarriers were fully characterized. The anti-cancer activity, cellular internalization, and then the cell death mechanism of prepared nanocarriers were determined and compared in vitro. Finally, tumor inhibitory effects, biodistribution and possible side effects of the nanocarriers were evaluated in immunocompromised C57BL/6 mice bearing human HT-29 tumors.
   Results: Nanocarriers were successfully synthesized with a mean final size diameter of 58.22 +/- 8.54 nm. Higher cytotoxicity and cellular uptake of targeted nanocarriers were shown in the EpCAM-positive HT-29 cells as compared to the EpCAM-negative CHO cells, indicating the efficacy of aptamer as a targeting agent. In vivo results in a humanized mouse model showed that targeted nanocarriers could effectively increase DOX accumulation in the tumor site, inhibit tumor growth, and reduce the adverse side effects.
   Conclusion: These results suggest that corporation of a magnetic core, gold gatekeeper, PEG and aptamer can strongly improve drug delivery performance and provide a theranostic DDS for efficient CRC therapy.
C1 [Iranpour, Sonia; Bahrami, Ahmad Reza; Matin, Maryam M.] Ferdowsi Univ Mashhad, Dept Biol, Fac Sci, Mashhad, Razavi Khorasan, Iran.
   [Bahrami, Ahmad Reza] Ferdowsi Univ Mashhad, Inst Biotechnol, Ind Biotechnol Res Grp, Mashhad, Razavi Khorasan, Iran.
   [Nekooei, Sirous] Mashhad Univ Med Sci, Fac Med, Dept Radiol, Mashhad, Razavi Khorasan, Iran.
   [Sh. Saljooghi, Amir] Ferdowsi Univ Mashhad, Fac Sci, Dept Chem, Mashhad, Razavi Khorasan, Iran.
   [Sh. Saljooghi, Amir; Matin, Maryam M.] Ferdowsi Univ Mashhad, Inst Biotechnol, Novel Diagnost & Therapeut Res Grp, Mashhad, Razavi Khorasan, Iran.
C3 Ferdowsi University Mashhad; Ferdowsi University Mashhad; Mashhad
   University of Medical Sciences; Ferdowsi University Mashhad; Ferdowsi
   University Mashhad
RP Matin, MM (corresponding author), Ferdowsi Univ Mashhad, Dept Biol, Fac Sci, Mashhad, Razavi Khorasan, Iran.; Saljooghi, AS (corresponding author), Ferdowsi Univ Mashhad, Fac Sci, Dept Chem, Mashhad, Razavi Khorasan, Iran.
EM saljooghi@um.ac.ir; matin@um.ac.ir
RI Saljooghi, Amir/AAB-6042-2021; M. Matin, Maryam/W-1884-2017
OI M. Matin, Maryam/0000-0002-7949-7712; Sh. Saljooghi,
   Amir/0000-0001-5764-469X
FU Ferdowsi University of Mashhad [3.51537]
FX This work was supported by Ferdowsi University of Mashhad, grant number:
   3.51537.
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NR 88
TC 30
Z9 32
U1 8
U2 67
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1477-3155
J9 J NANOBIOTECHNOL
JI J. Nanobiotechnol.
PD OCT 12
PY 2021
VL 19
IS 1
AR 314
DI 10.1186/s12951-021-01056-3
PG 22
WC Biotechnology & Applied Microbiology; Nanoscience & Nanotechnology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Science & Technology - Other
   Topics
GA WG1BZ
UT WOS:000706734800004
PM 34641857
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Chen, RM
   Chiou, YS
   Chong, QY
   Poh, HM
   Tan, TZ
   Zhang, MY
   Ma, L
   Zhu, T
   Pandey, V
   Basappa,
   Kumar, AP
   Lobie, PE
AF Chen, Ru-Mei
   Chiou, Yi-Shiou
   Chong, Qing-Yun
   Poh, Han-Ming
   Tan, Tuan-Zea
   Zhang, Meng-Yi
   Ma, Lan
   Zhu, Tao
   Pandey, Vijay
   Basappa
   Kumar, Alan Prem
   Lobie, Peter E.
TI Pharmacological Inhibition of TFF3 Enhances Sensitivity of CMS4
   Colorectal Carcinoma to 5-Fluorouracil through Inhibition of p44/42 MAPK
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE trefoil factor 3; CMS4 CRC; ERK1/2; 5-FU; cancer stem cell; targeted
   therapy
ID CONSENSUS MOLECULAR SUBTYPES; TREFOIL FACTOR-3 EXPRESSION; COLON-CANCER;
   IN-VITRO; CELLS; RESISTANCE; METASTASES; MIGRATION; PEPTIDES; PATHWAYS
AB Increased expression of trefoil factor 3 (TFF3) has been reported in colorectal carcinoma (CRC), being correlated with distant metastasis and poor clinical outcomes. Amongst the CRC subtypes, mesenchymal (CMS4) CRC is associated with the worst survival outcome. Herein, the functional roles of TFF3 and the pharmacological inhibition of TFF3 by a novel specific small molecule TFF3 inhibitor-2-amino-4-(4-(6-fluoro-5-methylpyridin-3-yl)phenyl)-5-oxo-4H,5H-pyrano[3,2-c]chromene-3-carbonitrile (AMPC) in CMS4 CRC was explored. Forced expression of TFF3 in CMS4 CRC cells promoted cell proliferation, cell survival, foci formation, invasion, migration, cancer stem cell like behaviour and growth in 3D Matrigel. In contrast, siRNA-mediated depletion of TFF3 or AMPC inhibition of TFF3 in CMS4 CRC cells decreased oncogenic behaviour as indicated by the above cell function assays. AMPC also inhibited tumour growth in vivo. The TFF3-stimulated oncogenic behaviour of CMS4 CRC cells was dependent on TFF3 activation of the p44/42 MAPK (ERK1/2) pathway. Furthermore, the forced expression of TFF3 decreased the sensitivity of CMS4 CRC cells to 5-fluorouracil (5-FU); while depleted TFF3 expression enhanced 5-FU sensitivity in CMS4 CRC cells. 5-FU treatment induced TFF3 expression in CMS4 CRC cells. AMPC, when used in combination with 5-FU in CMS4 CRC cells exhibited a synergistic inhibitory effect. In summary, this study provides functional evidence for TFF3 as a therapeutic target in CMS4 CRC.
C1 [Chen, Ru-Mei; Chong, Qing-Yun; Poh, Han-Ming; Tan, Tuan-Zea; Zhang, Meng-Yi; Kumar, Alan Prem; Lobie, Peter E.] Natl Univ Singapore, Canc Sci Inst Singapore, Singapore 117599, Singapore.
   [Chen, Ru-Mei; Poh, Han-Ming; Zhang, Meng-Yi; Kumar, Alan Prem] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Pharmacol, Singapore 117600, Singapore.
   [Chiou, Yi-Shiou; Ma, Lan; Pandey, Vijay; Lobie, Peter E.] Tsinghua Univ, TBSI, Shenzhen 518055, Guangdong, Peoples R China.
   [Zhang, Meng-Yi] Nankai Univ, State Key Lab Med Chem Biol, Coll Pharm, Tianjin 300350, Peoples R China.
   [Ma, Lan; Pandey, Vijay; Lobie, Peter E.] Shenzhen Bay Lab, Shenzhen 518055, Guangdong, Peoples R China.
   [Zhu, Tao] Univ Sci & Technol China, Hefei Natl Lab Phys Sci Microscale, Hefei 230027, Anhui, Peoples R China.
   [Zhu, Tao] Univ Sci & Technol China, Sch Life Sci, Hefei 230027, Anhui, Peoples R China.
   [Basappa] Univ Mysore, Dept Studies Organ Chem, Biol Chem Lab, Mysore 570006, Karnataka, India.
   [Kumar, Alan Prem] Natl Univ Singapore, Yong Loo Lin Sch Med, Canc Program Med Sci Cluster, Singapore 117599, Singapore.
C3 National University of Singapore; National University of Singapore;
   Tsinghua University; Nankai University; Shenzhen Bay Laboratory; Chinese
   Academy of Sciences; University of Science & Technology of China, CAS;
   Chinese Academy of Sciences; University of Science & Technology of
   China, CAS; University of Mysore; National University of Singapore
RP Kumar, AP; Lobie, PE (corresponding author), Natl Univ Singapore, Canc Sci Inst Singapore, Singapore 117599, Singapore.; Kumar, AP (corresponding author), Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Pharmacol, Singapore 117600, Singapore.; Lobie, PE (corresponding author), Tsinghua Univ, TBSI, Shenzhen 518055, Guangdong, Peoples R China.; Lobie, PE (corresponding author), Shenzhen Bay Lab, Shenzhen 518055, Guangdong, Peoples R China.; Kumar, AP (corresponding author), Natl Univ Singapore, Yong Loo Lin Sch Med, Canc Program Med Sci Cluster, Singapore 117599, Singapore.
EM chenrumei@u.nus.edu; chiouyishiou@gmail.com; csicqy@nus.edu.sg;
   Han_ming89@hotmail.com; csittz@nus.edu.sg; zhangmengyi@u.nus.edu;
   malan@sz.tsinghua.edu.cn; zhut@ustc.edu.cn; vijaypandey7@hotmail.com;
   salundibasappa@gmail.com; csiapk@nus.edu.sg; pelobie@sz.tsinghua.edu.cn
RI Pandey, Vijay/HPF-7092-2023; Zhu, Tao/JEF-1129-2023; Wang,
   Xintong/JJE-1189-2023; Ma, Lan/HNB-3827-2023; Tan, Tuan/I-9227-2019;
   basappa, basappa/AIC-5353-2022; Kumar, Alan/ABE-7492-2020
OI Kumar, Alan Prem/0000-0002-3754-5712; Basappa,
   Basappa/0000-0002-8844-468X
FU National Medical Research Council of Singapore; National Research
   Foundation Singapore; Singapore Ministry of Education under its Research
   Centres of Excellence initiative; Shenzhen Development and Reform
   Commission Subject Construction Project [[2017]1434]; Shenzhen Bay
   Laboratory; Department of Biotechnology; Vision group on Science and
   Technology (India)
FX This work was funded by grants from the National Medical Research
   Council of Singapore to A.P.K. and P.E.L. and by the National Research
   Foundation Singapore and the Singapore Ministry of Education under its
   Research Centres of Excellence initiative to Cancer Science Institute of
   Singapore, National University of Singapore to A.P.K. and P.E.L. The
   project was also supported by the Shenzhen Development and Reform
   Commission Subject Construction Project [2017]1434 to P.E.L., the
   Shenzhen Bay Laboratory and the Department of Biotechnology, and Vision
   group on Science and Technology (India) to B.
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   Zanardi E., 2015, SEMINARS ONCOLOGY
NR 50
TC 19
Z9 21
U1 3
U2 10
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 DEC
PY 2019
VL 20
IS 24
AR 6215
DI 10.3390/ijms20246215
PG 21
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA KB9XE
UT WOS:000506840100109
PM 31835445
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Freeling, JL
   Scholl, JL
   Eikanger, M
   Knoblich, C
   Potts, RA
   Anderson, DJ
   Rower, JE
   Farjoo, MH
   Zhao, HT
   Pillatzki, A
   Rezvani, K
AF Freeling, Jessica L.
   Scholl, Jamie L.
   Eikanger, Morgan
   Knoblich, Cole
   Potts, Rashaun A.
   Anderson, David J.
   Rower, Joseph E.
   Farjoo, Mohammad Hadi
   Zhao, Haotian
   Pillatzki, Angela
   Rezvani, Khosrow
TI Pre-clinical safety and therapeutic efficacy of a plant-based alkaloid
   in a human colon cancer xenograft model
SO CELL DEATH DISCOVERY
LA English
DT Article
ID BRAIN NEURONAL CULTURES; CYTOSOLIC HSP70; VERATRIDINE; MORTALIN;
   TOXICITY; SODIUM; DEATH; BLOOD; CELLS
AB A high-throughput drug screen revealed that veratridine (VTD), a natural plant alkaloid, induces expression of the anti-cancer protein UBXN2A in colon cancer cells. UBXN2A suppresses mortalin, a heat shock protein, with dominant roles in cancer development including epithelial-mesenchymal transition (EMT), cancer cell stemness, drug resistance, and apoptosis. VTD-dependent expression of UBXN2A leads to the deactivation of mortalin in colon cancer cells, making VTD a potential targeted therapy in malignant tumors with high levels of mortalin. VTD was used clinically for the treatment of hypertension in decades past. However, the discovery of newer antihypertensive drugs and concerns over potential neuro- and cardiotoxicity ended the use of VTD for this purpose. The current study aims to determine the safety and efficacy of VTD at doses sufficient to induce UBXN2A expression in a mouse model. A set of flow-cytometry experiments confirmed that VTD induces both early and late apoptosis in a dose-dependent manner. In vivo intraperitoneal (IP) administration of VTD at 0.1 mg/kg every other day (QOD) for 4 weeks effectively induced expression of UBXN2A in the small and large intestines of mice. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) assays on tissues collected from VTD-treated animals demonstrated VTD concentrations in the low pg/mg range. To address concerns regarding neuro- and cardiotoxicity, a comprehensive set of behavioral and cardiovascular assessments performed on C57BL/6NHsd mice revealed that VTD generates no detectable neurotoxicity or cardiotoxicity in animals receiving 0.1 mg/kg VTD QOD for 30 days. Finally, mouse xenograft experiments in athymic nude mice showed that VTD can suppress tumor growth. The main causes for the failure of experimental oncologic drug candidates are lack of sufficient safety and efficacy. The results achieved in this study support the potential utility of VTD as a safe and efficacious anti-cancer molecule.
C1 [Freeling, Jessica L.] Univ South Dakota, Div Basic Biomed Sci, Physiol Core Facil, Vermillion, SD USA.
   [Scholl, Jamie L.] Univ South Dakota, Ctr Brain & Behav Res, Div Basic Biomed Sci, Vermillion, SD USA.
   [Eikanger, Morgan; Knoblich, Cole; Potts, Rashaun A.; Rezvani, Khosrow] Univ South Dakota, Sanford Sch Med, Div Basic Biomed Sci, Vermillion, SD 57069 USA.
   [Anderson, David J.; Rower, Joseph E.] Univ Utah, Ctr Human Toxicol, Salt Lake City, UT USA.
   [Farjoo, Mohammad Hadi] Shahid Beheshti Univ Med Sci, Sch Med, Dept Pharmacol, Tehran, Iran.
   [Zhao, Haotian] New York Inst Technol, Coll Osteopath Med, Old Westbury, NY 11568 USA.
   [Pillatzki, Angela] South Dakota State Univ, Vet & Biomed Sci Dept, Anim Dis Res & Diagnost Lab, Brookings, SD 57007 USA.
C3 University of South Dakota; University of South Dakota; University of
   South Dakota; Utah System of Higher Education; University of Utah;
   Shahid Beheshti University Medical Sciences; New York Institute
   Technology; South Dakota State University
RP Rezvani, K (corresponding author), Univ South Dakota, Sanford Sch Med, Div Basic Biomed Sci, Vermillion, SD 57069 USA.
EM khosrow.rezvani@usd.edu
RI Pillatzki, Angela/W-9005-2019
OI Freeling, Jessica/0000-0002-1003-9174; Eikanger,
   Morgan/0000-0002-6435-6175; Rower, Joseph/0000-0003-3629-7902; Farjoo,
   Mohammad Hadi/0000-0001-7765-6970
FU National Institute of General Medical Sciences of the National
   Institutes of Health [U54GM128729]; National Cancer Institute of the
   National Institutes of Health [1R03CA223935-01]; Sanford School of
   Medicine, Research Enhancement & Academic Development (READ) funding
   program; National Institute of General Medical Sciences [U54 GM115458];
   New York Institute of Technology College of Osteopathic Medicine;
   Matthew Larson Foundation; NIH Institutional Development Award
   [5P20GM103548, 1P20GM103620-01A1]; NIH [R01 CA220551]; National Cancer
   Institute [R01CA220551] Funding Source: NIH RePORTER; National Institute
   of General Medical Sciences [U54GM128729, P20GM103620] Funding Source:
   NIH RePORTER
FX KR is supported by the DaCCoTA funding is supported by the National
   Institute of General Medical Sciences of the National Institutes of
   Health under award number U54GM128729 and the National Cancer Institute
   of the National Institutes of Health under award number 1R03CA223935-01.
   KR is also supported by the Sanford School of Medicine, Research
   Enhancement & Academic Development (READ) funding program. The
   subscription fee for the GraphPad Prism license used in this study is
   supported by the National Institute of General Medical Sciences, U54
   GM115458, which funds the Great Plains IDeA-CTR Network. HZ is supported
   by the New York Institute of Technology College of Osteopathic Medicine,
   Matthew Larson Foundation, NIH Institutional Development Awards
   (5P20GM103548 and 1P20GM103620-01A1), and NIH R01 CA220551.
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NR 55
TC 5
Z9 7
U1 2
U2 5
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2058-7716
J9 CELL DEATH DISCOV
JI Cell Death Discov.
PD MAR 28
PY 2022
VL 8
IS 1
AR 135
DI 10.1038/s41420-022-00936-3
PG 12
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 0J9VA
UT WOS:000780444900002
PM 35347121
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Kozlowska-Geller, MA
   Lewitowicz, P
   Gluszek, SZ
AF Kozlowska-Geller, Monika A.
   Lewitowicz, Piotr
   Gluszek, Stanislaw Z.
TI A FIVE-YEAR FOLLOW UP STUDY OF STAGE I-IV OF RECTAL CANCER WITH AN
   EMPHASIS ON EPIDERMAL GROWTH FACTOR OVER-EXPRESSION
SO POLISH JOURNAL OF PATHOLOGY
LA English
DT Article
DE EGFR; rectal cancer; follow up; immunohistochemistry
ID METASTATIC COLORECTAL-CANCER; FACTOR RECEPTOR; PREDICTIVE FACTORS;
   TARGETED THERAPY; EGFR ANTIBODIES; KRAS; RADIOTHERAPY; STRATEGIES;
   EFFICACY; IMPACT
AB The key pro-proliferative pathway, based on EGFR-KRAS/BRAF-myc, is seen as the main goal of personalized therapy in rectal cancer. The objective of the study is to assess the EGFR immunoreactivity in rectal cancer and to estimate its relationship with the clinical outcome, especially as a predictor of poor outcomes. Patients: applying exclusion criteria, 102 patients with stage I-IV rectal cancer, who had undergone scheduled surgery during the period 2005-2011, were included in the study. There was a follow-up study with a span of 5 years from the date of the surgery.
   Immunohistochemistry using EGFR (EGFR Ab10, Clone111.6) was performed to detect an overexpression of the targeted receptor. Digital analysis of positive reactions of membranes was performed utilizing Visiopharm (TM).
   The degree of EGFR intensity (log OR 0.854, OR 2.35, 95% CI: 1.14-4.85, p = 0.021) is a significant factor in the prognosis of death within 2 years of surgery. The OS curve showed a significant decrease after 40 months from the date of surgery in the cases where EGFR had a high expression. The ROC curve for the cancer stage, according to the UICC classification and EGFR expression, in order to predict a 2-year RFS, reached a high specificity value (ROC = 0.81, p = 0.0408).
   Immunohistochemical EGFR expression is inexpensive, specific and broadly available.
C1 [Kozlowska-Geller, Monika A.] Jan Kochanowski Univ, Coll Med, Inst Med Sci, Dept Physiol, Kielce, Poland.
   [Lewitowicz, Piotr] Jan Kochanowski Univ, Coll Med, Dept Surg & Surg Nursing, Kielce, Poland.
   [Gluszek, Stanislaw Z.] Jan Kochanowski Univ, Coll Med, Dept Pathol, Kielce, Poland.
C3 Jan Kochanowski University; Jan Kochanowski University; Jan Kochanowski
   University
RP Kozlowska-Geller, MA (corresponding author), Jan Kochanowski Univ, Coll Med, Al 9 Wiekow Kielc 19A, PL-25317 Kielce, Poland.
EM monika.kozlowska.chir@onet.pl
RI Stanisław, Gluszek/S-3303-2019; Lewitowicz, Piotr/O-7137-2015
FU  [024/RID/2018/19]
FX Project financed under the program of the Minister of Science and Higher
   Education called "Regional Initiative of Excellence" in the years
   2019-2022, project no. 024/RID/2018/19, amount of financing 11 999
   000,00 PLN.
CR Angulo B, 2014, EXPERT REV MOL DIAGN, V14, P517, DOI 10.1586/14737159.2014.910120
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NR 25
TC 2
Z9 2
U1 0
U2 0
PU VESALIUS UNIV MEDICAL PUBL
PI CRACOW
PA WISLISKO 1, CRACOW, 00000, POLAND
SN 1233-9687
J9 POL J PATHOL
JI Pol. J. Pathol.
PY 2021
VL 72
IS 2
BP 124
EP 129
DI 10.5114/PJP.2021.105639
PG 6
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA XM2YA
UT WOS:000728698100009
PM 34706519
OA gold
DA 2025-01-04
ER

PT J
AU Gumà, J
   Peña, K
   Riu, F
   Guilarte, C
   Hernandez, A
   Lucía, C
   Martínez-Madueño, F
   Miranda, MJ
   Cabezas, I
   Grifoll, M
   Peralta, S
   Serrano, S
   Muñoz, F
   Delamo, L
   Roig, B
   Borràs, J
   Badia, J
   Rodriguez-Balada, M
   Parada, D
AF Guma, Josep
   Pena, Karla
   Riu, Francesc
   Guilarte, Carmen
   Hernandez, Anna
   Lucia, Clara
   Martinez-Madueno, Francisca
   Miranda, Maria Jose
   Cabezas, Ines
   Grifoll, Marc
   Peralta, Sergio
   Serrano, Sara
   Munoz, Felix
   Delamo, Lola
   Roig, Barbara
   Borras, Joan
   Badia, Joan
   Rodriguez-Balada, Marta
   Parada, David
TI Utility of ctDNA Liquid Biopsies from Cancer Patients: An Institutional
   Study of 285 ctDNA Samples
SO CANCERS
LA English
DT Article
DE liquid biopsy; ctDNA; cancer; lung; colorectal; melanoma; precision
   medicine
ID CELL LUNG-CANCER; RAS MUTATIONS; OSIMERTINIB; SURVIVAL; MELANOMA
AB Simple Summary Liquid biopsy is a minimally invasive complementary tool useful in cancer patients for the early identification of treatment selection and resistance to cancer treatment, as well as in routine cancer follow-up. Due to its potential, it is necessary to promote and assess its implementation in the practice of precision medicine. Liquid biopsy has improved significantly over the last decade and is attracting attention as a tool that can complement tissue biopsy to evaluate the genetic landscape of solid tumors. In the present study, we evaluated the usefulness of liquid biopsy in daily oncology practice in different clinical contexts. We studied ctDNA and tissue biopsy to investigate EGFR, KRAS, NRAS, and BRAF mutations from 199 cancer patients between January 2016 and March 2021. The study included 114 male and 85 female patients with a median age of 68 years. A total of 122 cases were lung carcinoma, 53 were colorectal carcinoma, and 24 were melanoma. Liquid biopsy was positive for a potentially druggable driver mutation in 14 lung and colorectal carcinoma where tissue biopsy was not performed, and in two (3%) lung carcinoma patients whose tissue biopsy was negative. Liquid biopsy identified nine (45%) de novo EGFR-T790M mutations during TKI-treatment follow-up in lung carcinoma. BRAF-V600 mutation resurgence was detected in three (12.5%) melanoma patients during follow-up. Our results confirm the value of liquid biopsy in routine clinical oncologic practice for targeted therapy, diagnosis of resistance to treatment, and cancer follow-up.
C1 [Guma, Josep; Lucia, Clara; Martinez-Madueno, Francisca; Miranda, Maria Jose; Cabezas, Ines; Grifoll, Marc; Peralta, Sergio; Serrano, Sara; Munoz, Felix; Delamo, Lola; Roig, Barbara; Borras, Joan; Badia, Joan; Rodriguez-Balada, Marta] Hosp Univ St Joan de Reus, Inst Oncol Catalunya Sud, IISPV, URV, Reus 43204, Spain.
   [Guma, Josep; Pena, Karla; Riu, Francesc; Guilarte, Carmen; Hernandez, Anna; Lucia, Clara; Martinez-Madueno, Francisca; Miranda, Maria Jose; Cabezas, Ines; Grifoll, Marc; Peralta, Sergio; Serrano, Sara; Munoz, Felix; Delamo, Lola; Roig, Barbara; Borras, Joan; Badia, Joan; Rodriguez-Balada, Marta; Parada, David] Inst Invest Sanitaria Pere Virgili, Reus 43204, Spain.
   [Guma, Josep; Pena, Karla; Riu, Francesc; Guilarte, Carmen; Hernandez, Anna; Parada, David] Univ Rovira & Virgili, Fac Med & Ciencies Salut, Reus 43204, Spain.
   [Pena, Karla; Riu, Francesc; Guilarte, Carmen; Hernandez, Anna; Parada, David] Hosp Univ St Joan, Mol Pathol Unit, Dept Pathol, Reus 43204, Spain.
C3 Universitat Rovira i Virgili; Institut d'Investigacio Sanitaria Pere
   Virgili (IISPV); Universitat Rovira i Virgili; Institut d'Investigacio
   Sanitaria Pere Virgili (IISPV); Universitat Rovira i Virgili
RP Parada, D (corresponding author), Inst Invest Sanitaria Pere Virgili, Reus 43204, Spain.; Parada, D (corresponding author), Univ Rovira & Virgili, Fac Med & Ciencies Salut, Reus 43204, Spain.; Parada, D (corresponding author), Hosp Univ St Joan, Mol Pathol Unit, Dept Pathol, Reus 43204, Spain.
EM david.parada@urv.cat
RI Badia, Joan/JRX-7077-2023
OI Badia, Joan/0000-0001-7446-7365; Parada, David/0000-0002-8894-2312;
   Lucia Gozalvez, Clara/0000-0001-6965-4529; Borras,
   Joan/0000-0003-1315-0246; Grifoll, Marc/0000-0002-1948-328X;
   Rodriguez-Balada, Marta/0000-0002-2691-8819; Guma,
   Josep/0000-0001-7541-9832; Hernandez-Aguilera, Anna/0000-0003-0954-295X
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NR 32
TC 0
Z9 0
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 DEC
PY 2022
VL 14
IS 23
AR 5859
DI 10.3390/cancers14235859
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 6X0XP
UT WOS:000896146900001
PM 36497340
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Cleary, JM
   McRee, AJ
   Shapiro, GI
   Tolaney, SM
   O'Neil, BH
   Kearns, JD
   Mathews, S
   Nering, R
   MacBeath, G
   Czibere, A
   Sharma, S
   Korn, WM
AF Cleary, James M.
   McRee, Autumn J.
   Shapiro, Geoffrey I.
   Tolaney, Sara M.
   O'Neil, Bert H.
   Kearns, Jeffrey D.
   Mathews, Sara
   Nering, Rachel
   MacBeath, Gavin
   Czibere, Akos
   Sharma, Sunil
   Korn, W. Michael
TI A phase 1 study combining the HER3 antibody seribantumab (MM-121) and
   cetuximab with and without irinotecan
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE Seribantumab; Cetuximab; HER3; EGFR
ID METASTATIC COLORECTAL-CANCER; TYROSINE KINASE INHIBITORS; SQUAMOUS-CELL
   CARCINOMA; ACQUIRED-RESISTANCE; ANTITUMOR-ACTIVITY; TARGETED THERAPY;
   PLUS CETUXIMAB; LUNG-CANCER; RECEPTOR; EGFR
AB Background HER3/EGFR heterodimers have been implicated as a mode of resistance to EGFR-directed therapies. Methods This Phase 1 trial assessed the tolerability, maximum tolerated dose (MTD) and pharmacokinetic (PK) properties of the HER-3 antibody seribantumab in combination with cetuximab (Part I) or cetuximab and irinotecan (Part II) in patients with EGFR-dependent cancers. In Part I, escalating doses of seribantumab and cetuximab were administered. In Part II of the trial, escalating doses of seribantumab/cetuximab were combined with irinotecan 180 mg/m(2) administered every two weeks. Results 34 patients were enrolled in Part I (seribantumab/cetuximab) and 14 patients were enrolled in Part II (seribantumab/cetuximab/irinotecan). Common toxicities of seribantumab/cetuximab included acneiform rash, diarrhea, stomatitis, and paronychia. The MTD of Part I was seribantumab 40 mg/kg bolus, then 20 mg/kg weekly combined with cetuximab 400 mg/m(2) bolus, then 250 mg/m(2) IV weekly. Common toxicities reported in the seribantumab/cetuximab/irinotecan combination were similar to the Part I portion. However, toxicities were more frequent and severe with the triplet combination. There was one treatment-related death in Part II secondary to Grade 4 neutropenia and grade 3 diarrhea. Other dose-limiting toxicities in Part II were Grade 3 mucositis andGrade 3 diarrhea. Acholangiocarcinoma patient, previously untreated with EGFR-directed therapy, had a confirmed partial response (PR). One colorectal cancer patient, previously treated with EGFR-directed therapy, had an unconfirmed PR. Conclusions Seribantumab/cetuximab was well tolerated and patients experienced toxicities typical to EGFR inhibition. Unlike the seribantumab/cetuximab doublet, seribantumab/cetuximab/irinotecan was difficult to tolerate in this heavily pretreated population. There was limited efficacy of the combination therapy.
C1 [Cleary, James M.; Shapiro, Geoffrey I.; Tolaney, Sara M.] Dana Farber Canc Inst, Early Drug Dev Ctr, Boston, MA 02115 USA.
   [McRee, Autumn J.; O'Neil, Bert H.] Univ N Carolina, Chapel Hill, NC USA.
   [O'Neil, Bert H.] Indiana Univ, Simon Canc Ctr, Indianapolis, IN 46204 USA.
   [Kearns, Jeffrey D.; Mathews, Sara; Nering, Rachel; MacBeath, Gavin; Czibere, Akos] Merrimack Pharmaceut Inc, Cambridge, MA USA.
   [Sharma, Sunil] Huntsman Canc Inst, Salt Lake City, UT USA.
   [Korn, W. Michael] Univ Calif San Francisco, Box 1705, San Francisco, CA 94143 USA.
C3 Harvard University; Dana-Farber Cancer Institute; University of North
   Carolina; University of North Carolina Chapel Hill; Indiana University
   System; Indiana University Indianapolis; Merrimack Pharmaceuticals,
   Inc.; Utah System of Higher Education; University of Utah; Huntsman
   Cancer Institute; University of California System; University of
   California San Francisco
RP Korn, WM (corresponding author), Univ Calif San Francisco, Box 1705, San Francisco, CA 94143 USA.
EM Michael.Korn@ucsf.edu
RI Tolaney, S/AFZ-2612-2022; Shapiro, Geoffrey/IWL-8291-2023
OI MacBeath, Gavin/0000-0003-2585-6772; Shapiro,
   Geoffrey/0000-0002-3331-4095
FU Merrimack Pharmaceuticals, Inc.
FX Merrimack Pharmaceuticals, Inc.
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NR 35
TC 17
Z9 18
U1 0
U2 6
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 2017
VL 35
IS 1
BP 68
EP 78
DI 10.1007/s10637-016-0399-7
PG 11
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA EQ5AN
UT WOS:000398093300007
PM 27853996
DA 2025-01-04
ER

PT J
AU Pietrantonio, F
   Di Nicolantonio, F
   Schrock, AB
   Lee, J
   Morano, F
   Fucà, G
   Nikolinakos, P
   Drilon, A
   Hechtman, JF
   Christiansen, J
   Gowen, K
   Frampton, GM
   Gasparini, P
   Rossini, D
   Gigliotti, C
   Kim, ST
   Prisciandaro, M
   Hodgson, J
   Zaniboni, A
   Chiu, VK
   Milione, M
   Patel, R
   Miller, V
   Bardelli, A
   Novara, L
   Wang, L
   Pupa, SM
   Sozzi, G
   Ross, J
   Di Bartolomeo, M
   Bertotti, A
   Ali, S
   Trusolino, L
   Falcone, A
   de Braud, F
   Cremolini, C
AF Pietrantonio, F.
   Di Nicolantonio, F.
   Schrock, A. B.
   Lee, J.
   Morano, F.
   Fuca, G.
   Nikolinakos, P.
   Drilon, A.
   Hechtman, J. F.
   Christiansen, J.
   Gowen, K.
   Frampton, G. M.
   Gasparini, P.
   Rossini, D.
   Gigliotti, C.
   Kim, S. T.
   Prisciandaro, M.
   Hodgson, J.
   Zaniboni, A.
   Chiu, V. K.
   Milione, M.
   Patel, R.
   Miller, V.
   Bardelli, A.
   Novara, L.
   Wang, L.
   Pupa, S. M.
   Sozzi, G.
   Ross, J.
   Di Bartolomeo, M.
   Bertotti, A.
   Ali, S.
   Trusolino, L.
   Falcone, A.
   de Braud, F.
   Cremolini, C.
TI <i>RET</i> fusions in a small subset of advanced colorectal cancers at
   risk of being neglected
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE PET; colorectal cancer; gene fusions; targeted therapy; MSI high;
   prognosis
ID LANDSCAPE; MULTICENTER
AB Background
   Recognition of rare molecular subgroups is a challenge for precision oncology and may lead to tissue-agnostic approval of targeted agents. Here we aimed to comprehensively characterize the clinical, pathological and molecular landscape of RET rearranged metastatic colorectal cancer (mCRC).
   Patients and methods
   In this case series, we compared clinical, pathological and molecular characteristics of 24 RET rearranged mCRC patients with those of a control group of 291 patients with RET negative tumors. RET rearranged and RET negative mCRCs were retrieved by systematic literature review and by taking advantage of three screening sources: (i) Ignytas phase 1/1b study on RXDX-105 (NCT01877811), (ii) cohorts screened at two Italian and one South Korean Institutions and (iii) Foundation Medicine Inc. database. Next-generation sequencing data were analyzed for RET rearranged cases.
   Results
   RET fusions were more frequent in older patients (median age of 66 versus 60 years, P = 0.052), with ECOG PS 1-2 (90% versus 50%, P = 0.02), right-sided (55% versus 32%, P = 0.013), previously unresected primary tumors (58% versus 21%, P < 0.001), RAS and BRAF wild-type (100% versus 40%, P < 0.001) and MSI-high (48% versus 7%, P < 0.001). Notably, 11 (26%) out of 43 patients with right-sided, RAS and BRAF wild-type tumors harbored a RET rearrangement. At a median follow-up of 45.8 months, patients with RET fusion-positive tumors showed a significantly worse OS when compared with RET-negative ones (median OS 14.0 versus 38.0 months, HR: 4.59; 95% CI, 3.64-32.66; P < 0.001). In the multivariable model, RET rearrangements were still associated with shorter OS (HR: 2.97; 95% CI, 1.25-7.07; P = 0.014), while primary tumor location, RAS and BRAF mutations and MSI status were not.
   Conclusions
   Though very rare, RET rearrangements define a new subtype of mCRC that shows poor prognosis with conventional treatments and is therefore worth of a specific management.
C1 [Pietrantonio, F.; Morano, F.; Fuca, G.; Prisciandaro, M.; Di Bartolomeo, M.; de Braud, F.] Fdn IRCCS Ist Nazl Tumori, Dept Med Oncol, Milan, Italy.
   [Pietrantonio, F.; de Braud, F.] Univ Milan, Dept Oncol & Hematooncol, Milan, Italy.
   [Di Nicolantonio, F.; Gigliotti, C.; Bardelli, A.; Bertotti, A.; Trusolino, L.] Univ Torino, Dept Oncol, Candiolo, Italy.
   [Di Nicolantonio, F.; Gigliotti, C.; Bardelli, A.; Novara, L.; Bertotti, A.; Trusolino, L.] IRCCS, Candiolo Canc Inst FPO, ECMO, Candiolo, Italy.
   [Schrock, A. B.; Gowen, K.; Frampton, G. M.; Miller, V.; Ross, J.; Ali, S.] Fdn Med Inc, Clin Dev, Cambridge, MA USA.
   [Lee, J.; Kim, S. T.] Sungkyunkwan Univ, Dept Med, Samsung Med Ctr, Sch Med, Seoul, South Korea.
   [Nikolinakos, P.; Hodgson, J.] Univ Canc & Blood Ctr, Med Oncol, Athens, Greece.
   [Drilon, A.] Mem Sloan Kettering Canc Ctr, Dept Med, 1275 York Ave, New York, NY 10021 USA.
   [Hechtman, J. F.] Mem Sloan Kettering Canc Ctr, Dept Pathol, 1275 York Ave, New York, NY 10021 USA.
   [Christiansen, J.; Patel, R.] Ignyta Inc, Diagnost, San Diego, CA USA.
   [Gasparini, P.; Pupa, S. M.; Sozzi, G.] Fdn IRCCS Ist Nazl Tumori, Dept Expt Oncol & Mol Med, Milan, Italy.
   [Rossini, D.; Falcone, A.; Cremolini, C.] Univ Pisa, Dept Translat Res & New Technol Med & Surg, Pisa, Italy.
   [Zaniboni, A.] Fdn Poliambulanza, Dept Med Oncol, Brescia, Italy.
   [Chiu, V. K.] Univ New Mexico, Dept Internal Med, Albuquerque, NM 87131 USA.
   [Milione, M.] Fdn IRCCS Ist Nazl Tumori, Dept Diagnost Pathol & Lab Med, Milan, Italy.
   [Wang, L.] St Jude Childrens Res Hosp, Dept Pathol, 332 N Lauderdale St, Memphis, TN 38105 USA.
C3 Fondazione IRCCS Istituto Nazionale Tumori Milan; University of Milan;
   University of Turin; IRCCS Fondazione del Piemonte per l'Oncologia;
   Foundation Medicine; Sungkyunkwan University (SKKU); Samsung Medical
   Center; Memorial Sloan Kettering Cancer Center; Memorial Sloan Kettering
   Cancer Center; Fondazione IRCCS Istituto Nazionale Tumori Milan;
   University of Pisa; University of New Mexico; Fondazione IRCCS Istituto
   Nazionale Tumori Milan; St Jude Children's Research Hospital
RP Pietrantonio, F (corresponding author), Fdn IRCCS Ist Nazl Tumori, Dept Med Oncol, Med Oncol Unit, Via Venezian 1, I-20133 Milan, Italy.
EM filippo.pietrantonio@istitutotumori.mi.it
RI Lee, Jee/C-9646-2011; kim, st/O-5928-2014; Trusolino, Livio/A-3896-2011;
   de Braud, Filippo/B-9997-2017; Cremolini, Chiara/AAC-1889-2019; Fuca,
   Giovanni/AAF-2378-2019; Rossini, Daniele/GPW-8241-2022; Hechtman,
   Jaclyn/A-3277-2013; Falcone, Alfredo/G-5217-2013; Di Nicolantonio,
   Federica/A-2503-2011; Pietrantonio, Filippo/C-2180-2017; ,
   Lu/N-8128-2018; Morano, Federica/B-7910-2018; Gasparini,
   Patrizia/Q-7626-2016; Di Bartolomeo, Maria/D-1655-2017; BARDELLI,
   Alberto/J-9721-2018; Pupa, Serenella/K-6388-2016
OI CREMOLINI, CHIARA/0000-0002-0520-4841; Di Nicolantonio,
   Federica/0000-0001-9618-2010; Pietrantonio, Filippo/0000-0002-8530-8420;
   , Lu/0000-0002-0073-0666; Hechtman, Jaclyn/0000-0003-2645-0985;
   Gigliotti, Chiara/0000-0001-9225-2616; Bertotti,
   Andrea/0000-0001-8196-7608; Falcone, Alfredo/0000-0001-5840-2529;
   Prisciandaro, Michele/0000-0001-5596-469X; Morano,
   Federica/0000-0002-5306-3596; Rossini, Daniele/0009-0000-3777-8471;
   Frampton, Garrett/0000-0002-2361-2750; Trusolino,
   Livio/0000-0002-6379-3365; Gasparini, Patrizia/0000-0002-9548-3724; Di
   Bartolomeo, Maria/0000-0002-7954-6609; Fuca,
   Giovanni/0000-0002-1560-2253; BARDELLI, Alberto/0000-0003-1647-5070;
   Pupa, Serenella/0000-0002-4592-6830
FU Fondazione ARCO (Associazione Ricerche e Cure in Oncologia), Italy; AIRC
   [17707]; Associazione Italiana per la Ricerca sul Cancro [18532]
FX This work was supported by Fondazione ARCO (Associazione Ricerche e Cure
   in Oncologia), Italy and partly supported by grants AIRC IG n. 17707
   (FDN); Associazione Italiana per la Ricerca sul Cancro, Investigator
   Grant 18532 (LT). Fondazione Piemontese per la Ricerca sul Cancro-ONLUS,
   5 x 1000 Ministero della Salute 2011 (LT) and 2014 (LT); Transcan,
   TACTIC (LT).
CR BENJAMINI Y, 1995, J R STAT SOC B, V57, P289, DOI 10.1111/j.2517-6161.1995.tb02031.x
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NR 17
TC 76
Z9 81
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 JUN
PY 2018
VL 29
IS 6
BP 1394
EP 1401
DI 10.1093/annonc/mdy090
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GM8TQ
UT WOS:000438508100014
PM 29538669
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Chen, Y
   Xu, YY
   Jiang, HJ
   Wang, L
   Zhai, JW
   Zhang, T
   Yang, YF
AF Chen Yue
   Xu Yu-ying
   Jiang Hai-jun
   Wang Lei
   Zhai Jia-wei
   Zhang Tong
   Yang Yu-fei
TI Patients with Metastatic Colorectal Cancer after Failure of Second-Line
   Treatment May Benefit from Low-Dose Apatinib and S-1 Combined with
   Jianpi Bushen Jiedu Decoction
SO CHINESE JOURNAL OF INTEGRATIVE MEDICINE
LA English
DT Article
DE metastatic colorectal cancer; apatinib; S-1; Jianpi Bushen Jiedu
   Decoction; Chinese medicine; progression-free survival; clinical trial
ID DOUBLE-BLIND; SINGLE-ARM; PLACEBO; MULTICENTER; CAPSULE
AB Objective To evaluate the effect and safety of low-dose of apatinib and S-1 combined with Jianpi Bushen Jiedu Decoction (JBJD) in patients with metastatic colorectal cancer (mCRC) who have failed second or above lines treatment, in order to provide more treatment option for mCRC patients by integrated medicine. Methods Thirteen patients were selected from a single-arm, open-label clinical study from April 2019 to September 2020. The patients were treated with low-dose apatinib (250 mg, once a day) and S-1 (20 mg, twice a day) combined with JBJD for at least one cycle and were followed up to August 2021. The primary endpoint was disease progression-free survival (PFS). Disease control rate (DCR), objective response rate (ORR), and overall survival (OS) of patients were observed as the secondary endpoints. Adverse events were recorded as well. Results The average age of the 13 patients was 56.5 +/- 13.0 years and 76.9% were male. The median PFS and median OS were 4.6 and 8.3 months, respectively. The ORR was 7.7% (1/13) while the DCR was 61.5% (8/13). The common adverse events were hypertension, proteinuria, elevated transaminase, and thrombocytopenia. One patient experienced thrombocytopenia of grade 3. Conclusions Patients with mCRC after failure of the second or above lines of treatment may potentially benefit from the treatment of low-dose apatinib and S-1 combined with JBJD because of its similar effect as the standard dose of target therapy and relatively better safety. (Registration No. ChiCTR1900022673)
C1 [Chen Yue; Zhai Jia-wei] Beijing Univ Chinese Med, Grad Sch, Beijing 100029, Peoples R China.
   [Xu Yu-ying; Wang Lei; Zhang Tong; Yang Yu-fei] China Acad Chinese Med Sci, Xiyuan Hosp, Dept Oncol, Beijing 100091, Peoples R China.
   [Jiang Hai-jun] Cent Hosp Ankang City, Dept Oncol, Ankang 725000, Shaanxi, Peoples R China.
C3 Beijing University of Chinese Medicine; Xiyuan Hospital, CACMS; China
   Academy of Chinese Medical Sciences
RP Yang, YF (corresponding author), China Acad Chinese Med Sci, Xiyuan Hosp, Dept Oncol, Beijing 100091, Peoples R China.
EM yyf93@vip.sina.com
RI Zhang, tong/IAP-2587-2023; Yang, yufei/KHW-2735-2024
FU National Administration of Traditional Chinese Medicine: Qihuang Scholar
   [02045004]; Collaborative Pilot Project of Clinical Traditional Chinese
   and Western Medicine for Major and Difficult Diseases in 2019
   [070030003]
FX Supported by National Administration of Traditional Chinese Medicine:
   Qihuang Scholar (No. 02045004) and Collaborative Pilot Project of
   Clinical Traditional Chinese and Western Medicine for Major and
   Difficult Diseases in 2019 (No. 070030003)
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NR 34
TC 1
Z9 1
U1 0
U2 22
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1672-0415
EI 1993-0402
J9 CHIN J INTEGR MED
JI Chin. J. Integr. Med.
PD OCT
PY 2022
VL 28
IS 10
BP 924
EP 929
DI 10.1007/s11655-022-3676-7
EA MAY 2022
PG 6
WC Integrative & Complementary Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Integrative & Complementary Medicine
GA 4Z0CY
UT WOS:000790628200001
PM 35508862
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Li, C
   Xu, N
   Li, YQ
   Wang, Y
   Zhu, ZT
AF Li, Chen
   Xu, Na
   Li, Yu-Qiang
   Wang, Yu
   Zhu, Zhi-Tu
TI Inhibition of SW620 human colon cancer cells by upregulating miRNA-145
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE miRNA-145; Colorectal cancer; Targeted therapy; N-ras; Lentiviral vector
ID COLORECTAL-CANCER; MICRORNA SIGNATURES; STAGE-II; MIR-143/145;
   METASTASIS; RECURRENCE; EXPRESSION; CARCINOMA; BIOMARKER; SURVIVAL
AB AIM: To investigate the targeted inhibition of proliferation and migration of SW620 human colon cancer cells by upregulating miRNA-145 (miR-145).
   METHODS: Forty-five samples of colon cancer tissues and 45 normal control samples were obtained from the biological database of the First Affiliated Hospital of Liaoning Medical University. We performed quantitative analysis of miR-145 and N-ras expression in tissues; reverse transcriptase polymerase chain reaction analysis of miR-145 expression in SW620 colon cancer cells and normal colonic epithelial cells; construction of miR-145 lentiviral vector and determination of miR-145 expression in SW620 cells transduced with miR-145 vector; analysis of the effect of miR-145 overexpression on SW620 cell proliferation; analysis of the effect of miR-145 overexpression on SW620 cell migration using a wound healing assay; and analysis of the effect of miR-145 on N-ras expression using Western blotting.
   RESULTS: miR-145 expression was significantly downregulated in colon cancer tissues, with its expression in normal colonic tissues being 4-5-fold higher (two sample t test, P < 0.05), whereas N-ras expression showed the opposite trend. miR-145 expression in SW620 cells was downregulated, which was significantly lower compared to that in colonic epithelial cells (two sample t test, P < 0.05). miR-145 vector and control were successfully packaged; expression of miR-145 in SW620 cells transduced with miR-145 was 8.2-fold of that in control cells (two sample t test, P < 0.05). The proliferation of miR-145-transduced SW620 cells was significantly decreased compared to control cells (two sample t test, P < 0.05). At 48 h in the wound healing experiment, the migration indexes and controls were (97.27% +/- 9.25%) and (70.22% +/- 6.53%), respectively (two sample t test, P < 0.05). N-ras expression in miR-145-tranduced SW620 cells was significantly lower than others (one-way analysis of variance, P < 0.05).
   CONCLUSION: miR-145 is important in inhibiting colon cancer cell proliferation and migration. This is a good foundation for development of colon cancer therapy by targeting tumor suppressor miR-145.
C1 [Li, Chen; Li, Yu-Qiang; Wang, Yu] Liaoning Med Univ, Affiliated Hosp 1, Biobank, Jinzhou 121001, Liaoning Provin, Peoples R China.
   [Xu, Na] Liaoning Med Univ, Affiliated Hosp 1, Dept Radiol, Jinzhou 121001, Liaoning Provin, Peoples R China.
   [Zhu, Zhi-Tu] Liaoning Med Univ, Affiliated Hosp 1, Dept Oncol, 2 Wuduan,Renmin St, Jinzhou 121001, Liaoning Provin, Peoples R China.
C3 Jinzhou Medical University; Jinzhou Medical University; Jinzhou Medical
   University
RP Zhu, ZT (corresponding author), Liaoning Med Univ, Affiliated Hosp 1, Dept Oncol, 2 Wuduan,Renmin St, Jinzhou 121001, Liaoning Provin, Peoples R China.
EM zhuzhitu2014jz@hotmail.com
FU Liaoning Medical "Principal Fund" special fund clinical construction
   [XZJJ20130214]; Liaoning Provincial Science and Technology Department of
   Science and Technology Program [2013225305]
FX Supported by Liaoning Medical "Principal Fund" special fund clinical
   construction, No. XZJJ20130214; and Liaoning Provincial Science and
   Technology Department of Science and Technology Program, No. 2013225305.
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U1 1
U2 15
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD MAR 7
PY 2016
VL 22
IS 9
BP 2771
EP 2778
DI 10.3748/wjg.v22.i9.2771
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DG0ZH
UT WOS:000371794300011
PM 26973415
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Kuwata, T
AF Kuwata, Takeshi
TI Molecular classification and intratumoral heterogeneity of gastric
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SO PATHOLOGY INTERNATIONAL
LA English
DT Review
DE claudin 18.2; DNA mismatch repair; gastric cancer; HER2 microsatellite
   instability; intratumoral heterogeneity; molecular classification;
   molecular targeted therapy; PD-L1; precision medicine
ID EPSTEIN-BARR-VIRUS; EPITHELIAL-MESENCHYMAL TRANSITION; MICROSATELLITE
   INSTABILITY; TUMOR HETEROGENEITY; MISMATCH-REPAIR; OPEN-LABEL;
   GASTROESOPHAGEAL JUNCTION; CLINICAL-SIGNIFICANCE; COLORECTAL-CANCER;
   PLUS CHEMOTHERAPY
AB Gastric cancers frequently harbor striking histological complexity and diversity between lesions as well as within single lesions, known as inter- and intratumoral heterogeneity, respectively. The latest World Health Organization Classification of Tumors designated more than 30 histological subtypes for gastric epithelial tumors, assigning 12 subtypes for gastric adenocarcinoma (GAD). Meanwhile, recent advances in genome-wide analyses have provided molecular aspects to the histological classification of GAD, and consequently revealed different molecular traits underlying these histological subtypes. Moreover, accumulating knowledge of comprehensive molecular profiles has led to establishing molecular classifications of GAD, which are often associated with clinical biomarkers for therapeutics and prognosis. However, most of our knowledge of GAD molecular profiles is based on inter-tumoral heterogeneity, and the molecular profiles underlying intratumoral heterogeneity are yet to be determined. In this review, recently established molecular classifications of GAD are introduced in the aspect of pathological diagnosis and are discussed in the context of intratumoral heterogeneity.
C1 [Kuwata, Takeshi] Natl Canc Ctr Hosp East, Dept Genet Med & Serv, 6-5-1 Kashiwano Ha, Kashiwa, Chiba 2778577, Japan.
C3 National Cancer Center - Japan
RP Kuwata, T (corresponding author), Natl Canc Ctr Hosp East, Dept Genet Med & Serv, 6-5-1 Kashiwano Ha, Kashiwa, Chiba 2778577, Japan.
EM tkuwata@east.ncc.go.jp
FU JSPS KAKENHI;  [21K06939]
FX The author has been announced as the winner of The Japanese Society of
   Pathology; Pathology Research Award in 2020. This work was supported in
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NR 160
TC 1
Z9 1
U1 0
U2 0
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1320-5463
EI 1440-1827
J9 PATHOL INT
JI Pathol. Int.
PD JUN
PY 2024
VL 74
IS 6
BP 301
EP 316
DI 10.1111/pin.13427
EA APR 2024
PG 16
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA WC3J1
UT WOS:001206163700001
PM 38651937
OA hybrid
DA 2025-01-04
ER

PT J
AU Vassilev, ZP
   Fan, XZ
   Xu, JL
   Ostojic, H
   Barzi, A
AF Vassilev, Zdravko P.
   Fan, Xiaozhou
   Xu, Julie
   Ostojic, Helene
   Barzi, Afsaneh
TI Use of FOLFOXIRI Plus Bevacizumab and Subsequent Therapies in Metastatic
   Colorectal Cancer: An Age-Stratified Analysis
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE Chemotherapy; Electronic health records; Real-world data; Retrospective;
   Targeted therapy
ID COLON-CANCER; YOUNG-ADULTS; CHEMOTHERAPY
AB We conducted an analysis of electronic health records to assess FOLFOXIRI + bevacizumab (triplet + bev) use and subsequent therapies in adult patients with metastatic colorectal cancer. Results showed increasing triplet + bev use over time in patients aged < 65 years and administration of "new" subsequent therapies (not including any agents comprising triplet + bev) in over half of the study population, consistent with available evidence. Background: Treatment recommendations for metastatic colorectal cancer (mCRC) do not differ by age group; nevertheless, aggressive multiagent chemotherapy comprising FOLFOXIRI+bevacizumab (triplet+bev) is routinely administered in younger patients. This study analyzed real-world data on index triplet+bev use and subsequent systemic therapies. Materials and Methods: This retrospective, observational cohort study was conducted in patients aged >= 18 years with mCRC, who were initiated on triplet+bev. Data were derived from the Optum de-identified electronic health record dataset. Results: Of 36,056 patients, 14%, 36%, and 50% were aged 18-49, 50-64, and >= 65 years, respectively. During the study period (2010-2021), triplet+bev use increased in patients aged 18-49 years (1%-4%) but remained at approximately 3% and 1% in patients aged 50-64 and >= 65 years, respectively. Patient demographics and clinical characteristics varied slightly; of patients receiving triplet+bev (n = 921) versus nontriplet+bev (n = 35,132) most were male (57% vs. 52%), resided in the Midwest (54% vs. 49%) and Northeast (18% vs. 14%) US regions, and had secondary malignancies (86% vs. 73%). Following triplet+bev, most patients received subsequent therapies (including continued triplet component therapies; 97%) or subsequent "new" therapies (therapies that did not include any agents comprising triplet+bev; 57%), most frequently EGFR inhibitors (28%) and regorafenib (21%), with a similar trend among all age groups. Conclusions: Overall, this study shows that younger patients with mCRC are more likely to receive first-line triplet+bev. These results also reveal that nonchemotherapy options are often used beyond first-line triplet chemotherapy for patients with mCRC.
C1 [Vassilev, Zdravko P.; Fan, Xiaozhou] Bayer HealthCare Pharmaceut, 100 Bayer Blvd, Whippany, NJ 07981 USA.
   [Xu, Julie] Bayer Canada, Mississauga, ON, Canada.
   [Ostojic, Helene] Bayer Consumer Care, Basel, Switzerland.
   [Barzi, Afsaneh] City Hope Natl Med Ctr, Dept Med Oncol & Therapeut Res, Duarte, CA USA.
C3 Bayer AG; Bayer Healthcare Pharmaceuticals; Bayer AG; City of Hope
RP Vassilev, ZP (corresponding author), Bayer HealthCare Pharmaceut, 100 Bayer Blvd, Whippany, NJ 07981 USA.
EM zdravko.vassilev@bayer.com
RI Fan, Xiaozhou/J-6059-2019
FU OPEN Health Communications (London, UK) - Bayer
FX Medical writing support was provided by Robyn Fowler, PhD, Matthew
   Naylor, PhD, and Priya Popat, BSc, OPEN Health Communications (London,
   UK) and funded by Bayer, in accordance with Good Publication Practice
   (GPP) guidelines ( www.ismpp.org/gpp-2022) .
CR Akimoto N, 2021, NAT REV CLIN ONCOL, V18, P230, DOI 10.1038/s41571-020-00445-1
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NR 33
TC 1
Z9 1
U1 1
U2 1
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 2024
VL 23
IS 3
DI 10.1016/j.clcc.2024.05.001
EA AUG 2024
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA G4Q6A
UT WOS:001316505700001
PM 38853099
DA 2025-01-04
ER

PT J
AU Delle Cave, D
   Mangini, M
   Tramontano, C
   De Stefano, L
   Corona, M
   Rea, I
   De Luca, AC
   Lonardo, E
AF Delle Cave, Donatella
   Mangini, Maria
   Tramontano, Chiara
   De Stefano, Luca
   Corona, Marco
   Rea, Ilaria
   De Luca, Anna Chiara
   Lonardo, Enza
TI Hybrid Biosilica Nanoparticles for in-vivo Targeted Inhibition of
   Colorectal Cancer Growth and Label-Free Imaging
SO INTERNATIONAL JOURNAL OF NANOMEDICINE
LA English
DT Article
DE targeted drug delivery; Raman imaging; antibody quantification;
   biosilica nanoparticle; in vivo treatment; colorectal cancer
ID TGF-BETA; CELLS; FLUORESCENCE; RESISTANCE; EXPRESSION
AB Background: Metastasis-initiating cells are key players in progression, resistance, and relapse of colorectal cancer (CRC), by leveraging the regulatory relationship between Transforming Growth Factor-beta (TGF-(3) signaling and anti-L1 cell adhesion molecule (L1CAM). Methods: This study introduces a novel strategy for CRC targeted therapy and imaging based on the use of a hybrid nanosystem made of gold nanoparticles-covered porous biosilica further modified with the (L1CAM) antibody. Results: The nanosystem intracellularly delivers galunisertib (LY), a TGF-(3 inhibitor, aiming to inhibit epithelial-mesenchymal transition (EMT), a process pivotal for metastasis. Anti-L1CAM antibody-functionalized nanoparticles (NPs) target tumor-initiating cells expressing L1CAM, inhibiting cancer growth. The number of antibody molecules conjugated to the single NP is precisely quantified, revealing a high surface coverage that facilitates the tumor targeting. The therapeutic efficacy of the nanosystem is investigated in organoid-like cultures of CRC cells and in vivo mouse models, showing a significant reduction in tumor growth. The spatial distribution of NPs within CRC tumors from mice is investigated using a label-free optical approach based on Raman micro- spectroscopy. Conclusion: This research highlights the multifunctional capabilities of engineered biosilica NPs, which offer new insights in targeted CRC therapy and imaging, improving patient outcomes and paving the way for personalized therapies.
C1 [Delle Cave, Donatella; Corona, Marco; Lonardo, Enza] CNR, Inst Genet & Biophys, I-80131 Naples, Italy.
   [Mangini, Maria; De Luca, Anna Chiara] CNR, Inst Expt Endocrinol & Oncol G Salvatore, Unit 2, I-80131 Naples, Italy.
   [Tramontano, Chiara; De Stefano, Luca; Rea, Ilaria] CNR, Inst Appl Sci & Intelligent Syst, Unit Naples, I-80131 Naples, Italy.
C3 Consiglio Nazionale delle Ricerche (CNR); Istituto di Genetica e
   Biofisica "Adriano Buzzati-Traverso" (IGB-CNR); Consiglio Nazionale
   delle Ricerche (CNR); Consiglio Nazionale delle Ricerche (CNR); Istituto
   di Scienze Applicate e Sistemi Intelligenti "Eduardo Caianiello"
   (ISASI-CNR)
RP De Luca, AC (corresponding author), CNR, Inst Expt Endocrinol & Oncol G Salvatore, Unit 2, I-80131 Naples, Italy.; Rea, I (corresponding author), CNR, Inst Appl Sci & Intelligent Syst, Unit Naples, I-80131 Naples, Italy.
EM ilaria.rea@na.isasi.cnr.it; annachiara.deluca@cnr.it
RI Mangini, Maria/AAL-9201-2021; lonardo, enza/AAI-5726-2020; Tramontano,
   Chiara/JGM-9859-2023; corona, marco/ABH-7484-2022; Rea,
   Ilaria/ABC-4892-2020
OI Rea, Ilaria/0000-0003-0568-9911
FU AIRC Bridge Grant [27012]; AIRC IG [21420]; Fondazione Umberto Veronesi;
   Young Researchers-MSCA-PNR-MUR [MSCA_0000023]; FIMP; NextGenerationEU
   Project PNRR-SEE LIFE-Strengthening the Italian Infrastructure of
   Euro-Bioimaging [IR23-DD MUR 3264/21 CUPB53C22001810006];  [PNC
   0000001_D3 4 health]
FX We are grateful to members of the Animal House of IGB-ABT and
   Euro-Bioimaging Infrastructure at IEOS. We thank Annalisa Di Domenico
   (IGB) and Alessandro Esposito (IEOS) for their support in conducting
   some of the experiments during the revision of this work. This work was
   supported by: AIRC Bridge Grant #27012, Young Researchers-MSCA-PNR-MUR
   #MSCA_0000023 and PNC 0000001_D3 4 health to E.L.; AIRC IG grant #21420
   to A.C.D.L.; FIMP and Fondazione Umberto Veronesi to D.D.C. This work is
   partially supported by the NextGenerationEU Project PNRR-SEE
   LIFE-Strengthening the Italian Infrastructure of Euro-Bioimaging
   (IR23-DD MUR 3264/21 CUPB53C22001810006) .
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NR 38
TC 0
Z9 0
U1 2
U2 2
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-2013
J9 INT J NANOMED
JI Int. J. Nanomed.
PY 2024
VL 19
DI 10.2147/IJN.S480168
PG 20
WC Nanoscience & Nanotechnology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Pharmacology & Pharmacy
GA M7P9G
UT WOS:001359427900001
PM 39583322
OA gold
DA 2025-01-04
ER

PT J
AU Tang, XM
   Chen, H
   Liu, Y
   Huang, BL
   Zhang, XQ
   Yuan, JM
   He, X
AF Tang, Xue-Miao
   Chen, Hao
   Liu, Yu
   Huang, Bin-Lian
   Zhang, Xiu-Quan
   Yuan, Jian-Mei
   He, Xia
TI The cardiotoxicity of cetuximab as single therapy in Chinese
   chemotherapy-refractory metastatic colorectal cancer patients
SO MEDICINE
LA English
DT Article
DE cardiac safety; cetuximab; colorectal cancer; targeted therapy; toxicity
ID HIGH-DOSE CHEMOTHERAPY; TROPONIN-I; PLUS IRINOTECAN; ST DEPRESSION;
   SOLID TUMORS; DE-POINTES; RISK; DIAGNOSIS; TOXICITY; ISCHEMIA
AB The cardiac safety of cetuximab, particularly as single approach, has not been investigated extensively. This trial was designed to evaluate the cardiac safety of cetuximab as salvage monotherapy in Chinese chemotherapy-refractory metastatic colorectal cancer (mCRC) patients.
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   Cetuximab showed its cardiac safety as a single agent for chemotherapy-refractory mCRC patients. And TNI Ultra and ECG could be sensitive and convenient approaches for the surveillance of adverse events.
C1 [Tang, Xue-Miao; Zhang, Xiu-Quan; Yuan, Jian-Mei] Sun Yat Sen Univ, Ctr Canc, Dept Ultrasound & Electrocardiogram, Guangzhou, Guangdong, Peoples R China.
   [Chen, Hao; He, Xia] Sun Yat Sen Univ, Ctr Canc, Dept Clin Lab, Guangzhou, Guangdong, Peoples R China.
   [Huang, Bin-Lian] Sun Yat Sen Univ, Ctr Canc, Dept Radiat Oncol, Guangzhou, Guangdong, Peoples R China.
   [Liu, Yu] Sun Yat Sen Univ, Ctr Canc, Dept Nursing, Guangzhou, Guangdong, Peoples R China.
   [Tang, Xue-Miao; Chen, Hao; Liu, Yu; Huang, Bin-Lian; Zhang, Xiu-Quan; Yuan, Jian-Mei; He, Xia] State Key Lab Oncol Southern China, Guangzhou, Guangdong, Peoples R China.
   [Tang, Xue-Miao; Chen, Hao; Liu, Yu; Huang, Bin-Lian; Zhang, Xiu-Quan; Yuan, Jian-Mei; He, Xia] Collaborat Innovat Ctr Canc Med, Guangzhou, Guangdong, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen University;
   Sun Yat Sen University; State Key Lab Oncology South China
EM hexia@sysucc.org.cn
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NR 24
TC 12
Z9 16
U1 0
U2 4
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 JAN
PY 2017
VL 96
IS 3
AR e5946
DI 10.1097/MD.0000000000005946
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA EI4TR
UT WOS:000392486800035
PM 28099361
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Farooqi, MA
   Mahnoor, M
   Delgado, KM
   Dahlgren, WTT
   Kang, CU
   Farooqi, HMU
AF Farooqi, Muhammad Awais
   Mahnoor, Mahnoor
   Delgado, Kaylee Marie
   Dahlgren, Wylie Thien-Tam
   Kang, Chul-Ung
   Farooqi, Hafiz Muhammad Umer
TI Focused Ultrasound as Targeted Therapy for Colorectal Cancer: A
   Comprehensive Review
SO GASTROINTESTINAL DISORDERS
LA English
DT Review
DE therapeutic focused ultrasound; high-intensity focused ultrasound; tumor
   microenvironment; colorectal cancer
ID MEDIATED DRUG-DELIVERY; COLON-CANCER; EFFICACY; TRENDS; COMBINATION;
   STRATEGIES; ABLATION; SAFETY; VIRUS
AB Traditional cancer treatments have not significantly improved the survival rates for individuals with colorectal cancer. As a result, there is a dire need to explore novel treatment modalities that can target cancer-specific niches, transform cold colorectal tumors into hot ones, and disrupt the tumor niche. Therapeutic focused ultrasound, recognized for its capacity to induce thermal and mechanical impacts on tissue, can potentially eliminate cancer cells and elicit the body's anticancer reaction by disrupting the tumor microenvironment. This article provides an overview of recent developments in employing therapeutic focused ultrasound (TFUS) to enhance the body's natural defenses against colorectal cancers. It also discusses studies examining the utility of TFUS in treating colorectal cancer patients and recent research indicating its potential to stimulate the body's anticancer response in various in vitro and in vivo colorectal cancer models. Furthermore, it explores the therapeutic effects of TFUS on the immune system in colorectal cancers. This article also highlights the safety and effectiveness of TFUS in managing colorectal cancer, providing relief from pain, and potentially improving survival rates. Given the indications that TFUS may bolster the body's immune response and augment the impacts of TFUS therapy in clinical and preclinical colorectal cancer models, it has the potential to emerge as a pivotal tool in clinical settings.
C1 [Farooqi, Muhammad Awais; Kang, Chul-Ung] Jeju Natl Univ, Dept Mechatron Engn, Jeju 63243, South Korea.
   [Mahnoor, Mahnoor] Univ Turku, Dept Biomed, FI-20014 Turku, Finland.
   [Delgado, Kaylee Marie] Univ Calif Los Angeles, Dept Neurosci, Los Angeles, CA 90024 USA.
   [Dahlgren, Wylie Thien-Tam] Univ Calif Los Angeles, Dept Ecol & Evolutionary Biol, Los Angeles, CA 90024 USA.
   [Farooqi, Hafiz Muhammad Umer] Cedars Sinai Med Ctr, Board Governors Regenerat Med Inst, Los Angeles, CA 90048 USA.
C3 Jeju National University; University of Turku; University of California
   System; University of California Los Angeles; University of California
   System; University of California Los Angeles; Cedars Sinai Medical
   Center
RP Kang, CU (corresponding author), Jeju Natl Univ, Dept Mechatron Engn, Jeju 63243, South Korea.; Farooqi, HMU (corresponding author), Cedars Sinai Med Ctr, Board Governors Regenerat Med Inst, Los Angeles, CA 90048 USA.
EM zzmahn@utu.fi; wyliedahlgren@g.ucla.edu; cukang@jejunu.ac.kr;
   umer.farooqi@cshs.org
RI Farooqi, Muhammad Awais/JTT-0987-2023; FAROOQI, HAFIZ MUHAMMAD
   UMER/GLV-0825-2022
OI FAROOQI, HAFIZ MUHAMMAD UMER/0000-0002-1735-5911; Farooqi, Muhammad
   Awais/0000-0002-8035-9296; Delgado, Kaylee/0009-0006-7874-1310; Mahnoor,
   Mahnoor/0009-0007-5074-0495
FU Jeju National University
FX This work was supported by a research grant from Jeju National
   University in 2023.
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NR 87
TC 1
Z9 1
U1 3
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2624-5647
J9 GASTROINTEST DISORD
JI Gastrointest. Disord.
PD JUN
PY 2024
VL 6
IS 2
BP 380
EP 401
DI 10.3390/gidisord6020026
PG 22
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA WP2F2
UT WOS:001256005600001
OA gold
DA 2025-01-04
ER

PT J
AU Szymanska-Chabowska, A
   Swiatkowski, F
   Jankowska-Polanska, B
   Mazur, G
   Chabowski, M
AF Szymanska-Chabowska, Anna
   Swiatkowski, Filip
   Jankowska-Polanska, Beata
   Mazur, Grzegorz
   Chabowski, Mariusz
TI Nestin Expression as a Diagnostic and Prognostic Marker in Colorectal
   Cancer and Other Tumors
SO CLINICAL MEDICINE INSIGHTS-ONCOLOGY
LA English
DT Review
DE Predictive biomarker; malignant tumor; nestin; cancer stem cells;
   prognosis
ID STEM-CELL MARKERS; NEURAL STEM; POOR-PROGNOSIS; GROWTH-FACTOR; HUMAN
   GLIOMA; SURVIVAL; ANGIOGENESIS; BIOMARKERS; VIMENTIN; OVEREXPRESSION
AB Lung cancer, colon cancer, breast cancer, and prostate cancer are the leading causes of death in developed countries. Many cancers display non-specific signs in the early stage of the disease, thus making early diagnosis often difficult. We focused on nestin as a new biomarker of possible clinical importance in the early diagnosis and monitoring of cancer. The expression of nestin takes place at an early stage of neural differentiation, but no expression of the nestin gene can be revealed in normal, mature adult tissues. Nestin plays an important role in the development of the central nervous system and contributes to the organization and maintenance of cell shape. Nestin was found to be a marker of microvessel density, which in turn has proven to be a reliable prognostic factor for neoplastic malignancies in patients. Nestin expression correlates with an increased aggressiveness of tumor cells. The role of nestin in cancers of the colon and rectum, liver, central nervous system, lung cancer, breast cancer, melanoma, and other cancers has been reviewed in the literature. Associations between nestin expression and prognosis or drug-resistance may help in disease management. More research is needed to understand the molecular mechanisms of nestin expression and its role in possible targeted therapy.
C1 [Szymanska-Chabowska, Anna; Mazur, Grzegorz] Wroclaw Med Univ, Dept Internal Med Occupat Dis Hypertens & Clin On, Wroclaw, Poland.
   [Swiatkowski, Filip; Chabowski, Mariusz] 4th Mil Teaching Hosp, Dept Surg, 5 Weigla St, PL-50981 Wroclaw, Poland.
   [Jankowska-Polanska, Beata] Wroclaw Med Univ, Fac Hlth Sci, Dept Clin Nursing, Div Nervous Syst Dis, Wroclaw, Poland.
   [Chabowski, Mariusz] Wroclaw Med Univ, Fac Hlth Sci, Dept Clin Nursing, Div Oncol & Palliat Care, Wroclaw, Poland.
C3 Wroclaw Medical University; Wroclaw Medical University; Wroclaw Medical
   University
RP Chabowski, M (corresponding author), 4th Mil Teaching Hosp, Dept Surg, 5 Weigla St, PL-50981 Wroclaw, Poland.
EM mariusz.chabowski@gmail.com
RI Jankowska-Polanska, Beata Katarzyna/AAC-8354-2022; Chabowski,
   Mariusz/H-9847-2019; Szymanska-Chabowska, Anna/ABE-3330-2020
OI Szymanska-Chabowska, Anna/0000-0003-3615-6923; Jankowska-Polanska,
   Beata/0000-0003-1120-3535; Chabowski, Mariusz/0000-0002-9232-4525;
   Mazur, Grzegorz/0000-0001-6610-2008
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NR 76
TC 13
Z9 13
U1 0
U2 5
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
EI 1179-5549
J9 CLIN MED INSIGHTS-ON
JI Clin. Med. Insights-Oncol.
PD AUG
PY 2021
VL 15
AR 11795549211038256
DI 10.1177/11795549211038256
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA WG6JY
UT WOS:000707101600001
PM 34421318
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Cao, C
   Zhang, JH
   Yang, CH
   Xiang, LL
   Liu, WN
AF Cao, Chen
   Zhang, Junhui
   Yang, Chuanhua
   Xiang, Lili
   Liu, Wenneng
TI Silencing of long noncoding RNA UCA1 inhibits colon cancer invasion,
   migration and epithelial-mesenchymal transition and tumour formation by
   upregulating miR-185-5p in vitro and in vivo
SO CELL BIOCHEMISTRY AND FUNCTION
LA English
DT Article
DE colon cancer; HSP27; MAPK14; MAPKAPK2; miR-185-5p; urothelial
   carcinoma-associated 1
ID PROGRESSION; CELLS; PROLIFERATION; EXPRESSION
AB Colon cancer is the third most common malignancy in the world. Long-chain noncoding RNA urothelial carcinoma-associated 1 (UCA1) was abnormally expressed in colon cancer and participated in colon cancer by regulating multiple miRNAs. This study further explored the molecular mechanism of UCA1 in the development of colon cancer from both in vitro and in vivo. The results showed that UCA1 was highly expressed in colon cancer cells, while miR-185-5p was low expressed. Bioinformatics analysis showed that miR-185-5p was a target of UCA1, while MAPK14 was a target of miR-185-5p. Knockdown of UCA1 with shRNA (sh-UCA1) resulted in a significant increase in miR-185-5p and a significant decrease in MAPK14. In addition, sh-UCA1 inhibited invasion, migration and epithelial-mesenchymal transformation of colon cancer cells. Western blotting also showed that sh-UCA1 inactivated the MAPKAPK2/HSP27 pathway. Furthermore, animal studies have revealed that sh-UCA1 inhibited tumour formation in vivo and improved the survival rate of mice. Collectively, these results suggest that silencing UCA1 may inhibit the carcinogenesis and metastasis of colon cancer in vitro and in vivo by modulating miR-185-5p/MAPK14/MAPKAPK2/HSP27 axis. Significance of the study Colon cancer is the third largest malignant tumour worldwide. This study elucidated the role of urothelial carcinoma-associated 1 (UCA1) in colon cancer cells and its molecular mechanism. The present study suggests that silencing UCA1 may inhibit the invasion, migration, epithelial-mesenchymal transformation and tumour formation of colon cancer by upregulating miR-185-5p in vitro and in vivo. In summary, this study provides a new strategy for targeted therapy of colon cancer.
C1 [Cao, Chen; Zhang, Junhui; Yang, Chuanhua; Xiang, Lili] Sichuan Univ, West China Hosp 4, Dept Hyroid & Breast Surg, Chengdu, Sichuan, Peoples R China.
   [Liu, Wenneng] Sichuan Univ, West China Sch Publ Hlth, 18,Sect 3,Renmin South Rd, Chengdu 610000, Sichuan, Peoples R China.
   [Liu, Wenneng] Sichuan Univ, West China Hosp 4, 18,Sect 3,Renmin South Rd, Chengdu 610000, Sichuan, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University
RP Liu, WN (corresponding author), Sichuan Univ, West China Sch Publ Hlth, 18,Sect 3,Renmin South Rd, Chengdu 610000, Sichuan, Peoples R China.; Liu, WN (corresponding author), Sichuan Univ, West China Hosp 4, 18,Sect 3,Renmin South Rd, Chengdu 610000, Sichuan, Peoples R China.
EM gmkgdzbaywp@sina.com
RI zhang, junhui/HDN-6783-2022
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NR 32
TC 9
Z9 10
U1 0
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0263-6484
EI 1099-0844
J9 CELL BIOCHEM FUNCT
JI Cell Biochem. Funct.
PD MAR
PY 2020
VL 38
IS 2
BP 176
EP 184
DI 10.1002/cbf.3454
EA JAN 2020
PG 9
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA LH6MZ
UT WOS:000509467100001
PM 31989667
DA 2025-01-04
ER

PT J
AU Theyra-Enias, H
   Tumba, N
   Popoola, O
AF Theyra-Enias, H.
   Tumba, N.
   Popoola, O.
TI Management and Outcome of Colorectal Cancer in a Resource-Limited
   Setting: Ahmadu Bello University Teaching Hospital, Zaria, Nigeria
SO NIGERIAN JOURNAL OF CLINICAL PRACTICE
LA English
DT Article
DE Chemotherapy; colorectal cancer; Nigeria; radiotherapy; surgery;
   treatment outcome
ID COLON-CANCER; RADIOTHERAPY; CHALLENGES
AB Background: Colorectal cancer (CRC) is one of the most common malignancies seen in the Western World. It is increasing in developing countries due to adaptation of the western lifestyle with an incidence of 6% in Nigeria. Treatment options are dependent on the stage of disease at presentation, the performance status of the patient, and increasingly the molecular makeup of the tumor. There is a dearth of data on the treatment options obtainable for the management and outcome of CRC cases in Northwestern, Nigeria. Aim: The study assessed the treatment options and outcome of colorectal cancer patients in a tertiary institution, in Northwestern, Nigeria over a 10-year period. Patients and Methods: Between January 2006 and December 2015, data of one-hundred and twenty-two histologically confirmed colorectal cancer cases seen at the Surgery, Radiotherapy and Oncology Departments, ABUTH Zaria, were retrieved retrospectively from the case files and treatment cards of the patients at the health information unit of the hospital. The stage at disease presentation, treatment received, and outcome were analyzed. Results: Nearly a quarter of the patients fell within the age bracket 31-40 years with the median age being 41 years. While only 41% of the patients had their disease staged, 30.4% of the patients presented with advanced disease (Dukes'C + D). Only 95 cases received a form of surgery or the other. Colostomy however accounted for 28.4%. Eighty-nine of the patients received chemotherapy either as neoadjuvant, adjuvant or with palliative intent. External beam radiotherapy either with radical or palliative intent was received by 60 patients (49.2%). At 1-year follow-up sixty cases had been lost to follow up, and thirty-six cases had defaulted on one form of treatment. Conclusion: The study showed that stage at presentation and the available treatment options in the hospital informed treatment offered to the patients. However, surgery was readily performed due to the pattern of presentation and most patients benefited from just a diverting colostomy. Majority of the patients presented with rectal tumor which required radiotherapy as part of its treatment modality, although this is still a luxury in this part of the world. Chemotherapy is also readily available and often prescribed. Cost and limited facility for biomarker (K-ras) testing restrict the use of targeted therapy. Outcome at 1-year follow-up was poor with whereabouts of nearly half of the patients unknown.
C1 [Theyra-Enias, H.] Barau Dikko Teaching Hosp, Dept Radiol, Oncol Unit, Kaduna, Nigeria.
   [Tumba, N.] Bingham Univ, Dept Radiol, Plateau, Nigeria.
   [Popoola, O.] Fed Med Ctr, Dept Oncol, Jabi Abuja, Nigeria.
   [Theyra-Enias, H.] Barau Dikko Teaching Hosp, Dept Radiol, POB 9727 Lafiya Rd, Kaduna, Kaduna, Nigeria.
RP Theyra-Enias, H (corresponding author), Barau Dikko Teaching Hosp, Dept Radiol, POB 9727 Lafiya Rd, Kaduna, Kaduna, Nigeria.
RI TheyraEnias, Hadiza/LRC-0282-2024
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NR 34
TC 1
Z9 1
U1 0
U2 0
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, Maharashtra, INDIA
SN 1119-3077
J9 NIGER J CLIN PRACT
JI Niger. J. Clin. Pract.
PD JUN
PY 2022
VL 25
IS 6
BP 923
EP 930
DI 10.4103/njcp.njcp_1948_21
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 2G3SD
UT WOS:000813517100022
PM 35708435
DA 2025-01-04
ER

PT J
AU Lv, ZL
   Yan, R
   Lin, YX
   Gao, L
   Zhang, F
   Wang, Y
AF Lv, Zhilong
   Yan, Rui
   Lin, Yuexiao
   Gao, Lin
   Zhang, Fa
   Wang, Ying
TI A Disentangled Representation-Based Multimodal Fusion Framework
   Integrating Pathomics and Radiomics for KRAS Mutation Detection in
   Colorectal Cancer
SO BIG DATA MINING AND ANALYTICS
LA English
DT Article
DE Radiomics; Feature extraction; Pathology; Tumors; Transformers;
   Representation learning; Predictive models; KRAS mutation detection;
   multimodal feature fusion; pathomics; radiomics
ID PREDICTION; HISTOPATHOLOGY; CLASSIFICATION; IMAGES
AB Kirsten rat sarcoma viral oncogene homolog (namely KRAS) is a key biomarker for prognostic analysis and targeted therapy of colorectal cancer. Recently, the advancement of machine learning, especially deep learning, has greatly promoted the development of KRAS mutation detection from tumor phenotype data, such as pathology slides or radiology images. However, there are still two major problems in existing studies: inadequate single-modal feature learning and lack of multimodal phenotypic feature fusion. In this paper, we propose a Disentangled Representation-based Multimodal Fusion framework integrating Pathomics and Radiomics (DRMF-PaRa) for KRAS mutation detection. Specifically, the DRMF-PaRa model consists of three parts: (1) the pathomics learning module, which introduces a tissue-guided Transformer model to extract more comprehensive and targeted pathological features; (2) the radiomics learning module, which captures the generic hand-crafted radiomics features and the task-specific deep radiomics features; (3) the disentangled representation-based multimodal fusion module, which learns factorized subspaces for each modality and provides a holistic view of the two heterogeneous phenotypic features. The proposed model is developed and evaluated on a multi modality dataset of 111 colorectal cancer patients with whole slide images and contrast-enhanced CT. The experimental results demonstrate the superiority of the proposed DRMF-PaRa model with an accuracy of 0.876 and an AUC of 0.865 for KRAS mutation detection.
C1 [Lv, Zhilong; Gao, Lin] Xidian Univ, Sch Comp Sci & Technol, Xian 710071, Peoples R China.
   [Yan, Rui] Univ Sci & Technol China, Sch Biomed Engn, Hefei 230026, Peoples R China.
   [Lin, Yuexiao] Capital Med Univ, Beijing Chaoyang Hosp, Dept Gen Surg, Beijing 100020, Peoples R China.
   [Zhang, Fa] Beijing Inst Technol, Sch Med Technol, Beijing 100081, Peoples R China.
   [Wang, Ying] Capital Med Univ, Beijing Chaoyang Hosp, Dept Pathol, Beijing 100020, Peoples R China.
C3 Xidian University; Chinese Academy of Sciences; University of Science &
   Technology of China, CAS; Capital Medical University; Beijing Institute
   of Technology; Capital Medical University
RP Gao, L (corresponding author), Xidian Univ, Sch Comp Sci & Technol, Xian 710071, Peoples R China.; Zhang, F (corresponding author), Beijing Inst Technol, Sch Med Technol, Beijing 100081, Peoples R China.; Wang, Y (corresponding author), Capital Med Univ, Beijing Chaoyang Hosp, Dept Pathol, Beijing 100020, Peoples R China.
EM lvzhilong@xidian.edu.cn; yanrui@ustc.edu.cn; linyuexiao2506@163.com;
   lgao@mail.xidian.edu.cn; zhangfa@bit.edu.cn; wangying_blk@126.com
RI Zhang, Fa/LOS-2518-2024; Yan, Rui/ISB-7062-2023
OI Zhang, Fa/0000-0002-2081-9369
FU National Natural Science Foundation of China [61932018, 32241027,
   62072441, 62272326, 62132015, U22A2037]; Beijing Municipal
   Administration of Hospitals Incubating Program [PX2021013]
FX The research was supported by the National Natural Science Foundation of
   China (Nos. 61932018, 32241027, 62072441, 62272326, 62132015, and
   U22A2037) and the Beijing Municipal Administration of Hospitals
   Incubating Program (No. PX2021013).
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NR 48
TC 0
Z9 0
U1 8
U2 8
PU TSINGHUA UNIV PRESS
PI BEIJING
PA B605D, XUE YAN BUILDING, BEIJING, 100084, PEOPLES R CHINA
EI 2096-0654
J9 BIG DATA MIN ANAL
JI Big Data Min. Anal.
PD SEP
PY 2024
VL 7
IS 3
BP 590
EP 602
DI 10.26599/BDMA.2024.9020012
PG 13
WC Computer Science, Artificial Intelligence; Computer Science, Information
   Systems
WE Emerging Sources Citation Index (ESCI)
SC Computer Science
GA E9Y6D
UT WOS:001306486900006
OA gold
DA 2025-01-04
ER

PT J
AU Chen, DT
   Gu, KK
   Wang, HY
AF Chen, Datian
   Gu, Kaikai
   Wang, Huiyu
TI Optimizing sequential treatment with anti-EGFR and VEGF mAb in
   metastatic colorectal cancer: current results and controversies
SO CANCER MANAGEMENT AND RESEARCH
LA English
DT Review
DE anti-EGFR mAb; bevacizumab; treatment sequence; metastatic colorectal
   cancer
ID EARLY TUMOR SHRINKAGE; GROWTH-FACTOR RECEPTOR; KRAS WILD-TYPE; FOLFIRI
   PLUS CETUXIMAB; 1ST-LINE THERAPY; PHASE-III; ANTIANGIOGENIC THERAPY;
   RANDOMIZED PHASE-3; 2ND-LINE TREATMENT; PREDICTIVE-VALUE
AB Anti-EGFR mAb (cetuximab or panitumumab) and anti-VEGF mAb (bevacizumab) are the two main targeted agents available for RAS wild-type (WT) metastatic colorectal cancer (mCRC) treatment. Nonetheless, three head-to-head clinical trials evaluating anti-EGFR mAb vs -VEGF mAb in first-line treatment failed to conclude a uniform result. Recently, a few small clinical studies revealed that prior use of bevacizumab may impair the effect of cetuximab or panitumumab. Preclinical studies have also suggested that pretreatment with bevacizumab may lead to simultaneous resistance to anti-EGFR mAb. Therefore, we performed this review to summarize the available data regarding the optimal sequential treatment of anti-EGFR and -VEGF mAb for RAS or KRAS WT mCRC and discuss the potential mechanisms that may explain this phenomenon. Primary tumor location and early tumor shrinkage have emerged as new potential prognostic and predictive factors in mCRC. We also collected information to explore whether these factors affect the optimal sequencing of targeted therapy in mCRC. However, definite conclusions cannot be made, and we can only speculate on optimal treatment recommendations based on the contradictory results.
C1 [Chen, Datian] Haimen Peoples Hosp, Dept Oncol, Haimen, Peoples R China.
   [Gu, Kaikai] Haimen Hosp Tradit Chinese Med, Haimen, Peoples R China.
   [Wang, Huiyu] Nanjing Med Univ, Wuxi Peoples Hosp, 299 Qingyang Rd, Wuxi, Peoples R China.
C3 Nanjing Medical University; Jiangnan University
RP Wang, HY (corresponding author), Nanjing Med Univ, Wuxi Peoples Hosp, 299 Qingyang Rd, Wuxi, Peoples R China.
EM wanghuitu2011@126.com
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NR 87
TC 18
Z9 20
U1 1
U2 13
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 2019
VL 11
BP 1705
EP 1716
DI 10.2147/CMAR.S196170
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HM3YN
UT WOS:000459410800007
PM 30863179
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Yuan, LB
   Cheng, F
   Wu, Z
   Li, XD
   Shen, W
AF Yuan, Lebin
   Cheng, Fei
   Wu, Zhao
   Li, Xiaodong
   Shen, Wei
TI Homeobox B9 Promotes Colon Cancer Progression by Targeting SRSF3
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE HOXB9; Colon cancer; SRSF3; Progression; Prognosis
ID SPLICING FACTORS; CELL-PROLIFERATION; COLORECTAL-CANCER; MESSENGER-RNA;
   HOXB9; GENE; SRP20; OVEREXPRESSION; TUMORIGENICITY; TRANSCRIPTION
AB BackgroundHomeobox B9 (HOXB9) is one of the HOX family of transcription factors that are essential for cancer development and embryonic growth. However, the clinical importance and biological involvement of HOXB9 in colon cancer (CC) are not adequately understood.AimsTo investigate whether HOXB9 participates in the proliferation, invasion, and migration of CC.MethodsThis study investigated the function and clinical significance of HOXB9 mRNA and protein expression in CC. Furthermore, overexpression and knockdown experiments of HOXB9 were developed to explore their effects on CC cell transwell and proliferation. Moreover, a molecular mechanism of HOXB9 regulate serine/arginine-rich splicing factor 3 (SRSF3) was explored.ResultsHOXB9 expression was higher in CC cells and tissues at both the mRNA and protein levels. Poor survival in CC patients was significantly connected with high HOXB9 expression, which was also strongly associated with the TNM stage and lymph node metastases. Furthermore, in vitro CC cell proliferation, transwell were markedly aided by HOXB9 overexpression. Contrarily, HOXB9 knockdown had the reverse result and inhibited the formation of xenograft tumors in naked mice. Gene set enrichment analysis (GSEA) revealed a correlation between high HOXB9 expression and spliceosomes. JASPAR and GEPIA2.0, in addition to CHIP and dual-luciferase reporting assays, confirmed that HOXB9 targets the promoter of SRSF3 to enhance its expression. We also found that SRSF3 knockdown eliminated HOXB9 from cell proliferation and transwell.ConclusionWe characterized the function and mechanism of HOXB9 in regulating colon cancer growth, suggesting a novel molecular approach for colon cancer-targeted therapy.
C1 [Yuan, Lebin; Cheng, Fei; Wu, Zhao; Li, Xiaodong; Shen, Wei] Nanchang Univ, Affiliated Hosp 2, Dept Gen Surg, Nanchang 330006, Jiangxi, Peoples R China.
C3 Nanchang University
RP Shen, W (corresponding author), Nanchang Univ, Affiliated Hosp 2, Dept Gen Surg, Nanchang 330006, Jiangxi, Peoples R China.
EM ndefy95006@ncu.edu.cn
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NR 49
TC 3
Z9 3
U1 2
U2 6
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD AUG
PY 2023
VL 68
IS 8
BP 3324
EP 3340
DI 10.1007/s10620-023-07977-3
EA JUN 2023
PG 17
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA M6MA8
UT WOS:000998335400001
PM 37258980
DA 2025-01-04
ER

PT J
AU Mao, HR
   Zhou, JF
   Yan, L
   Zhang, SP
   Yu, DG
AF Mao, Hairong
   Zhou, Jianfeng
   Yan, Liang
   Zhang, Shuping
   Yu, Deng-Guang
TI Hybrid films loaded with 5-fluorouracil and Reglan for synergistic
   treatment of colon cancer via asynchronous dual-drug delivery
SO FRONTIERS IN BIOENGINEERING AND BIOTECHNOLOGY
LA English
DT Article
DE synergistic therapy; hybrid films; colon cancer; asynchronous dual-drug
   delivery; coaxial electrospraying; casting; tumor-targeted therapy
ID ELECTROSPUN NANOFIBERS; NANOPARTICLES; FABRICATION; PROGRESS; RELEASE
AB Combination therapy with oral administration of several active ingredients is a popular clinical treatment for cancer. However, the traditional method has poor convenience, less safety, and low efficiency for patients. The combination of traditional pharmaceutical techniques and advanced material conversion methods can provide new solutions to this issue. In this research, a new kind of hybrid film was created via coaxial electrospraying, followed by a casting process. The films were composed of Reglan and 5-fluorouracil (5-FU)-loaded cellulose acetate (CA) core-shell particles in a polyvinylpyrrolidone (PVP) film matrix. Microscopic observations of these films demonstrated a solid cross section loaded with core-shell particles. X-ray diffraction and Fourier-transform infrared tests verified that the Reglan and 5-FU loaded in the films showed amorphous states and fine compatibilities with the polymeric matrices, i.e., PVP and CA, respectively. In vitro dissolution tests indicated that the films were able to provide the desired asynchronous dual-drug delivery, fast release of Reglan, and sustained release of 5-FU. The controlled release mechanisms were shown to be an erosion mechanism for Reglan and a typical Fickian diffusion mechanism for 5-FU. The protocols reported herein pioneer a new approach for fabricating biomaterials loaded with multiple drugs, each with its own controlled release behavior, for synergistic cancer treatment.
C1 [Mao, Hairong] Zhengzhou Normal Univ, Coll Chem & Chem Engn, Zhengzhou, Henan, Peoples R China.
   [Zhou, Jianfeng; Zhang, Shuping; Yu, Deng-Guang] Univ Shanghai Sci & Technol, Sch Mat & Chem, Shanghai, Peoples R China.
   [Yan, Liang] Univ Shanghai Sci & Technol, Sch Opt Elect & Comp Engn, Shanghai, Peoples R China.
C3 Zhengzhou Normal University; University of Shanghai for Science &
   Technology; University of Shanghai for Science & Technology
RP Zhang, SP; Yu, DG (corresponding author), Univ Shanghai Sci & Technol, Sch Mat & Chem, Shanghai, Peoples R China.
EM zhang_lucy9999@vip.126.com; ydg017@usst.edu.cn
FU Biomed-Eng Crossing projects of the USST [HCXBCY-2023-042,
   XTCX-KJ-2023-44]; USST Medical-Engineering Cross Project
FX The author(s) declare that financial support was received for the
   research, authorship, and/or publication of this article. This work was
   financially supported by funds (HCXBCY-2023-042 and XTCX-KJ-2023-44),
   the Biomed-Eng Crossing projects of the USST (2023-2025), and the USST
   Medical-Engineering Cross Project (2023-2024).
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NR 117
TC 19
Z9 19
U1 16
U2 16
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-4185
J9 FRONT BIOENG BIOTECH
JI Front. Bioeng. Biotechnol.
PD JUN 13
PY 2024
VL 12
AR 1398730
DI 10.3389/fbioe.2024.1398730
PG 15
WC Biotechnology & Applied Microbiology; Engineering, Biomedical
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Engineering
GA WL0P8
UT WOS:001254910000001
PM 38938981
OA gold
DA 2025-01-04
ER

PT J
AU Fujiyoshi, K
   Yamamoto, G
   Takahashi, A
   Arai, Y
   Yamada, M
   Kakuta, M
   Yamaguchi, K
   Akagi, Y
   Nishimura, Y
   Sakamoto, H
   Akagi, K
AF Fujiyoshi, Kenji
   Yamamoto, Gou
   Takahashi, Akemi
   Arai, Yoshiko
   Yamada, Mina
   Kakuta, Miho
   Yamaguchi, Kensei
   Akagi, Yoshito
   Nishimura, Yoji
   Sakamoto, Hirohiko
   Akagi, Kiwamu
TI High concordance rate of <i>KRAS</i>/<i>BRAF</i> mutations. and MSI-H
   between primary colorectal cancer and corresponding metastases
SO ONCOLOGY REPORTS
LA English
DT Article
DE KRAS; BRAF; microsatellite instability; colorectal cancer; heterogeneity
ID FOLFOXIRI PLUS BEVACIZUMAB; 1ST-LINE TREATMENT; GENETIC-HETEROGENEITY;
   PIK3CA MUTATIONS; PRIMARY TUMORS; KRAS MUTATION; BRAF MUTATION;
   SURVIVAL; PANITUMUMAB; VEMURAFENIB
AB Genetic testing is needed for the treatment of colorectal cancer (CRC), especially molecular-targeted therapy. The effects of anti-EGFR therapy and prognosis are affected by the presence of KRAS mutations. However, whether primary CRC or metastatic tissues are appropriate in the analysis is still unclear. In the present study, we assessed the concordance of KRAS/BRAF mutation status and microsatellite instability (MSI) in primary CRC and corresponding metastases. This study enrolled 457 patients with surgically resected primary and corresponding metastatic CRC (499 synchronous metastases and 57 metachronous metastases) and seven local recurrences, and KRAS/BRAF mutation and MSI status were analysed for these tumours. The concordance rates of KRAS mutation, BRAF mutation, wild-type, MSI-H and MSS between primary CRC and corresponding metastases were 93.9% (214/228), 100% (30/30), 99.3% (304/306), 87.5% (21/24) and 100% (137/137), respectively. These high concordance rates were not different between synchronous and metachronous metastases. In conclusion, a high concordance of KRAS/BRAF mutation status and MSI status was observed between primary CRC and corresponding metastases in this study. Either primary CRC or metastatic tissues can be used for testing KRAS/BRAF mutation status and MSI status.
C1 [Fujiyoshi, Kenji; Yamamoto, Gou; Takahashi, Akemi; Arai, Yoshiko; Yamada, Mina; Kakuta, Miho; Akagi, Kiwamu] Saitama Canc Ctr, Div Mol Diag & Canc Prevent, 818 Komuro, Ina, Saitama 3620806, Japan.
   [Fujiyoshi, Kenji; Akagi, Yoshito] Kurume Univ, Dept Surg, Fukuoka 8300011, Japan.
   [Yamaguchi, Kensei] Japanese Fdn Canc Res, Canc Inst Hosp, Dept Gastrointestinal Oncol, Tokyo 1358550, Japan.
   [Nishimura, Yoji; Sakamoto, Hirohiko] Saitama Canc Ctr, Div Gastroenterol Surg, Ina, Saitama 3620806, Japan.
C3 Kurume University; Japanese Foundation for Cancer Research
RP Akagi, K (corresponding author), Saitama Canc Ctr, Div Mol Diag & Canc Prevent, 818 Komuro, Ina, Saitama 3620806, Japan.
EM akagi@cancer-c.pref.saitama.jp
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NR 38
TC 60
Z9 63
U1 1
U2 6
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 FEB
PY 2017
VL 37
IS 2
BP 785
EP 792
DI 10.3892/or.2016.5323
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EJ3BU
UT WOS:000393086900016
PM 28000889
OA Bronze
DA 2025-01-04
ER

PT J
AU Fan, LC
   Teng, HW
   Shiau, CW
   Tai, WT
   Hung, MH
   Yang, SH
   Jiang, JK
   Chen, KF
AF Fan, Li-Ching
   Teng, Hao-Wei
   Shiau, Chung-Wai
   Tai, Wei-Tien
   Hung, Man-Hsin
   Yang, Shung-Haur
   Jiang, Jeng-Kai
   Chen, Kuen-Feng
TI Regorafenib (Stivarga) pharmacologically targets epithelial-mesenchymal
   transition in colorectal cancer
SO ONCOTARGET
LA English
DT Article
DE regorafenib; EMT; SHP-1; STAT3; CRC
ID E-CADHERIN; EXPRESSION; SORAFENIB; STAT3; EMT; ANGIOGENESIS;
   PHOSPHATASE; COMPLEX; GROWTH; SHP-1
AB Epithelial-to-mesenchymal transition (EMT) is well-known to evoke cancer invasion/metastasis, leading to a high frequency of mortality in patients with metastatic colorectal cancer (mCRC). Protein tyrosine phosphatase (PTPase)-targeted therapy has been identified as a novel cancer therapeutic. Previously, we proved that sorafenib with anti-EMT potency prevents TGF-beta 1-induced EMT/invasion by directly activating SH2-domain-containing phosphatase 1 (SHP-1)-dependent p-STAT3(Tyr705) suppression in hepatocellular carcinoma. Regorafenib has a closely related chemical structure as sorafenib and is approved for the pharmacotherapy of mCRC. Herein, we evaluate whether regorafenib activates PTPase SHP-1 in the same way as sorafenib to abolish EMT-related invasion/metastasis in CRC. Notably, regorafenib exerted potent anti-EMT activity to curb TGF-beta 1-induced EMT/invasion in vitro as well inhibited lung metastatic outgrowth of SW480 mesenchymal cells in vivo. Mechanistically, regorafenib-enhanced SHP-1 activity significantly impeded TGF-beta 1-induced EMT/invasion via low p-STAT3Tyr705 level as proved by a SHP-1 inhibitor or siRNA-mediated SHP-1 depletion. Conversely, overexpression of SHP-1 further enhanced the inhibitory effects of regorafenib on TGF-beta 1-induced p-STAT3Tyr705 and EMT/invasion. Regorafenib directly activates SHP-1 by potently relieving the autoinhibited N-SH2 domain of SHP-1 to inhibit TGF-beta 1-induced p-STAT3Tyr705 and EMT/invasion. Importantly, the clinical evidence indicated that SHP-1 was positively correlated with E-cadherin and that significantly determined the overall survival of CRC patients. This result further confirms our in vitro data that SHP-1 is a negative regulatory PTPase in EMT regulation and serves as a pharmacological target for mCRC therapy. Collectively, activating PTPase SHP-1 by regorafenib focusing on its anti-EMT activity might be a useful pharmacotherapy for mCRC.
C1 [Fan, Li-Ching; Tai, Wei-Tien; Chen, Kuen-Feng] Natl Taiwan Univ Hosp, Dept Med Res, Taipei, Taiwan.
   [Fan, Li-Ching; Tai, Wei-Tien; Chen, Kuen-Feng] Natl Taiwan Univ Hosp, Natl Ctr Excellence Clin Trial & Res, Taipei, Taiwan.
   [Teng, Hao-Wei] Taipei Vet Gen Hosp, Div Hematol & Oncol, Dept Med, Taipei, Taiwan.
   [Shiau, Chung-Wai] Natl Yang Ming Univ, Inst Biopharmaceut Sci, Taipei, Taiwan.
   [Hung, Man-Hsin] Taipei Vet Gen Hosp, Div Med Oncol, Dept Oncol, Taipei, Taiwan.
   [Yang, Shung-Haur; Jiang, Jeng-Kai] Taipei Vet Gen Hosp, Div Colon & Rectal Surg, Dept Surg, Taipei, Taiwan.
   [Teng, Hao-Wei; Hung, Man-Hsin; Yang, Shung-Haur; Jiang, Jeng-Kai] Natl Yang Ming Univ, Sch Med, Taipei, Taiwan.
C3 National Taiwan University; National Taiwan University Hospital;
   National Taiwan University; National Taiwan University Hospital; Taipei
   Veterans General Hospital; National Yang Ming Chiao Tung University;
   Taipei Veterans General Hospital; Taipei Veterans General Hospital;
   National Yang Ming Chiao Tung University
RP Chen, KF (corresponding author), Natl Taiwan Univ Hosp, Dept Med Res, Taipei, Taiwan.; Chen, KF (corresponding author), Natl Taiwan Univ Hosp, Natl Ctr Excellence Clin Trial & Res, Taipei, Taiwan.
EM kfchen1970@ntu.edu.tw
RI Wang, Yuhui/JTT-7711-2023; chen, yian/IWM-4310-2023
OI Hung, Man Hsin/0000-0002-7449-5857
FU Ministry of Science and Technology, Taiwan [MOST 105-2314-B-002-190-MY2,
   MOST 103-2622-B-002-006, MOST 103-2325-B-002-016, 104C101-62]; College
   of Medicine, National Taiwan University
FX This work was supported by grants MOST 105-2314-B-002-190-MY2, MOST
   103-2622-B-002-006, MOST 103-2325-B-002-016, and 104C101-62 from the
   Ministry of Science and Technology, Taiwan and College of Medicine,
   National Taiwan University.
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NR 24
TC 37
Z9 40
U1 0
U2 5
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 SEP 27
PY 2016
VL 7
IS 39
BP 64136
EP 64147
DI 10.18632/oncotarget.11636
PG 12
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EB2DN
UT WOS:000387167800104
PM 27580057
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Seo, MK
   Cairns, J
AF Seo, Mikyung Kelly
   Cairns, John
TI How are we evaluating the cost-effectiveness of companion biomarkers for
   targeted cancer therapies? A systematic review
SO BMC CANCER
LA English
DT Review
DE Biomarker; Companion biomarker; Companion diagnostic; Precision
   medicine; Targeted therapy; Oncology; Cancer; Economic evaluation;
   Health economics; Cost-effectiveness; Systematic review
ID METASTATIC COLORECTAL-CANCER; SHARED DECISION-MAKING; ECONOMIC
   EVALUATIONS; 1ST-LINE TREATMENT; PROCESS UTILITY; PERSPECTIVE
AB Background Despite the increasing economic assessment of biomarker-guided therapies, no clear agreement exists whether existing methods are sufficient or whether different methods might produce different cost-effectiveness results. This study aims to examine current practices of modeling companion biomarkers when assessing the cost-effectiveness of targeted cancer therapies. It investigates the current methods in modeling the characteristics of companion diagnostics based on existing economic evaluations of biomarker-guided therapies in cancer. Methods A literature search was performed using Medline, Embase, EconLit, Cochrane library for economic evaluations of biomarker-guided therapies with companion diagnostics in cancer. Preferred Reporting Items of Systematic Reviews and Meta-Analyses (PRISMA) guidelines were followed. Studies were selected using pre-specified eligibility criteria based on the PICO framework. To make the included studies more comparable, we qualitatively synthesized the data under nine domains of methods where consensus was deemed lacking. Results Only four of the twenty-two studies included in this review were found to be of good quality with respect to incorporating the characteristics of companion biomarkers in economic evaluations. However, many evaluations focused on a pre-selected patient group rather than including all patients regardless of their biomarker status. Companion biomarker characteristics captured in evaluations were often limited to the cost or the accuracy of the test. Often, only the costs of biomarker testing were modelled. Clinical outcomes and health state utilities were often not included due to the limited data generated by clinical trials. Methods of economic evaluation were not applied consistently in assessments of companion cancer biomarkers for targeted therapies. It was also shown that conflicting cost-effectiveness results were likely depending on what comparator arm was chosen and what comparison structure was designed in the model. Conclusion We found no consistent approach applied in assessing the value of companion biomarker tests and including the characteristics of biomarkers in an economic evaluation of targeted oncology therapies. Currently, many economic evaluations fail to capture the full value of companion biomarkers beyond sensitivity/specificity and cost related to biomarker testing.
C1 [Seo, Mikyung Kelly; Cairns, John] London Sch Hyg & Trop Med, Fac Publ Hlth & Policy, Dept Hlth Serv Res & Policy, London, England.
   [Seo, Mikyung Kelly; Cairns, John] Univ Bergen, Ctr Canc Biomarkers CCBIO, Bergen, Norway.
   [Seo, Mikyung Kelly] Imperial Coll London, Dept Surg & Canc, Fac Med, London, England.
   [Seo, Mikyung Kelly] Univ Cambridge, Sch Clin Med, Dept Publ Hlth & Primary Care, Cambridge, England.
C3 University of London; London School of Hygiene & Tropical Medicine;
   University of Bergen; Imperial College London; University of Cambridge
RP Seo, MK (corresponding author), London Sch Hyg & Trop Med, Fac Publ Hlth & Policy, Dept Hlth Serv Res & Policy, London, England.; Seo, MK (corresponding author), Univ Bergen, Ctr Canc Biomarkers CCBIO, Bergen, Norway.
EM mk.seo@imperial.ac.uk
RI Cairns, John/AAD-1168-2020
OI Seo, Mikyung (Kelly)/0000-0003-4746-2264; Cairns,
   John/0000-0001-6442-0440
FU Centre for Cancer Biomarkers (CCBIO), Centre of Excellence at the
   Faculty of Medicine and Dentistry, University of Bergen
FX Mikyung Kelly Seo receives a PhD studentship from the Centre for Cancer
   Biomarkers (CCBIO), Centre of Excellence at the Faculty of Medicine and
   Dentistry, University of Bergen. No sources of funding were used to
   conduct this study or prepare this manuscript.
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NR 65
TC 7
Z9 7
U1 1
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 SEP 1
PY 2021
VL 21
IS 1
AR 980
DI 10.1186/s12885-021-08725-4
PG 21
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Oncology
GA UL2FP
UT WOS:000692473400002
PM 34470603
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhou, HM
   Guo, RX
   Wang, CF
AF Zhou, Hongmei
   Guo, Ruixia
   Wang, Chunfang
TI RETRACTED: Long non-coding RNA NEAT1 accelerates cell progression in
   cervical cancer by regulating the miR-889-3p/E2F7 axis through the
   activation of the PI3K/AKT pathway (Retracted article. See vol. 11, pg.
   5025, 2021)
SO RSC ADVANCES
LA English
DT Article; Retracted Publication
ID INHIBITS PROLIFERATION; COLORECTAL-CANCER; MICRORNA-889; INVASION
AB Cervical cancer (CC) is a common malignant gynecological cancer that is frequently diagnosed in women. Apparently, long noncoding RNA nuclear-enriched autosomal transcript 1 (NEAT1) has been identified as a tumor promoter in multiple cancers. Our research is focused on the effects of lncRNA NEAT1 on cell progression in cervical cancer and the potential molecular mechanism of NEAT1 for CC cell progression. The levels of NEAT1, MicroRNA (miR)-889-3p and E2F transcription factor 7 (E2F7) in CC tumors and cells were measured by a quantitative real-time polymerase chain reaction (qRT-PCR). The interaction of miR-889-3p with NEAT1 and E2F7 was validated by a luciferase reporter system and a RNA immunoprecipitation (RIP) assay, respectively. Cell counting kit-8 (CCK-8) and flow cytometry were used for cell proliferation and apoptosis evaluation. Cell migration and invasion were examined by a transwell assay. The protein expressions of E2F7, AKT, phospho-AKT (p-AKT), phosphatidylinositol 3-kinase (PI3K) and phosphorylated PI3K (p-PI3K) were analyzed by western blot assay. Animal models were established by subcutaneously injecting the Me180 cells stably transfected with sh-NEAT1 and sh-NC. The expressions of NEAT1 and E2F7 were up-regulated, whereas the expression of miR-889-3p was down-regulated in the CC tumors and cells when compared with those in normal tumors and cells. The interaction between miR-889-3p and NEAT1 or E2F7 was proved by luciferase reporter system and RIP assay. In addition, the miR-889-3p inhibitor attenuated the NEAT1 silencing-induced inhibition effects on cell proliferation, migration, and invasion and the promotion effects on apoptosis in CC. Consistently, E2F7 reversed the miR-889-3p-mediated inhibition on cell progression in CC. Moreover, NEAT1 modulated cell behavior by targeting the miR-889-3p/E2F7 axis through the PI3K/AKT pathway. Finally, the intervention of NEAT1 hindered tumor growth in vivo. Thus, NEAT1 contributes to cell progression in CC by targeting miR-889-3p to facilitate the E2F7 expression through the activation of the PI3K/AKT pathway, representing an alternative targeted therapy of CC.
C1 [Zhou, Hongmei; Guo, Ruixia; Wang, Chunfang] Zhengzhou Univ, Affiliated Hosp 1, Dept Gynecol, 1 East Jianshe Rd, Zhengzhou 450052, Henan, Peoples R China.
C3 Zhengzhou University
RP Zhou, HM (corresponding author), Zhengzhou Univ, Affiliated Hosp 1, Dept Gynecol, 1 East Jianshe Rd, Zhengzhou 450052, Henan, Peoples R China.
EM 13526528555@163.com
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NR 30
TC 6
Z9 6
U1 0
U2 3
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
EI 2046-2069
J9 RSC ADV
JI RSC Adv.
PD OCT 27
PY 2019
VL 9
IS 59
BP 34627
EP 34635
DI 10.1039/c9ra07039g
PG 9
WC Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA JK2NV
UT WOS:000494684600060
PM 35529988
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Hocke, S
   Guo, Y
   Job, A
   Orth, M
   Ziesch, A
   Lauber, K
   De Toni, EN
   Gress, TM
   Herbst, A
   Göke, B
   Gallmeier, E
AF Hocke, Sandra
   Guo, Yang
   Job, Albert
   Orth, Michael
   Ziesch, Andreas
   Lauber, Kirsten
   De Toni, Enrico N.
   Gress, Thomas M.
   Herbst, Andreas
   Goeke, Burkhard
   Gallmeier, Eike
TI A synthetic lethal screen identifies ATR-inhibition as a novel
   therapeutic approach for POLD1-deficient cancers
SO ONCOTARGET
LA English
DT Article
DE ATR; POLD1; synthetic lethality; DNA repair; targeted therapy
ID DNA-POLYMERASE DELTA; CELL-CYCLE PROGRESSION; ATAXIA-TELANGIECTASIA;
   REPLICATION STRESS; REPAIR; MUTATIONS; COLON; CHECKPOINT; CHROMATIN;
   APOPTOSIS
AB The phosphoinositide 3-kinase-related kinase ATR represents a central checkpoint regulator and mediator of DNA-repair. Its inhibition selectively eliminates certain subsets of cancer cells in various tumor types, but the underlying genetic determinants remain enigmatic. Here, we applied a synthetic lethal screen directed against 288 DNA-repair genes using the well-defined ATR knock-in model of DLD1 colorectal cancer cells to identify potential DNA-repair defects mediating these effects. We identified a set of DNA-repair proteins, whose knockdown selectively killed ATR-deficient cancer cells. From this set, we further investigated the profound synthetic lethal interaction between ATR and POLD1. ATR-dependent POLD1 knockdown-induced cell killing was reproducible pharmacologically in POLD1-depleted DLD1 cells and a panel of other colorectal cancer cell lines by using chemical inhibitors of ATR or its major effector kinase CHK1. Mechanistically, POLD1 depletion in ATR-deficient cells caused caspase-dependent apoptosis without preceding cell cycle arrest and increased DNA-damage along with impaired DNA-repair. Our data could have clinical implications regarding tumor genotype-based cancer therapy, as inactivating POLD1 mutations have recently been identified in small subsets of colorectal and endometrial cancers. POLD1 deficiency might thus represent a predictive marker for treatment response towards ATR- or CHK1-inhibitors that are currently tested in clinical trials.
C1 [Hocke, Sandra; Guo, Yang; Ziesch, Andreas; De Toni, Enrico N.; Herbst, Andreas; Goeke, Burkhard; Gallmeier, Eike] Univ Munich, Dept Med 2, D-81377 Munich, Germany.
   [Job, Albert; Gress, Thomas M.; Gallmeier, Eike] Univ Marburg, Univ Hosp Marburg, Dept Gastroenterol Endocrinol & Metab, D-35043 Marburg, Germany.
   [Orth, Michael; Lauber, Kirsten] Univ Munich, Dept Radiotherapy & Radiat Oncol, D-81377 Munich, Germany.
C3 University of Munich; University Hospital of Giessen & Marburg; Philipps
   University Marburg; University of Munich
RP Gallmeier, E (corresponding author), Univ Munich, Dept Med 2, D-81377 Munich, Germany.; Gallmeier, E (corresponding author), Univ Marburg, Univ Hosp Marburg, Dept Gastroenterol Endocrinol & Metab, D-35043 Marburg, Germany.
EM Eike.Gallmeier@med.uni-marburg.de
RI , Thomas/AAD-4757-2020; De Toni, Enrico/C-6496-2008; Orth,
   Michael/AAQ-7299-2021
OI Orth, Michael/0000-0002-4608-7151; Gress, Thomas/0000-0002-9333-5461;
   Guo, Yang/0000-0001-5259-7871
FU DFG (Forderprogramm fur Forschung und Lehre) [Ga762/3-1, 762/3-2]; DFG
   (MMW-Fund)
FX This work was supported by grants to EG (DFG Ga762/3-1 and 762/3-2,
   Forderprogramm fur Forschung und Lehre, MMW-Fund).
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NR 67
TC 29
Z9 39
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 FEB 9
PY 2016
VL 7
IS 6
BP 7080
EP 7095
DI 10.18632/oncotarget.6857
PG 16
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DM1RE
UT WOS:000376123100052
PM 26755646
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Kow, AWC
AF Kow, Alfred Wei Chieh
TI Hepatic metastasis from colorectal cancer
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Colorectal liver metastasis (CRLM); systemic chemotherapy; liver
   resection; liver transplantation; liver targeted therapy
ID PORTAL-VEIN LIGATION; ASSOCIATING LIVER PARTITION; GROWTH-FACTOR
   RECEPTOR; RADIOFREQUENCY ABLATION; ARTERIAL INFUSION; REPEAT
   HEPATECTOMY; STAGED HEPATECTOMY; SURGICAL MARGIN; STELLATE CELLS;
   PHASE-II
AB Colorectal cancer (CRC) is one of the most common cancers in the world. About two third of patients with CRC will develop distant recurrence at some point in time. Liver is the most common site where distant metastasis takes place. While the overall survival (OS) of patients with metastatic CRC was poor about 3 decades ago, there has been tremendous improvement in this area in the recent years. With the advent of effective systemic chemotherapy and biologic agents and better understanding of the biological behaviour of the tumour, aggressive treatment strategies such as metastatectomy of the liver metastases (or lung metastases) are now acceptable. More importantly, it has transformed the way how stage IV CRCs are being managed. From predominantly palliative as the primary aim, a comprehensive multidisciplinary approach is now the mainstay of treatment with very successful outcomes. Combination of systemic therapies with liver resection has been shown to be effective in providing promising survival benefits. In addition, other adjunctive modalities in targeting the liver metastases such as ablation, combining resection and ablation, transarterial chemoembolization, stereotactic body radiotherapy (SBRT), hepatic artery perfusion, etc. have also been demonstrated variable outcome in treating colorectal liver metastasis (CRLM). Very recently, transplant oncologists have also explored using liver transplantation as a treatment modality for unresectable CRLM, which has demonstrated very good long-term survival in well selected cases. The new paradigm in the treatment of metastatic CRC has dawned.
C1 [Kow, Alfred Wei Chieh] Natl Univ Hlth Syst, Dept Surg, Div Hepatopancreaticobiliary Surg & Liver Transpl, Singapore, Singapore.
   [Kow, Alfred Wei Chieh] Natl Univ Singapore, Dept Surg, Singapore, Singapore.
C3 National University of Singapore; National University of Singapore
RP Kow, AWC (corresponding author), Natl Univ Singapore Hosp, Univ Surg Cluster, Div Hepatobiliary & Pancreat Surg & Liver Transpl, 1E,Kent Ridge Rd,NUHS Tower Block,Level 8, Singapore 119228, Singapore.
EM alfred_kow@nuhs.edu.sg
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NR 178
TC 114
Z9 118
U1 1
U2 15
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 DEC
PY 2019
VL 10
IS 6
BP 1274
EP 1298
DI 10.21037/jgo.2019.08.06
PG 25
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA JW7GR
UT WOS:000503216800028
PM 31949948
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Giordano, G
   Parcesepe, P
   D'Andrea, MR
   Coppola, L
   Di Raimo, T
   Remo, A
   Manfrin, E
   Fiorini, C
   Scarpa, A
   Amoreo, CA
   Conciatori, F
   Milella, M
   Caruso, FP
   Cerulo, L
   Porras, A
   Pancione, M
AF Giordano, Guido
   Parcesepe, Pietro
   D'Andrea, Mario Rosario
   Coppola, Luigi
   Di Raimo, Tania
   Remo, Andrea
   Manfrin, Erminia
   Fiorini, Claudia
   Scarpa, Aldo
   Amoreo, Carla Azzurra
   Conciatori, Fabiana
   Milella, Michele
   Caruso, Francesca Pia
   Cerulo, Luigi
   Porras, Almudena
   Pancione, Massimo
TI JAK/Stat5-mediated subtype-specific lymphocyte antigen 6 complex, locus
   G6D (LY6G6D) expression drives mismatch repair proficient colorectal
   cancer
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Article
DE LY6G6D; Colorectal cancer; Microsatellite-stable; Immune resistance
ID CONSENSUS MOLECULAR SUBTYPES; CHROMOSOMAL INSTABILITY; MEK INHIBITORS;
   RESISTANCE; CELLS; PROGRESSION; SURVIVAL; STAT5; COLON; LY6E
AB BackgroundHuman microsatellite-stable (MSS) colorectal cancers (CRCs) are immunologically cold tumour subtypes characterized by reduced immune cytotoxicity. The molecular linkages between immune-resistance and human MSS CRC is not clear.MethodsWe used transcriptome profiling, in silico analysis, immunohistochemistry, western blot, RT-qPCR and immunofluorescence staining to characterize novel CRC immune biomarkers. The effects of selective antagonists were tested by in vitro assays of long term viability and analysis of kinase active forms using anti-phospho antibodies.ResultsWe identified the lymphocyte antigen 6 complex, locus G6D (LY6G6D) as significantly overexpressed (around 15-fold) in CRC when compared with its relatively low expression in other human solid tumours. LY6G6D up-regulation was predominant in MSS CRCs characterized by an enrichment of immune suppressive regulatory T-cells and a limited repertoire of PD-1/PD-L1 immune checkpoint receptors. Coexpression of LY6G6D and CD15 increases the risk of metastatic relapse in response to therapy. Both JAK-STAT5 and RAS-MEK-ERK cascades act in concert as key regulators of LY6G6D and Fucosyltransferase 4 (FUT4), which direct CD15-mediated immune-resistance. Momelotinib, an inhibitor of JAK1/JAK2, consistently abrogated the STAT5/LY6G6D axis in vitro, sensitizing MSS cancer cells with an intact JAK-STAT signaling, to efficiently respond to trametinib, a MEK inhibitor used in clinical setting. Notably, colon cancer cells can evade JAK2/JAK1-targeted therapy by a reversible shift of the RAS-MEK-ERK pathway activity, which explains the treatment failure of JAK1/2 inhibitors in refractory CRC.ConclusionsCombined targeting of STAT5 and MAPK pathways has superior therapeutic effects on immune resistance. In addition, the new identified LY6G6D antigen is a promising molecular target for human MSS CRC.
C1 [Giordano, Guido] Casa Sollievo Sofferenza IRCCS, Oncol Unit, San Giovanni Rotondo, Italy.
   [Giordano, Guido; D'Andrea, Mario Rosario; Coppola, Luigi; Di Raimo, Tania] San Filippo Neri Hosp, Med Oncol & Anat Pathol Unit, Rome, Italy.
   [Parcesepe, Pietro; Manfrin, Erminia; Fiorini, Claudia; Scarpa, Aldo] Univ & Hosp Trust Verona, Dept Diagnost & Publ Hlth, Sect Pathol, Verona, Italy.
   [Remo, Andrea] Mater Salutis Hosp AULSS9, Pathol Unit, Legnago Verona, Italy.
   [Amoreo, Carla Azzurra] IRCCS Regina Elena Natl Canc Inst, Pathol, Via Elio Chianesi 53, I-00144 Rome, Italy.
   [Conciatori, Fabiana; Milella, Michele] IRCCS Regina Elena Canc Inst, Med Oncol, Via Elio Chianesi 53, I-00144 Rome, Italy.
   [Caruso, Francesca Pia; Cerulo, Luigi; Pancione, Massimo] Univ Sannio, Dept Sci & Technol, Via PortArsa 11, I-82100 Benevento, Italy.
   [Caruso, Francesca Pia] BIOGEM Scrl, Bioinformat Lab, Avellino, Italy.
   [Porras, Almudena; Pancione, Massimo] Univ Complutense Madrid, Dept Biochem & Mol Biol, Fac Pharm, Madrid, Spain.
   [Porras, Almudena] Hosp Clin San Carlos IdISSC, Hlth Res Inst, Madrid, Spain.
C3 IRCCS Casa Sollievo Della Sofferenza; San Filippo Neri Hospital;
   University of Verona; Azienda Ospedaliera Universitaria Integrata
   Verona; ULSS 9 Scaligera; Ospedale Mater Salutis di Legnago; University
   of Sannio; Complutense University of Madrid; Hospital Clinico San Carlos
RP Giordano, G (corresponding author), Casa Sollievo Sofferenza IRCCS, Oncol Unit, San Giovanni Rotondo, Italy.; Pancione, M (corresponding author), Univ Sannio, Dept Sci & Technol, Via PortArsa 11, I-82100 Benevento, Italy.; Porras, A; Pancione, M (corresponding author), Univ Complutense Madrid, Dept Biochem & Mol Biol, Fac Pharm, Madrid, Spain.
EM giordano.guido81@gmail.com; maporras@ucm.es;
   massimo.pancione@unisannio.it
RI Pancione, Massimo/AAF-2109-2019; AMOREO, CARLA/K-5375-2018; Milella,
   Michele/ABH-8606-2020; Remo, Andrea/Q-7746-2016; manfrin,
   erminia/P-2645-2016; Porras, Almudena/N-2121-2015; Conciatori,
   Fabiana/AAU-2657-2020; Scarpa, Aldo/K-6832-2016; Giordano,
   Guido/IQU-6240-2023
OI Caruso, Francesca Pia/0000-0002-2206-1459; Conciatori,
   Fabiana/0000-0002-8579-5222; PANCIONE, Massimo/0000-0003-1728-8816;
   Scarpa, Aldo/0000-0003-1678-739X; Giordano, Guido/0000-0002-9310-1075
FU Italian Ministry of University and Research (MiUR) "FFABR" [4982];
   Spanish Ministry of Science, Innovation and Universities
   [SAF2013-48210-C2-02, SAF2016-76588-C2-1-R]
FX This work was supported by Italian Ministry of University and Research
   (MiUR) "FFABR" (n. 4982) to M.P. and by Grants SAF2013-48210-C2-02 and
   SAF2016-76588-C2-1-R to A.P. from the Spanish Ministry of Science,
   Innovation and Universities.
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NR 37
TC 29
Z9 31
U1 0
U2 8
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1756-9966
J9 J EXP CLIN CANC RES
JI J. Exp. Clin. Cancer Res.
PD JAN 22
PY 2019
VL 38
AR 28
DI 10.1186/s13046-018-1019-5
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HI4PV
UT WOS:000456433600001
PM 30670049
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Azad, A
   Sulaiman, WMAW
   Almoustafa, H
   Dayoob, M
   Kumarasamy, V
   Subramaniyan, V
   Alshehri, JM
   Khan, AA
AF Azad, Abul Kalam
   Sulaiman, Wan Mohd Azizi Wan
   Almoustafa, Hassan
   Dayoob, Mohamad
   Kumarasamy, Vinoth
   Subramaniyan, Vetriselvan
   Alshehri, Jamilah M.
   Khan, Azmat Ali
TI A dataset of microstructure features of electro-hydrodynamic assisted
   5-fluorouracil-grafted alginate microbeads and physicochemical
   properties for effective colon targeted carriers drug delivery
SO DATA IN BRIEF
LA English
DT Article
DE 5-fluorouracil; Electrospray; Microbeads; pH sensitive delivery; Sodium
   alginate
AB 5-Fluorouracil (5 -FU) has been the primary drug used in chemotherapy for colorectal carcinoma, and localizing the drug would be effective in avoiding its side effects and improving therapeutic outcomes. One approach to achieve this is by encapsulating the drug in microbeads. Alginate microbeads, in particular, exhibit promising pH-sensitive properties, making them an attractive option for colon targeting. Thus, the main aim of this study is to formulate and characterize 5-FU-encapsulated alginate microbeads as a pH-sensitive drug delivery system for controlled release in the gastrointestinal tract. In this study, the alginate microbeads encapsulating 5 -FU was manufactured using electrospray methods. This method offers the advantages of promoting the formulation of uniformly small -sized microbeads with improved performance in terms of swelling and diffusion rates. The size and shape of the 5 -FU microbeads are 394.23 +/- 3.077 mu m and have a spherical factor of 0.026 +/- 0.022, respectively, which are considered acceptable and indicative of a spherical shape. The microbeads' encapsulation efficiency was found to be 69.65 +/- 0.18%, which is considered high in comparison to other literature. The attenuated total reflectance - Fourier transform infrared spectroscopy (ATR-FTIR) data confirmed the complexation of sodium alginate with calcium ions, along with the encapsulation of 5 -FU in the microbeads matrix. The 5 -FU microbeads displayed pH -dependent swelling, exhibiting less swelling in simulated gastric fluid (SGF) than in simulated intestinal fluid (SIF). Additionally, the release of 5 -FU from the microbeads is pH -dependent, with the cumulative percentage drug release being higher in simulated intestinal fluid than in SGF. The data indicate that the 5 -FU microbeads can be utilized for the delivery of 5 -FU in colon -targeted therapy, potentially leading to improved tumor treatment. (c) 2024 The Author(s). Published by Elsevier Inc. This is an open access article under the CC BY license ( http://creativecommons.org/licenses/by/4.0/ )
C1 [Azad, Abul Kalam; Sulaiman, Wan Mohd Azizi Wan] Univ Coll MAIWP Int, Kuala Lumpur 68100, Malaysia.
   [Almoustafa, Hassan] Univ Malaya, Fac Med, Dept Pharmacolgy, Kuala Lumpur 50603, Malaysia.
   [Dayoob, Mohamad] MAHSA Univ, Fac Pharm, Jenjarom 42610, Selangor, Malaysia.
   [Kumarasamy, Vinoth] Univ Kebangsaan Malaysia, Fac Med, Dept Parasitol & Med Entomol, Jalan Yaacob Latif, Kuala Lumpur 56000, Malaysia.
   [Subramaniyan, Vetriselvan] Monash Univ, Jeffrey Cheah Sch Med & Hlth Sci, Pharmacol Unit, Jalan Lagoon Selatan, Bandar Sunway 47500, Selangor, Malaysia.
   [Alshehri, Jamilah M.; Khan, Azmat Ali] King Saudi Univ, Coll Pharm, Dept Pharmaceut Chem, Pharmaceut Biotechnol Lab, Riyadh 11451, Saudi Arabia.
C3 Universiti Malaya; Mahsa University; Universiti Kebangsaan Malaysia;
   Monash University; Monash University Malaysia
RP Azad, A (corresponding author), Univ Coll MAIWP Int, Kuala Lumpur 68100, Malaysia.
EM azad2011iium@gmail.com
RI Khan, Prof. Azmat Ali/Q-2841-2016; Almoustafa, Hassan/ABK-0389-2022;
   Dayoob, Mohamad/JFK-9650-2023; subramaniyan, vetriselvan/AAC-5548-2020;
   Kumarasamy, Vinoth/AAQ-1554-2020; Azad, Abul/AAN-6501-2020; Alshehri,
   Jamilah/GRX-7699-2022; Azad, Abul/I-2953-2013
OI Vetriselvan, Subramaniayan/0000-0002-9629-9494; Almoustafa,
   Hassan/0000-0002-2549-1761; Azad, Abul/0000-0003-4874-1169; Kumarasamy,
   Vinoth/0000-0002-8895-1796
FU Researchers Supporting Project at King Saud University, Riyadh, Saudi
   Arabia [RSP2024R339]
FX This work was funded by the Researchers Supporting Project Number
   (RSP2024R339) at King Saud University, Riyadh 11451, Saudi Arabia.
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NR 13
TC 2
Z9 2
U1 1
U2 2
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2352-3409
J9 DATA BRIEF
JI Data Brief
PD APR
PY 2024
VL 53
AR 110202
DI 10.1016/j.dib.2024.110202
EA FEB 2024
PG 13
WC Multidisciplinary Sciences
WE Emerging Sources Citation Index (ESCI)
SC Science & Technology - Other Topics
GA OR9Y4
UT WOS:001209132300001
PM 38439989
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Farahani, RK
   Soleimanpour, S
   Golmohammadi, M
   Soleimanpour-lichaei, HR
AF Farahani, Roya Kishani
   Soleimanpour, Samereh
   Golmohammadi, Maryam
   Soleimanpour-lichaei, Hamid Reza
TI PIWIL2 Regulates the Proliferation, Apoptosis and Colony Formation of
   Colorectal Cancer Cell Line
SO IRANIAN JOURNAL OF BIOTECHNOLOGY
LA English
DT Article
DE Apoptosis; Colorectal Cancer (CRC); PIWIL2; Proliferation
ID MOLECULAR TARGET; EXPRESSION; CYCLE; KI67; OVEREXPRESSION; FAMILY; STAT3
AB Background: Tumor cells proliferation and apoptosis inhibition are the mechanisms through which the Colorectal Cancer (CRC) progression, metastasis and chemoresistance are promoted pathologically, offering clinical advantages for characterizing their molecular regulators.Objectives: In this study, to unravel the role of PIWIL2 as a potential CRC oncogenic regulator, we examined the effect of its overexpression on proliferation, apoptosis and colony formation of SW480 colon cancer cell line.Material and Methods: Established SW480-P (overexpression of PIWIL2) and SW480-control (SW480-empty vector) cell lines were cultured in DMEM containing 10% FBS with 1% penicillin-streptomycin. The total DNA and RNA was extracted for further experiments. Real-Time PCR and western blotting assay were performed to measure the differential expression of proliferation associated genes including the expression of cell cycle and anti-apoptotic genes as well as Ki-67 and PIWIL2 in both cell lines. Cell proliferation was determined using MTT assay, doubling time assay and the colony formation rate of transfected cells was measured with the 2D colony formation assay.Results: At the molecular level, PIWIL2 overexpression was associated with significant up-regulation of cyclin D1, STAT3, BCL2-L1, BCL2-L2 and Ki-67 genes. MTT and doubling time assay showed that PIWIL2 expression induced time-related effects on proliferation rate of SW480 cells. Moreover, SW480-P cells had markedly greater capacity to form colonies.Conclusions: PIWIL2 plays important roles to promote cancer cell proliferation and colonization via the cell cycle acceleration and inhibition of apoptosis, the mechanisms through which this gene seems to contribute to CRC development, metastasis and chemoresistance, hence potentially highlighting PIWIL2 targeted therapy as a valuable tool for CRC treatment.
C1 [Farahani, Roya Kishani; Soleimanpour, Samereh; Golmohammadi, Maryam; Soleimanpour-lichaei, Hamid Reza] Natl Inst Genet Engn & Biotechnol NIGEB, Inst Med Biotechnol, Dept Stem Cells & Regenerat Med, Tehran, Iran.
RP Soleimanpour-lichaei, HR (corresponding author), Natl Inst Genet Engn & Biotechnol NIGEB, Inst Med Biotechnol, Dept Stem Cells & Regenerat Med, Tehran, Iran.
EM hrs@nigeb.ac.ir
OI Soleimanpour Lichaei, Hamidreza/0000-0003-0173-958X; kishani farahani,
   roya/0000-0002-6889-777X
FU National Institute of Genetic Engineering and Biotechnology [443];
   Gilrayan co., Ltd. [GRI-16-121]; Zistpooyesh knowledge-based company
   [ZPSP/19-10]
FX PIWIL2 seemingly contributes to CRC development, metastasis and
   chemoresistance, all proving PIWIL2 as a valuable tool for target
   therapy of CRC. Acknowledgements This study was supported by research
   grants from National Institute of Genetic Engineering and Biotechnology
   (Grant no. 443) and Gilrayan co., Ltd. (Grant no. GRI-16-121) and
   Zistpooyesh knowledge-based company (ZPSP/19-10) .
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NR 38
TC 3
Z9 3
U1 1
U2 1
PU NATL INST GENETIC ENGINEERING & BIOTECHNOLOGY
PI TEHRAN
PA PAJOOHESH BLVD, TEHRAN-KARAJ HWY, 17 KM, TEHRAN, IRAN
SN 1728-3043
J9 IRAN J BIOTECHNOL
JI Iran. J. Biotechnol.
PD JAN
PY 2023
VL 21
IS 1
BP 37
EP 44
AR e3176
DI 10.30498/ijb.2022.307054.3176
PG 9
WC Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology
GA G9VY2
UT WOS:000992558800002
PM 36811102
DA 2025-01-04
ER

PT J
AU Jin, B
   Wu, XA
   Xu, G
   Xing, JL
   Wang, YX
   Yang, HY
   Du, SD
   Mao, YL
AF Jin, Bao
   Wu, Xiang'an
   Xu, Gang
   Xing, Jiali
   Wang, Yuxin
   Yang, Huayu
   Du, Shunda
   Mao, Yilei
TI Evolutions of the Management of Colorectal Cancer Liver Metastasis: A
   Bibliometric Analysis
SO JOURNAL OF CANCER
LA English
DT Article
DE colorectal cancer liver metastasis (CRCLM); bibliometric analysis;
   therapy; management; citation
ID BODY RADIATION-THERAPY; RESECTION; TRIAL
AB Background: Tremendous progress has been made in the treatment of colorectal cancer liver metastasis (CRCLM) in recent decades, and thousands of papers have been published. Therefore, we conducted a bibliometric analysis of articles related to CRCLM treatment to explore its evolution.
   Materials and Methods: The Clarivate Analytics Web of Science (WOS) Core Collection database was searched through June 2020 using terms related to CRCLM treatment. We analyzed the bibliographic information of the literature related to CRCLM treatment and explored the research topics to understand its evolution over time.
   Results: We identified 3436 records related to CRCLM treatment in the WOS database. The total number of times these documents were cited ranged 0-2352, and the years of publication spanned 1976-2020. The greatest numbers of articles were published in the United States, Japan, and France. Among institutions, Memorial Sloan-Kettering Cancer Center, MD Anderson Cancer Center, and Oslo University Hospital published the most articles. Regarding authors, Jarnagin WR, Adam R, Vauthey JN published the most articles. The research topics of these articles included systemic chemotherapy, molecular targeted therapy, the outcome of liver resection, prognosis prediction, hepatic artery infusion, radiofrequency ablation, and two-stage hepatectomy.
   Conclusion: Bibliometric analysis of studies related to CRCLM treatment can help doctors and researchers quickly understand the development trend in this field. These data emphasize the current management of patients with CRCLM, and they can potentially guide the direction of future research.
C1 Peking Union Med Coll PUMC, Peking Union Med Coll Hosp PUMCH, Dept Liver Surg, Beijing 100730, Peoples R China.
   Chinese Acad Med Sci CAMS, Beijing 100730, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Peking Union Medical College
RP Du, SD; Mao, YL (corresponding author), PUMC, Peking Union Med Coll PUMC Hosp, Dept Liver Surg, Beijing 100730, Peoples R China.; Du, SD; Mao, YL (corresponding author), Chinese Acad Med Sci, Beijing 100730, Peoples R China.
EM dushd@pumch.cn; pumch-liver@hotmail.com
RI Xu, Gang/C-9762-2013
FU National Natural Science Foundation of China [81972698]; Chinese Academy
   of Medical Sciences (CAMS) Initiative for Innovative Medicine
   [2017-I2M-4-002]; Chen Xiao-Ping Foundation for the Development of
   Science and Technology of Hubei Province [CXPJJH11900001-2019215]
FX H This work was supported by the National Natural Science Foundation of
   China (Grant No. 81972698), Chinese Academy of Medical Sciences (CAMS)
   Initiative for Innovative Medicine (Grant No. 2017-I2M-4-002) and Chen
   Xiao-Ping Foundation for the Development of Science and Technology of
   Hubei Province (Grant No. CXPJJH11900001-2019215).
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NR 47
TC 8
Z9 8
U1 2
U2 38
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 2021
VL 12
IS 12
BP 3660
EP 3670
DI 10.7150/jca.52842
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RZ4TW
UT WOS:000648591100023
PM 33995641
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Bolduc, F
   Turcotte, MA
   Perreault, JP
AF Bolduc, Francois
   Turcotte, Marc-Antoine
   Perreault, Jean-Pierre
TI The Small Nuclear Ribonucleoprotein Polypeptide A (SNRPA) binds to the
   G-quadruplex of the BAG-1 5′UTR
SO BIOCHIMIE
LA English
DT Article
DE G-quadruplex; SNRPA; Gene regulation; RNA binding Proteins; RNA
   structure; Cancer
ID U1A PROTEIN; RNA; IDENTIFICATION; EXPRESSION
AB The protein "BCL-2-associated athanogene-1" (BAG-1), which exists in multiple isoforms, promotes cancer cell survival and is overexpressed in many different cancers. As a result, BAG-1-targeted therapy appears to be a promising strategy with which to treat cancer. It has previously been shown that the 5'UTR of the BAG-1 mRNA contains a guanine rich region that folds into a G-quadruplex structure which can modulate both its cap-dependent and its cap-independent translation. Accumulating data regarding G-quadruplex binding proteins suggest that these proteins can play a central role in gene expression. Consequently, the identification of the proteins that could potentially bind to the G-quadruplex of the BAG-1 mRNA was undertaken. Label-free RNA pulldown assays were performed using protein extracts from colorectal cancer cells and this leads to the detection of RNA G4 binding proteins by LC-MS/MS. The use of G-quadruplex containing RNA, as well as of a mutated version, ensured that the proteins identified were specific for the RNA G-quadruplex structure and not just general RNA binding proteins. Following confirmation of the interaction, the Small Nuclear Ribonucleoprotein Polypeptide A (SNRPA) was shown to bind directly to the BAG-1 mRNA through the G-quadruplex, and knock down experiments in colorectal cancer cells suggested that it can modulate the expression level of BAG-1. (c) 2020 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
C1 [Bolduc, Francois; Turcotte, Marc-Antoine; Perreault, Jean-Pierre] Univ Sherbrooke, Dept Biochim & Genom Fonct, RNA Grp, Pavillon Rech Appl Canc,3201 Jean Mignault, Sherbrooke, PQ J1E 4K8, Canada.
C3 University of Sherbrooke
RP Perreault, JP (corresponding author), Univ Sherbrooke, Dept Biochim & Genom Fonct, RNA Grp, Pavillon Rech Appl Canc,3201 Jean Mignault, Sherbrooke, PQ J1E 4K8, Canada.
EM jean-pierre.perreault@usherbrooke.ca
FU Natural Sciences and Engineering Research Council of Canada
   [RGPIN-155219-17]
FX This work was supported by funding from the Natural Sciences and
   Engineering Research Council of Canada (RGPIN-155219-17) to JPP, who is
   a member of the Centre de Recherche du CHUS.
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NR 28
TC 18
Z9 19
U1 0
U2 6
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0300-9084
EI 1638-6183
J9 BIOCHIMIE
JI Biochimie
PD SEP
PY 2020
VL 176
BP 122
EP 127
DI 10.1016/j.biochi.2020.06.013
PG 6
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA NE4AY
UT WOS:000562540900013
PM 32629040
OA hybrid
DA 2025-01-04
ER

PT J
AU Chen, MC
   Lee, NH
   Hsu, HH
   Ho, TJ
   Tu, CC
   Chen, RJ
   Lin, YM
   Viswanadha, VP
   Kuo, WW
   Huang, CY
AF Chen, Ming-Cheng
   Lee, Nien-Hung
   Hsu, Hsi-Hsien
   Ho, Tsung-Jung
   Tu, Chuan-Chou
   Chen, Ray-Jade
   Lin, Yueh-Min
   Viswanadha, Vijaya Padma
   Kuo, Wei-Wen
   Huang, Chih-Yang
TI Inhibition of NF-B and metastasis in irinotecan (CPT-11)-resistant LoVo
   colon cancer cells by thymoquinone via JNK and p38
SO ENVIRONMENTAL TOXICOLOGY
LA English
DT Article
DE CPT-11-R LoVo colon cancer cells; JNK; NF-B; p38; Thymoquinone
ID FACTOR-KAPPA-B; PANCREATIC-CANCER; ANTITUMOR-ACTIVITY; ACTIVATION; DRUG;
   ADENOCARCINOMA; SUPPRESSION; EXPRESSION; RESISTANCE; THERAPIES
AB Clinically used chemotherapeutics can effectively eliminate most tumor cells. However, they cause unwanted side effects and result in chemoresistance. To overcome such problems, phytochemicals are now used to treat cancers by means of targeted therapy. Thymoquinone (TQ) is used to treat different cancers (including colon cancer) and is an NF-B inhibitor. Irinotecan resistant (CPT-11-R) LoVo colon cancer cell line was previous constructed by step-wise CPT-11 challenges to un-treated parental LoVo cells and expresses EGFR/IKK//NF-B pathway. TQ resulted in reduced total and phosphorylation of IKK/ and NF-B and decreased metastasis in CPT-11-R cells. TQ not only reduced activity of ERK1/2 and PI3K but also activated JNK and p38. Furthermore, TQ was also found to suppress metastasis through activation of JNK and p38. Therefore, TQ suppressed metastasis through NF-B inhibition and activation of JNK and p38 in CPT-11-R LoVo colon cancer cells. (c) 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 669-678, 2017.
C1 [Chen, Ming-Cheng] Taichung Vet Gen Hosp, Div Colorectal Surg, Taichung, Taiwan.
   [Lee, Nien-Hung; Huang, Chih-Yang] China Med Univ, Grad Inst Basic Med Sci, Taichung, Taiwan.
   [Hsu, Hsi-Hsien] Mackay Mem Hosp, Div Colorectal Surg, Taipei, Taiwan.
   [Hsu, Hsi-Hsien] Mackay Med, Nursing & Management Coll, Taipei, Taiwan.
   [Ho, Tsung-Jung] China Med Univ, Beigang Hosp, Chinese Med Dept, Yunlin, Taiwan.
   [Tu, Chuan-Chou] Armed Force Taichung Gen Hosp, Dept Internal Med, Div Chest Med, Taichung, Taiwan.
   [Chen, Ray-Jade] Taipei Med Univ, Sch Med, Dept Surg, Taipei, Taiwan.
   [Lin, Yueh-Min] Changhua Christian Hosp, Dept Pathol, Changhua, Taiwan.
   [Lin, Yueh-Min] Jen Teh Jr Coll Med Nursing & Management, Dept Med Technol, Miaoli, Taiwan.
   [Viswanadha, Vijaya Padma] Bharathiar Univ, Dept Biotechnol, Coimbatore, Tamil Nadu, India.
   [Kuo, Wei-Wen] China Med Univ, Dept Biol Sci & Technol, Taichung, Taiwan.
   [Huang, Chih-Yang] China Med Univ, Grad Inst Chinese Med Sci, Taichung, Taiwan.
   [Huang, Chih-Yang] Asia Univ, Dept Hlth & Nutr Biotechnol, Taichung, Taiwan.
C3 Taichung Veterans General Hospital; China Medical University Taiwan;
   Mackay Memorial Hospital; Mackay Junior College of Medicine, Nursing &
   Management; China Medical University Taiwan; Taipei Medical University;
   Changhua Christian Hospital; Bharathiar University; China Medical
   University Taiwan; China Medical University Taiwan; Asia University
   Taiwan
RP Huang, CY (corresponding author), China Med Univ, Grad Inst Basic Med Sci, Taichung, Taiwan.; Huang, CY (corresponding author), China Med Univ, Grad Inst Chinese Med Sci, Taichung, Taiwan.; Huang, CY (corresponding author), Asia Univ, Dept Hlth & Nutr Biotechnol, Taichung, Taiwan.
EM cyhuang@mail.cmu.edu.tw
RI Viswanadha, Vijaya/ABG-4936-2020; Chen, Ray/GRJ-6736-2022
OI Huang, Chih-Yang/0000-0003-2347-0411; Lee, Nien-Hung/0000-0001-5423-8880
FU Taiwan Ministry of Health and Welfare Clinical Trial and Research Center
   of Excellence [MOHW105-TDU-B-212-133019]
FX Contract grant sponsor: Taiwan Ministry of Health and Welfare Clinical
   Trial and Research Center of Excellence.Contract grant number:
   MOHW105-TDU-B-212-133019.
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NR 34
TC 39
Z9 40
U1 0
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1520-4081
EI 1522-7278
J9 ENVIRON TOXICOL
JI Environ. Toxicol.
PD FEB
PY 2017
VL 32
IS 2
BP 669
EP 678
DI 10.1002/tox.22268
PG 10
WC Environmental Sciences; Toxicology; Water Resources
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Environmental Sciences & Ecology; Toxicology; Water Resources
GA EK3AX
UT WOS:000393799500027
PM 27060453
DA 2025-01-04
ER

PT J
AU O'Connell, E
   Reynolds, IS
   McNamara, DA
   Prehn, JHM
   Burke, JP
AF O'Connell, E.
   Reynolds, I. S.
   McNamara, D. A.
   Prehn, J. H. M.
   Burke, J. P.
TI Microsatellite instability and response to neoadjuvant chemoradiotherapy
   in rectal cancer: A systematic review and meta-analysis
SO SURGICAL ONCOLOGY-OXFORD
LA English
DT Review
DE Microsatelliteinstability; Rectalcancer; Neoadjuvantchemoradiotherapy;
   Pathologicalcompleteresponse
ID ADJUVANT CHEMOTHERAPY; COLORECTAL-CANCER; PREOPERATIVE
   CHEMORADIOTHERAPY; TUMOR RESPONSE; COLON-CANCER; CARCINOMAS; EXPRESSION;
   MUTATIONS; ADENOCARCINOMA; RADIOTHERAPY
AB Background: Response to neoadjuvant chemoradiotherapy (CRT) in locally advanced rectal cancer is variable. Identification of biomarkers to predict response is desirable in order to provide prognostic information and targeted therapy. Several studies have investigated microsatellite instability (MSI) as a predictor of response to CRT with contradictory results. This study aims to clarify the effect of MSI status on response to CRT in locally advanced rectal cancer through systematic review and meta-analysis.
   Methods: A systematic search of PubMed, Embase and Cochrane databases was performed for all studies relating to MSI and response to CRT in rectal cancer using the search algorithm (Microsatellite Instability) AND (Chemoradiotherapy) AND (Rectal Cancer). From each included study the number of patients with MSI tumors and Microsatellite Stable (MSS) tumors and the numbers achieving pathological complete response (pCR) were recorded. Pooled outcome measures were determined using a random effects model and the odds ratio estimated with variance and 95% confidence interval.
   Results: Nine published studies were identified reporting data on MSI and its effect on outcome after CRT for locally advanced rectal cancer. Five studies describing 5,877 patients included data on MSI and the number of patients achieving pCR. There was no significant association between MSI and pCR (MSI Vs MSS: 10.1% Vs 6.6%, OR 1.38, 95% CI: 0.7-2.72, p = 0.35).
   Conclusion: This meta-analysis concludes that there appears to be no significant difference in pCR rate following CRT in patients with MSI versus MSS rectal tumors.
C1 [O'Connell, E.; Reynolds, I. S.; McNamara, D. A.; Burke, J. P.] Beaumont Hosp, Dept Colorectal Surg, Dublin 9, Ireland.
   [McNamara, D. A.] Royal Coll Surgeons Ireland, Dept Surg, Dublin 2, Ireland.
   [O'Connell, E.; Reynolds, I. S.; Prehn, J. H. M.] Royal Coll Surgeons Ireland, Dept Physiol & Med Phys, Dublin 2, Ireland.
C3 Royal College of Surgeons - Ireland; Royal College of Surgeons - Ireland
RP Burke, JP (corresponding author), Beaumont Hosp, Dept Colorectal Surg, Dublin 9, Ireland.
EM emerpoconnell@rcsi.com; Johnburke@rcsi.ie
RI Reynolds, Ian/AAF-6332-2020; Prehn, Jochen/A-3928-2010
OI McNamara, Deborah/0000-0003-3975-0485; Reynolds, Ian
   Sean/0000-0002-8790-2538
FU Bon Secours Hospital through the RCSI StAR MD program; Beaumont Hospital
   Colorectal Research Trust
FX This work was supported by the Bon Secours Hospital through the RCSI
   StAR MD program and the Beaumont Hospital Colorectal Research Trust. The
   funding sources had no influence of the design, conduct or submission
   for publication of this article.
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NR 43
TC 24
Z9 24
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 2020
VL 34
BP 57
EP 62
DI 10.1016/j.suronc.2020.03.009
PG 6
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA NQ1CI
UT WOS:000570604400010
PM 32891354
DA 2025-01-04
ER

PT J
AU Banerjee, A
   Deka, D
   Muralikumar, M
   Sun-Zhang, A
   Bisgin, A
   Christopher, C
   Zhang, H
   Sun, XF
   Pathak, S
AF Banerjee, Antara
   Deka, Dikshita
   Muralikumar, Makalakshmi
   Sun-Zhang, Alexander
   Bisgin, Atil
   Christopher, Cynthia
   Zhang, Hong
   Sun, Xiao-Feng
   Pathak, Surajit
TI A concise review on miRNAs as regulators of colon cancer stem cells and
   associated signalling pathways
SO CLINICAL & TRANSLATIONAL ONCOLOGY
LA English
DT Review
DE miRNA; Theranostic; Colon cancer; Cancer stem cells; Targeted therapy
ID TUMOR MICROENVIRONMENT; BETA-CATENIN; MICRORNAS; EXPRESSION; RNA;
   METASTASIS; GROWTH; NICHE; PROTEINS; SURVIVAL
AB Despite recent therapy advances and a better understanding of colon cancer biology, it remains one of the major causes of death. The cancer stem cells, associated with the progression, metastasis, and recurrence of colon cancer, play a major role in promoting the development of tumour and are found to be chemo resistant. The stroma of the tumour, which makes up the bulk of the tumour mass, is composed of the tumour microenvironment. With the advent of theranostic and the development of personalised medicine, miRNAs are becoming increasingly important in the context of colon malignancies. A holistic understanding of the regulatory roles of miRNAs in cancer cells and cancer stem cells will allow us to design effective strategies to regulate miRNAs, which could lead to improved clinical translation and creating a potent colon cancer treatment strategy. In this review paper, we briefly discuss the history of miRNA as well as the mechanisms of miRNA and cancer stem cells that contribute to the tumour growth, apoptosis, and advancement of colon cancer. The usefulness of miRNA in colorectal cancer theranostic is further concisely reviewed. We conclude by holding a stance in addressing the prospects and possibilities for miRNA by the disclosure of recent theranostic approaches aimed at eradicating cancer stem cells and enhancing overall cancer treatment outcomes.
C1 [Banerjee, Antara; Deka, Dikshita; Muralikumar, Makalakshmi; Christopher, Cynthia; Pathak, Surajit] Chettinad Hosp & Res Inst CHRI, Chettinad Acad Res & Educ CARE, Fac Allied Hlth Sci, Dept Med Biotechnol, Chennai 603103, India.
   [Sun-Zhang, Alexander] Karolinska Inst, Dept Oncol Pathol, S-17177 Solna, Sweden.
   [Bisgin, Atil] Cukurova Technopolis, InfoGenom R&D Labs, Adana, Turkiye.
   [Bisgin, Atil] Cukurova Univ, AGENTEM Adana Genet Dis Diag & Treatment Ctr, Med Fac, Med Genet Dept, Adana, Turkiye.
   [Zhang, Hong] Orebro Univ, Sch Med, Dept Med Sci, S-70182 Orebro, Sweden.
   [Sun, Xiao-Feng] Linkoping Univ, Dept Biomed & Clin Sci, Div Oncol, S-58183 Linkoping, Sweden.
C3 Karolinska Institutet; Cukurova University; Orebro University; Linkoping
   University
RP Banerjee, A (corresponding author), Chettinad Hosp & Res Inst CHRI, Chettinad Acad Res & Educ CARE, Fac Allied Hlth Sci, Dept Med Biotechnol, Chennai 603103, India.; Sun, XF (corresponding author), Linkoping Univ, Dept Biomed & Clin Sci, Div Oncol, S-58183 Linkoping, Sweden.
EM antara.banerjee27@gmail.com; xiao-feng.sun@liu.se
RI sun, xiao/KUD-2253-2024; Banerjee, Antara/AAH-4044-2020; Deka,
   Dikshita/JYP-3230-2024; BISGIN, ATIL/G-5001-2018; Pathak,
   Surajit/AAH-4022-2020
OI Bisgin, Atil/0000-0002-2053-9076; Banerjee, Antara/0000-0002-5519-6878
FU DST Inspire research student grant [190963]; Chettinad academy of
   Research and Education [004/Regr/AR-Research/2022-05]
FX This work was supported by the DST Inspire research student grant with
   award number 190963 and Departmental Seed Grants to Dr. Antara Banerjee
   from Chettinad academy of Research and Education with reference
   number-Ref.No.004/Regr/AR-Research/2022-05.
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NR 83
TC 4
Z9 4
U1 2
U2 7
PU SPRINGER INT PUBL AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 1699-048X
EI 1699-3055
J9 CLIN TRANSL ONCOL
JI Clin. Transl. Oncol.
PD DEC
PY 2023
VL 25
IS 12
BP 3345
EP 3356
DI 10.1007/s12094-023-03200-x
EA APR 2023
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA W4IE2
UT WOS:000973381400001
PM 37086351
DA 2025-01-04
ER

PT J
AU Cao, WG
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AF Cao, Weiguo
   Xu, Yaping
   Chang, Lianpeng
   Gong, Yuhua
   Li, Liren
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   Zhang, Xin
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   Zhou, Jiaolin
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   Chu, Yuxing
   Guan, Yanfang
   Chen, Yongsheng
   Wang, Jiayin
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   Yang, Ling
   Yi, Xin
   Cheng, Yong
TI Genotyping of Circulating Tumor DNA Reveals the Clinically Actionable
   Mutation Landscape of Advanced Colorectal Cancer
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID LIQUID BIOPSIES; HETEROGENEITY; PROGRESS; AGE
AB Circulating tumor DNA (ctDNA) enables genomic profiling of colorectal cancer. We investigated therapeutic targets by performing ca/NA panel-captured sequencing of 152 blood samples from advanced stage patients, from which somatic mutations and potentially actionable targets were evaluated. An additional 11 matched tissue samples were retrospectively obtained to verify target validity. The mutation frequencies of 1,127 collective genetic variants identified in our study strongly correlated with those of multiple public databases (Pearson R-2 = 0,92, P< 0.0001). The clonal fraction of driver genes was 90.3%, which was significantly higher than that of potential passenger genes (58.12%). Totally, 90 drug-sensitive genes from 56 patients (36.84%) were identified, including recurring targets PIK3CA, FBXW7, EGFR, BRAT, and NRAS. Various resistance mechanisms of anti-EGIR antibodies were revealed via ctDNA profiling, with 29 patients individually exhibiting multiple mechanisms, suggesting considerable resistance heterogeneity in our study population. Of the matched tissue/blood pairs, 88.14% of tissue-derived mutations were detected in ctDNA, and 88.9% of actionable targets were validated The mutational landscape of ctDNA was highly consistent with tissue databases, and ctDNA profiling showed favorable concordance with tumor tissues in our matched analysis. Thus, comprehensive ctDNA genotyping is a promising noninvasive alternative to biopsy-derived analysis for determining targeted therapy in advanced colorectal cancer.
C1 [Cao, Weiguo] Shanghai Jiao Tong Univ, Sch Med, Dept Radiat Oncol, Ruijin Hosp, Shanghai, Peoples R China.
   [Xu, Yaping; Chang, Lianpeng; Gong, Yuhua; Liu, Dan; Yi, Yuting; Dai, Pingping; Zhu, Chenchen; Liu, Tao; Chu, Yuxing; Guan, Yanfang; Chen, Yongsheng; Xia, Xuefeng; Yang, Ling; Yi, Xin] Geneplus Beijing Inst, Beijing, Peoples R China.
   [Li, Liren] Sun Yat Sen Univ, Colorectal Canc Ctr, Guangzhou, Guangdong, Peoples R China.
   [Mo, Xianwei] Guangxi Med Univ, Tumour Hosp, Dept Gastrointestinal Surg, Nanning, Peoples R China.
   [Zhang, Xin] Guangzhou Med Univ, Dept Thorac Surg, Hosp 1, Guangzhou, Guangdong, Peoples R China.
   [Lin, Guole; Zhou, Jiaolin] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Peking Union Med Coll, Dept Gen Surg, Beijing, Peoples R China.
   [Liu, Tao; Chu, Yuxing; Guan, Yanfang; Chen, Yongsheng; Wang, Jiayin] Xi An Jiao Tong Univ, Sch Elect & Informat Engn, Dept Comp Sci & Technol, Xian, Shaanxi, Peoples R China.
   [Cheng, Yong] Chongqing Med Univ, Dept Gastrointestinal Surg, Affiliated Hosp 1, 1 Youyi Rd, Chongqing 400000, Peoples R China.
C3 Shanghai Jiao Tong University; Sun Yat Sen University; Guangxi Medical
   University; Guangzhou Medical University; Chinese Academy of Medical
   Sciences - Peking Union Medical College; Peking Union Medical College;
   Peking Union Medical College Hospital; Xi'an Jiaotong University;
   Chongqing Medical University
RP Cao, WG (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Dept Radiat Oncol, Ruijin Hosp, Shanghai, Peoples R China.; Cheng, Y (corresponding author), Chongqing Med Univ, Dept Gastrointestinal Surg, Affiliated Hosp 1, 1 Youyi Rd, Chongqing 400000, Peoples R China.
EM caowg52@hotmail.com; chengyongcq@aliyun.com
RI Zhou, Jiaolin/AAV-4465-2021; Li, Liren/HGF-3027-2022; Wang,
   Jiayin/HJP-0287-2023
OI Li, Li-ren/0000-0002-2803-3803
FU National Science Foundation of China [31701150]
FX The authors would like to acknowledge Yao Su, PhD, and Zhihua Pei, MSc,
   for their assistance with data analysis and figure generation. W. Cao
   received a grant from the National Science Foundation of China (grant
   no.: 31701150).
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NR 36
TC 15
Z9 16
U1 0
U2 6
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 JUN
PY 2019
VL 18
IS 6
BP 1158
EP 1167
DI 10.1158/1535-7163.MCT-18-1247
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IB5ES
UT WOS:000470294700013
PM 31015309
OA Bronze
DA 2025-01-04
ER

PT J
AU Michel, P
   Boige, V
   Andre, T
   Aparicio, T
   Bachet, JB
   Dahan, L
   Guimbaud, R
   Lepage, C
   Manfredi, S
   Tougeron, D
   Taieb, J
   Selves, J
   Le Malicot, K
   Di Fiore, F
   Maillard, E
AF Michel, Pierre
   Boige, Valerie
   Andre, Thierry
   Aparicio, Thomas
   Bachet, Jean Baptiste
   Dahan, Laetitia
   Guimbaud, Rosine
   Lepage, Come
   Manfredi, Sylvain
   Tougeron, David
   Taieb, Julien
   Selves, Janick
   Le Malicot, Karine
   Di Fiore, Frederic
   Maillard, Emilie
TI Aspirin versus placebo in stage III or high-risk stage II colon cancer
   with <i>PIK3CA</i> mutation: A French randomised double-blind phase III
   trial (PRODIGE 50-ASPIK)
SO DIGESTIVE AND LIVER DISEASE
LA English
DT Article
DE Aspirin; Colorectal cancer; PI3KCA mutation
ID COLORECTAL-CANCER; ADJUVANT CHEMOTHERAPY; SURVIVAL; OXALIPLATIN;
   DIAGNOSIS; FLUOROURACIL; BEVACIZUMAB; METASTASIS; LEUCOVORIN; EXPRESSION
AB Oxaliplatin-based adjuvant chemotherapy is standard of care for radically resected stage III colon cancer and an accepted option for high-risk stage II. Two recent retrospective studies strongly suggested that low-dose aspirin used (100 mg/d) after surgical resection of colorectal cancer with a PIK3CA mutation could act as a targeted therapy with a major protective effect on the risk of recurrence.
   We propose a double-blind randomized phase III study to evaluate aspirin (100 mg/d during 3 years or until recurrence) versus placebo. Main inclusion criteria are patients aged 18 or 20, stage III or high risk stage II.
   The primary endpoint of the study is 3-year disease-free survival (DFS). Hypotheses are to improve 3-years DFS from placebo: 72% to aspirin: 83% (HR = 0.56). 94 events and 264 patients with PIK3CA mutation are required. The secondary endpoints are DFS at 5 years, the overall survival rate at 5 years, grade 3-4 severe bleeding. (C) 2017 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
C1 [Michel, Pierre] Normandie Univ, Rouen Univ Hosp, Dept Hepatogastroenterol, IRON Grp,Inserm 1245,UNIROUEN, Rouen, France.
   [Boige, Valerie] Gustave Roussy, Dept Oncol Med, Villejuif, France.
   [Andre, Thierry] Univ Paris 06, St Antoine Hosp, Dept Med Oncol, Paris, France.
   [Aparicio, Thomas] Univ Paris 07, St Louis Hosp, AP HP, Dept Gastroenterol & Digest Oncol,Sorbonne Paris, Paris, France.
   [Bachet, Jean Baptiste] Univ Paris 06, Hop Pitie Salpetriere, AP HP, Dept Hepatogastroenterol & Digest Oncol, Paris, France.
   [Dahan, Laetitia] Aix Marseille Univ, AP HM, Dept Digest Oncol, Marseille, France.
   [Guimbaud, Rosine] Paul Sabatier Univ, Univ Hosp Toulouse, Dept Med Oncol, Toulouse, France.
   [Lepage, Come; Manfredi, Sylvain] Burgundy Franche Conte Univ, Univ Hosp Dijon, Dept Hepatogastroenterol & Oncol Digest, INSERM LNC UMR EPICAD 1231, Dijon, France.
   [Tougeron, David] Univ Poitiers Hosp, Gastroenterol Dept Hepatogastroenterol, Poitiers, France.
   [Taieb, Julien] Univ Paris 05, Dept Digest Oncol, Hop Europeen Georges Pompidou, Paris, France.
   [Selves, Janick] Paul Sabatier Univ, Univ Hosp Toulouse, Dept Pathol, Toulouse, France.
   [Le Malicot, Karine; Maillard, Emilie] French Federat Digest Oncol FFCD, INSERM LCN UMR EPICAD 1231, Dijon, France.
   [Di Fiore, Frederic] Normandie Univ, Dept Hepatogastroenterol, Rouen Univ Hosp, UNIROUEN,Inserm 1245,IRON Grp,Dept Med Oncol,Ctr, Rouen, France.
C3 Institut National de la Sante et de la Recherche Medicale (Inserm);
   Universite de Rouen Normandie; CHU de Rouen; UNICANCER; Gustave Roussy;
   Sorbonne Universite; Assistance Publique Hopitaux Paris (APHP); Hopital
   Universitaire Saint-Antoine - APHP; Assistance Publique Hopitaux Paris
   (APHP); Universite Paris Cite; Assistance Publique Hopitaux Paris
   (APHP); Hopital Universitaire Pitie-Salpetriere - APHP; Sorbonne
   Universite; Aix-Marseille Universite; Assistance Publique-Hopitaux de
   Marseille; Universite de Toulouse; Universite Toulouse III - Paul
   Sabatier; CHU de Toulouse; CHU Dijon Bourgogne; Institut Agro; AgroSup
   Dijon; Universite de Bourgogne; Institut National de la Sante et de la
   Recherche Medicale (Inserm); CHU Poitiers; Universite de Poitiers;
   Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Europeen Georges-Pompidou - APHP; Universite de
   Toulouse; Universite Toulouse III - Paul Sabatier; CHU de Toulouse;
   Institut Agro; AgroSup Dijon; Institut National de la Sante et de la
   Recherche Medicale (Inserm); Universite de Bourgogne; Universite de
   Rouen Normandie; CHU de Rouen; Institut National de la Sante et de la
   Recherche Medicale (Inserm)
RP Michel, P (corresponding author), Normandie Univ, Rouen Univ Hosp, Dept Hepatogastroenterol, IRON Grp,Inserm 1245,UNIROUEN, Rouen, France.
EM pierre.michel@chu-rouen.fr
RI tougeron, david/ABF-3217-2020; BACHET, Jean-Baptiste/N-6943-2017; André,
   Thierry/N-8830-2017; Dahan, Laetitia/M-3441-2016; Selves,
   Janick/M-7719-2014
OI Le Malicot, Karine/0000-0002-3226-8525; tougeron,
   david/0000-0002-8065-9635; Andre, Thierry/0000-0002-5103-7095; taieb,
   julien/0000-0002-9955-4753
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NR 27
TC 14
Z9 14
U1 0
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1590-8658
EI 1878-3562
J9 DIGEST LIVER DIS
JI Dig. Liver Dis.
PD MAR
PY 2018
VL 50
IS 3
BP 305
EP 307
DI 10.1016/j.dld.2017.12.023
PG 3
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GA8ZR
UT WOS:000428631100015
PM 29402752
DA 2025-01-04
ER

PT J
AU Mo, SB
   Cai, GX
AF Mo, Shaobo
   Cai, Guoxiang
TI Multidisciplinary Treatment for Colorectal Peritoneal Metastases: Review
   of the Literature
SO GASTROENTEROLOGY RESEARCH AND PRACTICE
LA English
DT Review
ID HYPERTHERMIC INTRAPERITONEAL CHEMOTHERAPY; DISEASE SEVERITY SCORE;
   TRIFUNCTIONAL ANTIBODY CATUMAXOMAB; SYSTEMATIC 2ND-LOOK SURGERY;
   INDOCYANINE GREEN USAGE; DIFFUSION-WEIGHTED MRI; CYTOREDUCTIVE SURGERY;
   CANCER INDEX; LIVER METASTASES; SURFACE MALIGNANCIES
AB Peritoneum is one of the common sites of metastasis in advanced stage colorectal cancer patients. Colorectal cancer patients with peritoneal metastases (PM) are traditionally believed to have poor prognosis, which indicates it is of no value to adopt surgical treatment. With the advancement of surgical techniques, hyperthermic intraperitoneal chemotherapy (HIPEC), and multidisciplinary treatment in recent years, the cognition and treatment strategies of colorectal peritoneal metastases (CPM) have changed dramatically. In terms of prognosis, CPM under the palliative systemic treatment shows an inferior outcome compared with nonperitoneal metastasis. Nevertheless, some CPM patients amenable to the complete peritoneal cytoreductive surgery (CRS) combined with HIPEC may achieve long-term survival. The prognostic factors of CPM comprise peritoneal carcinomatosis index (PCI), completeness of cytoreduction score (CC score), the presence of extraperitoneal metastasis (liver, etc.), Peritoneal Surface Disease Severity Score (PSDSS), Japanese peritoneal staging, and so forth. Taken together, literature data suggest that a multimodality approach combining complete peritoneal CRS plus HIPEC, systemic chemotherapy, and targeted therapy may be the best treatment option for PM from colorectal cancer.
C1 [Mo, Shaobo; Cai, Guoxiang] Fudan Univ, Shanghai Canc Ctr, Dept Colorectal Surg, Shanghai 200032, Peoples R China.
   [Mo, Shaobo; Cai, Guoxiang] Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai 200032, Peoples R China.
C3 Fudan University; Fudan University
RP Cai, GX (corresponding author), Fudan Univ, Shanghai Canc Ctr, Dept Colorectal Surg, Shanghai 200032, Peoples R China.; Cai, GX (corresponding author), Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai 200032, Peoples R China.
EM gxcai@fudan.edu.cn
RI CAI, GUOXIANG/LKK-9614-2024
OI Cai, Guoxiang/0000-0002-7772-7078
FU Department of Colorectal Surgery, Fudan University Shanghai Cancer
   Center
FX This work was supported by Department of Colorectal Surgery, Fudan
   University Shanghai Cancer Center.
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NR 72
TC 14
Z9 19
U1 0
U2 3
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1687-6121
EI 1687-630X
J9 GASTROENT RES PRACT
JI Gastroenterol. Res. Pract.
PY 2016
VL 2016
AR 1516259
DI 10.1155/2016/1516259
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA EH8CG
UT WOS:000391998600001
PM 28105045
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Lv, YB
   Lin, SQ
   Liu, MS
   Wang, LH
   Wang, XY
   Cui, L
   Xu, JG
AF Lv, Yangbo
   Lin, Shuiquan
   Liu, Mingsheng
   Wang, Lihui
   Wang, Xiaoyu
   Cui, Li
   Xu, Jianguang
TI Impacts of pre-existing diabetes mellitus on colorectal cancer in a mice
   model
SO CANCER MEDICINE
LA English
DT Article
DE colorectal cancer; diabetes mellitus; gut microbiota; T-cell
   infiltration; transcriptome
ID CELLS; RISK; MORTALITY
AB Background: Although diabetes mellitus (DM) is regarded as a risk factor of colorectal cancer (CRC), the impacts of pre-existing DM on CRC without drug intervention remain unknown. The purpose of this study was to investigate and analyze the effects of diabetes mellitus (DM) on colorectal cancer (CRC). And, to further explore the influencing factors and the mechanisms of DM affects CRC progression.Methods: In this study, we investigated the effects of DM on CRC progression in a streptozotocin-induced DM mice model. Furthermore, we evaluated the change of T cells levels using flow cytometry and indirect immunofluorescence. We assessed the alternation of gut microbiome and the transcriptional response using 16s rRNA sequencing and RNA-seq.Results: Results showed that the mice survival time was significantly decreased in CRC complicated with DM group (DM-CRC), compared with only tumor bearing mice (CRC group). Furthermore, we found that DM could affect the immune response by changing the infiltration of CD4(+) T cells, CD8(+) T cells and mucosal-associated invariant T cell (MAIT) in the CRC progression. In addition, DM could induce gut microbiome dysbiosis and change the transcriptional response in CRC complicated with DM.Conclusion: For the first time, the effects of DM on CRC were systematically characterized in a mice model. Our findings highlight the effects of pre-existing DM on CRC, and these findings should facilitate further studies in exploring and developing potentially targeted therapy for CRC in diabetic patients. Our results suggest that the effects induced by DM should be considered in the treatment for CRC complicated with DM patients.
C1 [Lv, Yangbo; Lin, Shuiquan; Liu, Mingsheng; Wang, Lihui] Wenzhou Med Univ, Quzhou Peoples Hosp, Quzhou Affiliated Hosp, Dept Colorectal Surg, Quzhou, Zhejiang, Peoples R China.
   [Wang, Xiaoyu; Cui, Li] Shanghai Jiao Tong Univ, Sch Agr & Biol, Shanghai Key Lab Vet Biotechnol, Shanghai, Peoples R China.
   [Xu, Jianguang] Wenzhou Med Univ, Quzhou Peoples Hosp, Quzhou Affiliated Hosp, Dept Gastroenterol, Quzhou, Zhejiang, Peoples R China.
C3 Wenzhou Medical University; Shanghai Jiao Tong University; Wenzhou
   Medical University
RP Lv, YB (corresponding author), Wenzhou Med Univ, Quzhou Peoples Hosp, Quzhou Affiliated Hosp, Dept Colorectal Surg, Quzhou, Zhejiang, Peoples R China.; Cui, L (corresponding author), Shanghai Jiao Tong Univ, Sch Agr & Biol, Shanghai Key Lab Vet Biotechnol, Shanghai, Peoples R China.; Xu, JG (corresponding author), Wenzhou Med Univ, Quzhou Peoples Hosp, Quzhou Affiliated Hosp, Dept Gastroenterol, Quzhou, Zhejiang, Peoples R China.
EM lyb20110115@163.com; lcui@sjtu.edu.cn; 12689513@qq.com
RI wang, lili/HDL-7210-2022; ming, liu/ABC-9262-2021
FU Shanghai Science and Technology Innovation Action [21140901400]
FX Shanghai Science and Technology Innovation Action, Grant/Award Number:
   21140901400
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NR 35
TC 3
Z9 3
U1 0
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD MAY
PY 2023
VL 12
IS 10
BP 11641
EP 11650
DI 10.1002/cam4.5868
EA MAR 2023
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA I2DG4
UT WOS:000962203000001
PM 36999930
OA gold
DA 2025-01-04
ER

PT J
AU Zhang, RW
   Ma, JL
   Avery, JT
   Sambandam, V
   Nguyen, TH
   Xu, B
   Suto, MJ
   Boohaker, RJ
AF Zhang, Ruowen
   Ma, Jinlu
   Avery, Justin T.
   Sambandam, Vijaya
   Nguyen, Theresa H.
   Xu, Bo
   Suto, Mark J.
   Boohaker, Rebecca J.
TI GLI1 Inhibitor SRI-38832 Attenuates Chemotherapeutic Resistance by
   Downregulating NBS1 Transcription in BRAF<SUP>V600E</SUP> Colorectal
   Cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colorectal cancer; 5-FU resistance; DNA damage repair; GLI1 target gene;
   novel GLI1 inhibitor; target therapy
ID DISRUPTS HOMOLOGOUS RECOMBINATION; HEDGEHOG PATHWAY; DNA-DAMAGE;
   MUTATIONS; SURVIVAL; GROWTH; GENE; BRAF; MEDULLOBLASTOMA; BEVACIZUMAB
AB Resistance to radiation and chemotherapy in colorectal cancer (CRC) patients contribute significantly to refractory disease and disease progression. Herein, we provide mechanistic rationale for acquired or inherent chemotherapeutic resistance to the anti-tumor effects of 5-fluorouracil (5-FU) that is linked to oncogenic GLI1 transcription activity and NBS1 overexpression. Patients with high levels of GLI1 also expressed high levels of NBS1. Non-canonical activation of GLI1 is driven through oncogenic pathways in CRC, like the BRAF(V600E) mutation. GLI1 was identified as a novel regulator of NBS1 and discovered that by knocking down GLI1 levels in vitro, diminished NBS1 expression, increased DNA damage/apoptosis, and re-sensitization of 5-FU resistant cancer to treatment was observed. Furthermore, a novel GLI1 inhibitor, SRI-38832, which exhibited pharmacokinetic properties suitable for in vivo testing, was identified. GLI1 inhibition in a murine BRAF(V600E) variant xenograft model of CRC resulted in the same down-regulation of NBS1 observed in vitro as well as significant reduction of tumor growth/burden. GLI1 inhibition could therefore be a therapeutic option for 5-FU resistant and BRAF(V600E) variant CRC patients.
C1 [Zhang, Ruowen; Avery, Justin T.; Sambandam, Vijaya; Nguyen, Theresa H.; Suto, Mark J.; Boohaker, Rebecca J.] Southern Res, Div Drug Discovery, Birmingham, AL USA.
   [Ma, Jinlu] Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Radiat Oncol, Xian, Peoples R China.
   [Xu, Bo] Tianjin Med Univ Canc Inst & Hosp, Tianjin, Peoples R China.
C3 Xi'an Jiaotong University; Tianjin Medical University
RP Boohaker, RJ (corresponding author), Southern Res, Div Drug Discovery, Birmingham, AL USA.
EM rboohaker@southernresearch.org
RI zhang, ying/HJB-1230-2022
OI Avery, Justin/0000-0001-6792-0803; Zhang, Ruowen/0000-0003-1403-2356
FU National Institutes of Health [5RO1CA183921-05]; Southern Research,
   Birmingham, Alabama
FX This work was supported by The National Institutes of Health
   [5RO1CA183921-05] and by Southern Research, Birmingham, Alabama.
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NR 52
TC 14
Z9 14
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 28
PY 2020
VL 10
AR 241
DI 10.3389/fonc.2020.00241
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LB6KL
UT WOS:000524742600001
PM 32185127
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Rankin, A
   Klempner, SJ
   Erlich, R
   Sun, JX
   Grothey, A
   Fakih, M
   George, TJ
   Lee, J
   Ross, JS
   Stephens, PJ
   Miller, VA
   Ali, SM
   Schrock, AB
AF Rankin, Andrew
   Klempner, Samuel J.
   Erlich, Rachel
   Sun, James X.
   Grothey, Axel
   Fakih, Marwan
   George, Thomas J., Jr.
   Lee, Jeeyun
   Ross, Jeffrey S.
   Stephens, Philip J.
   Miller, Vincent A.
   Ali, Siraj M.
   Schrock, Alexa B.
TI Broad Detection of Alterations Predicted to Confer Lack of Benefit From
   EGFR Antibodies or Sensitivity to Targeted Therapy in Advanced
   Colorectal Cancer
SO ONCOLOGIST
LA English
DT Article
DE KRAS; Colon cancer; Biomarker; Genomic profiling; Epidermal growth
   factor receptor; Cetuximab
ID CETUXIMAB PLUS IRINOTECAN; 1ST-LINE TREATMENT; KRAS MUTATIONS;
   ACQUIRED-RESISTANCE; RAS MUTATIONS; OPEN-LABEL; BRAF; CARCINOMA;
   IDENTIFICATION; BEVACIZUMAB
AB Introduction. A KRAS mutation represented the first genomic biomarker to predict lack of benefit from anti-epidermal growth factor receptor (EGFR) antibody therapy in advanced colorectal cancer (CRC). Expanded RAS testing has further refined the treatment approach, but understanding of genomic alterations underlying primary and acquired resistance is limited and further study is needed.
   Materials and Methods. We prospectively analyzed 4,422 clinical samples from patients with advanced CRC, using hybrid-capture based comprehensive genomic profiling (CGP) at the request of the individual treating physicians. Comparison with prior molecular testing results, when available, was performed to assess concordance.
   Results. We identified a RAS/RAF pathway mutation or amplification in 62% of cases, including samples harboring KRAS mutations outside of the codon 12/13 hotspot region in 6.4% of cases. Among cases with KRAS non-codon 12/13 alterations for which prior test results were available, 79 of 90 (88%) were not identified by focused testing. Of 1,644 RAS/RAF wild-type cases analyzed by CGP, 31% harbored a genomic alteration (GA) associated with resistance to anti-EGFR therapy in advanced CRC including mutations in PIK3CA, PTEN, EGFR, and ERBB2. We also identified other targetable GA, including novel kinase fusions, receptor tyrosine kinase amplification, activating point mutations, as well as micro-satellite instability.
   Conclusion. Extended genomic profiling reliably detects alterations associated with lack of benefit to anti-EGFR therapy in advanced CRC, while simultaneously identifying alterations potentially important in guiding treatment. The use of CGP during the course of clinical care allows for the refined selection of appropriate targeted therapies and clinical trials, increasing the chance of clinical benefit and avoiding therapeutic futility.
C1 [Rankin, Andrew; Erlich, Rachel; Sun, James X.; Ross, Jeffrey S.; Stephens, Philip J.; Miller, Vincent A.; Ali, Siraj M.; Schrock, Alexa B.] Fdn Med Inc, 150 Second St,Second Floor, Cambridge, MA 02141 USA.
   [Klempner, Samuel J.] Angeles Clin & Res Inst, Los Angeles, CA USA.
   [Grothey, Axel] Mayo Clin, Ctr Canc, Rochester, MN USA.
   [Fakih, Marwan] City Hope Natl Med Ctr, Ctr Comprehens Canc, Duarte, CA USA.
   [George, Thomas J., Jr.] Univ Florida, Coll Med, Gainesville, FL USA.
   [Lee, Jeeyun] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Hematol & Oncol, Seoul, South Korea.
   [Ross, Jeffrey S.] Albany Med Coll, Dept Pathol & Lab Med, Albany, NY 12208 USA.
C3 Foundation Medicine; Angeles Clinic & Research Institute; Mayo Clinic;
   City of Hope; State University System of Florida; University of Florida;
   Sungkyunkwan University (SKKU); Samsung Medical Center; Albany Medical
   College
RP Schrock, AB (corresponding author), Fdn Med Inc, 150 Second St,Second Floor, Cambridge, MA 02141 USA.
EM aschrock@Foundationmedicine.com
RI Klempner, Samuel/U-2235-2019; Ali, Siraj/AAE-2958-2019; Lee,
   Jee/C-9646-2011; George, Thomas/L-9119-2019
OI George, Thomas/0000-0002-6249-9180; Klempner,
   Samuel/0000-0002-4062-0808; Fakih, Marwan/0000-0002-6554-5488
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NR 58
TC 26
Z9 28
U1 0
U2 4
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 NOV
PY 2016
VL 21
IS 11
BP 1306
EP 1314
DI 10.1634/theoncologist.2016-0148
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EC0IF
UT WOS:000387782600008
PM 27682134
OA Bronze, Green Published
DA 2025-01-04
ER

PT J
AU Matsuda, T
   Yamashita, K
   Hasegawa, H
   Oshikiri, T
   Hosono, M
   Higashino, N
   Yamamoto, M
   Matsuda, Y
   Kanaji, S
   Nakamura, T
   Suzuki, S
   Sumi, Y
   Kakeji, Y
AF Matsuda, Takeru
   Yamashita, Kimihiro
   Hasegawa, Hiroshi
   Oshikiri, Taro
   Hosono, Masayoshi
   Higashino, Nobuhide
   Yamamoto, Masashi
   Matsuda, Yoshiko
   Kanaji, Shingo
   Nakamura, Tetsu
   Suzuki, Satoshi
   Sumi, Yasuo
   Kakeji, Yoshihiro
TI Recent updates in the surgical treatment of colorectal cancer
SO ANNALS OF GASTROENTEROLOGICAL SURGERY
LA English
DT Review
DE colorectal cancer; laparoscopic surgery; lateral pelvic lymph node
   dissection; robotic surgery; transanal total mesorectal excision
ID TOTAL MESORECTAL EXCISION; LOW-RECTAL-CANCER; LYMPH-NODE DISSECTION;
   LAPAROSCOPIC-ASSISTED RESECTION; MISMATCH REPAIR STATUS; SHORT-TERM
   OUTCOMES; MRC CLASICC TRIAL; NEOADJUVANT CHEMORADIOTHERAPY; STAGE-II;
   COLON-CANCER
AB Because of recent advances in medical technology and new findings of clinical trials, treatment options for colorectal cancer are evolutionally changing, even in the last few years. Therefore, we need to update the treatment options and strategies so that patients can receive optimal and tailored treatment. The present review aimed to elucidate the recent global trends and update the surgical treatment strategies in colorectal cancer by citing the literature published in the last 2 years, namely 2016 and 2017. Although laparoscopic surgery is still considered the most common approach for the treatment of colorectal cancer, new surgical technologies such as transanal total mesorectal excision, robotic surgery, and laparoscopic lateral pelvic lymph node dissection are emerging. However, with the recent evidence, superiority of the laparoscopic approach to the open approach for rectal cancer seems to be controversial. Surgeons should notice the risk of adverse outcomes associated with unfounded and uncontrolled use of these novel techniques. Many promising results are accumulating in preoperative and postoperative treatment including chemotherapy, chemoradiotherapy, and targeted therapy. Development of new biomarkers seems to be essential for further improvement in the treatment outcomes of colorectal cancer patients.
C1 [Matsuda, Takeru] Kobe Univ, Div Minimally Invas Surg, Dept Surg, Grad Sch Med, Kobe, Hyogo, Japan.
   [Yamashita, Kimihiro; Hasegawa, Hiroshi; Oshikiri, Taro; Hosono, Masayoshi; Higashino, Nobuhide; Yamamoto, Masashi; Matsuda, Yoshiko; Kanaji, Shingo; Nakamura, Tetsu; Suzuki, Satoshi; Kakeji, Yoshihiro] Kobe Univ, Div Gastrointestinal Surg, Dept Surg, Grad Sch Med, Kobe, Hyogo, Japan.
   [Sumi, Yasuo] Kobe Univ, Div Int Clin Canc Res, Dept Surg, Grad Sch Med, Kobe, Hyogo, Japan.
C3 Kobe University; Kobe University; Kobe University
RP Matsuda, T (corresponding author), Kobe Univ, Div Minimally Invas Surg, Dept Surg, Grad Sch Med, Kobe, Hyogo, Japan.
EM takerumatsuda@nifty.com
RI Nakamura, Tetsu/W-3864-2019; Yamashita, Kimihiro/J-4396-2014
OI Hasegawa, Hiroshi/0000-0003-1545-0509; Nakamura,
   Tetsu/0000-0003-2653-9234; Kanaji, Shingo/0000-0002-8698-8923
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NR 69
TC 69
Z9 72
U1 0
U2 10
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA POSTFACH 101161, 69451 WEINHEIM, GERMANY
SN 2475-0328
J9 ANN GASTROENT SURG
JI Ann. Gastroent. Surg.
PD MAR
PY 2018
VL 2
IS 2
BP 129
EP 136
DI 10.1002/ags3.12061
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GX0HT
UT WOS:000447391700006
PM 29863145
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Gherman, A
   Balacescu, L
   Gheorghe-Cetean, S
   Vlad, C
   Balacescu, O
   Irimie, A
   Lisencu, C
AF Gherman, Alexandra
   Balacescu, Loredana
   Gheorghe-Cetean, Sinziana
   Vlad, Catalin
   Balacescu, Ovidiu
   Irimie, Alexandru
   Lisencu, Cosmin
TI Current and New Predictors for Treatment Response in Metastatic
   Colorectal Cancer. The Role of Circulating miRNAs as Biomarkers
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE chemotherapy; prediction; treatment response; biomarkers; microRNA;
   colorectal cancer
ID ESMO CONSENSUS GUIDELINES; THYMIDYLATE SYNTHASE; 1ST-LINE TREATMENT;
   MICROSATELLITE INSTABILITY; CHEMOTHERAPY EFFICACY; CLINICAL-OUTCOMES;
   GENE-EXPRESSION; BRAF MUTATION; GROWTH-FACTOR; CELL-GROWTH
AB Colorectal cancer (CRC) is the third most frequently diagnosed cancer in the world. More than half of all CRC patients will eventually develop metastases and require treatment accordingly, but few validated predictive factors for response to systemic treatments exist. In order to ascertain which patients benefit from specific treatments, there is a strong need for new and reliable biomarkers. We conducted a comprehensive search using the PUBMED database, up to December 2019, in order to identify relevant studies on predictive biomarkers for treatment response in metastatic CRC. We will herein present the currently used and potential biomarkers for treatment response and bring up-to-date knowledge on the role of circulating microRNAs, associated with chemotherapy and targeted therapy regimens used in metastatic CRC treatment. Molecular, tumor-related, disease-related, clinical, and laboratory predictive markers for treatment response were identified, mostly proposed, with few validated. Several circulating microRNAs have already proven their role of prediction for treatment response in CRC, but future clinical studies are needed to confirm their role as biomarkers across large cohorts of patients.
C1 [Gherman, Alexandra; Balacescu, Loredana; Balacescu, Ovidiu] Univ Med & Pharm Iuliu Hatieganu, Dept Med Oncol 11, 34-36 Republicii St, Cluj Napoca 400015, Romania.
   [Balacescu, Loredana; Balacescu, Ovidiu] Oncol Inst Prof Dr Ion Chiricuta, Dept Funct Genom Prote & Expt Pathol, 34-36 Republicii St, Cluj Napoca 400015, Romania.
   [Gheorghe-Cetean, Sinziana] Iuliu Hatieganu Univ Med & Pharm, Dept Gen & Inorgan Chem, 4 Louis Pasteur St, Cluj Napoca 400012, Romania.
   [Vlad, Catalin; Irimie, Alexandru; Lisencu, Cosmin] IuliuHatieganu Univ Med & Pharm, Dept Oncol Surg & Gynecol Oncol 11, 34-36 Republicii St, Cluj Napoca 400015, Romania.
   [Vlad, Catalin; Irimie, Alexandru; Lisencu, Cosmin] Oncol Inst Prof Dr Ion Chiricuta, Dept Surg, 34-36 Republicii St, Cluj Napoca 400015, Romania.
C3 Iuliu Hatieganu University of Medicine & Pharmacy; Oncology Institute
   Prof. Dr. Ion Chiricuta; Iuliu Hatieganu University of Medicine &
   Pharmacy; Oncology Institute Prof. Dr. Ion Chiricuta
RP Balacescu, O (corresponding author), Univ Med & Pharm Iuliu Hatieganu, Dept Med Oncol 11, 34-36 Republicii St, Cluj Napoca 400015, Romania.; Balacescu, O (corresponding author), Oncol Inst Prof Dr Ion Chiricuta, Dept Funct Genom Prote & Expt Pathol, 34-36 Republicii St, Cluj Napoca 400015, Romania.; Vlad, C (corresponding author), IuliuHatieganu Univ Med & Pharm, Dept Oncol Surg & Gynecol Oncol 11, 34-36 Republicii St, Cluj Napoca 400015, Romania.; Vlad, C (corresponding author), Oncol Inst Prof Dr Ion Chiricuta, Dept Surg, 34-36 Republicii St, Cluj Napoca 400015, Romania.
EM allexandragherman@gmail.com; loredanabalacescu@yahoo.com;
   cetean.sinziana@umfcluj.ro; catalinvlad@yahoo.it;
   ovidiubalacescu@iocn.ro; airimie@umfcluj.ro; cosminlisencu@yahoo.com
RI Balacescu, Ovidiu/C-9728-2014; Gherman, Alexandra/AAH-2689-2020
OI Balacescu, Ovidiu/0000-0003-0253-7103; Balacescu,
   Loredana/0000-0003-2946-7758
FU BIOGENONCO grant [105774, 10/01.09.2016]
FX The authors A.G., L.B and O.B. were supported by the BIOGENONCO grant,
   10/01.09.2016 (MySMIS-Code: 105774).
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NR 74
TC 12
Z9 12
U1 1
U2 13
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 MAR
PY 2020
VL 21
IS 6
AR 2089
DI 10.3390/ijms21062089
PG 22
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA LJ0UU
UT WOS:000529890200185
PM 32197436
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhang, YJ
   Zhou, L
   Tan, JW
   Liu, JL
   Shan, XQ
   Ma, Y
AF Zhang, Yajie
   Zhou, Lu
   Tan, Jingwei
   Liu, Jianling
   Shan, Xiaoqing
   Ma, Yong
TI Laser-triggered collaborative chemophotothermal effect of gold
   nanoparticles for targeted colon cancer therapy
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Targeted therapy; Photothermal effect; Doxorubicin; Colon cancer therapy
ID DRUG-RELEASE; IN-VITRO; NUCLEOLIN; DELIVERY; LIGHT; PROTEIN; AS1411;
   SMART; SIZE; DNA
AB Nanotechnology has shown advantages for cancer treatment. Multimodal nanoparticles (NPs) combining chemotherapy and photothermal therapy are promising and elicit synergetic benefit. However, there were still less multifunctional nanomaterials with good targeting and anti-tumor property applied as the colon cancer therapeutic strategy. In this study, we designed the gold NPs modified with AS1411 and DNA riched of GC intercalation (hairpin DNA) with doxorubicin (DOX) for targeted chemotherapy and NIR laser-triggered chemophotothermal effect (PTT). We took advantage of PTT effect to realize DOX release from hairpin DNA. We also demonstrated AS1411 based NPs exhibited remarkable targeted binding towards SW480 colon cancer cells in vitro and enhanced uptake inside the cells. Strikingly, AS1411 based NPs exhibited the most efficient cytotoxicity and markedly enhanced inhibition effect on cells proliferation to SW480 cells under laser exposure when compared to the NPs merely with PTT or chemotherapy. Our study appears to provide an alternative nano-platform with good targeted and chemo-photothermal therapy against colon cancer.
C1 [Zhang, Yajie; Zhou, Lu; Tan, Jingwei; Liu, Jianling; Shan, Xiaoqing; Ma, Yong] China Med Univ, Sch Fundamental Sci, Dept Chem, Shenyang 110122, Peoples R China.
   [Zhang, Yajie] China Med Univ, Dept Gastroenterol, Shengjing Hosp, Shenyang 110004, Peoples R China.
C3 China Medical University; China Medical University
RP Ma, Y (corresponding author), China Med Univ, Sch Fundamental Sci, Dept Chem, Shenyang 110122, Peoples R China.
EM mayong@lnu.edu.cn
RI zhang, yajie/GVT-3956-2022
FU National Natural Science Foundation of China [21372262]; Basic Research
   Program of Higher Education of Liaoning Province of China [LQNK201742]
FX This research was supported by the National Natural Science Foundation
   of China (Grant No. 21372262) and Basic Research Program of Higher
   Education of Liaoning Province of China (Grant No. LQNK201742).
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NR 41
TC 18
Z9 18
U1 2
U2 35
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 OCT
PY 2020
VL 130
AR 110492
DI 10.1016/j.biopha.2020.110492
PG 9
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA OH6JX
UT WOS:000582697900012
PM 32682110
OA gold
DA 2025-01-04
ER

PT J
AU Cruz-Nova, P
   Ancira-Cortez, A
   Ferro-Flores, G
   Ocampo-García, B
   Gibbens-Bandala, B
AF Cruz-Nova, Pedro
   Ancira-Cortez, Alejandra
   Ferro-Flores, Guillermina
   Ocampo-Garcia, Blanca
   Gibbens-Bandala, Brenda
TI Controlled-Release Nanosystems with a Dual Function of Targeted Therapy
   and Radiotherapy in Colorectal Cancer
SO PHARMACEUTICS
LA English
DT Review
DE nanoparticle system; colorectal cancer; combined therapy
ID GOLD NANOPARTICLES; DRUG; CHEMORADIOTHERAPY; CAMPTOTHECIN; STRATEGIES;
   RETENTION; CITRATE; CRLX101; TOOLS
AB Nanoparticles are excellent platforms for several biomedical applications, including cancer treatment. They can incorporate different molecules to produce combinations of chemotherapeutic agents, radionuclides, and targeting molecules to improve the therapeutic strategies against cancer. These specific nanosystems are designed to have minimal side effects on healthy cells and better treatment efficacy against cancer cells when compared to chemotherapeutics, external irradiation, or targeted radiotherapy alone. In colorectal cancer, some metal and polymeric nanoparticle platforms have been used to potentialize external radiation therapy and targeted drug delivery. Polymeric nanoparticles, liposomes, albumin-based nanoparticles, etc., conjugated with PEG and/or HLA, can be excellent platforms to increase blood circulation time and decrease side effects, in addition to the combination of chemo/radiotherapy, which increases therapeutic efficacy. Additionally, radiolabeled nanoparticles have been conjugated to target specific tissues and are mainly used as agents for diagnosis, drug/gene delivery systems, or plasmonic photothermal therapy enhancers. This review aims to analyze how nanosystems are shaping combinatorial therapy and evaluate their status in the treatment of colorectal cancer.
C1 [Cruz-Nova, Pedro; Ancira-Cortez, Alejandra; Ferro-Flores, Guillermina; Ocampo-Garcia, Blanca; Gibbens-Bandala, Brenda] Inst Nacl Invest Nucl, Dept Mat Radiact, Carretera Mexico Toluca S N, Ocoyoacac 52750, Mexico.
RP Ocampo-García, B; Gibbens-Bandala, B (corresponding author), Inst Nacl Invest Nucl, Dept Mat Radiact, Carretera Mexico Toluca S N, Ocoyoacac 52750, Mexico.
EM pedro.cruz.comecyt@inin.gob.mx; alejandra.a.servicios@inin.gob.mx;
   guillermina.ferro@inin.gob.mx; blanca.ocampo@inin.gob.mx;
   brenda.g.servicios@inin.gob.mx
RI Cruz-Nova, Pedro/AAQ-7981-2021; Ancira-Cortez, Alejandra/AAQ-8494-2021;
   Ocampo-Garcia, Blanca/L-3127-2019; FERRO-FLORES, GUILLERMINA/Q-8630-2019
OI Cruz-Nova, Pedro/0000-0001-5719-7324; Ancira-Cortez,
   Alejandra/0000-0001-8772-1078; Gibbens-Bandala,
   Brenda/0000-0003-2419-0307; Ocampo-Garcia, Blanca/0000-0002-5831-8412;
   FERRO-FLORES, GUILLERMINA/0000-0003-0296-7605
FU COMECyT (Consejo Mexiquense de Ciencia y Tecnologia del Estado de
   Mexico) [CAT2021-0036]
FX Pedro Cruz-Nova acknowledges the COMECyT (Consejo Mexiquense de Ciencia
   y Tecnologia del Estado de Mexico) for the CAT2021-0036 grant.
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NR 112
TC 12
Z9 12
U1 6
U2 51
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1999-4923
J9 PHARMACEUTICS
JI Pharmaceutics
PD MAY
PY 2022
VL 14
IS 5
AR 1095
DI 10.3390/pharmaceutics14051095
PG 24
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 1O5UX
UT WOS:000801398100001
PM 35631681
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Pilonis, ND
   Januszewicz, W
   di Pietro, M
AF Pilonis, Nastazja Dagny
   Januszewicz, Wladyslaw
   di Pietro, Massimiliano
TI Confocal laser endomicroscopy in gastro-intestinal endoscopy: technical
   aspects and clinical applications
SO TRANSLATIONAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Review
DE Confocal laser endomicroscopy (CLE); image enhanced endoscopy;
   esophageal cancer; stomach cancer; colon cancer; inflammatory bowel
   disease (IBD); pancreatic cancer; fluorescent endoscopy
ID GASTRIC INTESTINAL METAPLASIA; INFLAMMATORY-BOWEL-DISEASE; IN-VIVO
   DIAGNOSIS; CROHNS-DISEASE; INTEROBSERVER AGREEMENT; VIRTUAL
   CHROMOENDOSCOPY; ULCERATIVE-COLITIS; BILIARY STRICTURES;
   BARRETTS-ESOPHAGUS; DIRECT VISUALIZATION
AB Confocal laser endomicroscopy (CLE) is an advanced endoscopic imaging technology that provides a magnified, cellular level view of gastrointestinal epithelia. In conjunction with topical or intravenous fluorescent dyes, CLE allows for an "optical biopsy" for real-time diagnosis. Two different CLE system have been used in clinical endoscopy, probe-based CLE (pCLE) and endoscope-based CLE (eCLE). Using pCLE, the device can be delivered: (I) into the luminal gastrointestinal tract through the working channel of standard endoscopes; (II) into extraluminal cystic and solid parenchymal lesions through an endoscopic ultrasound (EUS) needle; or (III) into the biliary system through an endoscopic retrograde cholangiopancreatography (ERCP) accessory channel. With eCLE, the probe is directly integrated into the tip of a conventional endoscope, however, these endoscopes are no longer commercially available. CLE has moderate to high diagnostic accuracy for neoplastic and inflammatory conditions through the gastrointestinal tract including: oesophageal, gastric and colonic neoplasia, pancreatic cysts and solid lesions, malignant pancreatobiliary strictures and inflammatory bowel disease. Some studies have demonstrated the diagnostic benefit of CLE imaging when combined with either conventional white light endoscopy or advanced imaging technologies. Therefore, optical biopsies using CLE can resolve diagnostic dilemmas in some cases where conventional imaging fails to achieve conclusive results. CLE could also reduce the requirement for extensive tissue sampling during surveillance procedures. In the future, CLE in combination with molecular probes, could allow for the molecular characterization of diseases and assess response to targeted therapy. However, the narrow field of view, high capital costs and specialized operator training requirements remain the main limitations. Future multi-center, randomized trials with a focus on conventional diagnostic applications, cost-effectiveness and standardized training will be required for definitive evidence. The objective of this review is to evaluate the technical aspects and current applications of CLE in patients with gastrointestinal and pancreatobiliary diseases and discuss future directions for this technique.
C1 [Pilonis, Nastazja Dagny; di Pietro, Massimiliano] Univ Cambridge, MRC Canc Unit, Cambridge Biomed Campus,Box197, Cambridge CB2 0XZ, England.
   [Pilonis, Nastazja Dagny; Januszewicz, Wladyslaw] Med Ctr Postgrad Educ, Dept Gastroenterol Hepatol & Clin Oncol, Warsaw, Poland.
   [Pilonis, Nastazja Dagny; di Pietro, Massimiliano] Maria Sklodowska Curie Mem Canc Ctr & Inst Oncol, Dept Gastroenterol Oncol, Warsaw, Poland.
C3 University of Cambridge; Centre of Postgraduate Medical Education -
   Poland; Maria Sklodowska-Curie National Research Institute of Oncology
RP di Pietro, M (corresponding author), Univ Cambridge, MRC Canc Unit, Cambridge Biomed Campus,Box197, Cambridge CB2 0XZ, England.
EM md460@mrc-cu.cam.ac.uk
RI Januszewicz, Wladyslaw/AAK-2119-2020
OI Pilonis, Nastazja Dagny/0000-0003-3806-8679
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NR 95
TC 40
Z9 46
U1 10
U2 27
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
EI 2415-1289
J9 TRANSL GASTROENT HEP
JI Transl. Gastroenterol. Hepatol.
PD JAN
PY 2022
VL 7
AR 7
DI 10.21037/tgh.2020.04.02
EA MAR 2020
PG 20
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA ZS9GL
UT WOS:000675481900001
PM 35243116
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Rasmy, A
   Fayed, A
   Omar, A
   Fahmy, N
AF Rasmy, Ayman
   Fayed, Alaa
   Omar, Ayman
   Fahmy, Nermin
TI Effect of <i>KRAS</i> mutational status on disease behavior and
   treatment outcome in patients with metastatic colorectal cancer:
   intratumor heterogeneity and mutational status
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Colorectal cancer (CRC); molecular study; KRAS; prognostic and
   predictive factors chemotherapy/target therapy; progression-free
   survival (PFS); overall survival (OS)
ID RAS MUTATIONS; CETUXIMAB; STATISTICS
AB Background: Nowadays, the outcomes of metastatic colorectal cancer (mCRC) have considerably improved. Genetic studies evaluating KRAS mutational status are important in the personalized therapy era to understand disease heterogeneity, disease behaviors, and treatment outcomes.
   Methods: This multicenter retrospective study evaluated 360 patients with mCRC treated at three oncology centers in Saudi Arabia and Egypt between February 2011 and December 2015. Patients were treated with bevacizumab and cetuximab according to guidelines. Therapy outcome, time to progression, and disease-associated death were assessed. KRAS mutational status was evaluated by testing exons 12 and 13.
   Results: Approximately 220 (61.1%) cases were of wild-type KRAS, whereas KRAS mutation was noted in 38.9%. KRAS mutation was common in the descending colon, whereas a low incidence of the KRAS mutation was observed in the ascending colon (P<0.001). Among patients with KRAS mutation, 64.3% initially presented as emergency cases with obstruction/perforation (P=0.002), and 62.9% had hepatic or pulmonary metastasis. The progression-free survival (ITS) was 10.7 months. Cases without KRAS mutation showed a higher PFS than did those with KRAS mutation (mean PFS: 11.5 vs. 9.6 months, P=0.001). The overall survival was 23.2 months. The survival varied considerably according to KRAS type: patients without mutation survived for 25.0 months and those with mutation survived for 19.6 months (P<0.001). Disease-related death occurred in 132 (36.7%) cases, approximately 57.1% of them (80 cases) had KRAS mutations (P=0.001).
   Conclusions: A major association between KRAS mutational status and both disease behavior and treatment outcomes was found in this study. Patients with KRAS mutation show advanced disease presentation, with lower PFS and overall survival.
C1 [Rasmy, Ayman] Zagazig Univ Hosp, Med Oncol, Zagazig, Egypt.
   [Rasmy, Ayman] King Saud Med City, Oncol Dept, Riyadh, Saudi Arabia.
   [Rasmy, Ayman] King Fahad Specialist Hosp, Oncol Dept, Dammam, Saudi Arabia.
   [Fayed, Alaa] Zagazig Univ, Clin Oncol Dept, Zagazig, Egypt.
   [Omar, Ayman; Fahmy, Nermin] Suez Canal Univ, Clin Oncol & Nucl Med Dept, Ismailia, Egypt.
   [Omar, Ayman; Fahmy, Nermin] King Faisal Specialist Hosp & Res Ctr, Oncol Dept, Riyadh, Saudi Arabia.
C3 Egyptian Knowledge Bank (EKB); Zagazig University; King Saud Medical
   City; Egyptian Knowledge Bank (EKB); Zagazig University; Egyptian
   Knowledge Bank (EKB); Suez Canal University; King Faisal Specialist
   Hospital & Research Center
RP Rasmy, A (corresponding author), Zagazig Univ, Zagazig, Egypt.
EM ay_rasmy@yahoo.com
RI Rasmy, Ayman/AFU-8429-2022
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NR 18
TC 8
Z9 10
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 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD OCT
PY 2019
VL 10
IS 5
BP 886
EP 895
DI 10.21037/jgo.2019.05.04
PG 10
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA JB0KV
UT WOS:000488243500008
PM 31602326
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Seidlitz, T
   Stange, DE
AF Seidlitz, Therese
   Stange, Daniel E.
TI Gastrointestinal cancer organoids-applications in basic and
   translational cancer research
SO EXPERIMENTAL AND MOLECULAR MEDICINE
LA English
DT Review
ID COMPREHENSIVE MOLECULAR CHARACTERIZATION; STEM-CELL NICHE;
   COLORECTAL-CANCER; HUMAN COLON; HUMAN LIVER; IN-VITRO; TUMOR; MODELS;
   MOUSE; TRANSPLANTATION
AB Cancer is a major health problem and a leading cause of death worldwide. Early cancer detection and continuous changes in treatment strategies have improved overall patient survival. The recent development of targeted drugs offers new opportunities for personalized cancer treatment. Nevertheless, individualized treatment is accompanied by the need for biomarkers predicting the response of a patient to a certain drug. One of the most promising breakthroughs in recent years that might help to overcome this problem is the organoid technology. Organoid cultures exhibit self-renewal capacity, self-organization, and long-term proliferation, while recapitulating many aspects of their primary tissue. Generated patient-derived organoid (PDO) libraries constitute "living" biobanks, allowing the in-depth analysis of tissue function, development, tumor initiation, and cancer pathobiology. Organoids can be derived from all gastrointestinal tissues, including esophageal, gastric, liver, pancreatic, small intestinal and colorectal tissues, and cancers of these tissues. PDOs are amenable to various techniques, including sequencing analyses, drug screening, targeted therapy testing, tumor microenvironment studies, and genetic engineering capabilities. In this review, we discuss the different applications of gastrointestinal organoids in basic cancer biology and clinical translation.
   Cancer: personalized models of gastrointestinal tumors Three-dimensional mini-organs or "organoids" derived from patients with gastrointestinal tumors can offer new insights into cancer biology and guide the selection of appropriate therapies. By cultivating gastrointestinal tumor cells with an appropriate combination of growth factors, researchers can generate organoids that recapitulate key features of the original malignancy in miniature. Therese Seidlitz and Daniel E. Stange from the University Hospital Carl Gustav Carus in Dresden, Germany have reviewed the use of such models for cancer research and clinical care. These organoids can be used to identify the treatment strategies most likely to be effective in a given patient, or to assess differences between primary tumors and their metastases. Researchers can also genetically manipulate organoids made from healthy tissue to study the biological pathways that contribute to tumor development and disease progression in cancer patients.
C1 [Seidlitz, Therese; Stange, Daniel E.] Tech Univ Dresden, Dept Visceral Thorac & Vasc Surg, Fac Med, Dresden, Germany.
   [Seidlitz, Therese; Stange, Daniel E.] Tech Univ Dresden, Univ Hosp Carl Gustav Carus, Dresden, Germany.
   [Stange, Daniel E.] Natl Ctr Tumor Dis NCT, Dresden, Germany.
   [Stange, Daniel E.] German Canc Res Ctr, Heidelberg, Germany.
   [Stange, Daniel E.] Helmholtz Zentrum Dresden Rossendorf HZDR, Dresden, Germany.
C3 Technische Universitat Dresden; Technische Universitat Dresden; Carl
   Gustav Carus University Hospital; Helmholtz Association; German Cancer
   Research Center (DKFZ); Ruprecht Karls University Heidelberg; Helmholtz
   Association; German Cancer Research Center (DKFZ); Helmholtz
   Association; Helmholtz-Zentrum Dresden-Rossendorf (HZDR)
RP Stange, DE (corresponding author), Tech Univ Dresden, Dept Visceral Thorac & Vasc Surg, Fac Med, Dresden, Germany.; Stange, DE (corresponding author), Tech Univ Dresden, Univ Hosp Carl Gustav Carus, Dresden, Germany.; Stange, DE (corresponding author), Natl Ctr Tumor Dis NCT, Dresden, Germany.; Stange, DE (corresponding author), German Canc Res Ctr, Heidelberg, Germany.; Stange, DE (corresponding author), Helmholtz Zentrum Dresden Rossendorf HZDR, Dresden, Germany.
EM daniel.stange@uniklinikum-dresden.de
RI Stange, Daniel/O-1837-2015
OI Seidlitz, Therese/0000-0001-7367-5525
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NR 88
TC 20
Z9 21
U1 1
U2 34
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 1226-3613
EI 2092-6413
J9 EXP MOL MED
JI Exp. Mol. Med.
PD OCT
PY 2021
VL 53
IS 10
BP 1459
EP 1470
DI 10.1038/s12276-021-00654-3
EA OCT 2021
PG 12
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine
GA WS5ID
UT WOS:000708379400006
PM 34663939
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Li, S
   Cong, XL
   Gao, HY
   Lan, XW
   Li, ZG
   Wang, WP
   Song, SB
   Wang, YM
   Li, CF
   Zhang, HF
   Xue, YW
   Zhao, YZ
AF Li, Sen
   Cong, Xiliang
   Gao, Hongyu
   Lan, Xiuwen
   Li, Zhiguo
   Wang, Wenpeng
   Song, Shubin
   Wang, Yimin
   Li, Chunfeng
   Zhang, Hongfeng
   Xue, Yingwei
   Zhao, Yuzhou
TI Tumor-associated neutrophils induce EMT by IL-17a to promote migration
   and invasion in gastric cancer cells
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Article
DE Gastric cancer; Neutrophils; IL-17a; Epithelial mesenchymal transition;
   Migration and invasion
ID EPITHELIAL-MESENCHYMAL TRANSITION; COLORECTAL-CANCER; LYMPHOCYTE RATIO;
   PATHWAY; PROGRESSION; METASTASIS; ANGIOGENESIS; INFLAMMATION;
   FIBROBLASTS; ACTIVATION
AB PurposeEpithelial to mesenchymal transition (EMT) can contribute to gastric cancer (GC) progression and recurrence following therapy. Tumor-associated neutrophils (TANs) are associated with poor outcomes in a variety of cancers. However, it is not clear whether TANs interact with the EMT process during GC development.MethodsImmunohistochemistry was performed to examine the distribution and levels of CD66+neutrophils in samples from 327 patients with GC. CD66b+TANs were isolated either directly from GC cell suspensions or were conditioned from healthy donor peripheral blood polymorphonuclear neutrophils (PMNs) stimulated with tumor tissue culture supernatants (TTCS) and placed into co-culture with MKN45 or MKN74 cells, after which migration, invasion and EMT were measured. Interleukin-17a (IL-17a) was blocked with a polyclonal antibody, and the STAT3 pathway was blocked with the specific inhibitor AG490.ResultsNeutrophils were widely distributed in gastric tissues of patients with GC and were enriched predominantly at the invasion margin. Neutrophil levels at the invasion margin were an independent predictor of poor disease-free survival (DFS) and disease-specific survival (DSS). IL-17a+neutrophils constituted a large portion of IL-17a-producing cells in GC, and IL-17a was produced at the highest levels in co-culture compared with that in TANs not undergoing co-culture. TANs enhanced the migration, invasion and EMT of GC cells through the secretion of IL-17a, which activated the Janus kinase 2/signal transducers and activators of transcription (JAK2/STAT3) pathway in GC cells, while deprivation of IL-17a using a neutralizing antibody or inhibition of the JAK2/STAT3 pathway with AG490 markedly reversed these TAN-induced phenotypes in GC cells induced by TANs.ConclusionsNeutrophils correlate with tumor stage and predict poor prognosis in GC. TANs produce IL-17a, which promotes EMT of GC cells through JAK2/STAT3 signalling. Blockade of IL-17a signalling with a neutralizing antibody inhibits TAN-stimulated activity in GC cells. Therefore, IL-17a-targeted therapy might be used to treat patients with GC.
C1 [Li, Sen; Zhao, Yuzhou] Zhengzhou Univ, Affiliated Canc Hosp, Dept Gen Surg, 127 Dong Ming Rd, Zhengzhou 450008, Henan, Peoples R China.
   [Li, Sen; Cong, Xiliang; Gao, Hongyu; Lan, Xiuwen; Li, Zhiguo; Song, Shubin; Wang, Yimin; Li, Chunfeng; Zhang, Hongfeng; Xue, Yingwei] Harbin Med Univ, Dept Gastroenterol Surg, Canc Hosp, 150 Ha Ping Rd, Harbin 150081, Heilongjiang, Peoples R China.
   [Wang, Wenpeng] Chinese Acad Med Sci, Dept Gynecol Oncol, Canc Hosp, Beijing, Peoples R China.
   [Wang, Wenpeng] Peking Union Med Coll, Beijing, Peoples R China.
C3 Zhengzhou University; Harbin Medical University; Chinese Academy of
   Medical Sciences - Peking Union Medical College; Chinese Academy of
   Medical Sciences - Peking Union Medical College; Peking Union Medical
   College
RP Zhao, YZ (corresponding author), Zhengzhou Univ, Affiliated Canc Hosp, Dept Gen Surg, 127 Dong Ming Rd, Zhengzhou 450008, Henan, Peoples R China.; Xue, YW (corresponding author), Harbin Med Univ, Dept Gastroenterol Surg, Canc Hosp, 150 Ha Ping Rd, Harbin 150081, Heilongjiang, Peoples R China.
EM xueyingwei@hrbmu.edu.cn; 15776835073@163.com
RI Li, zhiguo/AGZ-7951-2022; Wang, Wenpeng/HRC-9099-2023
OI Zhang, Hongfeng/0009-0001-3186-3357
FU Harbin Medical University Cancer Hospital [Nn10PY2017-03]
FX This study was supported by a grant from the Harbin Medical University
   Cancer Hospital. No: Nn10PY2017-03.
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NR 45
TC 185
Z9 204
U1 5
U2 43
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 7
PY 2019
VL 38
AR 6
DI 10.1186/s13046-018-1003-0
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HG7EE
UT WOS:000455150800001
PM 30616627
OA gold, Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Vigarios, E
   Epstein, JB
   Sibaud, V
AF Vigarios, Emmanuelle
   Epstein, Joel B.
   Sibaud, Vincent
TI Oral mucosal changes induced by anticancer targeted therapies and immune
   checkpoint inhibitors
SO SUPPORTIVE CARE IN CANCER
LA English
DT Review
DE Mucosal changes; Oral cavity; Mucositis; Stomatitis; Mucosal
   sensitivity; Dysgeusia; Xerostomia; Lichenoid reaction; Hyperkeratotic
   lesion; Oral squamous cell carcinoma; Benign migratory glossitis;
   Hyperpigmentation; Angiogenesis inhibitors; EGFR inhibitors; BRAF
   inhibitors; mTOR inhibitors; BCR-ABL inhibitor; Cancer; Targeted
   therapies; Immune checkpoint inhibitors; Immunotherapy; Oral adverse
   events; Osteonecrosis of jaw; mIAS; Telangiectasias; Anti-PD-1
ID RENAL-CELL CARCINOMA; METASTATIC COLORECTAL-CANCER; MEDICATION-RELATED
   OSTEONECROSIS; CLINICAL-PRACTICE GUIDELINES; PLATINUM-BASED THERAPY;
   LONG-TERM SAFETY; PHASE-III TRIAL; OPEN-LABEL; LUNG-CANCER; ADVERSE
   EVENTS
AB Development of biological targeted therapies and immune checkpoint inhibitors has redefined the treatment for many cancers; however, the increasing use of new protocols has led to physicians observing a new spectrum of toxicities. To date, oral adverse events induced by these new anticancer therapies have been mainly reported using nonspecific terminology ("stomatitis," "mucosal inflammation," "mucositis") and remain poorly characterized, with the exception of mammalian target of rapamycin (mTOR) inhibitor-associated stomatitis. Oral toxicities of targeted therapies often display very characteristic features which clearly differ from classic oral injuries observed with cytotoxic chemotherapy and/or radiotherapy. In addition, they frequently affect more than 20% of treated patients and can lead to a significant morbidity or permanent treatment discontinuation. Oral mucosal toxicities described in this review include mTOR inhibitor-associated stomatitis (mIAS); stomatitis, benign migratory glossitis, and osteonecrosis of the jaw associated with multi-targeted kinase inhibitors of the VEGF and PDGF receptors; mucositis induced by EGFR inhibitors (in monotherapy or in combination with head and neck radiotherapy and/or chemotherapy); hyperkeratotic lesions with BRAF inhibitors; pigmentary changes and lichenoid reactions secondary to imatinib; and more recent data on the "Osler-Weber-Rendu-like syndrome" described with the antibody-drug conjugate, TDM-1. Finally, we provide, to our knowledge, the first available structured data on oral toxicities induced by the new recently FDA-and EMA-approved monoclonal antibodies targeting PD-1. Clinical management of these targeted therapy-related oral changes is also discussed.
C1 [Vigarios, Emmanuelle; Sibaud, Vincent] Inst Univ Canc Toulouse Oncopole, Inst Claudius Regaud, Dept Oral Med, 1 Ave Irene Joliot Curie, F-31059 Toulouse, France.
   [Vigarios, Emmanuelle] UFR Odontol 1, 1 Chemin Maraichers, F-31062 Toulouse, France.
   [Epstein, Joel B.] Cedars Sinai Hlth Syst, Samuel Oschin Comprehens Canc Inst, Los Angeles, CA USA.
   [Epstein, Joel B.] City Hope Natl Med Ctr, Otolaryngol & Head & Neck Surg, 1500 E Duarte Rd, Duarte, CA 91010 USA.
   [Sibaud, Vincent] Inst Univ Canc Toulouse Oncopole, Inst Claudius Regaud, Oncodermatol Dept, Toulouse, France.
C3 UNICANCER; Institut Claudius Regaud; Cedars Sinai Medical Center; City
   of Hope; UNICANCER; Institut Claudius Regaud
RP Vigarios, E (corresponding author), Inst Univ Canc Toulouse Oncopole, Inst Claudius Regaud, Dept Oral Med, 1 Ave Irene Joliot Curie, F-31059 Toulouse, France.; Vigarios, E (corresponding author), UFR Odontol 1, 1 Chemin Maraichers, F-31062 Toulouse, France.
EM vigarios.emmanuelle@iuct-oncopole.fr
RI Sibaud, Vincent/P-6270-2014; Vigarios, Emmanuelle/A-7576-2015
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NR 182
TC 114
Z9 124
U1 0
U2 29
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 MAY
PY 2017
VL 25
IS 5
BP 1713
EP 1739
DI 10.1007/s00520-017-3629-4
PG 27
WC Oncology; Health Care Sciences & Services; Rehabilitation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Health Care Sciences & Services; Rehabilitation
GA ER9NM
UT WOS:000399153200040
PM 28224235
OA Bronze
DA 2025-01-04
ER

PT J
AU Bang, H
   Lee, MS
   Sung, M
   Choi, J
   An, S
   Kim, SH
   Lee, SE
   Choi, YL
AF Bang, Heejin
   Lee, Mi-Sook
   Sung, Minjung
   Choi, Juyoung
   An, Sungbin
   Kim, Seok-Hyung
   Lee, Seung Eun
   Choi, Yoon-La
TI <i>NTRK</i> Fusions in 1113 Solid Tumors in a Single Institution
SO DIAGNOSTICS
LA English
DT Article
DE NTRK fusion; TRK immunohistochemistry; next-generation sequencing; TRK
   inhibitors; lung cancer; colon cancer; inflammatory myofibroblastic
   tumor
ID INFLAMMATORY MYOFIBROBLASTIC TUMORS; PAN-TRK IMMUNOHISTOCHEMISTRY;
   ETV6-NTRK3 GENE FUSION; ROS1; ALK; REARRANGEMENT; ENTRECTINIB;
   EXPRESSION; CARCINOMA
AB Simple Summary: Recently, there has been increasing interest in identifying NTRK fusions in various tumors, as they are therapeutically targetable driver mutations. In tumor types with low-frequency NTRK fusions, recent recommendations on NTRK testing recommend pan-Trk immunohistochemistry (IHC) as the initial screening test to validate pan-Trk expression cases with next- generation sequencing (NGS) assays. This retrospective study was conducted on 1113 solid tumor samples (510 non-small cell lung cancers, 503 colorectal cancers, and 100 inflammatory myofibroblastic tumors) to evaluate using pan-Trk IHC assay, and TRK expression cases were followed by validation with NGS. We investigated the accuracy of an IHC assay in detecting NTRK fusions and characterizing the clinicopathological and molecular features of NTRK-rearranged common tumors. Despite its rarity, this study confirms the importance of identifying potential target groups based on the pathological and immunohistochemical characteristics of NTRK fusion-driven solid tumors for effective targeted therapy.
   Most NTRK fusions occur at very low frequencies in various common cancers. Recent recommendations on NTRK testing recommend immunohistochemistry (IHC) as the initial test for tumor types with a low frequency of NTRK fusions. This study investigated the accuracy of an IHC assay to detect NTRK fusions and characterize the clinicopathological and molecular features of NTRK-rearranged tumors. This retrospective study was conducted on 1113 solid tumor samples known to harbor no oncogenic driver alterations, including 510 non-small cell lung cancers (NSCLC), 503 colorectal cancers (CRC), and 79 inflammatory myofibroblastic tumors (IMT). Additionally, 21 ALK expression-positive cases were included. TRK expression was evaluated using a pan-Trk IHC assay, and positive cases were validated using NGS. TRK expression was observed in three NSCLCs (0.6%), six CRCs (1.2%), and six IMTs (6%). NTRK fusions were finally detected in two NSCLCs (0.4%), six CRCs (1.2%), and one IMT (1%). In NSCLC and CRC, the majority of NTRK fusions were readily discernible due to diffuse moderate-to-strong cytoplasmic staining on pan-Trk IHC. In IMT, focal weak nuclear staining indicated the presence of NTRK fusion. Therefore, the utility of pan-Trk IHC should be assessed considering that the difference in performance depends on tumor type.
C1 [Bang, Heejin; Lee, Seung Eun] Konkuk Univ, Med Ctr, Sch Med, Dept Pathol, Seoul 05030, South Korea.
   [Lee, Mi-Sook; Sung, Minjung; Choi, Juyoung; An, Sungbin; Choi, Yoon-La] Sungkyunkwan Univ, Samsung Med Ctr, Sch Med, Lab Theranot & Mol Pathol, Seoul 06351, South Korea.
   [Lee, Mi-Sook; An, Sungbin; Choi, Yoon-La] Sungkyunkwan Univ, Dept Hlth Sci & Technol, SAIHST, Seoul 06351, South Korea.
   [Kim, Seok-Hyung; Choi, Yoon-La] Sungkyunkwan Univ, Samsung Med Ctr, Sch Med, Dept Pathol & Translat Genom, Seoul 06351, South Korea.
C3 Konkuk University; Konkuk University Medical Center; Sungkyunkwan
   University (SKKU); Samsung Medical Center; Sungkyunkwan University
   (SKKU); Sungkyunkwan University (SKKU); Samsung Medical Center
RP Lee, SE (corresponding author), Konkuk Univ, Med Ctr, Sch Med, Dept Pathol, Seoul 05030, South Korea.; Choi, YL (corresponding author), Sungkyunkwan Univ, Samsung Med Ctr, Sch Med, Lab Theranot & Mol Pathol, Seoul 06351, South Korea.; Choi, YL (corresponding author), Sungkyunkwan Univ, Dept Hlth Sci & Technol, SAIHST, Seoul 06351, South Korea.; Choi, YL (corresponding author), Sungkyunkwan Univ, Samsung Med Ctr, Sch Med, Dept Pathol & Translat Genom, Seoul 06351, South Korea.
EM mars-21@hanmail.net; misook98@gmail.com; mjsung0111@gmail.com;
   juyoung.choi92@gmail.com; been9312@naver.com; platoshkim@daum.net;
   20150063@kuh.ac.kr; ylachoi@skku.edu
RI Lee, MI-Sook/HKO-0279-2023
OI lee, seungeun/0000-0002-7459-0061
FU National Research Foundation of Korea - Korean government
   [NRF-2016R1A5A2945889, 2021R1A2C4002158, 2022R1A2C2006322]
FX This study was supported by grants from National Research Foundation of
   Korea funded by the Korean government (NRF-2016R1A5A2945889,
   2021R1A2C4002158, and 2022R1A2C2006322).
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NR 41
TC 6
Z9 6
U1 0
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4418
J9 DIAGNOSTICS
JI Diagnostics
PD JUN
PY 2022
VL 12
IS 6
AR 1450
DI 10.3390/diagnostics12061450
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 2K2EZ
UT WOS:000816157100001
PM 35741260
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Sulaiman, S
   Arafat, K
   Iratni, R
   Attoub, S
AF Sulaiman, Shahrazad
   Arafat, Kholoud
   Iratni, Rabah
   Attoub, Samir
TI PTC-209 Anti-Cancer Effects Involved the Inhibition of STAT3
   Phosphorylation
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Article
DE PTC-219; Frondoside-A; cisplatin; Bmi-1; STAT3
ID STEM-CELLS; GROWTH; BMI1; FRONDOSIDE; INVASION
AB Introduction: Lung, breast, and colorectal cancers are the leading causes of cancer-related deaths despite many therapeutic options, including targeted therapy and immunotherapies. Methods: Here, we investigated the impact of PTC-209, a small-molecule Bmi-1 inhibitor, on human cancer cell viability alone and in combination with anticancer drugs, namely, cisplatin, oxaliplatin, 5-fluorouracil, camptothecin, and Frondoside-A and its impact on cellular migration and colony growth in vitro and on tumor growth in ovo. Results: We demonstrate that PTC-209 causes a concentration- and time-dependent decrease in the cellular viability of lung cancer cells (LNM35 and A549), breast cancer cells (MDA-MB-231 and T47D), and colon cancer cells (HT-29, HCT8/S11, and HCT-116). Similarly, treatment with PTC-209 significantly decreased the growth of LNM35, A549, MDA-MB-231, and HT-29 clones and colonies in vitro and LNM35 and A549 tumor growth in the in ovo tumor xenograft model. PTC-209 at the non-toxic concentrations significantly reduced the migration of lung (LNM35 and A549) and breast (MDA-MB-231) cancer cells. Moreover, we show that PTC-209, at a concentration of 1 mu M, enhances the anti-cancer effects of Frondoside-A in lung, breast, and colon cancer cells, as well as the effect camptothecin in breast cancer cells and the effect of cisplatin in lung cancer cells in vitro. However, PTC-209 failed to enhance the anti-cancer effects of oxaliplatin and 5-fluorouracil in colon cancer cells. Treatment of lung, breast, and colon cancer cells with PTC-209 (1 and 2.5 mu M) for 48 h showed no caspase-3 activation, but a decrease in the cell number below the seeding level suggests that PTC-209 reduces cellular viability probably through inhibition of cell proliferation and induction of cell death via a caspase-3-independent mechanism. Molecular mechanism analysis revealed that PTC-209 significantly inhibited the STAT3 phosphorylation by decreasing the expression level of gp130 as early as 30 min post-treatment. Conclusion: Our findings identify PTC-209 as a promising anticancer agent for the treatment of solid tumors either alone and/or in combination with the standard cytotoxic drugs cisplatin and camptothecin and the natural product Frondoside-A.
C1 [Sulaiman, Shahrazad; Arafat, Kholoud; Attoub, Samir] United Arab Emirates Univ, Coll Med & Hlth Sci, Dept Pharmacol & Therapeut, Al Ain, U Arab Emirates.
   [Iratni, Rabah] United Arab Emirates Univ, Coll Sci, Dept Biol, Al Ain, U Arab Emirates.
   [Attoub, Samir] INSERM, Paris, France.
C3 United Arab Emirates University; United Arab Emirates University;
   Institut National de la Sante et de la Recherche Medicale (Inserm)
RP Attoub, S (corresponding author), United Arab Emirates Univ, Coll Med & Hlth Sci, Dept Pharmacol & Therapeut, Al Ain, U Arab Emirates.; Attoub, S (corresponding author), INSERM, Paris, France.
EM samir.attoub@uaeu.ac.ae
RI Attoub, Samir/N-6852-2018
FU CMHS grant [31M275]; Terry Fox UAE [21M081]
FX This work was supported by the CMHS grant (31M275) and partly supported
   by the Terry Fox UAE grant (21M081). 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 22
TC 8
Z9 9
U1 0
U2 8
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 OCT 21
PY 2019
VL 10
AR 1199
DI 10.3389/fphar.2019.01199
PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA JL2TP
UT WOS:000495385000001
PM 31695609
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kasi, PM
   Afghan, MK
   Bellizzi, AM
   Chan, CH
AF Kasi, Pashtoon M.
   Afghan, Maaz Khan
   Bellizzi, Andrew M.
   Chan, Carlos H. F.
TI Larotrectinib in Mismatch-Repair-Deficient TRK Fusion-Positive
   Metastatic Colon Cancer After Progression on Immunotherapy
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Article
DE ntrk fusion; pembrolizumab; mismatch repair deficiency; microsatellite
   instability; liquid biopsy; larotrectinib; ipilimumab; colorectal
   cancer; circulating tumor dna
ID STAGE-II; NIVOLUMAB; PETACC-3; BRAF
AB A 43-year-old woman presented with recurrent metastatic colon cancer with metastases to the peritoneum after having initially been diagnosed with stage IIB colon cancer and deferring adjuvant chemotherapy. Circulating tumor DNA (ctDNA)-based liquid biopsy testing revealed microsatellite instability-high (MSI-H) status, which was also confirmed on tissue testing. This patient then underwent four cycles of pembrolizumab and two cycles of ipilimumab and nivolumab (CTLA-4 rescue) with, unfortunately, progression of the disease. The patient was subsequently treated with larotrectinib, given the findings of TRK fusion-positive cancer on next-generation sequencing (NGS), and she was able to undergo curative surgery two months later that showed complete pathologic response. She continues to have no evidence of disease years later as well as no detectable ctDNA on NGS as well as tumor-informed minimal residual disease platforms. This case represents a marked and durable response to larotrectinib in a patient with deficiency in mismatch repair/MSI-H metastatic colorectal cancer harboring an NTRKfusion, bringing to light the potential for use of larotrectinib in earlier treatment lines in patients, and/or choice of targeted therapy versus immunotherapy in this patient subset.
C1 [Kasi, Pashtoon M.] Weill Cornell Med, Oncology, New York, NY 10065 USA.
   [Afghan, Maaz Khan] Bolan Med Coll Complex Hosp, Oncol, Quetta, Pakistan.
   [Bellizzi, Andrew M.] Univ Iowa, Holden Comprehens Canc Ctr, Pathol, Iowa City, IA USA.
   [Chan, Carlos H. F.] Univ Iowa, Holden Comprehens Canc Ctr, Surg, Iowa City, IA USA.
C3 Cornell University; Weill Cornell Medicine; University of Iowa;
   University of Iowa
RP Kasi, PM (corresponding author), Weill Cornell Med, Oncology, New York, NY 10065 USA.
EM pmk4001@med.cornell.edu
RI Kasi, Pashtoon/M-2569-2019
OI Afghan, Muhammad Maaz Khan/0009-0005-5778-4971
CR André T, 2020, NEW ENGL J MED, V383, P2207, DOI 10.1056/NEJMoa2017699
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NR 23
TC 3
Z9 3
U1 0
U2 0
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD JUL 7
PY 2022
VL 14
IS 7
AR e26648
DI 10.7759/cureus.26648
PG 5
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA 3C1NV
UT WOS:000828398300028
PM 35815302
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Ezenkwa, US
   Ogun, GO
   Mashor, MI
   Ogunbiyi, OJ
AF Ezenkwa, Uchenna Simon
   Ogun, Gabriel Olabiyi
   Mashor, Mbwas Isaac
   Ogunbiyi, Olufemi John
TI EpCAM expression negatively regulates E-cadherin function in colorectal
   carcinomas
SO ECANCERMEDICALSCIENCE
LA English
DT Article
DE epithelial cell adhesion molecule; E-cadherin; colorectal carcinoma
ID CELL-ADHESION; CANCER; ANTIGEN; COLON; CAM
AB Background: This study aimed to characterise epithelial cell adhesion molecule (EpCAM) expression patterns in colorectal carcinomas (CRC) from Nigerian patients, its association with E-cadherin and tumour characteristics, to forecast patient selection for anti-EpCAM therapy among whom no data existed previously. Methods: Tissue microarray blocks of formalin-fixed and paraffin-embedded CRC tissues, with their non-cancer margins of resection, were sectioned and stained with EpCAM and E-cadherin primary antibodies. Scoring for antibody staining was done semiquantitatively by combining staining proportion and intensity. The outcome was correlated with patient age, gender and tumour histological parameters with p & LE; 0.05 regarded as statistically significant.Results: Sixty-three carcinoma tissues had staining status for the two markers and were included in this study. Of these, 36 (57.1%) showed positive EpCAM expression (immu-noscore & GE;3) out of which 83% (30/36 positive cases) were overexpressed (combined immunoscore & GE;4) while 12 (19%) tissues were positive for E-cadherin. Non-tumour mar- gins of resection tissues showed less EpCAM positivity in 24% (6/25) of histospots. The difference in staining between tumour and non-tumour margin tissues with EpCAM was significant (p < 0.001). Also, EpCAM overexpression was significantly associated with reduced E-cadherin (p < 0.035) expression in tumour cells. Tumour extent within the gut wall was equal (50% each) for early and late pT stages among EpCAM overexpressing tumours but two-thirds (8/12) of cases expressing E-cadherin had later pT stage para-doxically, while distant metastasis was negligible among tumours bearing both markers. Also, tumours overexpressing EpCAM had significant association with tumour-associated lymphocytes (p < 0.02 each). Conclusion: CRC in this study preferentially overexpress EpCAM over E-cadherin whose strong cell-cell contact inhibitory role is weakened even when expressed, resulting in further local tumour spread. This, and the observed immune response, supports targeted therapy among eligible patients.
C1 [Ezenkwa, Uchenna Simon] Fed Med Ctr Azare, Azare 751101, Bauchi, Nigeria.
   [Ogun, Gabriel Olabiyi; Ogunbiyi, Olufemi John] Univ Coll Hosp, Dept Pathol, Ibadan 200285, Oyo, Nigeria.
   [Mashor, Mbwas Isaac] Bringham Univ, Dept Pathol, Jos 930105, Plateau, Nigeria.
RP Ogunbiyi, OJ (corresponding author), Univ Coll Hosp, Dept Pathol, Ibadan 200285, Oyo, Nigeria.
EM fogunbiyi@gmail.com
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NR 34
TC 0
Z9 0
U1 0
U2 0
PU eCancer Global Foundation
PI Bristol
PA 13 King Square Avenue, Bristol, UNITED KINGDOM
SN 1754-6605
J9 ECANCERMEDICALSCIENC
JI eCancerMedicalScience
PD JUL 6
PY 2023
VL 17
AR 1569
DI 10.3332/ecancer.2023.1569
PG 11
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA L9JH7
UT WOS:001026349500001
PM 37533952
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Sun, LT
   Meng, C
   Zhang, ZT
   Luo, Y
   Yang, ZY
   Yao, HW
AF Sun, Liting
   Meng, Cong
   Zhang, Zhongtao
   Luo, Yao
   Yang, Zhengyang
   Yao, Hongwei
TI Opportunities and challenges of indocyanine green in gastrointestinal
   cancers for intraoperative and nano-medicine application
SO CANCER NANOTECHNOLOGY
LA English
DT Review
DE Gastrointestinal cancers; Indocyanine green; Sentinel lymph node;
   Nanoparticle; Target delivery
ID SENTINEL NODE NAVIGATION; EARLY GASTRIC-CANCER; RECTAL-CANCER; PERFUSION
   ASSESSMENT; LYMPH-NODES; BLUE-DYE; SURGERY; RESECTION; NANOPARTICLES;
   MANAGEMENT
AB The morbidity and mortality of gastrointestinal tumours remain high worldwide. Surgical resection is currently the most critical radical therapeutic schedule, while postoperative complications and sentinel lymph node (SLN) identification are closely related to the outcome. Indocyanine green (ICG)-mediated fluorescence imaging is increasingly being used in gastrointestinal surgery. It has been embraced by various surgical disciplines as a potential method to improve lymph node detection and enhance surgical field visualization. ICG can passively concentrate in SLN because of enhanced permeation and retention effects. After excitation by near-infrared light devices, SLN can display higher intensity fluorescence, helping visualization for better lymph node dissection. In addition, visual assessment of intestinal blood flow through ICG may reduce the incidence of anastomotic leakage. Although it has good clinical application, ICG-imaging still faces some problems, such as a higher false-negative rate, poorly targeted biodistribution, and lower fluorescence contrast, due to the lack of active tumour targeting. Thus, different ICG-coupled nanoparticles with inherent characteristics or functional modification-enhanced SLN identification features for gastrointestinal cancers bring benefit through active tumour targeting, superior tumour-background ratio, and high resolution. Nano-ICG combined with potential substances, including enhanced imaging contrast and/or combination therapy (chemotherapy, targeted therapy, immunotherapy, etc.), have been packaged and accumulated in the tumour area through active targeting for multimodal imaging and treatment. In this review, we outline the intraoperative application and possible future nanodirections of ICG in gastrointestinal cancer. The prospects and challenges of nano-ICG diagnostic and therapeutic methods in clinical applications are also discussed.
C1 [Sun, Liting; Meng, Cong; Zhang, Zhongtao; Yang, Zhengyang; Yao, Hongwei] Capital Med Univ, Beijing Friendship Hosp, Dept Gen Surg, Beijing, Peoples R China.
   [Sun, Liting; Meng, Cong; Zhang, Zhongtao; Yang, Zhengyang; Yao, Hongwei] Natl Clin Res Ctr Digest Dis, Beijing, Peoples R China.
   [Luo, Yao] Sichuan Univ, West China Hosp, Dept Lab Med, Chengdu, Peoples R China.
C3 Capital Medical University; Sichuan University
RP Yang, ZY; Yao, HW (corresponding author), Capital Med Univ, Beijing Friendship Hosp, Dept Gen Surg, Beijing, Peoples R China.; Yang, ZY; Yao, HW (corresponding author), Natl Clin Res Ctr Digest Dis, Beijing, Peoples R China.; Luo, Y (corresponding author), Sichuan Univ, West China Hosp, Dept Lab Med, Chengdu, Peoples R China.
EM luoyao@scu.edu.cn; doctoryangzy@163.com; yaohongwei@ccmu.edu.cn
RI Yang, Zhengyang/V-6233-2019; Zhang, Zhongtao/AAE-2185-2021; Luo,
   Yao/HSE-6408-2023
OI Yao, Hongwei/0000-0003-3995-6520; Yang, Zhengyang/0000-0002-2640-9619;
   Luo, Yao/0000-0002-4542-3504
FU National Key Technologies RD Program
FX We thank Figdraw (www.figdraw.com) for supporting some figures drawing.
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NR 99
TC 0
Z9 0
U1 14
U2 40
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 2024
VL 15
IS 1
AR 12
DI 10.1186/s12645-024-00251-9
PG 22
WC Oncology; Nanoscience & Nanotechnology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Science & Technology - Other Topics
GA GY2Q3
UT WOS:001156174000001
OA gold
DA 2025-01-04
ER

PT J
AU Geng, YT
   Xia, W
   Zheng, X
   Chen, LJ
   Zhou, Y
   Feng, J
   Yuan, Y
   Zhang, MY
   Lu, JW
   Wei, SS
   Hu, WW
AF Geng, Yiting
   Xia, Wei
   Zheng, Xiao
   Chen, Lujun
   Zhou, You
   Feng, Jun
   Yuan, Ye
   Zhang, Mingyue
   Lu, Jianwen
   Wei, Shanshan
   Hu, Wenwei
TI Targeted delivery of FAK siRNA by engineered exosomes to reverse
   cetuximab resistance via activating paraptosis in colon cancer
SO APOPTOSIS
LA English
DT Article
DE Colorectal cancer; Cetuximab resistance; Paraptosis; FAK; Engineered
   exosome
ID FOCAL-ADHESION KINASE; THERAPY; LANDSCAPE; CELLS; KRAS
AB BackgroundCetuximab is extensively used in the treatment of metastatic colorectal cancer (mCRC). However, resistance poses a significant challenge to successful therapy. Recently, paraptosis, a non-classical programmed cell death, has garnered increased attention for its potential application value in antitumor treatments. We aimed to identify the essential pathways and signaling molecules involved in paraptosis inhibition and select them as therapeutic targets in cetuximab resistance. Additionally, engineered exosome technology is used as a drug delivery system with both targeted and effector properties.ResultsBy comparing the differential expression of paraptosis-related genes between drug-resistant colon cancer cells and sensitive cells, it was observed that the paraptosis level induced by cetuximab was significantly downregulated in drug-resistant cells. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis identified the focal adhesion kinase (FAK) signaling pathway as a key pathway involved in the suppression of paraptosis. The biological function of FAK in cetuximab-resistant cells was investigated through cell morphology observation, CCK-8 assay, colony formation assay, RT-qPCR, Western Blot, and loss-of-function experiments. The results showed that the FAK signaling pathway was significantly upregulated in cetuximab-resistant colon cancer cells, and siRNA interference targeting FAK could notably inhibit cell proliferation while upregulating the paraptosis level. Based on this, engineered colon cancer cells targeted and FAK siRNA loaded exosomes (CT-Exo-siFAK1) were constructed. In vitro experiments, CT-Exo-siFAK1 could effectively activate paraptosis and inhibit the proliferation of drug-resistant colon cancer cells. In vivo experiments also confirmed that CT-Exo-siFAK1 significantly suppressed tumor growth and metastasis while upregulating the paraptosis level.ConclusionThis study suggests that FAK signaling pathway-mediated inhibition of paraptosis levels is crucial in the sensitivity of cetuximab targeted therapy in colon cancer, and the use of engineered exosomes to deliver FAK siRNA may be an effective strategy to reverse cetuximab resistance.
C1 [Geng, Yiting; Xia, Wei; Feng, Jun; Yuan, Ye; Zhang, Mingyue; Lu, Jianwen; Wei, Shanshan; Hu, Wenwei] Soochow Univ, Dept Oncol, Affiliated Hosp 3, 185 Juqian St, Changzhou 213003, Peoples R China.
   [Zheng, Xiao; Chen, Lujun; Zhou, You; Hu, Wenwei] Soochow Univ, Affiliated Hosp 3, Jiangsu Engn Res Ctr Tumor Immunotherapy, Changzhou 213003, Peoples R China.
   [Zheng, Xiao; Chen, Lujun; Zhou, You] Soochow Univ, Affiliated Hosp 3, Tumor Biol Diag & Treatment Ctr, Changzhou 213003, Peoples R China.
   [Zheng, Xiao; Chen, Lujun; Zhou, You] Soochow Univ, Inst Cell Therapy, Changzhou 213003, Peoples R China.
C3 Soochow University - China; Soochow University - China; Soochow
   University - China; Soochow University - China
RP Hu, WW (corresponding author), Soochow Univ, Dept Oncol, Affiliated Hosp 3, 185 Juqian St, Changzhou 213003, Peoples R China.; Hu, WW (corresponding author), Soochow Univ, Affiliated Hosp 3, Jiangsu Engn Res Ctr Tumor Immunotherapy, Changzhou 213003, Peoples R China.
EM gyt1986@suda.edu.cn; xiawei9938@163.com; zhengxiao923@163.com;
   clj_sz@163.com; zhouyounew@163.com; sudafj92@sina.com;
   yuanye.198705@163.com; zhangmingyue0817@163.com; a17648241356@163.com;
   wss19855827821@163.com; huwenwei@suda.edu.cn
RI Lu, Jianwen/AAG-9842-2019; zhang, ying/HJB-1230-2022
FU National Natural Science Foundation of China [82002479]; Role of
   Beta-glucans in Regulating the Intratumoral Microbiota of Colorectal
   Adenomatous Polyps [ZD202302:KY20241785]; Changzhou "14th Five-Year
   Plan" High-level Health Personnel Training Project [2022260: KY20221354,
   KY20221355]
FX This work was supported by the National Natural Science Foundation of
   China (No. 82002479), the Role of Beta-glucans in Regulating the
   Intratumoral Microbiota of Colorectal Adenomatous Polyps
   (ZD202302:KY20241785), Changzhou "14th Five-Year Plan" High-level Health
   Personnel Training Project (No. 2022260: KY20221354, KY20221355).
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NR 48
TC 0
Z9 0
U1 7
U2 7
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1360-8185
EI 1573-675X
J9 APOPTOSIS
JI Apoptosis
PD DEC
PY 2024
VL 29
IS 11-12
BP 1959
EP 1977
DI 10.1007/s10495-024-01986-x
EA JUL 2024
PG 19
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA L6D8Y
UT WOS:001263593400001
PM 38960944
OA hybrid
DA 2025-01-04
ER

PT J
AU Li, J
   Jiang, JL
   Chen, YM
   Lu, WQ
AF Li, Jia
   Jiang, Ji Ling
   Chen, Yi Mei
   Lu, Wei Qi
TI KLF2 inhibits colorectal cancer progression and metastasis by inducing
   ferroptosis via the PI3K/AKT signaling pathway
SO JOURNAL OF PATHOLOGY CLINICAL RESEARCH
LA English
DT Article
DE colorectal cancer; KLF2; ferroptosis; metastasis; pathway
ID CELL LUNG-CANCER; ACTIVATION; PROLIFERATION; TRANSCRIPTION; CONTRIBUTES;
   APOPTOSIS; PROMOTES; GPX4
AB Kruppel-like factor 2 (KLF2) belongs to the zinc finger family and is thought to be a tumor suppressor gene due to its low expression in various cancer types. However, its functional role and molecular pathway involvement in colorectal cancer (CRC) are not well defined. Herein, we investigated the potential mechanism of KLF2 in CRC cell invasion, migration, and epithelial-mesenchymal transition (EMT). We utilized the TCGA and GEPIA databases to analyze the expression of KLF2 in CRC patients and its correlation with different CRC stages and CRC prognosis. RT-PCR, western blot, and immunohistochemistry assays were used to measure KLF2 expression. Gain-of-function assays were performed to evaluate the role of KLF2 in CRC progression. Moreover, mechanistic experiments were conducted to investigate the molecular mechanism and involved signaling pathways regulated by KLF2. Additionally, we also conducted a xenograft tumor assay to evaluate the role of KLF2 in tumorigenesis. KLF2 expression was low in CRC patient tissues and cell lines, and low expression of KLF2 was associated with poor CRC prognosis. Remarkably, overexpressing KLF2 significantly inhibited the invasion, migration, and EMT capabilities of CRC cells, and tumor growth in xenografts. Mechanistically, KLF2 overexpression induced ferroptosis in CRC cells by regulating glutathione peroxidase 4 expression. Moreover, this KLF2-dependent ferroptosis in CRC cells was mediated by inhibiting the PI3K/AKT signaling pathway that resulted in the suppression of invasion, migration, and EMT of CRC cells. We report for the first time that KLF2 acts as a tumor suppressor in CRC by inducing ferroptosis via inhibiting the PI3K/AKT signaling pathway, thus providing a new direction for CRC prognosis assessment and targeted therapy.
C1 [Li, Jia; Jiang, Ji Ling] Shenzhen Tradit Chinese Med Hosp, Dept Gen Surg, Shenzhen, Peoples R China.
   [Chen, Yi Mei] Shenzhen Women & Childrens Hlth Care Hosp, Dept Breast Surg, Shenzhen, Peoples R China.
   [Lu, Wei Qi] Guangzhou Univ Chinese Med, Dept Gastrointestinal Surg, Affiliated Hosp 1, 16 Airport Rd, Guangzhou 510405, Peoples R China.
C3 Shenzhen Traditional Chinese Medicine Hospital; Guangzhou University of
   Chinese Medicine
RP Lu, WQ (corresponding author), Guangzhou Univ Chinese Med, Dept Gastrointestinal Surg, Affiliated Hosp 1, 16 Airport Rd, Guangzhou 510405, Peoples R China.
EM luweiqi9749@163.com
RI chen, yimei/KHX-1520-2024
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NR 44
TC 22
Z9 22
U1 2
U2 12
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2056-4538
J9 J PATHOL CLIN RES
JI J. Pathol. Clin. Res.
PD SEP
PY 2023
VL 9
IS 5
BP 423
EP 435
DI 10.1002/cjp2.325
EA MAY 2023
PG 13
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA N8MY4
UT WOS:001033204800001
PM 37147883
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Durslewicz, J
   Klimaszewska-Wisniewska, A
   Antosik, P
   Kasperska, A
   Grzanka, D
   Szylberg, T
   Szylberg, L
AF Durslewicz, Justyna
   Klimaszewska-Wisniewska, Anna
   Antosik, Paulina
   Kasperska, Anna
   Grzanka, Dariusz
   Szylberg, Tadeusz
   Szylberg, Lukasz
TI Detection of BRAF V600E Mutation in Ganglioglioma and Pilocytic
   Astrocytoma by Immunohistochemistry and Real-Time PCR-Based Idylla Test
SO DISEASE MARKERS
LA English
DT Article
ID DYSEMBRYOPLASTIC NEUROEPITHELIAL TUMORS; BRAF(V600E) MUTATION;
   COLORECTAL-CARCINOMA; BRAF-V600E MUTATION; MELANOMA; PROTEIN; SYSTEM;
   TRANSCRIPT; LANDSCAPE; RELEVANCE
AB The BRAF V600E mutation is an important oncological target in certain central nervous system (CNS) tumors, for which a possible application of BRAF-targeted therapy grows continuously. In the present study, we aim to determine the prevalence of BRAF V600E mutations in a series of ganglioglioma (GG) and pilocytic astrocytoma (PA) cases. Simultaneously, we decided to verify whether the combination of fully automated tests-BRAF-VE1 immunohistochemistry (IHC) and Idylla BRAF mutation assay-may be useful to accurately predict it in the case of specified CNS tumors. The study included 49 formalin-fixed, paraffin-embedded tissues, of which 15 were GG and 34 PA. Immunohistochemistry with anti-BRAF V600E (VE1) antibody was performed on tissue sections using the VentanaBenchMark ULTRA platform. All positive or equivocal cases on IHC and selected negative ones were further assessed using the Idylla BRAF mutation assay coupled with the Idylla platform. The BRAF-VE1 IHC was positive in 6 (6/49; 12.3%) and negative in 39 samples (39/49; 79.6%). The interpretation of immunostaining results was complicated in 4 cases, of which 1 tested positive for the Idylla BRAF mutation assay. Therefore, the overall positivity rate was 14.3%. This included 2 cases of GG and 5 cases of PA. Our study found that BRAF V600E mutations are moderately frequent in PA and GG and that for these tumor entities, IHC VE1 is suitable for screening purposes, but all negative, equivocal, and weak positive cases should be further tested with molecular biology techniques, of which the Idylla system seems to be a promising tool.
C1 [Durslewicz, Justyna; Klimaszewska-Wisniewska, Anna; Antosik, Paulina; Kasperska, Anna; Grzanka, Dariusz; Szylberg, Lukasz] Nicolaus Copernicus Univ Torun, Dept Clin Pathomorphol, Fac Med, Coll Med Bydgoszcz, PL-85092 Bydgoszcz, Poland.
   [Szylberg, Tadeusz; Szylberg, Lukasz] 10th Mil Res Hosp & Polyclin, PL-85681 Bydgoszcz, Poland.
C3 Nicolaus Copernicus University; Ludwik Rydygier Collegium Medicum
RP Klimaszewska-Wisniewska, A (corresponding author), Nicolaus Copernicus Univ Torun, Dept Clin Pathomorphol, Fac Med, Coll Med Bydgoszcz, PL-85092 Bydgoszcz, Poland.
EM justyna.durslewicz@op.pl; ania.klimaszewska@op.pl;
   paulina.antosik@cm.umk.pl; kasperskaanna@o2.pl; d_gr@me.com;
   tadeusz.szylberg@10wsk.mil.pl; l.szylberg@cm.umk.pl
RI Antosik, Paulina/IWM-2870-2023; Grzanka, Dariusz/N-5612-2014;
   Durślewicz, Justyna/JVO-1456-2024; Klimaszewska-Wisniewska,
   Anna/H-6679-2014
OI Antosik, Paulina/0000-0002-7099-8115; Durslewicz,
   Justyna/0000-0001-7301-5324; Klimaszewska-Wisniewska,
   Anna/0000-0002-8493-3806
FU Nicolaus Copernicus University, Collegium Medicum, Bydgoszcz [141]
FX The study was supported by research tasks no. 141 within the framework
   of basal research activity (Nicolaus Copernicus University, Collegium
   Medicum, Bydgoszcz).
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NR 66
TC 7
Z9 7
U1 0
U2 1
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
PD AUG 17
PY 2020
VL 2020
AR 8880548
DI 10.1155/2020/8880548
PG 10
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 NR4UX
UT WOS:000571560400001
PM 32879641
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Li, HW
   Yang, L
   Yang, Q
   Liang, Z
   Su, WM
   Yu, LL
AF Li, Haiwen
   Yang, Li
   Yang, Quan
   Liang, Zhu
   Su, Wenmei
   Yu, Lili
TI Integration of osimertinib-targeted EGFR gene-associated differential
   gene expression in constructing a prognostic model for lung
   adenocarcinoma
SO FUNCTIONAL & INTEGRATIVE GENOMICS
LA English
DT Article
DE Lung adenocarcinoma; EGFR-TKI resistance; <italic>CCT6A</italic>;
   <italic>KCTD12</italic>; Prognostic model
ID COLON-CANCER; OPEN-LABEL; CHEMOTHERAPY; MULTICENTER; GEFITINIB; SURVIVAL
AB Lung adenocarcinoma (LUAD) is one of the deadliest cancers. Epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI)-targeted therapy is an important approach for treating LUAD. However, the development of acquired resistance poses a serious clinical challenge. Our objective was to explore the differentially expressed genes (DEGs) associated with EGFR and detect biomarkers for diagnosing and treating osimertinib resistance in LUAD patients. LUAD datasets were downloaded from public databases. Differential expression analysis was performed to screen DEGs, and prognostic modules were constructed by Cox regression. Enrichment analysis, gene regulatory network analysis and immune microenvironment analysis were employed to explore the underlying mechanisms in LUAD. Finally, the expression of prognosis module genes (PMGs) was validated in 8 LUAD tissue specimens and 5 cell lines by qRT-PCR. In total, 13 differential module genes (BIRC3, CCT6A, CPLX2, GLCCI1, GSTA1, HLA-DQB2, ID1, KCTD12, MUC15, NOTUM, NT5E, TCIM, and TM4SF4) were screened for the construction of a prognostic module. Notably, CCT6A and KCTD12 demonstrated excellent accuracy in the diagnosis of LUAD. Immune dysregulation and BIRC3, HLA-DQB2, KCTD12, and NT5E expression were significantly associated with invasive immune cells in LUAD patients. The expression level of CCT6A was highest in PC9-OR and H1975-OR cells, while the expression level of KCTD12 was highest in paracancerous tissue and HBE cells. The constructed prognostic model showed promise in predicting the survival of LUAD patients. Notably, KCTD12 and CCT6A might be candidate biomarkers for improving diagnostic performance and guiding individualized therapy for EGFR-TKI-resistant LUAD patients.
C1 [Li, Haiwen; Yang, Li; Su, Wenmei; Yu, Lili] Macau Univ Sci & Technol, Fac Chinese Med, Macau 999078, Peoples R China.
   [Yu, Lili] Macau Univ Sci & Technol, State Key Lab Qual Res Chinese Med, Macau 999078, Peoples R China.
   [Yang, Quan; Su, Wenmei] Guangdong Med Univ, Dept Pulm Oncol, Affiliated Hosp, 57 South Renmin Rd, Zhanjiang 524000, Guangdong, Peoples R China.
   [Li, Haiwen] Guangdong Med Univ, Dept Head & Neck Oncol, Affiliated Hosp, Zhanjiang 524000, Guangdong, Peoples R China.
   [Yang, Li] Guangdong Med Univ, Affiliated Hosp, Dept Digest Oncol, Zhanjiang 524000, Guangdong, Peoples R China.
   [Liang, Zhu] Guangdong Med Univ, Dept Cardiovasc & Thorac Surg, Affiliated Hosp, Zhanjiang 524000, Guangdong, Peoples R China.
C3 Macau University of Science & Technology; Macau University of Science &
   Technology; Guangdong Medical University; Guangdong Medical University;
   Guangdong Medical University; Guangdong Medical University
RP Su, WM; Yu, LL (corresponding author), Macau Univ Sci & Technol, Fac Chinese Med, Macau 999078, Peoples R China.; Yu, LL (corresponding author), Macau Univ Sci & Technol, State Key Lab Qual Res Chinese Med, Macau 999078, Peoples R China.; Su, WM (corresponding author), Guangdong Med Univ, Dept Pulm Oncol, Affiliated Hosp, 57 South Renmin Rd, Zhanjiang 524000, Guangdong, Peoples R China.
EM suwenmei123@hotmail.com; llyu@must.edu.mo
RI Li, Haiwen/ITR-8920-2023
FU National Natural Science Foundation of China
FX We thanks all the contributors to the public database.
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NR 35
TC 0
Z9 0
U1 2
U2 2
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1438-793X
EI 1438-7948
J9 FUNCT INTEGR GENOMIC
JI Funct. Integr. Genomics
PD DEC
PY 2024
VL 24
IS 6
AR 226
DI 10.1007/s10142-024-01499-5
PG 26
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA P0G3H
UT WOS:001374799000001
PM 39661202
OA hybrid
DA 2025-01-04
ER

PT J
AU Hao, YX
   Li, YM
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   Zhang, H
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   Xiao, WH
AF Hao, Yi-Xin
   Li, Yong-Mei
   Ye, Ming
   Guo, Yan-Yan
   Li, Qiu-Wen
   Peng, Xiu-Mei
   Wang, Qi
   Zhang, Shu-Fang
   Zhao, Hui-Xia
   Zhang, He
   Li, Guang-Hui
   Zhu, Jian-Hua
   Xiao, Wen-Hua
TI KRAS and BRAF mutations in serum exosomes from patients with colorectal
   cancer in a Chinese population
SO ONCOLOGY LETTERS
LA English
DT Article
DE Kirsten rat sarcoma viral oncogene homolog; BRAF serine/threonine kinase
   proto-oncogene; mutation; exosome; colorectal cancer
ID TUMOR-DERIVED EXOSOMES; DIAGNOSTIC BIOMARKERS; CLINICAL-SIGNIFICANCE;
   OVARIAN-CANCER; NUCLEIC-ACIDS; BLOOD-PLASMA; STOOL DNA; MICRORNAS;
   CELLS; IDENTIFICATION
AB The efficacy of epidermal growth factor receptor targeted therapy is significantly associated with Kirsten rat sarcoma viral oncogene homolog (KRAS) and B-raf serine/threonine kinase proto-oncogene (BRAE) mutation in patients with colorectal cancer (CRC), for which the standard gene testing is currently performed using tumor tissue DNA. The aim of the present study was to compare the presence of KRAS and BRAE mutations in the serum exosome and primary tumor tissue from patients with CRC Genomic DNA were extracted from the tumor tissues of 35 patients with histologically-confirmed CRC and exosomal mRNA were obtained from peripheral blood, which were collected from the corresponding patients prior to surgery. Three mutations in the KRAS gene (codons 12, 13 and 61) and a mutation in the BRAF gene (codon 600) were detected using a polymerase chain reaction-based sequencing method and their presence were compared between tumor tissues and the matched serum exosomes. The KRAS mutation rates in tumor tissues and the matched serum exosomes were 57.6 and 42.4%, respectively, which was not significantly different (P=0.063). The detection rate of the BRAE mutation was 24.2 and 18.2% in tumor tissues and the matched serum exosomes, respectively, and there was no significant difference (P=0.500). The patients with CRC that had a KRAS mutation of codon 12 in exon 2 in their tumor tissues and serum exosomes were significantly older compared with those without this mutation (tumor tissue, P=0.002; serum exosome, P=0.022). The sensitivity of KRAS and BRAE imitation detection using exosomal mRNA was 73.7 and 75%, respectively. The specificity of the detected mutations exhibited an efficiency of 100%, and the total consistency rate was 94.9 and 93.9% for KRAS and BRAE mutations, respectively. These results suggested that serum exosomal mRNA may be used as a novel source for the rapid and non-invasive genotyping of patients with CRC.
C1 [Hao, Yi-Xin; Ye, Ming; Guo, Yan-Yan; Li, Qiu-Wen; Peng, Xiu-Mei; Wang, Qi; Zhang, Shu-Fang; Zhao, Hui-Xia; Zhang, He; Li, Guang-Hui; Zhu, Jian-Hua; Xiao, Wen-Hua] Peoples Liberat Army, Affiliated Hosp 1, Dept Oncol, Gen Hosp, 51 Fucheng Rd, Beijing 100039, Peoples R China.
   [Li, Yong-Mei] Second Mil Med Univ, Changhai Hosp, Dept Oncol, Shanghai 200433, Peoples R China.
C3 Chinese People's Liberation Army General Hospital; Naval Medical
   University
RP Hao, YX; Xiao, WH (corresponding author), Peoples Liberat Army, Affiliated Hosp 1, Dept Oncol, Gen Hosp, 51 Fucheng Rd, Beijing 100039, Peoples R China.
EM 15901537871@163.com; w_hxiao@hotmail.com
RI Hao, Yixin/A-5435-2018; JianHua.Zhu, JianHua.Zhu/ADE-5187-2022; li,
   guanghui/JNS-0836-2023
FU First Affiliated Hospital of The People's Liberation Army General
   Hospital (Beijing, China)
FX The present study was supported by the The First Affiliated Hospital of
   The People's Liberation Army General Hospital (Beijing, China). The
   authors would like to thank Dr Ning Dong (The First Affiliated Hospital
   of The People's Liberation Army General Hospital) for aiding with
   exosome collection and exosomal eDNA synthesis and Dr Jayashri Ghosh
   (Temple University, Philadelphia, PA, USA) for her assistance in editing
   the language.
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NR 58
TC 37
Z9 43
U1 1
U2 17
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 2017
VL 13
IS 5
BP 3608
EP 3616
DI 10.3892/ol.2017.5889
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EU6FQ
UT WOS:000401129800103
PM 28521461
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Younis, S
   Javed, Q
   Blumenberg, M
AF Younis, Sidra
   Javed, Qamar
   Blumenberg, Miroslav
TI Transcriptional changes associated with resistance to inhibitors of
   epidermal growth factor receptor revealed using metaanalysis
SO BMC CANCER
LA English
DT Article
DE Development of resistance; Erlotinib; Gefitinib; Metabolic changes;
   Targeted therapy
ID TYROSINE KINASE INHIBITORS; ACQUIRED-RESISTANCE; TARGETED THERAPIES;
   COLORECTAL-CANCER; TUMOR-GROWTH; LUNG-CANCER; KRAS; EGF; METABOLISM;
   MUTATIONS
AB Background: EGFR is important in maintaining metabolic homeostasis in healthy cells, but in tumors it activates downstream signaling pathways, causing proliferation, angiogenesis, invasion and metastasis. Consequently, EGFR is targeted in cancers using reversible, irreversible or antibody inhibitors. Unfortunately, tumors develop inhibitor resistance by mutations or overexpressing EGFR, or its ligand, or activating secondary, EGFR-independent pathways.
   Methods: Here we present a global metaanalysis comparing transcriptional profiles from matched pairs of EGFR inhibitor-sensitive vs. -resistant cell lines, using 15 datasets comprising 274 microarrays. We also analyzed separately pairs of cell lines derived using reversible, irreversible or antibody inhibitors.
   Results: The metaanalysis identifies commonalities in cell lines resistant to EGFR inhibitors: in sensitive cell lines, the ontological categories involving the ErbB receptors pathways, cell adhesion and lipid metabolism are overexpressed; however, resistance to EGFR inhibitors is associated with overexpression of genes for ErbB receptors-independent oncogenic pathways, regulation of cell motility, energy metabolism, immunity especially inflammatory cytokines biosynthesis, cell cycle and responses to exogenous and endogenous stimuli. Specifically in Gefitinib-resistant cell lines, the immunity-associated genes are overexpressed, whereas in Erlotinib-resistant ones so are the mitochondrial genes and processes. Unexpectedly, lines selected using EGFR-targeting antibodies overexpress different gene ontologies from ones selected using kinase inhibitors. Specifically, they have reduced expression of genes for proliferation, chemotaxis, immunity and angiogenesis.
   Conclusions: This metaanalysis suggests that 'combination therapies' can improve cancer treatment outcomes. Potentially, use of mitochondrial blockers with Erlotinib, immunity blockers with Gefitinib, tyrosine kinase inhibitors with antibody inhibitors, may have better chance of avoiding development of resistance.
C1 [Younis, Sidra; Blumenberg, Miroslav] RO Perelman Dept Dermatol, New York, NY 10016 USA.
   [Younis, Sidra; Blumenberg, Miroslav] Dept Biochem & Mol Pharmacol, New York, NY USA.
   [Younis, Sidra; Blumenberg, Miroslav] NYU, Langone Med Ctr, Inst Canc, New York, NY USA.
   [Younis, Sidra; Javed, Qamar] Quaid I Azam Univ, Dept Biochem, Islamabad 45320, Pakistan.
   [Blumenberg, Miroslav] NYU, Sch Med, New York, NY 10016 USA.
C3 NYU Langone Medical Center; New York University; Quaid I Azam
   University; New York University
RP Blumenberg, M (corresponding author), RO Perelman Dept Dermatol, New York, NY 10016 USA.
EM Miroslav.Blumenberg@nyumc.org
OI Blumenberg, Miroslav/0000-0002-8672-7774
FU IRSIP, Higher Education Commission, Islamabad, Pakistan; R.O. Perelman
   Department of Dermatology, NYU Medical School, New York, USA
FX IRSIP, Higher Education Commission, Islamabad, Pakistan, and the R.O.
   Perelman Department of Dermatology, NYU Medical School, New York, USA.
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NR 36
TC 5
Z9 5
U1 0
U2 8
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD MAY 7
PY 2015
VL 15
AR 369
DI 10.1186/s12885-015-1337-3
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CI0LM
UT WOS:000354428600001
PM 25948104
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Gharib, A
   Faezizadeh, Z
   Mesbah-Namin, SAR
   Saravani, R
AF Gharib, Amir
   Faezizadeh, Zohreh
   Mesbah-Namin, Seyed Ali Reza
   Saravani, Ramin
TI Experimental treatment of breast cancer-bearing BALB/c mice by
   artemisinin and transferrin-loaded magnetic nanoliposomes
SO PHARMACOGNOSY MAGAZINE
LA English
DT Article
DE Artemisinin; breast cancer; in vivo; magnetic nanoliposome; transferrin
ID IN-VITRO; SYSTEMIC CHEMOTHERAPY; COLORECTAL-CANCER; CELLS;
   NANOPARTICLES; LIPOSOMES; APOPTOSIS; OSTEOSARCOMA; CYTOTOXICITY;
   DOXORUBICIN
AB Background: The combination of artemisinin and transferrin exhibits versatile anticancer activities. In previous, we successfully prepared artemisinin and transferrin-loaded magnetic nanoliposomes and evaluated their anti-proliferative activity against MCF-7 and MDA-MB-231 cell lines in vitro. In this study, we investigate the in vivo anti-breast cancer activity of artemisinin and transferrin-loaded magnetic nanoliposome against breast transplanted tumors in BALB/c mice model. Materials and Methods: Artemisinin and transferrin-loaded magnetic nanoliposomes were prepared and characterized for some physiochemical properties. Pieces of tumor tissue from the breast cancer-bearing BALB/c mice were transplanted subcutaneously to the syngeneic female BALB/c mice. In the presence of the external magnet that placed at the breast tumor site, the tissue distribution and tumor-suppressing effects of prepared nanoliposomes on tumor growth was evaluated. Results: The prepared nanoliposomes have fine spherical shape, rough surface, nano-sized diameter and magnetic properties. At 2 h after treatment, the intravenous administration of artemisinin and transferrin-loaded magnetic nanoliposomes followed using the magnetic.eld approximately produced 10- and 5.5-fold higher levels of artemisinin and transferrin in the tumors, respectively, compared with free artemisinin and transferrin. Moreover, in the presence of an external magnetic field, the prepared nanoliposomes could significantly induce apoptosis in the mice breast cancer cells as well as could reduce tumor volume in tumorized mice at 15 days after treatment. Conclusion: The data suggested that the artemisinin and transferrin-loaded magnetic nanoliposomes would be a good choice for the breast tumor-targeted therapy, due to its high targeting efficiency.
C1 [Gharib, Amir; Faezizadeh, Zohreh] Islamic Azad Univ, Dept Lab Sci, Borujerd Branch, Borujerd 14515775, Iran.
   [Mesbah-Namin, Seyed Ali Reza] Tarbiat Modares Univ, Dept Clin Biochem, Fac Med Sci, Tehran, Iran.
   [Saravani, Ramin] Zahedan Univ Med Sci, Sch Med, Dept Biochem, Zahedan, Iran.
C3 Islamic Azad University; Tarbiat Modares University; Zahedan University
   of Medical Sciences
RP Gharib, A (corresponding author), Islamic Azad Univ, Fac Med Sci, Borujerd Branch, Dept Lab Sci, Modares St, Borujerd 14515775, Iran.
EM amirgharib@gmail.com
RI Mesbah-Namin, Seyed/ABG-8442-2022; Saravani, Ramin/AAH-7568-2021
OI Gharib, Amir/0000-0003-2370-4548
FU Iran National Science Foundation (INSF) [91001200]
FX The author gratefully acknowledges financial support from the Iran
   National Science Foundation (INSF) under grant agreement no: 91001200.
   Conflict of Interest: None declared.
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NR 31
TC 19
Z9 20
U1 1
U2 57
PU MEDKNOW PUBLICATIONS & MEDIA PVT LTD
PI MUMBAI
PA B-9, KANARA BUSINESS CENTRE, OFF LINK RD, GHAKTOPAR-E, MUMBAI, 400075,
   INDIA
SN 0973-1296
EI 0976-4062
J9 PHARMACOGN MAG
JI Pharmacogn. Mag.
PD MAY
PY 2015
VL 11
IS 42
SU 1
BP S117
EP S122
DI 10.4103/0973-1296.157710
PG 6
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA CL0AF
UT WOS:000356600100015
PM 26109756
OA Green Published
DA 2025-01-04
ER

PT J
AU Chen, BX
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AF Chen, Baoxiang
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   Hong, Yuntian
   Tian, Shunhua
   Zhai, Xiang
   Chen, Quanjiao
   Ren, Xianghai
   Fan, Lifang
   Xie, Xiaoyu
   Jiang, Congqing
TI m5C regulator-mediated modification patterns and tumor microenvironment
   infiltration characterization in colorectal cancer: One step closer to
   precision medicine
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE 5-methylcytosine; RNA methylation; colorectal cancer; immune
   infiltrates; tumor microenvironment; precision medicine
ID IMMUNE CELLS; T-CELLS; INNATE; IMMUNOTHERAPY; INFLAMMATION; RNA
AB Background The RNA modification 5-methylcytosine (m5C) is one of the most prevalent post-transcriptional modifications, with increasing evidence demonstrating its extensive involvement in the tumorigenesis and progression of various cancers. Colorectal cancer (CRC) is the third most common cancer and second leading cause of cancer-related deaths worldwide. However, the role of m5C modulators in shaping tumor microenvironment (TME) heterogeneity and regulating immune cell infiltration in CRC requires further clarification. Results The transcriptomic sequencing data of 18 m5C regulators and clinical data of patients with CRC were obtained from The Cancer Genome Atlas (TCGA) and systematically evaluated. We found that 16 m5C regulators were differentially expressed between CRC and normal tissues. Unsupervised cluster analysis was then performed and revealed two distinct m5C modification patterns that yielded different clinical prognoses and biological functions in CRC. We demonstrated that the m5C score constructed from eight m5C-related genes showed excellent prognostic performance, with a subsequent independent analysis confirming its predictive ability in the CRC cohort. Then we developed a nomogram containing five clinical risk factors and the m5C risk score and found that the m5C score exhibited high prognostic prediction accuracy and favorable clinical applicability. Moreover, the CRC patients with low m5C score were characterized by "hot" TME exhibiting increased immune cell infiltration and higher immune checkpoint expression. These characteristics were highlighted as potential identifiers of suitable candidates for anticancer immunotherapy. Although the high m5C score represented the non-inflammatory phenotype, the CRC patients in this group exhibited high level of sensitivity to molecular-targeted therapy. Conclusion Our comprehensive analysis indicated that the novel m5C clusters and scoring system accurately reflected the distinct prognostic signature, clinicopathological characteristics, immunological phenotypes, and stratifying therapeutic opportunities of CRC. Our findings, therefore, offer valuable insights into factors that may be targeted in the development of precision medicine-based therapeutic strategies for CRC.
C1 [Chen, Baoxiang; Hong, Yuntian; Tian, Shunhua; Zhai, Xiang; Ren, Xianghai; Xie, Xiaoyu; Jiang, Congqing] Wuhan Univ, Dept Colorectal & Anal Surg, Zhongnan Hosp, Wuhan, Peoples R China.
   [Chen, Baoxiang; Hong, Yuntian; Tian, Shunhua; Zhai, Xiang; Ren, Xianghai; Xie, Xiaoyu; Jiang, Congqing] Wuhan Univ, Clin Ctr Intestinal & Colorectal Dis Hubei Prov Z, Zhongnan Hosp, Wuhan, Peoples R China.
   [Chen, Baoxiang; Hong, Yuntian; Tian, Shunhua; Zhai, Xiang; Ren, Xianghai; Xie, Xiaoyu; Jiang, Congqing] Wuhan Univ, Hubei Key Lab Intestinal & Colorectal Dis Zhongna, Zhongnan Hosp, Wuhan, Peoples R China.
   [Xi, Yiqing] Wuhan Univ, Dept Breast & Thyroid Surg, Zhongnan Hosp, Wuhan, Peoples R China.
   [Zhao, Jianhong] Wuhan Univ, Coll Life Sci, Hubei Key Lab Cell Homeostasis, Wuhan, Peoples R China.
   [Zhao, Jianhong] Wuhan Univ, Med Res Inst, Frontier Sci Ctr Immunol & Metab, Wuhan, Peoples R China.
   [Chen, Quanjiao] Chinese Acad Sci, Wuhan Inst Virol, CAS Ctr Influenza Res & Early Warning, CAS Key Lab Special Pathogens & Biosafety, Wuhan, Peoples R China.
   [Fan, Lifang] Huazhong Univ Sci & Technol, Hubei Canc Hosp, Dept Pathol, Tongji Med Coll, Wuhan, Peoples R China.
C3 Wuhan University; Wuhan University; Wuhan University; Wuhan University;
   Wuhan University; Wuhan University; Chinese Academy of Sciences; Wuhan
   Institute of Virology, CAS; Huazhong University of Science & Technology
RP Ren, XH; Xie, XY; Jiang, CQ (corresponding author), Wuhan Univ, Dept Colorectal & Anal Surg, Zhongnan Hosp, Wuhan, Peoples R China.; Ren, XH; Xie, XY; Jiang, CQ (corresponding author), Wuhan Univ, Clin Ctr Intestinal & Colorectal Dis Hubei Prov Z, Zhongnan Hosp, Wuhan, Peoples R China.; Ren, XH; Xie, XY; Jiang, CQ (corresponding author), Wuhan Univ, Hubei Key Lab Intestinal & Colorectal Dis Zhongna, Zhongnan Hosp, Wuhan, Peoples R China.; Fan, LF (corresponding author), Huazhong Univ Sci & Technol, Hubei Canc Hosp, Dept Pathol, Tongji Med Coll, Wuhan, Peoples R China.
EM xianghai_ren@qq.com; 1577418746@qq.com; zn004356@whu.edu.cn;
   wb002554@whu.edu.cn
RI Hong, Yuntian/JJG-1945-2023; Li, Mengqi/HPF-6473-2023; Zhao,
   Jianhong/L-4798-2018; Ren, Xianghai/K-5032-2018
OI zhao, jianhong/0009-0006-7408-7462; Ren, Xianghai/0000-0001-8092-6687
FU Enginerring construction project of improving diagnosis and treatment
   ability of difficult diseases (oncology) [ZLYNXM202012]; Joint
   Foundation of Health Commission of Hubei Province [znpy2019086]; Wu
   Jieping Medical Research Foundation
FX This work was supported by Enginerring construction project of improving
   diagnosis and treatment ability of difficult diseases (oncology) (Grant
   No. ZLYNXM202012), Joint Foundation of Health Commission of Hubei
   Province (Grant No. znpy2019086), and Wu Jieping Medical Research
   Foundation (No.320.6750.2021-11-8).
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NR 55
TC 14
Z9 14
U1 0
U2 8
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 DEC 1
PY 2022
VL 13
AR 1049435
DI 10.3389/fimmu.2022.1049435
PG 19
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA I1IA7
UT WOS:001000370800001
PM 36532062
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Mohammadpour, S
   Esfahani, AT
   Sarpash, S
   Vakili, F
   Zafarjafarzadeh, N
   Mashaollahi, A
   Pardakhtchi, A
   Nazemalhosseini-Mojarad, E
AF Mohammadpour, Somayeh
   Esfahani, Amir Torshizi
   Sarpash, SeyedKasra
   Vakili, Fatemeh
   Zafarjafarzadeh, Nikta
   Mashaollahi, Amirhesam
   Pardakhtchi, Ali
   Nazemalhosseini-Mojarad, Ehsan
TI Hippo Signaling Pathway in Colorectal Cancer: Modulation by Various
   Signals and Therapeutic Potential
SO ANALYTICAL CELLULAR PATHOLOGY
LA English
DT Review
DE colorectal neoplasms; hippo pathway; therapy; tumorigenesis; YAP/TAZ
ID INHIBITS TUMORIGENESIS; INDUCED ACTIVATION; OXIDATIVE STRESS;
   GENE-EXPRESSION; YAP; PROTEIN; PROMOTES; PROGNOSIS; YAP/TAZ; TAZ
AB Colorectal cancer (CRC) stands as a significant global health issue, marked by elevated occurrence and mortality statistics. Despite the availability of various treatments, including chemotherapy, radiotherapy, and targeted therapy, CRC cells often exhibit resistance to these interventions. As a result, it is imperative to identify the disease at an earlier stage and enhance the response to treatment by acquiring a deeper comprehension of the processes driving tumor formation, aggressiveness, metastasis, and resistance to therapy. The Hippo pathway plays a critical role in facilitating the initiation of tumorigenesis and frequently experiences disruption within CRC because of genetic mutations and modified expression in its fundamental constituents. Targeting upstream regulators or core Hippo pathway components may provide innovative therapeutic strategies for modulating Hippo signaling dysfunction in CRC. To advance novel therapeutic techniques for CRC, it is imperative to grasp the involvement of the Hippo pathway in CRC and its interaction with alternate signaling pathways, noncoding RNAs, gut microbiota, and the immune microenvironment. This review seeks to illuminate the function and control of the Hippo pathway in CRC, ultimately aiming to unearth innovative therapeutic methodologies for addressing this ailment.
C1 [Mohammadpour, Somayeh; Esfahani, Amir Torshizi] Shahid Beheshti Univ Med Sci, Res Inst Gastroenterol & Liver Dis, Basic & Mol Epidemiol Gastrointestinal Disorders R, Tehran, Iran.
   [Sarpash, SeyedKasra; Vakili, Fatemeh; Zafarjafarzadeh, Nikta; Mashaollahi, Amirhesam; Pardakhtchi, Ali] Islamic Azad Univ, Fac Adv Sci & Technol, Dept Cellular & Mol Biol, Med Sci, Tehran, Iran.
   [Nazemalhosseini-Mojarad, Ehsan] Shahid Beheshti Univ Med Sci, Res Inst Gastroenterol & Liver Dis, Gastroenterol & Liver Dis Res Ctr, Tehran, Iran.
C3 Shahid Beheshti University Medical Sciences; Islamic Azad University;
   Shahid Beheshti University Medical Sciences
RP Nazemalhosseini-Mojarad, E (corresponding author), Shahid Beheshti Univ Med Sci, Res Inst Gastroenterol & Liver Dis, Gastroenterol & Liver Dis Res Ctr, Tehran, Iran.
EM s.mohamadpour@miau.ac.ir; amir_esfahani90@yahoo.com;
   kasra.sarpash@outlook.com; fatm.vakili@gmail.com; niktazafar@gmail.com;
   amirhesammashaollahi@gmail.com; ali.pardakhtchi90@gmail.com;
   ehsanmojarad@gmail.com
RI Nazemalhosseini-Moja, ehsan/HGF-3165-2022
OI nazemalhosseini-mojarad, ehsan/0000-0001-8914-004X
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NR 161
TC 0
Z9 0
U1 3
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2210-7177
EI 2210-7185
J9 ANAL CELL PATHOL
JI Anal. Cell. Pathol.
PD OCT 11
PY 2024
VL 2024
AR 5767535
DI 10.1155/2024/5767535
PG 17
WC Oncology; Cell Biology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology; Pathology
GA J3S9V
UT WOS:001336306300001
PM 39431199
OA gold
DA 2025-01-04
ER

PT J
AU Ying, JM
   Lin, C
   Wu, J
   Guo, L
   Qiu, T
   Ling, Y
   Shan, L
   Zhou, HT
   Zhao, DB
   Wang, J
   Liang, JW
   Zhao, JJ
   Jiao, YC
   Lu, N
   Zhao, H
AF Ying, Jianming
   Lin, Chen
   Wu, Jian
   Guo, Lei
   Qiu, Tian
   Ling, Yun
   Shan, Ling
   Zhou, Haitao
   Zhao, Dongbing
   Wang, Jian
   Liang, Jianwei
   Zhao, Jianjun
   Jiao, Yuchen
   Lu, Ning
   Zhao, Hong
TI <i>Anaplastic Lymphoma Kinase</i> Rearrangement in Digestive Tract
   Cancer: Implication for Targeted Therapy in Chinese Population
SO PLOS ONE
LA English
DT Article
ID CELL LUNG-CANCER; ALK; GENE; CRIZOTINIB; SPECTRIN; EXPRESSION; FUSION;
   IDENTIFICATION; CHEMOTHERAPY; PROTEINS
AB Background
   Anaplastic lymphoma kinase (ALK) rearrangements define a subgroup of lung cancer which is eligible to targeted kinase inhibition. The aim of this study is to observe the incidence rate of ALK fusion in a large cohort of Chinese digestive tract cancer patients.
   Patients and Methods
   Tissue microarray (TMA) was constructed from 808 digestive tract cancer cases, including 169 esophageal squamous cell carcinoma, 182 gastric cancer and 457 colorectal cancer (CRC) cases. We tested all cases for ALK expression via a fully automated immunohistochemistry (IHC) assay. The IHC-positive cases were subjected to fluorescence in situ hybridization (FISH), real-time polymerase chain reaction (qRT-PCR), target gene enrichment and sequencing for confirmation of ALK gene rearrangement and discovery of novel fusion partner.
   Results
   Among the tested cases, 2 (0.44%) CRC cases showed positive both by IHC and FISH. By qRT-PCR, EML4-ALK fusion was found in one IHC-positive CRC case. In another IHC-positive CRC case, target gene enrichment and sequencing revealed ALK was fused to a novel partner, spectrin beta non-erythrocytic 1 (SPTBN1). One gastric cancer case showed partially positive IHC result, but no fusion was found by FISH and gene sequencing.
   Conclusions
   The incidence rate of ALK gene fusion in Chinese CRC patients was 0.44%, but not detectable in gastric and esophageal cancers. The novel SPTBN1-ALK fusion, together with other ALK fusion genes, may become a potential target for anti-ALK therapy.
C1 [Ying, Jianming; Guo, Lei; Qiu, Tian; Ling, Yun; Shan, Ling; Lu, Ning] Chinese Acad Med Sci, Canc Hosp, Dept Pathol, Beijing 100730, Peoples R China.
   [Lin, Chen; Zhou, Haitao; Zhao, Dongbing; Wang, Jian; Liang, Jianwei; Zhao, Jianjun; Zhao, Hong] Chinese Acad Med Sci, Canc Hosp, Dept Abdominal Surg Oncol, Beijing 100730, Peoples R China.
   [Wu, Jian] MyGenostics Inc, Baltimore, MD USA.
   [Jiao, Yuchen] Chinese Acad Med Sci, Lab Cell & Mol Biol, Canc Inst, Beijing 100730, Peoples R China.
   [Jiao, Yuchen] Chinese Acad Med Sci, State Key Lab Mol Oncol, Canc Inst, Beijing 100730, Peoples R China.
   [Jiao, Yuchen] Chinese Acad Med Sci, Canc Hosp, Beijing 100730, Peoples R China.
   [Jiao, Yuchen] Peking Union Med Coll, Beijing 100021, 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; Cancer Institute & Hospital - CAMS;
   Chinese Academy of Medical Sciences - Peking Union Medical College;
   Chinese Academy of Medical Sciences - 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; Peking Union Medical College
RP Zhao, H (corresponding author), Chinese Acad Med Sci, Canc Hosp, Dept Abdominal Surg Oncol, Beijing 100730, Peoples R China.
EM jiaoyuchen@cicams.ac.cn; nlu03@126.com; zhaohong9@sina.com
RI Qiu, Tian/JGM-7268-2023; jiao, yuchen/H-6313-2011; Guo,
   Lei/AEU-0178-2022; Zhao, Hong/IUQ-0043-2023; Zhang,
   Hongyang/IAR-1565-2023; Ling, Yun/JMP-6953-2023
FU Natural Basic Research Program of China [2014CB542002]; National Natural
   Science Foundation of China [31470073, 81201967]; Beijing Natural
   Science Foundation [7144238]; Beijing Nova PrograM [2009A69]
FX This study was supported by grants from the Natural Basic Research
   Program of China (973 program 2014CB542002) and the National Natural
   Science Foundation of China (31470073), National Natural Science
   Foundation of China (81201967), the Beijing Natural Science Foundation
   (7144238) and Beijing Nova Program (No. 2009A69). MyGenostics Inc.,
   provided support in the form of salaries for author Jian Wu, but did not
   have any additional role in the study design, data collection and
   analysis, decision to publish, or preparation of the manuscript. The
   specific roles of this author is articulated in the 'author
   contributions' section. This study was supported by grants from the
   Natural Basic Research Program of China (973 program 2014CB542002) and
   the National Natural Science Foundation of China (31470073), National
   Natural Science Foundation of China (81201967), the Beijing Natural
   Science Foundation (7144238) and Beijing Nova Program (No. 2009A69).
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NR 30
TC 20
Z9 21
U1 1
U2 14
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 17
PY 2015
VL 10
IS 12
AR e0144731
DI 10.1371/journal.pone.0144731
PG 11
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA CY9JO
UT WOS:000366723400021
PM 26678488
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Vande Perre, P
   Siegfried, A
   Corsini, C
   Bonnet, D
   Toulas, C
   Hamzaoui, N
   Selves, J
   Chipoulet, E
   Hoffmann, JS
   Uro-Coste, E
   Guimbaud, R
AF Vande Perre, P.
   Siegfried, A.
   Corsini, C.
   Bonnet, D.
   Toulas, C.
   Hamzaoui, N.
   Selves, J.
   Chipoulet, E.
   Hoffmann, J. S.
   Uro-Coste, E.
   Guimbaud, R.
TI Germline mutation p.N363K in POLE is associated with an increased risk
   of colorectal cancer and giant cell glioblastoma
SO FAMILIAL CANCER
LA English
DT Article
DE POLE; Polymerase epsilon; PPAP; Proofreading; Glioblastoma; Giant cells
ID TUMORS; BRAIN
AB Germline mutations of the POLE gene are responsible for polymerase proofreading-associated polyposis syndrome (PPAP). These mutations were hypothesised to predispose to extra-gastrointestinal tumours (ovary, endometrium, brain), but this association has not been confirmed so far. We report a family with an autosomal dominant inheritance of PPAP due to a c.1089C>A; p.Asn363Lys mutation in the proofreading exonuclease domain of POLE. Ten patients presenting a history of colorectal tumours and three patients with polyposis are indexed in this family. Three carriers (including siblings and a distant cousin at 30, 45 and 52 respectively) and another member (at 37 not tested) presented glioblastoma. This is the second family reported to carry this mutation. Among the four glioblastomas in the family that we report, both show similar pathology: giant cell glioblastoma. These cases suggest that the c.1089C>A germline POLE mutation may confer an increased risk of brain cancer [incidence 17.4% (4/23) in mutation carriers combining the two families]. More observations are needed to support this hypothesis. It seems that not all mutations of POLE are equally associated with extra-gastrointestinal tumours. Although carriers of a mutation responsible for PPAP should benefit from screening for colorectal and uterine cancer, due to the rapid evolution of glioblastoma the value of neurological follow-up and brain imaging screening remains questionable. Nevertheless, considering the limitations of standard therapy for glioblastoma, mutation status could be useful for targeting therapy. The biological mechanism linking POLE mutation to glioblastoma remains to be determined.
C1 [Vande Perre, P.] CHU Toulouse, Hop Purpan, Serv Genet Med, Toulouse, France.
   [Vande Perre, P.; Bonnet, D.; Toulas, C.; Chipoulet, E.; Guimbaud, R.] IUCT Oncopole, Inst Claudius Regaud, Oncogenet, Toulouse, France.
   [Vande Perre, P.; Selves, J.; Hoffmann, J. S.; Uro-Coste, E.; Guimbaud, R.] Univ Toulouse III Paul Sabatier, Toulouse, France.
   [Siegfried, A.; Selves, J.; Uro-Coste, E.] CHU Toulouse, IUCT O, Dept Pathol, Toulouse, France.
   [Corsini, C.] CHU Montpellier, Dept Genet Med, Serv Oncogenet, Montpellier, France.
   [Bonnet, D.; Chipoulet, E.; Guimbaud, R.] CHU Toulouse, Pole Digestif IUCT Rangueil Larrey, Oncol Digest, Toulouse, France.
   [Siegfried, A.; Toulas, C.; Selves, J.; Hoffmann, J. S.; Uro-Coste, E.; Guimbaud, R.] CRCT, UMR 1037, Toulouse, France.
   [Hamzaoui, N.] Hop Cochin, Serv Biochim & Genet Mol, Paris, France.
C3 CHU de Toulouse; Universite de Toulouse; Universite Toulouse III - Paul
   Sabatier; UNICANCER; Institut Claudius Regaud; Universite de Toulouse;
   Universite Toulouse III - Paul Sabatier; Universite de Toulouse;
   Universite Toulouse III - Paul Sabatier; CHU de Toulouse; Universite de
   Montpellier; CHU de Montpellier; Universite de Toulouse; Universite
   Toulouse III - Paul Sabatier; CHU de Toulouse; Universite de Toulouse;
   Universite Toulouse III - Paul Sabatier; Institut National de la Sante
   et de la Recherche Medicale (Inserm); Assistance Publique Hopitaux Paris
   (APHP); Universite Paris Cite; Hopital Universitaire Cochin - APHP
RP Guimbaud, R (corresponding author), IUCT Oncopole, Inst Claudius Regaud, Oncogenet, Toulouse, France.; Guimbaud, R (corresponding author), Univ Toulouse III Paul Sabatier, Toulouse, France.; Guimbaud, R (corresponding author), CHU Toulouse, Pole Digestif IUCT Rangueil Larrey, Oncol Digest, Toulouse, France.; Guimbaud, R (corresponding author), CRCT, UMR 1037, Toulouse, France.
EM guimbaud.r@chu-toulouse.fr
RI Pierre, VANDE PERRE/CAI-1270-2022; Hoffmann, Jean-Sebastien/O-9183-2014
OI Hoffmann, Jean-Sebastien/0000-0003-2222-354X; Hamzaoui,
   Nadim/0000-0003-4630-9401; Vande Perre, Pierre/0000-0001-7595-7243
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NR 11
TC 25
Z9 25
U1 0
U2 3
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1389-9600
EI 1573-7292
J9 FAM CANCER
JI Fam. Cancer
PD APR
PY 2019
VL 18
IS 2
BP 173
EP 178
DI 10.1007/s10689-018-0102-6
PG 6
WC Oncology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Genetics & Heredity
GA HS4MS
UT WOS:000463838100005
PM 30368636
DA 2025-01-04
ER

PT J
AU Auzanneau, C
   Bacq, D
   Bellera, C
   Blons, H
   Boland, A
   Boucheix, M
   Bourdon, A
   Chollet, E
   Chomienne, C
   Deleuze, JF
   Delmas, C
   Dinart, D
   Espérou, H
   Geillon, F
   Geneste, D
   Italiano, A
   Jean, D
   Khalifa, E
   Laizet, Y
   Laurent-Puig, P
   Lethimonnier, F
   Lévy-Marchal, C
   Lucchesi, C
   Malle, C
   Mancini, P
   Mathoulin-Pélissier, S
   Meyer, V
   Marie-Ange, P
   Perkins, G
   Sellan-Albert, S
   Soubeyran, I
   Wallet, C
AF Auzanneau, Celine
   Bacq, Delphine
   Bellera, Carine
   Blons, Helene
   Boland, Anne
   Boucheix, Marlene
   Bourdon, Aurelien
   Chollet, Emmanuelle
   Chomienne, Christine
   Deleuze, Jean-Francois
   Delmas, Christelle
   Dinart, Derek
   Esperou, Helene
   Geillon, Flore
   Geneste, Damien
   Italiano, Antoine
   Jean, Delphine
   Khalifa, Emmanuel
   Laizet, Yec'han
   Laurent-Puig, Pierre
   Lethimonnier, Franck
   Levy-Marchal, Claire
   Lucchesi, Carlo
   Malle, Carine
   Mancini, Pierre
   Mathoulin-Pelissier, Simone
   Meyer, Vincent
   Marie-Ange, Palomares
   Perkins, Geraldine
   Sellan-Albert, Sabrina
   Soubeyran, Isabelle
   Wallet, Cedric
CA FGM 2025 Workflow Study Grp
TI Feasibility of high-throughput sequencing in clinical routine cancer
   care: lessons from the cancer pilot project of the France Genomic
   Medicine 2025 plan
SO ESMO OPEN
LA English
DT Article
DE WES; RNA sequencing; next-generation sequencing; targeted therapy;
   clinical practice; guidelines
ID RECOMMENDATIONS; EXOME
AB Background Whole exome sequencing and RNA sequencing (WES/RNASeq) should now be implemented in the clinical practice in order to increase access to optimal care for cancer patients. Providing results to Tumour Boards in a relevant time frame-that is, compatible with the clinical pathway-is crucial. Assessing the feasibility of this implementation in the French care system is the primary objective of the Multipli study, as one of the four pilot projects of the national France Genomic Medicine 2025 (FGM 2025) plan. The Multipli study encompasses two innovative trials which will be driven in around 2400 patients suffering from a soft-tissue sarcoma (Multisarc) or a metastatic colorectal carcinoma (Acompli).
   Methods Prior to launching the FGM 2025 cancer pilot study itself, the performance of the Multipli genomic workflow has been evaluated through each step, from the samples collection to the Molecular Tumour Board (MTB) report. Two Multipli-assigned INCa-labelled molecular genetics centres, the CEA-CNRGH sequencing platform and the Institut Bergonie's Bioinformatics Platform were involved in a multicentric study. The duration of each step of the genomic workflow was monitored and bottlenecks were identified.
   Results Thirty barriers which could affect the quality of the samples, sequencing results and the duration of each step of the genomic pathway were identified and mastered. The global turnaround time from the sample reception to the MTB report was of 44 calendar days.
   Conclusion Our results demonstrate the feasibility of tumour genomic analysis by WES/RNASeq within a time frame compatible with the current cancer patient care. Lessons learnt from the Multipli WES/RNASeq Platforms Workflow Study will constitute guidelines for the forthcoming Multipli study and more broadly for the future clinical routine practice in the first two France Genomic Medicine 2025 platforms.
C1 [Auzanneau, Celine; Boucheix, Marlene; Khalifa, Emmanuel; Soubeyran, Isabelle] Inst Bergonie, Unite Pathol Mol, Bordeaux, France.
   [Auzanneau, Celine; Bourdon, Aurelien; Geneste, Damien; Italiano, Antoine; Khalifa, Emmanuel; Laizet, Yec'han; Lucchesi, Carlo; Mancini, Pierre; Soubeyran, Isabelle] Inst Natl Sante & Rech Med, Inst Bergonie, U1218, Bordeaux, France.
   [Bacq, Delphine; Boland, Anne; Deleuze, Jean-Francois; Meyer, Vincent; Marie-Ange, Palomares] Commissariat Energie Atom & Energies Alternat, Inst Biol Francois Jacob, Ctr Natl Rech Genet Humaine, Evry, France.
   [Bellera, Carine; Dinart, Derek; Mathoulin-Pelissier, Simone; Sellan-Albert, Sabrina; Wallet, Cedric] Univ Bordeaux, Inst Sante Publ Epidemiol & Dev, Bordeaux, France.
   [Bellera, Carine; Dinart, Derek; Jean, Delphine; Mathoulin-Pelissier, Simone; Sellan-Albert, Sabrina; Wallet, Cedric] Inst Natl Sante & Rech Med, CIC EC1401 EUCLID, Bordeaux, France.
   [Blons, Helene] Hop Europeen Georges Pompidou, Serv Pharmacogenet & Oncol Mol, Paris, France.
   [Blons, Helene; Laurent-Puig, Pierre; Perkins, Geraldine] Inst Natl Sante & Rech Med, Ctr Univ St Peres, U1147, Paris, France.
   [Bourdon, Aurelien; Geneste, Damien; Laizet, Yec'han; Lucchesi, Carlo; Mancini, Pierre] Inst Bergonie, Unite Bioinformat, Bordeaux, France.
   [Chollet, Emmanuelle; Chomienne, Christine] Alliance Natil Sci Vie & Sante, ITMO Canc, Paris, France.
   [Chomienne, Christine] Inst Natl Canc, Boulogne, France.
   [Deleuze, Jean-Francois] Commissariat Energie Atom & Energies Alternat, US39, Ctr Reference Innovat & Expertise, Evry, France.
   [Delmas, Christelle; Esperou, Helene; Levy-Marchal, Claire; Malle, Carine] Inst Natl Sante & Rech Med, Pole Rech Clin, Inst Sante Publ, Paris, France.
   [Geillon, Flore] Federat Francophone Cancerol Digest, Dijon, France.
   [Italiano, Antoine] Inst Bergonie, Unites Essais Clin Phase Precoce & Sarcomes, Bordeaux, France.
   [Laurent-Puig, Pierre] Hop Europeen Georges Pompidou, Serv Genet Med & Clin, Paris, France.
   [Lethimonnier, Franck] Alliance Natl Sci Vie & Sante, ITMO Technol Sante, Paris, France.
   [Perkins, Geraldine] HEGP, Serv Genet Med & Clin, Paris, Ile De France, France.
C3 UNICANCER; Institut Bergonie; UNICANCER; Institut Bergonie; Universite
   de Bordeaux; Institut National de la Sante et de la Recherche Medicale
   (Inserm); CEA; Universite de Bordeaux; Institut National de la Sante et
   de la Recherche Medicale (Inserm); Assistance Publique Hopitaux Paris
   (APHP); Universite Paris Cite; Hopital Universitaire Europeen
   Georges-Pompidou - APHP; Institut National de la Sante et de la
   Recherche Medicale (Inserm); Universite Paris Cite; UNICANCER; Institut
   Bergonie; Institut National du Cancer (INCA) France; CEA; Institut
   National de la Sante et de la Recherche Medicale (Inserm); Universite de
   Bourgogne; UNICANCER; Institut Bergonie; Assistance Publique Hopitaux
   Paris (APHP); Universite Paris Cite; Hopital Universitaire Europeen
   Georges-Pompidou - APHP; Assistance Publique Hopitaux Paris (APHP);
   Universite Paris Cite; Hopital Universitaire Europeen Georges-Pompidou -
   APHP
RP Chomienne, C (corresponding author), Alliance Natil Sci Vie & Sante, ITMO Canc, Paris, France.; Chomienne, C (corresponding author), Inst Natl Canc, Boulogne, France.
EM christine.chomienne@inserm.fr
RI LUCCHESI, Carlo/HMD-4808-2023; Bellera, Carine/E-7531-2014; Italiano,
   Antoine/JRW-6637-2023; Dinart, Derek/GNP-8649-2022; MALLE,
   Carine/AAF-7305-2019; Laurent-Puig, Pierre/B-2226-2013
OI MALLE, Carine/0000-0002-6824-1383; CHOMIENNE,
   Christine/0000-0001-5513-5752; Lucchesi, Carlo/0000-0001-6657-2341;
   Laurent-Puig, Pierre/0000-0001-8475-5459
FU French 3rd National Cancer Plan (2014-2019); French National Institute
   for Health and Medical Research (Inserm); National Center of Human
   Genomics Research/French Alternative Energies and Atomic Energy
   Commission (CNRGH/CEA); Multipli-assigned INCa-labelled molecular
   genetics centers (Institut Bergonie; Multipli-assigned INCa-labelled
   molecular genetics center (Hopital europeen Georges-Pompidou)
FX The French 3rd National Cancer Plan (2014-2019), the French National
   Institute for Health and Medical Research (Inserm), the National Center
   of Human Genomics Research/French Alternative Energies and Atomic Energy
   Commission (CNRGH/CEA), the Multipli-assigned INCa-labelled molecular
   genetics centers (Institut Bergonie and Hopital europeen
   Georges-Pompidou).
CR [Anonymous], 2019, DECONFINEMENT PROGRE
   [Anonymous], 2019, CITING PHARMGKB
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NR 19
TC 5
Z9 5
U1 0
U2 2
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2059-7029
J9 ESMO OPEN
JI ESMO Open
PY 2020
VL 5
IS 4
AR e000744
DI 10.1136/esmoopen-2020-000744
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PR9OC
UT WOS:000607559100001
PM 32713836
OA Green Published
DA 2025-01-04
ER

PT J
AU Pohl, M
   Schmiegel, W
AF Pohl, Michael
   Schmiegel, Wolff
TI Therapeutic Strategies in Diseases of the Digestive Tract-2015 and
   Beyond Targeted Therapies in Colon Cancer Today and Tomorrow
SO DIGESTIVE DISEASES
LA English
DT Article
DE Colorectal cancer; Acquired resistance; Targeted therapies; Mismatch
   repair
ID COLORECTAL-CANCER; 1ST-LINE TREATMENT; EGFR BLOCKADE; COMBINED BRAF;
   OPEN-LABEL; SURVIVAL; BEVACIZUMAB; METASTASES; INHIBITION; DABRAFENIB
AB Background: Colorectal cancer (CRC) is the third most common cancer type in Western countries. Significant progress has been made in the last decade in the therapy of metastatic CRC (mCRC) with a median overall survival (OS) of patients exceeding 30 months. The integration of biologic targeted therapies and anti-epidermal growth factor receptor (EGFR) monoclonal antibodies (MABs) in the treatment of patients with genomically selected all-RAS wild-type mCRC leads to a significant progress in advanced incurable disease state. After the introduction of the anti-VEGF MAB bevacizumab, the FDA approved with ramucirumab the second antiangiogenic MAB for the mCRC treatment. Further new drugs are on the horizon and new diagnostic tools will be introduced soon. Key Messages: Molecular heterogeneity of mCRC has been recognized as pivotal in the evolution of clonal populations during anti-EGFR therapies. Mutations in RAS genes predict a lack of response to anti-EGFR MABs. Mutations in the mitogen-activated protein kinase-phosphoinositide 3-kinase pathways like BRAF or PIK3CA mutations or HER2/ERBB2 or MET amplifications bypass EGFR signaling and also may confer resistance to anti-EGFR MABs. HER2/ERBB2 amplification is a further driver of resistance to anti-EGFR MABs in mCRC. The phase II study of HER2 Amplification for Colo-Rectal Cancer Enhanced Stratification (HERACLES) discovers that a dual HER2-targeted therapy may be an option for HER2-amplified mCRC. The mismatch repair deficiency predicts responsiveness to an immune checkpoint blockade with the anti-PD-1 immune checkpoint inhibitor pembrolizumab. Conclusions: The understanding of primary (de novo) and secondary (acquired) resistance to anti-EGFR therapies, new targeted therapies, immuno-oncology and about predictive biomarkers in mCRC is guiding the development of rational therapeutic strategies. Combinations of targeted therapies are necessary to effectively treat drug-resistant cancers. Liquid biopsy is an upcoming new tool in the primary diagnosis and follow-up analysis of mutations in circulating tumor DNA. (C) 2016 S. Karger AG, Basel
C1 [Pohl, Michael; Schmiegel, Wolff] Univ Klinikum Knappsch Krankenhaus, Dept Med, Bochum, Germany.
C3 Ruhr University Bochum
RP Schmiegel, W (corresponding author), Univ Klinikum Knappsch Krankenhaus Bochum, Dept Med, Schornau 23-25, DE-44892 Bochum, Germany.
EM meduni-kkh@rub.de
FU Amgen; Merck Serono; Roche; Lilly; Sanofi-Aventis; Baxalta; Celgene; MCI
   Munchen; Novartis; Alexion; Janssen-Cilag; AiCuris; Apceth; AstraZeneca;
   Indivumed; Ganymed
FX M.P. has received consulting fees or honoraria and has served as a
   speaker or advisory board member for Amgen, Merck Serono, Roche, Lilly,
   Sanofi-Aventis, Baxalta, Celgene, MCI Munchen, Novartis, Alexion,
   Janssen-Cilag.W.S. has received consulting fees or has an advisory role
   for: AiCuris, Amgen, Apceth, AstraZeneca, Indivumed, Merck Serono,
   Roche; and obtained honoraria from: Abbott, Falk Foundation, GSB GmbH,
   Lilly Deutschland GmbH, MedCongress, Merck Serono, MCI, Pfizer, Roche,
   Sanofi Aventis, Siemens Healthcare; and obtained research funding from
   Ganymed, Novartis, Roche; and has cooperations with: Sysmex.
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NR 25
TC 21
Z9 22
U1 1
U2 13
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0257-2753
EI 1421-9875
J9 DIGEST DIS
JI Dig. Dis.
PY 2016
VL 34
IS 5
BP 574
EP 579
DI 10.1159/000445267
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DP8VQ
UT WOS:000378776400018
PM 27332557
DA 2025-01-04
ER

PT J
AU Gall, L
   Jardi, F
   Lammens, L
   Piñero, J
   Souza, TM
   Rodrigues, D
   Jennen, DGJ
   de Kok, TM
   Coyle, L
   Chung, SW
   Ferreira, S
   Jo, H
   Beattie, KA
   Kelly, C
   Duckworth, CA
   Pritchard, DM
   Pin, C
AF Gall, Louis
   Jardi, Ferran
   Lammens, Lieve
   Pinero, Janet
   Souza, Terezinha M.
   Rodrigues, Daniela
   Jennen, Danyel G. J.
   de Kok, Theo M.
   Coyle, Luke
   Chung, Seung-Wook
   Ferreira, Sofia
   Jo, Heeseung
   Beattie, Kylie A.
   Kelly, Colette
   Duckworth, Carrie A.
   Pritchard, D. Mark
   Pin, Carmen
TI A dynamic model of the intestinal epithelium integrates multiple sources
   of preclinical data and enables clinical translation of drug-induced
   toxicity
SO CPT-PHARMACOMETRICS & SYSTEMS PHARMACOLOGY
LA English
DT Article
ID PEGYLATED LIPOSOMAL DOXORUBICIN; METASTATIC COLORECTAL-CANCER;
   RECEPTOR-TYROSINE KINASE; SOFT-TISSUE SARCOMAS; STEM-CELLS; IN-VITRO;
   CITRULLINE; MARKER; GEFITINIB; PLASMA
AB We have built a quantitative systems toxicology modeling framework focused on the early prediction of oncotherapeutic-induced clinical intestinal adverse effects. The model describes stem and progenitor cell dynamics in the small intestinal epithelium and integrates heterogeneous epithelial-related processes, such as transcriptional profiles, citrulline kinetics, and probability of diarrhea. We fitted a mouse-specific version of the model to quantify doxorubicin and 5-fluorouracil (5-FU)-induced toxicity, which included pharmacokinetics and 5-FU metabolism and assumed that both drugs led to cell cycle arrest and apoptosis in stem cells and proliferative progenitors. The model successfully recapitulated observations in mice regarding dose-dependent disruption of proliferation which could lead to villus shortening, decrease of circulating citrulline, increased diarrhea risk, and transcriptional induction of the p53 pathway. Using a human-specific epithelial model, we translated the cytotoxic activity of doxorubicin and 5-FU quantified in mice into human intestinal injury and predicted with accuracy clinical diarrhea incidence. However, for gefitinib, a specific-molecularly targeted therapy, the mice failed to reproduce epithelial toxicity at exposures much higher than those associated with clinical diarrhea. This indicates that, regardless of the translational modeling approach, preclinical experimental settings have to be suitable to quantify drug-induced clinical toxicity with precision at the structural scale of the model. Our work demonstrates the usefulness of translational models at early stages of the drug development pipeline to predict clinical toxicity and highlights the importance of understanding cross-settings differences in toxicity when building these approaches.
C1 [Gall, Louis; Pin, Carmen] AstraZeneca, Clin Pharmacol & Quantitat Pharmacol, Clin Pharmacol & Safety Sci, R&D, Cambridge, England.
   [Jardi, Ferran; Lammens, Lieve] Janssen Pharmaceut NV, Preclin Sci & Translat Safety, Beerse, Belgium.
   [Pinero, Janet] UPF, Hosp del Mar Med Res Inst IMIM, Res Programme Biomed Informat GRIB, Barcelona 08003, Spain.
   [Souza, Terezinha M.; Rodrigues, Daniela; Jennen, Danyel G. J.; de Kok, Theo M.] Maastricht Univ, GROW Sch Oncol & Dev Biol, Dept Toxicogen, Maastricht, Netherlands.
   [Coyle, Luke; Chung, Seung-Wook] Boehringer Ingelheim Int GmbH, Ridgefield, CT USA.
   [Ferreira, Sofia; Jo, Heeseung] Certara UK Ltd, Simcyp Div, Sheffield, England.
   [Beattie, Kylie A.] GSK, Target & Syst Safety, Nonclin Safety, In Vivo In Vitro Translat, Stevenage, England.
   [Kelly, Colette; Duckworth, Carrie A.; Pritchard, D. Mark] Univ Liverpool, Inst Syst Mol & Integrat Biol, Liverpool, England.
C3 AstraZeneca; Johnson & Johnson; Johson & Johnson Belgium; Janssen
   Pharmaceuticals; Pompeu Fabra University; Hospital del Mar Research
   Institute; Hospital del Mar; Maastricht University; Certara UK Ltd;
   GlaxoSmithKline; University of Liverpool
RP Pin, C (corresponding author), AstraZeneca, Clin Pharmacol & Quantitat Pharmacol, Clin Pharmacol & Safety Sci, R&D, Cambridge, England.
EM carmen.pin@astrazeneca.com
RI Duckworth, Carrie/K-7302-2014; Piñero, Janet/O-6583-2016; jardi,
   ferran/LTE-4251-2024; pin, carmen/C-8959-2014
OI Pritchard, David Mark/0000-0001-7971-3561; Gall,
   Louis/0000-0002-1805-2357; Jennen, Danyel/0000-0002-8618-2487
FU TransQST consortium; Innovative Medicines Initiative 2 Joint
   Undertaking; European Union; EFPIA;  [116030]
FX The authors acknowledge financial support from TransQST consortium. This
   project has received funding from the Innovative Medicines Initiative 2
   Joint Undertaking under grant agreement No. 116030. This Joint
   Undertaking receives support from the European Union & apos;s Horizon
   2020 research and innovation program and EFPIA.
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NR 64
TC 3
Z9 3
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2163-8306
J9 CPT-PHARMACOMET SYST
JI CPT-PHARMACOMET. SYST. PHARMACOL.
PD OCT
PY 2023
VL 12
IS 10
BP 1511
EP 1528
DI 10.1002/psp4.13029
EA SEP 2023
PG 18
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA X6IG1
UT WOS:001066396400001
PM 37621010
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zheng, YT
   Yang, HY
   Li, T
   Zhao, B
   Shao, TF
   Xiang, XQ
   Cai, WM
AF Zheng, Yuan-ting
   Yang, Hui-ying
   Li, Tao
   Zhao, Bei
   Shao, Teng-fei
   Xiang, Xiao-qiang
   Cai, Wei-min
TI Amiloride sensitizes human pancreatic cancer cells to erlotinib <i>in
   vitro</i> through inhibition of the PI3K/AKT signaling pathway
SO ACTA PHARMACOLOGICA SINICA
LA English
DT Article
DE amiloride; erlotinib; pancreatic cancer; drug synergism; targeted
   therapy; PI3K/AKT signaling pathway
ID FACTOR RECEPTOR INHIBITOR; PHASE-III TRIAL; LUNG-CANCER;
   COLORECTAL-CANCER; EXPERIMENTAL CARCINOGENESIS; EGFR MUTATIONS; RAS
   MUTATIONS; GEMCITABINE; THERAPY; CYTOTOXICITY
AB Aim: Blockade of EGFR by EGFR tyrosine kinase inhibitors such as erlotinib is insufficient for effective treatment of human pancreatic cancer due to independent activation of the Akt pathway, while amiloride, a potassium-sparing diuretic, has been found as a potential Akt inhibitor. The aim of this study was to investigate the anticancer effects of combined amiloride with erlotinib against human pancreatic cancer cells in vitro.
   Methods: Cell proliferation, colony formation, cell cycle and apoptosis were analyzed in 4 human pancreatic cancer cell lines Bxpc-3, PANC-1, Aspc-1 and CFPAC-1 treated with erlotinib or amiloride alone, or in their combination. The synergistic analysis for the effects of combinations of amiloride and erlotinib was performed using Chou-Talalay's combination index isobolographic method.
   Results: Amiloride (10, 30, and 100 mu mol/L) concentration-dependently potentiated erlotinib-induced inhibition of cell proliferation and colony formation in the 4 pancreatic cancer cell lines. Isobolographic analysis confirmed that combinations of amiloride and erlotinib produced synergistic cytotoxic effects. Amiloride significantly potentiated erlotinib-induced G(0)/G(1) cell-cycle arrest and apoptosis in Bxpc-3 and PANC-1 cells. Amiloride inhibited EGF-stimulated phorsphorylation of AKT, and significantly enhanced erlotinib-induced downregulation of phorsphorylation of EGFR, AKT, PI3K P85 and GSK 3 beta in Bxpc-3 and PANC-1 cells.
   Conclusion: Amiloride sensitizes human pancreatic cancer cells to erlotinib in vitro through inhibition of the PI3K/AKT signaling pathway. Treatment of pancreatic cancer patients with combination of erlotinib and amiloride merits further investigation.
C1 [Zheng, Yuan-ting; Yang, Hui-ying; Li, Tao; Zhao, Bei; Shao, Teng-fei; Xiang, Xiao-qiang; Cai, Wei-min] Fudan Univ, Sch Pharm, Dept Clin Pharm, Shanghai 201203, Peoples R China.
C3 Fudan University
RP Cai, WM (corresponding author), Fudan Univ, Sch Pharm, Dept Clin Pharm, Shanghai 201203, Peoples R China.
EM weimincai@fudan.edu.cn
RI li, tao/W-7441-2019; Zheng, Yufan/KGL-8964-2024; Shao,
   Tengfei/LGY-0284-2024; Cai, Weimin/I-4442-2015
OI Cai, Weimin/0000-0002-0342-4912
FU National Natural Science Foundation of China [81102459]; Fundamental
   Research Funds for the Central Universities
FX We sincerely appreciate Dr Li-xin Wu (Fudan-Zhangjiang New Drug R&D
   Joint Platform, Shanghai, China) for assistance with cell cycle
   analysis. The project was supported by the National Natural Science
   Foundation of China (81102459) and the Fundamental Research Funds for
   the Central Universities.
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NR 29
TC 26
Z9 27
U1 0
U2 22
PU ACTA PHARMACOLOGICA SINICA
PI SHANGHAI
PA 294 TAI-YUAN RD, SHANGHAI, 200031, PEOPLES R CHINA
SN 1671-4083
EI 1745-7254
J9 ACTA PHARMACOL SIN
JI Acta Pharmacol. Sin.
PD MAY
PY 2015
VL 36
IS 5
BP 614
EP 626
DI 10.1038/aps.2015.4
PG 13
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA CH2YY
UT WOS:000353893100009
PM 25864651
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Mizukami, T
   Togashi, Y
   Naruki, S
   Banno, E
   Terashima, M
   de Velasco, MA
   Sakai, K
   Yoneshige, A
   Hayashi, H
   Fujita, Y
   Tomida, S
   Nakajima, TE
   Fujino, T
   Boku, N
   Ito, A
   Nakagawa, K
   Nishio, K
AF Mizukami, Takuro
   Togashi, Yosuke
   Naruki, Saeko
   Banno, Eri
   Terashima, Masato
   de Velasco, Marco A.
   Sakai, Kazuko
   Yoneshige, Azusa
   Hayashi, Hidetoshi
   Fujita, Yoshihiko
   Tomida, Shuta
   Nakajima, Takako Eguchi
   Fujino, Takashi
   Boku, Narikazu
   Ito, Akihiko
   Nakagawa, Kazuhiko
   Nishio, Kazuto
TI Significance of FGF9 gene in resistance to anti-EGFR therapies targeting
   colorectal cancer: A subset of colorectal cancer patients with
   <i>FGF9</i> upregulation may be resistant to anti-EGFR therapies
SO MOLECULAR CARCINOGENESIS
LA English
DT Article
DE colorectal cancer; FGF9; anti-EGFR therapy; drug resistance; KRAS
ID GROWTH-FACTOR 9; 1ST-LINE TREATMENT; CETUXIMAB; AMPLIFICATION;
   EXPRESSION; MUTATIONS; CARCINOMA; TUMORS; OVEREXPRESSION; FLUOROURACIL
AB Although fibroblast growth factor (FGF) signals are strongly associated with malignancy, limited information is available regarding the role of the FGF9 signal in colorectal cancer (CRC). In this study, we investigated the frequency of FGF9 amplification in CRC clinical specimens and the association between the FGF9 gene and resistance to anti-EGFR therapies. In clinical samples, an FGF9 copy number gain of 5 copies was observed at a frequency of 8/145 (5.5%) and tended to be related to wild-type KRAS (7/96, 7.3%). Furthermore, FGF9 amplification was not observed in any of the samples from the 15 responders to anti-EGFR therapies but was observed in one sample from the seven non-responders with wild-type KRAS, and two samples from non-responders also had high FGF9 mRNA expression levels. FGF9 amplification was validated using a fluorescence in situ hybridization (FISH) analysis, and FGF9-amplified sections showed readily detectable signals originating from FGF9 protein when examined using immunohistochemistry. In both the in vitro and in vivo experiments using FGF9-overexpressing CRC cell lines, FGF9 overexpression induced strong resistance to anti-EGFR therapies via the enforced FGFR signal, and this resistance was cancelled by the application of an FGFR inhibitor. Considering these results, the FGF9 gene may play an important role in resistance to anti-EGFR therapies in patients with CRC, and such resistance might be overcome by combined treatment with an anti-FGFR inhibitor. These findings strongly encourage the development of FGFR-targeted therapy for CRC patients with FGF9 gene upregulation. (c) 2016 Wiley Periodicals, Inc.
C1 [Mizukami, Takuro; Togashi, Yosuke; Banno, Eri; Terashima, Masato; de Velasco, Marco A.; Sakai, Kazuko; Hayashi, Hidetoshi; Fujita, Yoshihiko; Tomida, Shuta; Nishio, Kazuto] Kinki Univ, Dept Genome Biol, Sch Med, 377-2 Ohno Higashi, Osaka, Japan.
   [Mizukami, Takuro; Nakajima, Takako Eguchi; Boku, Narikazu] St Marianna Univ, Dept Clin Oncol, Sch Med, Kawasaki, Kanagawa, Japan.
   [Naruki, Saeko; Fujino, Takashi] St Marianna Univ, Dept Pathol, Sch Med, Kawasaki, Kanagawa, Japan.
   [Yoneshige, Azusa; Ito, Akihiko] Kinki Univ, Dept Pathol, Sch Med, Osaka, Japan.
   [Hayashi, Hidetoshi; Nakagawa, Kazuhiko] Kinki Univ, Dept Med Oncol, Sch Med, Osaka, Japan.
C3 Kindai University (Kinki University); Saint Marianna University; Saint
   Marianna University; Kindai University (Kinki University); Kindai
   University (Kinki University)
RP Tomida, S; Boku, N (corresponding author), Kinki Univ, Dept Genome Biol, Sch Med, 377-2 Ohno Higashi, Osaka, Japan.
EM shuta.tomida@okayama-u.ac.jp; nboku@ncc.go.jp
RI Togashi, Yosuke/KEH-7959-2024; NAKAGAWA, KAZUHIKO/ADM-9196-2022;
   NAKAJIMA, TAKAKO/AAY-4544-2020; De Velasco, Marco Antonio/R-1022-2019
OI Fujino, Takashi/0000-0002-0953-7379; De Velasco, Marco
   Antonio/0000-0002-4011-6572; Yoneshige, Azusa/0009-0007-4638-8476
FU Applied Research for Innovative Treatment of Cancer program
   [15ck0106018h0002]; Japan Agency for Medical Research and Development
   (AMED) [15H06754]; Grants-in-Aid for Scientific Research [15K15113,
   15H06754] Funding Source: KAKEN
FX The authors thank Mr. Shinji Kurashimo, Mr. Yoshihiro Mine, Ms. Eiko
   Honda, Ms. Tomoko Kitayama, Ms. Ayaka Kurumatani, and Dr. Yoshimi Hosono
   for their technical assistance. This research was supported by the
   Applied Research for Innovative Treatment of Cancer program
   (15ck0106018h0002) (K. Nishio) of the Japan Agency for Medical Research
   and Development (AMED) established by the Ministry of Health, Labour and
   Welfare of Japan and Grant-in-Aid for Research Activity start-up
   (15H06754) (Y. Togashi).
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NR 42
TC 17
Z9 18
U1 0
U2 23
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0899-1987
EI 1098-2744
J9 MOL CARCINOGEN
JI Mol. Carcinog.
PD JAN
PY 2017
VL 56
IS 1
BP 106
EP 117
DI 10.1002/mc.22476
PG 12
WC Biochemistry & Molecular Biology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA EE9EZ
UT WOS:000389930000008
PM 26916220
DA 2025-01-04
ER

PT J
AU Itzhaki, E
   Hadad, E
   Moskovits, N
   Stemmer, SM
   Margel, S
AF Itzhaki, Ella
   Hadad, Elad
   Moskovits, Neta
   Stemmer, Salomon M.
   Margel, Shlomo
TI Tumor-Targeted Fluorescent Proteinoid Nanocapsules Encapsulating
   Synergistic Drugs for Personalized Cancer Therapy
SO PHARMACEUTICALS
LA English
DT Article
DE personalized cancer therapy; proteinoids; RGD polymers; synergistic
   drugs; nanocapsules; targeted delivery
ID 4/6 INHIBITOR PALBOCICLIB; BREAST-CANCER; AMINO-ACIDS; THERMAL
   COPOLYMERIZATION; DELIVERY APPLICATIONS; NANOPARTICLES; LETROZOLE;
   SYSTEMS; RGD; COMBINATION
AB Personalized cancer treatment based on specific mutations offers targeted therapy and is preferred over "standard" chemotherapy. Proteinoid polymers produced by thermal step-growth polymerization of amino acids may form nanocapsules (NCs) that encapsulate drugs overcoming miscibility problems and allowing passive targeted delivery with reduced side effects. The arginine-glycine-glutamic acid (RGD) sequence is known for its preferential attraction to alpha v beta 3 integrin, which is highly expressed on neovascular endothelial cells that support tumor growth. Here, tumor-targeted RGD-based proteinoid NCs entrapping a synergistic combination of Palbociclib (Pal) and Alpelisib (Alp) were synthesized by self-assembly to induce the reduction of tumor cell growth in different types of cancers. The diameters of the hollow and drug encapsulating poly(RGD) NCs were 34 +/- 5 and 22 +/- 3 nm, respectively; thereby, their drug targeted efficiency is due to both passive and active targeting. The encapsulation yield of Pal and Alp was 70 and 90%, respectively. In vitro experiments with A549, MCF7 and HCT116 human cancer cells demonstrate a synergistic effect of Pal and Alp, controlled release and dose dependence. Preliminary results in a 3D tumor spheroid model with cells derived from patient-derived xenografts of colon cancer illustrate disassembly of spheroids, indicating that the NCs have therapeutic potential.
C1 [Itzhaki, Ella; Hadad, Elad; Margel, Shlomo] Bar Ilan Univ, Inst Nanotechnol & Adv Mat BINA, Dept Chem, IL-5290002 Ramat Gan, Israel.
   [Moskovits, Neta; Stemmer, Salomon M.] Rabin & Felsenstein Med Ctr, Davidoff Ctr, Beilinson Campus, IL-49100 Petah Tiqwa, Israel.
   [Stemmer, Salomon M.] Tel Aviv Univ, Sackler Fac Med, IL-6997801 Tel Aviv, Israel.
C3 Bar Ilan University; Rabin Medical Center; Tel Aviv University
RP Margel, S (corresponding author), Bar Ilan Univ, Inst Nanotechnol & Adv Mat BINA, Dept Chem, IL-5290002 Ramat Gan, Israel.
EM elaeli3543@gmail.com; eladha300@gmail.com; neta.moskovits@gmail.com;
   stemmer@post.tau.ac.il; Shlomo.margel@biu.ac.il
OI stemmer, salomon/0000-0002-8733-3929; Margel, Shlomo/0000-0001-6524-8179
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NR 74
TC 6
Z9 6
U1 1
U2 14
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1424-8247
J9 PHARMACEUTICALS-BASE
JI Pharmaceuticals
PD JUL
PY 2021
VL 14
IS 7
AR 648
DI 10.3390/ph14070648
PG 19
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA TO1TT
UT WOS:000676704000001
PM 34358074
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Liao, X
   Song, G
   Xu, ZH
   Bu, Y
   Chang, F
   Jia, FG
   Xiao, XL
   Ren, XJ
   Zhang, M
   Jia, QG
AF Liao, Xia
   Song, Ge
   Xu, Zihan
   Bu, Yang
   Chang, Fan
   Jia, Fengan
   Xiao, Xuelian
   Ren, Xuejiao
   Zhang, Mei
   Jia, Qingan
TI Oxaliplatin resistance is enhanced by saracatinib via upregulation
   Wnt-ABCG1 signaling in hepatocellular carcinoma
SO BMC CANCER
LA English
DT Article
DE Hepatocellular carcinoma; Oxaliplatin resistance; Saracatinib; Wnt
   signaling; ABCG1
ID COLORECTAL-CANCER; SRC; DOXORUBICIN; INHIBITION; EXPRESSION; GROWTH;
   CELLS
AB Background Chemo-resistance in hepatocellular carcinoma (HCC) is a major problem, and acquired drug resistance prevents cancer therapies from achieving complete responses. Molecular targeting therapy presents an opportunity to impede tumor through combination or sequential therapy, while the accurate effect is vague. Methods The efficacy of combinations between oxaliplatin and anti-cancer molecular targeting drugs was screened. Strangely, the combined chemotherapy with oxaliplatin and saracatinib induced significantly antagonistic effects. Then the antitumor effects of combined treatment with saracatinib and oxaliplatin were confirmed in wide type HCC as well as in saracatinib- and oxaliplatin-resistant HCC. RNA sequencing was used to explore the resistance mechanism, and the roles of ATP-binding cassette transporter G1 (ABCG1) and Wnt signaling in oxaliplatin resistance were confirmed. Results Chemotherapy with oxaliplatin and saracatinib individually induced strong anti-HCC effects, while combined or sequential treatment of HCC cells with these two drugs exhibited reduced efficacy compared to treatment with the single drugs. And it was saracatinib treatment caused oxaliplatin resistance. RNA sequencing revealed 458 genes that were altered by treatment with saracatinib and oxaliplatin. Of these, the gene encoding ABCG1 and Wnt-associated genes were significantly upregulated. Upregulation of ABCG1 and oxaliplatin resistance were associated with activation of Wnt signaling. Interference with ABCG1 expression or inhibition of Wnt signaling resulted in reversal of the saracatinib-induced oxaliplatin resistance in HCC. Conclusions These studies demonstrated that combined or sequential chemotherapy with oxaliplatin and saracatinib reduced antitumor efficacy, and this antagonism was attributed to the activation of Wnt signaling and upregulation of ABCG1 by saracatinib.
C1 [Liao, Xia; Song, Ge] Xi An Jiao Tong Univ, Dept Nutr, Affiliated Hosp 1, Xian 710061, Peoples R China.
   [Xu, Zihan] Shaanxi Prov Peoples Hosp, Dept Burns & Plast Surg, Xian 710068, Peoples R China.
   [Bu, Yang] Ningxia Med Univ, Gen Hosp, Dept Hepatobiliary Surg, Yinchuan 750001, Ningxia, Peoples R China.
   [Chang, Fan; Jia, Fengan] Shaanxi Inst Microbiol, Metabolite Res Ctr, Xian 710043, Peoples R China.
   [Xiao, Xuelian; Zhang, Mei; Jia, Qingan] Xi An Jiao Tong Univ, Dept Hepatobiliary Surg, Affiliated Hosp 1, 277 West Yanta Rd, Xian 710061, Peoples R China.
   [Ren, Xuejiao] Yanan Univ, Med Coll, Yanan 716000, Peoples R China.
C3 Xi'an Jiaotong University; Xi'an Medical University; Ningxia Medical
   University; Xi'an Jiaotong University; Yanan University
RP Jia, QG (corresponding author), Xi An Jiao Tong Univ, Dept Hepatobiliary Surg, Affiliated Hosp 1, 277 West Yanta Rd, Xian 710061, Peoples R China.
EM qajia66@163.com
RI xu, zihan/KHZ-4930-2024
FU National Natural Science Foundation of China [81502694]; Fundamental
   Research Funds for the Central Universities [1191329835]; Postdoctoral
   Science Foundation of China [2015 M570330]; Key projects of Ningxia
   Natural Science Foundation [NZ15130]
FX This research project was mainly supported by the National Natural
   Science Foundation of China (81502694). This research project was also
   partly supported by the Fundamental Research Funds for the Central
   Universities (1191329835), Postdoctoral Science Foundation of China
   (2015 M570330), and Key projects of Ningxia Natural Science Foundation
   (NZ15130). The funders had no role in the study design, data collection
   and interpretation, or decision to submit the work for publication.
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JI BMC Cancer
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WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KL8EV
UT WOS:000513651200001
PM 31931755
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Nieto-Jiménez, C
   Sanvicente, A
   Díaz-Tejeiro, C
   Moreno, V
   de Sá, A
   Calvo, E
   Martínez-López, J
   Pérez-Segura, P
   Ocaña, A
AF Nieto-Jimenez, Cristina
   Sanvicente, Adrian
   Diaz-Tejeiro, Cristina
   Moreno, Victor
   Lopez de Sa, Alfonso
   Calvo, Emiliano
   Martinez-Lopez, Joaquin
   Perez-Segura, Pedro
   Ocana, Alberto
TI Uncovering therapeutic opportunities in the clinical development of
   antibody-drug conjugates
SO CLINICAL AND TRANSLATIONAL MEDICINE
LA English
DT Review
DE ADC; clinical approach; new therapies; targeted therapy
ID CANCER
AB IntroductionAntibody-drug conjugates (ADCs) are a family of therapeutic agents that have demonstrated clinical activity in several indications.Material and methodsIn this article, we performed a deep analysis of their clinical landscape matched with public genomic human datasets from tumour antigen targets (TATs), to identify empty areas for clinical development.ResultsWe observed that TATs used in haematological malignancies were more specific than the ones developed in solid cancers. Those included CD19, CD22, CD30, CD33 and CD79b. In solid tumours, we identified TATs, with approved ADCs, widely expressed in non-explored niche indications like Enfortumab vedotin (anti-Nectin4) in lung or cervical cancer; Tisotumab vedotin (anti-TF) in glioblastoma or pancreatic cancer; and Sacituzumab govitecan (anti-TROP2) in pancreatic, gastric, thyroid or endometrial cancer, among others. Similarly, niche indications for ADCs in clinical development included targets for CD71, PSMA, PTK7 or CD74, in tumours like breast, lung, stomach or colon. Some of these TATs were essential for the survival of tumour cells like CD71, PSMA and PTK7.ConclusionsIn summary, our study opens the door for further evaluation of ADCs in several indications not explored before.
   & BULL; Most ongoing Antibody-drug conjugates (ADCs) have a classical structure, with a minority of them with specific formats & BULL; ADCs against TAAs of haematological malignancies are more specific than those for solid tumours.& BULL; Niche indications for ADCs included targets for CD71, PSMA, PTK7 or CD74, in breast, lung, stomach or colon cancer.& BULL; Some of these TAAs are essential genes like CD71, PSMA and PTK7 & BULL; This study opens the door for further evaluation of ADCs in non-explored indications.image
C1 [Nieto-Jimenez, Cristina; Sanvicente, Adrian; Diaz-Tejeiro, Cristina; Lopez de Sa, Alfonso; Perez-Segura, Pedro; Ocana, Alberto] Inst Invest Sanitaria San Carlos IdISSC, Hosp Clin San Carlos HCSC, Expt Therapeut Unit, Madrid 28040, Spain.
   [Sanvicente, Adrian] Univ Complutense, Fac Ciencias Quim, Madrid, Spain.
   [Moreno, Victor; Calvo, Emiliano; Ocana, Alberto] Hosp Fdn Jimenez Diaz, START Madrid FJD, Madrid, Spain.
   [Martinez-Lopez, Joaquin] Hosp Univ 12 Octubre, Ctr Nacl Invest Oncol H12O CNIO, Spanish Natl Canc Res Ctr, Haematol Malignancies Clin Res Unit, Madrid, Spain.
   [Martinez-Lopez, Joaquin] Univ Complutense, Hosp Univ Octubre 12, Inst Invest Sanitaria Hosp Octubre Imas 12 12, Dept Hematol, Madrid, Spain.
   [Ocana, Alberto] Ctr Invest Biomed Red Oncol CIBERONC, Breast Canc, Madrid, Spain.
C3 Complutense University of Madrid; Fundacion Jimenez Diaz; Centro
   Nacional de Investigaciones Oncologicas (CNIO); Hospital Universitario
   12 de Octubre; Hospital Universitario 12 de Octubre; Complutense
   University of Madrid; CIBER - Centro de Investigacion Biomedica en Red;
   CIBERONC
RP Nieto-Jiménez, C; Ocaña, A (corresponding author), Inst Invest Sanitaria San Carlos IdISSC, Hosp Clin San Carlos HCSC, Expt Therapeut Unit, Madrid 28040, Spain.
EM cnietoj@salud.madrid.org
RI martinez, joaquin/AAN-6939-2020; Nieto, Cristina/AFV-2076-2022; Moreno,
   Victor/A-1697-2010
OI Lopez-de-Sa, Alfonso/0000-0003-0742-1150; Nieto Jimenez,
   Cristina/0000-0002-3463-1439; Ocana, Alberto/0000-0002-1067-9630;
   Martinez-Lopez, Joaquin/0000-0001-7908-0063; Sanvicente Garcia,
   Adrian/0000-0002-6511-2498
FU Thanks to my family Raquel Pez, Mateo, Pablo, Rodrigo and Ines Ocana
   Pez, for their continuous support.
FX Instituto de Salud Carlos III, Grant/Award Number: PI19/00808; CRIS
   CANCER foundation, Grant/Award Number: PPS.C02CRIS/AOF.C01CRISr Thanks
   to my family Raquel Paez, Mateo, Pablo, Rodrigo and Ines Ocana Paez, for
   their continuous support.
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NR 25
TC 7
Z9 8
U1 2
U2 9
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 SEP
PY 2023
VL 13
IS 9
AR e1329
DI 10.1002/ctm2.1329
PG 10
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA S2ZP6
UT WOS:001069907800001
PM 37740463
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Raveendran, A
   Surendran, SP
   Ser, J
   Alam, K
   Cho, H
   Jeong, YY
AF Raveendran, Athira
   Surendran, Suchithra Poilil
   Ser, Jinhui
   Alam, Khurshed
   Cho, Hoonsung
   Jeong, Yong Yeon
TI Heptamethine Cyanine Dye MHI-148-Mediated Drug Delivery System to
   Enhance the Anticancer Efficiency of Paclitaxel
SO INTERNATIONAL JOURNAL OF NANOMEDICINE
LA English
DT Article
DE cancer therapy; colon cancer; bioconjugation; fluorescent dye;
   paclitaxel
ID CELL LUNG-CANCER; IR-780 DYE; HYPOXIA; RELEASE; TARGETS
AB Introduction: Paclitaxel (PTX) is a conventional chemotherapeutic drug that effectively treats various cancers. The cellular uptake and therapeutic potential of PTX are limited by its slow penetration and low solubility in water. The development of cancer chemotherapy methods is currently facing considerable challenges with respect to the delivery of the drugs, particularly in targeting the tumor site without exerting detrimental effects on the healthy surrounding cells. One possibility for improving the therapeutic potential is through the development of tumor-targeted delivery methods. Methods: We successfully synthesized paclitaxel-MHI-148 conjugates (PTX-MHI) by coupling PTX with the tumor-targeting heptamethine cyanine dye MHI-148. Synthesis and purification were characterized using the absorbance spectrum and the results of time-of-flight mass spectrometry. Cellular uptake and cytotoxicity studies were conducted in vitro and in vivo. Results: PTX-MHI accumulates in tumor cells but not in normal cells, as observed by in vitro near-infrared fluorescent (NIRF) imaging along with in vivo NIRF imaging and organ biodis-tribution studies. We observed that MHI-148-conjugated PTX shows greater efficiency in cancer cells than PTX alone, even in the absence of light treatment. PTX-MHI could also be used for specific drug delivery to intracellular compartments, such as the mitochondria and lysosomes of cancer cells, to improve the outcomes of tumor-targeting therapy. Conclusion: The results indicated that PTX-MHI-mediated cancer therapy exerts an excel-lent inhibitory effect on colon carcinoma (HT-29) cell growth with low toxicity in normal fibroblasts (NIH3T3).
C1 [Raveendran, Athira; Ser, Jinhui; Alam, Khurshed; Cho, Hoonsung] Chonnam Natl Univ, Dept Mat Sci & Engn, Gwangju 61186, South Korea.
   [Surendran, Suchithra Poilil] Chonnam Natl Univ Med Sch, Dept Biomed Sci, Hwasun 58128, South Korea.
   [Jeong, Yong Yeon] Chonnam Natl Univ Hwasun Hosp, Dept Radiol, Hwasun 58128, South Korea.
C3 Chonnam National University; Chonnam National University; Chonnam
   National University; Chonnam National University Hospital
RP Cho, H (corresponding author), Chonnam Natl Univ, Dept Mat Sci & Engn, Gwangju 61186, South Korea.; Jeong, YY (corresponding author), Chonnam Natl Univ Hwasun Hosp, Dept Radiol, Hwasun 58128, South Korea.
EM cho.hoonsung@jnu.ac.kr; yjeong@jnu.ac.kr
OI Raveendran, Athira/0000-0002-4853-4330; Ser, Jinhui/0000-0002-8673-7374;
   Alam, Khurshed/0000-0001-8115-4711; Poilil Surendran,
   Suchithra/0000-0002-5457-7716
FU Technology Innovation Program - Ministry of Trade, Industry & Energy
   (MOTIE, Korea) [20003822]; Basic Science Research Program through the
   National Research Foundation of Korea (NRF) - Ministry of Education
   [2018R1D1A1B07049867, 2021R1F1A1064062]
FX This work was supported by the Technology Innovation Program (or
   Industrial Strategic Technology Development Program-Development of Core
   Industrial Technology) (20003822, Development of Navigation System
   Technologies of Micro Nano Robots with Drug for Brain Disease Therapy)
   funded By the Ministry of Trade, Industry & Energy (MOTIE, Korea) and by
   the Basic Science Research Program through the National Research
   Foundation of Korea (NRF) funded by the Ministry of Education
   (2018R1D1A1B07049867, 2021R1F1A1064062).
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NR 43
TC 6
Z9 6
U1 1
U2 14
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-2013
J9 INT J NANOMED
JI Int. J. Nanomed.
PY 2021
VL 16
BP 7169
EP 7180
DI 10.2147/IJN.S325322
PG 12
WC Nanoscience & Nanotechnology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Pharmacology & Pharmacy
GA WM5SZ
UT WOS:000711146300001
PM 34707356
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Chen, WY
   Yan, HJ
   Li, XD
   Ge, KL
   Wu, J
AF Chen, Wenyu
   Yan, Haijiao
   Li, Xiaodong
   Ge, Kele
   Wu, Jun
TI Circulating tumor DNA detection and its application status in gastric
   cancer: a narrative review
SO TRANSLATIONAL CANCER RESEARCH
LA English
DT Review
DE Circulating tumor DNA (ctDNA); gastric cancer (GC); liquid biopsy;
   epigenetics
ID CELL-FREE DNA; MICROSATELLITE INSTABILITY; COLORECTAL-CANCER;
   CLINICAL-SIGNIFICANCE; PROGNOSTIC-FACTOR; LIQUID BIOPSIES; PLASMA DNA;
   QUANTIFICATION; RESISTANCE; MUTATIONS
AB Circulating tumor DNA (ctDNA) is the small genomic fragment released by tumor cells into the circulating system, which carries the gene variation features, such as mutation, insertion, deletion, rearrangement, copy number variation (CNV) and methylation, rendering it an important biomarker. It can be used not only to diagnose certain types of solid tumors, but also to monitor the therapeutic response and explore the minimal residual disease (MRD) and resistant mutation of targeted therapy. Therefore, ctDNA detection may become the preferred non-invasive tumor screening method. For patients who cannot receive further gene detection due to insufficient or restricted sample collection with the defined pathological diagnosis, ctDNA detection can be carried out to determine the gene mutation type, with no need for repeated sampling. Gastric cancer (GC) is a malignancy with extremely high morbidity and mortality, and its genesis and development are the consequence of interactions of multiple factors, including environment, diet, heredity, helicobacter pylori infection, chronic inflammatory infiltration, and precancerous lesion. As the research on GC moves forward, the existing research mainly focuses on genetic and epigenetic changes, including DNA methylation, histone modification, non-coding RNA changes, gene mutation, gene heterozygosity loss and microsatellite instability. This paper aimed to summarize the contents of ctDNA detection, its application status in GC and clinical significance.
C1 [Chen, Wenyu; Yan, Haijiao; Li, Xiaodong; Ge, Kele; Wu, Jun] Soochow Univ, Affiliated Hosp 3, Dept Oncol, Juqian St, Changzhou 213003, Peoples R China.
C3 Soochow University - China
RP Wu, J (corresponding author), Soochow Univ, Affiliated Hosp 3, Dept Oncol, Juqian St, Changzhou 213003, Peoples R China.
EM wujun1408@126.com
RI Li, Xiaodong/AAA-5808-2021; Chen, Wenyu/IQV-0732-2023
FU Key Program of the Changzhou Commission of Health [ZD2017]; Young
   Talents of the Changzhou Commission of Health [QN201902]
FX This study was supported by the grants from the Key Program of the
   Changzhou Commission of Health (ZD2017, to Dr. H Yan), and the Young
   Talents of the Changzhou Commission of Health (QN201902, to Dr. X Li).
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NR 43
TC 9
Z9 9
U1 2
U2 21
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 JAN
PY 2021
VL 10
IS 1
BP 529
EP 536
DI 10.21037/tcr-20-2856
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QB8AP
UT WOS:000614359600049
PM 35116282
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Rizeq, B
   Sif, S
   Nasrallah, GK
   Ouhtit, A
AF Rizeq, Balsam
   Sif, Said
   Nasrallah, Gheyath K.
   Ouhtit, Allal
TI Novel role of BRCA1 interacting C-terminal helicase 1 (<i>BRIP1)</i>in
   breast tumour cell invasion
SO JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
LA English
DT Article
DE breast cancer; BRIP1; invasion; metastasis; proliferation; targeted
   therapy
ID N-ACETYLGLUCOSAMINYLTRANSFERASE-V; COMPARATIVE-GENOMIC-HYBRIDIZATION;
   CHROMOSOMAL IMBALANCES; COLORECTAL-CANCER; MESSENGER-RNA; DNA GAINS;
   GENE; BRIP1; OVEREXPRESSION; METASTASIS
AB Breast cancer (BC) is the most common malignancy and the leading cause of death in women worldwide. Only 5%-10% of mutations in BRCA genes are associated with familial breast tumours in Eastern countries, suggesting the contribution of other genes. Using a microarray gene expression profiling study of BC, we have recently identifiedBRIP1(fivefold up-regulation) as a potential gene associated with BC progression in the Omani population. AlthoughBRIP1regulates DNA repair and cell proliferation, the precise role ofBRIP1in BC cell invasion/metastasis has not been explored yet; this prompted us to test the hypothesis thatBRIP1promotes BC cell proliferation and invasion. Using a combination of cellular and molecular approaches, our results revealed differential overexpression ofBRIP1in different BC cell lines. Functional assays validated further the physiological relevance ofBRIP1in tumour malignancy, and siRNA-mediatedBRIP1knockdown significantly reduced BC cell motility by targeting key motility-associated genes. Moreover, down-regulation ofBRIP1expression significantly attenuated cell proliferation via cell cycle arrest. Our study is the first to show the novel function ofBRIP1in promoting BC cell invasion by regulating expression of various downstream target genes. Furthermore, these findings provide us with a unique opportunity to identifyBRIP1-induced pro-invasive genes that could serve as biomarkers and/or targets to guide the design of appropriate BC targeted therapies.
C1 [Rizeq, Balsam; Sif, Said; Ouhtit, Allal] Qatar Univ, Coll Arts & Sci, Dept Biol & Environm Sci, Doha, Qatar.
   [Rizeq, Balsam; Nasrallah, Gheyath K.] Qatar Univ, Biomed Res Ctr, Doha, Qatar.
   [Nasrallah, Gheyath K.] Qatar Univ, Coll Hlth Sci, Biomed Sci Dept, Doha, Qatar.
C3 Qatar University; Qatar University; Qatar University
RP Ouhtit, A (corresponding author), Qatar Univ, Coll Arts & Sci, Dept Biol & Environm Sci, Doha, Qatar.
EM aouhtit@qu.edu.qa
RI Nasrallah, Gheyath/H-7949-2019; Sif, Said/AAE-5554-2019; rizeq,
   balsam/AAF-5318-2020
OI Sif, Said/0000-0001-6268-1145; Nasrallah, Gheyath/0000-0001-9252-1038
FU Qatar University [QUST-2-CAS-2017-16, QUST-CASSPR-15/16-14,
   QUUG-CAS-DBES-15/16-22, QUST-1-CAS-2019-2]; Qatar National Library
   (QNL); QNL; Ali Al-Suwaidi Trading Est./PhD [CAS00010]
FX Qatar University, Grant/Award Number: QUST-2-CAS-2017-16,
   QUST-CASSPR-15/16-14, QUUG-CAS-DBES-15/16-22 and QUST-1-CAS-2019-2;
   Qatar National Library (QNL), The publication was funded by QNL; Ali
   Al-Suwaidi Trading Est./PhD, Grant/Award Number: CAS00010
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NR 56
TC 9
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U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1582-1838
EI 1582-4934
J9 J CELL MOL MED
JI J. Cell. Mol. Med.
PD OCT
PY 2020
VL 24
IS 19
BP 11477
EP 11488
DI 10.1111/jcmm.15761
EA SEP 2020
PG 12
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA OH1OW
UT WOS:000565913600001
PM 32888398
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Peng, L
   Yuan, XQ
   Jiang, BY
   Tang, ZL
   Li, GC
AF Peng, Li
   Yuan, Xiaoqing
   Jiang, Binyuan
   Tang, Zaili
   Li, Guan-Cheng
TI LncRNAs: key players and novel insights into cervical cancer
SO TUMOR BIOLOGY
LA English
DT Review
DE LncRNA; Cervical cancer; Dysregulation; Function; Mechanism; ceRNA; EMT;
   EZH2; GAS5; HOTAIR; LncRNA-ANRIL; LncRNA-CCHE1; LncRNA-EBIC; LncRNA-LET;
   m6A; MALAT1; MEG3; NEAT2; TUSC8; Xist
ID LONG NONCODING RNA; COMPETING ENDOGENOUS RNA; POOR-PROGNOSIS;
   CELL-PROLIFERATION; HUMAN-PAPILLOMAVIRUS; GASTRIC-CANCER;
   COLORECTAL-CANCER; EPIGENETIC REGULATION; DECREASED EXPRESSION;
   CARCINOMA CELLS
AB Cervical cancer contributed the second highest number of deaths in female cancers, exceeded only by breast cancer, carrying high risks of morbidity and mortality. There was a great need and urgency in searching novel treatment targets and prognosis biomarkers to improve the survival rate of cervical cancer patients. Many long non-coding RNAs (lncRNAs) were emerging as pivotal regulators in various biological processes and took vitally an effect on the oncogenesis and progression of cervical cancer. In this review, we summarized the origin and overview function of lncRNAs; highlighted the roles of lncRNAs in cervical cancer in terms of prognosis and tumor progression, invasion and metastasis, apoptosis, and radio-resistance; and outlined the molecular mechanisms of lncRNAs in cervical cancer from the aspects of the interaction of lncRNAs with proteins/mRNAs (especially in HPV protein) and miRNAs, as well as RNA N-methyladenosine (m6A) methylation of lncRNAs. Meanwhile, the application of lncRNAs as biomarkers in cervical cancer prognosis and predictors for metastasis was also discussed. An overview of these researches will be valuable for broadening horizons into mechanisms, selection of meritorious biomarkers for diagnosis as well as prognosis, and future targeted therapy of cervical cancer.
C1 [Peng, Li; Jiang, Binyuan; Li, Guan-Cheng] Cent S Univ, Canc Res Inst, Changsha 410078, Hunan, Peoples R China.
   [Peng, Li; Jiang, Binyuan; Li, Guan-Cheng] Natl Hlth & Family Planning Commiss, Key Lab Carcinogenesis, Changsha 410078, Hunan, Peoples R China.
   [Peng, Li; Jiang, Binyuan; Li, Guan-Cheng] Minist Educ, Key Lab Carcinogenesis & Canc Invas, Changsha 410078, Hunan, Peoples R China.
   [Yuan, Xiaoqing] Cent S Univ, Xiangya Hosp, Dept Clin Pharmacol, Changsha 410008, Hunan, Peoples R China.
   [Yuan, Xiaoqing] Cent S Univ, Inst Clin Pharmacol, Hunan Key Lab Pharmacogenet, Changsha 410078, Hunan, Peoples R China.
   [Tang, Zaili] Univ South China, Affiliated Hosp 1, Dept Med Record Management & Stat, Hengyang 421002, Peoples R China.
C3 Central South University; Central South University; Central South
   University; University of South China
RP Li, GC (corresponding author), Cent S Univ, Canc Res Inst, Changsha 410078, Hunan, Peoples R China.; Li, GC (corresponding author), Natl Hlth & Family Planning Commiss, Key Lab Carcinogenesis, Changsha 410078, Hunan, Peoples R China.; Li, GC (corresponding author), Minist Educ, Key Lab Carcinogenesis & Canc Invas, Changsha 410078, Hunan, Peoples R China.
EM libsun@163.com
RI yuan, xq/KTI-7992-2024
OI Peng, Li/0000-0001-5358-6736
FU Fundamental Research Funds for the Central Universities of Central South
   University [2015zzts096]; Science and Technology Department Research
   Foundation of Hunan province [12JJ2052]; Open-End Fund for the Valuable
   and Precision Instruments of Central South University [CSU2C2013048]
FX This work was supported by the Fundamental Research Funds for the
   Central Universities of Central South University (2015zzts096), the
   Science and Technology Department Research Foundation of Hunan province
   (12JJ2052), and the Open-End Fund for the Valuable and Precision
   Instruments of Central South University (CSU2C2013048). Also, we thank
   Doctor Hui Xie and Junsong Chen for critical reading and reviewing the
   manuscript.
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NR 91
TC 182
Z9 191
U1 0
U2 133
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1010-4283
EI 1423-0380
J9 TUMOR BIOL
JI Tumor Biol.
PD MAR
PY 2016
VL 37
IS 3
BP 2779
EP 2788
DI 10.1007/s13277-015-4663-9
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DK4QJ
UT WOS:000374903500001
PM 26715267
DA 2025-01-04
ER

PT J
AU Guadagni, S
   Fiorentini, G
   Clementi, M
   Palumbo, G
   Chiominto, A
   Cappelli, S
   Masedu, F
   Valenti, M
AF Guadagni, Stefano
   Fiorentini, Giammaria
   Clementi, Marco
   Palumbo, Giancarlo
   Chiominto, Alessandro
   Cappelli, Sonia
   Masedu, Francesco
   Valenti, Marco
TI Melphalan hypoxic perfusion with hemofiltration for melanoma
   locoregional metastases in the pelvis
SO JOURNAL OF SURGICAL RESEARCH
LA English
DT Article
DE Melanoma; Melphalan; Pelvic perfusion; Hypoxia; Stopflow
ID ISOLATED LIMB PERFUSION; BALLOON-OCCLUSION TECHNIQUE;
   NECROSIS-FACTOR-ALPHA; IN-TRANSIT MELANOMA; RECURRENT MELANOMA;
   MALIGNANT-MELANOMA; MITOMYCIN-C; REGIONAL CHEMOTHERAPY; RECTAL-CANCER;
   SURVIVAL
AB Background: For patients with melanoma metastases in the pelvic and groin regions, the median survival time (MST) was 8 mo with old treatments, whereas today is approximately 20 mo with new target therapy and novel immunotherapy. Unfortunately, approximately 30% of patients are nonresponsive to these new drugs.
   Materials and methods: Thirty-six patients, previously progressing after standard treatments, collectively received 146 melphalan (30 mg/m(2)) hypoxic pelvic perfusions with hemofiltration, in association with palliative excision in most cases.
   Results: The median follow-up time was 15 mo. Among 36 patients, three patients were alive without evidence of disease after 62, 95, and 118 mo, respectively. Thirty-three patients died of melanoma. The overall MST was 15 mo. The 5-y survival rate was 8%. The MST was 37 mo for stage IIIB; 19 mo for stage IIIC; and 6 mo for stage IV. The MST was 11 mo for patients with >= 1 mitosis per mm(2) and 20 mo for patients with <1 mitosis per mm(2); 17 mo for patients who received excision and 7 mo for patients who did not receive excision; and 19.5 mo for patients who received >2 treatments and 7.5 mo for patients who received <= 2 treatments.
   Conclusions: Pelvic/inguinal perfusion is a safe and feasible treatment for patients with
C1 [Guadagni, Stefano; Cappelli, Sonia; Masedu, Francesco; Valenti, Marco] Univ Aquila, Dept Appl Clin Sci & Biotechnol, I-67100 Laquila, Italy.
   [Fiorentini, Giammaria] Osped Riuniti Marche Nord, Dept Oncol & Hematol, Pesaro, Italy.
   [Clementi, Marco; Palumbo, Giancarlo] Univ Aquila, Dept Life Hlth & Environm Sci, Laquila, Italy.
   [Chiominto, Alessandro] S Salvatore Hosp, Dept Pathol, Laquila, Italy.
C3 University of L'Aquila; University of L'Aquila
RP Guadagni, S (corresponding author), Univ Aquila, Dept Appl Clin Sci & Biotechnol, I-67100 Laquila, Italy.
EM stefano.guadagni@univaq.it
RI VALENTI, MARCO/AAO-1383-2020; Palumbo, Giancarlo/J-5219-2012; Clementi,
   Marco/P-8582-2016; Guadagni, Stefano/P-6471-2016; Valenti,
   Marco/F-4818-2015; MASEDU, Francesco/M-2989-2015
OI Clementi, Marco/0000-0002-9652-5148; Palumbo,
   Giancarlo/0000-0002-5464-7497; Guadagni, Stefano/0000-0001-8525-084X;
   Valenti, Marco/0000-0001-9043-3456; MASEDU,
   Francesco/0000-0003-0290-5324
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NR 48
TC 7
Z9 7
U1 0
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0022-4804
EI 1095-8673
J9 J SURG RES
JI J. Surg. Res.
PD JUL
PY 2017
VL 215
BP 114
EP 124
DI 10.1016/j.jss.2017.03.066
PG 11
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA FA3RZ
UT WOS:000405363400018
PM 28688635
DA 2025-01-04
ER

PT J
AU Su, YC
   Wu, CC
   Su, CC
   Hsieh, MC
   Cheng, CL
   Yang, YHK
AF Su, Yi-Chia
   Wu, Chih-Chien
   Su, Chien-Chou
   Hsieh, Meng-Che
   Cheng, Ching-Lan
   Kao Yang, Yea-Huei
TI Comparative Effectiveness of Bevacizumab versus Cetuximab in Metastatic
   Colorectal Cancer Patients without Primary Tumor Resection
SO CANCERS
LA English
DT Article
DE metastatic colorectal cancer; bevacizumab; cetuximab; primary tumor
   resection
ID 1ST-LINE TREATMENT; COMORBIDITY INDEX; PLUS CETUXIMAB; CHEMOTHERAPY;
   SURVIVAL; EFFICACY; IMPROVEMENT; TAIWAN
AB Simple Summary The current metastatic colorectal cancer guidelines suggest intensive systemic chemotherapy with a targeted agent, rather than surgical resection, as first-line treatment for primary colorectal tumor and distant metastasis. However, results of comparative efficacy between bevacizumab and cetuximab remain controversial. This study aimed to assess the effectiveness of both therapies in patients who did not undergo primary tumor resection. Among patients treated with targeted agents, primary tumor resection was associated with lower mortality among those who received both bevacizumab and cetuximab. Among patients that did not undergo primary tumor resection, multivariable analysis for conversion surgery showed that the cetuximab group had a significantly higher metastasectomy rate. In these patients, cetuximab-based therapy was associated with significantly better survival compared to bevacizumab-based therapy. Cetuximab also yielded a higher conversion surgery rate. Primary tumor resection may be unfeasible in metastatic colorectal cancer. We determined the effects of bevacizumab and cetuximab therapies on survival or conversion surgery in patients with metastatic colorectal cancer who did not undergo primary tumor resection. This retrospective cohort study enrolled 8466 patients who underwent first-line bevacizumab- or cetuximab-based therapy. We analyzed the data of both therapies in patients who did not undergo primary tumor resection. Overall survival after targeted therapy plus chemotherapy was assessed. The groups were matched using propensity score matching and weighting. Cetuximab resulted in lower mortality than bevacizumab (hazard ratio (HR) = 0.75); however, it did not have the same effect in patients that underwent primary tumor resection (HR = 0.95) after propensity score weighting. Among patients treated with targeted agents, primary tumor resection was associated with lower mortality among those who received both bevacizumab (HR = 0.60) and cetuximab (HR = 0.75). Among patients that did not undergo primary tumor resection, multivariable analysis for conversion surgery showed that the cetuximab group (HR = 1.82) had a significantly higher metastasectomy rate. In these patients, cetuximab-based therapy was associated with significantly better survival compared with bevacizumab-based therapy. Cetuximab also yielded a higher conversion surgery rate. These findings demonstrate the importance of stratification by primary tumor resection in the application of current treatment guidelines and initiation of future clinical trials.
C1 [Su, Yi-Chia] Kaohsiung Vet Gen Hosp, Dept Pharm, Kaohsiung 813414, Taiwan.
   [Su, Yi-Chia; Cheng, Ching-Lan; Kao Yang, Yea-Huei] Natl Cheng Kung Univ, Inst Clin Pharm & Pharmaceut Sci, Sch Pharm, Coll Med, Tainan 701401, Taiwan.
   [Su, Yi-Chia] Shu Zen Jr Coll Med & Management, Dept Nursing, Kaohsiung 821004, Taiwan.
   [Wu, Chih-Chien] Kaohsiung Vet Gen Hosp, Div Colorectal Surg, Dept Surg, Kaohsiung 813414, Taiwan.
   [Wu, Chih-Chien] Natl Yang Ming Chiao Tung Univ, Sch Med, Dept Surg, Taipei 112304, Taiwan.
   [Su, Chien-Chou] Natl Cheng Kung Univ, Natl Cheng Kung Univ Hosp, Clin Innovat Ctr, Tainan 701006, Taiwan.
   [Su, Chien-Chou; Cheng, Ching-Lan] Natl Cheng Kung Univ, Natl Cheng Kung Univ Hosp, Dept Pharm, Coll Med, Tainan 701006, Taiwan.
   [Hsieh, Meng-Che] Canc Hosp, Dept Hematol & Oncol, Kaohsiung 824005, Taiwan.
   [Hsieh, Meng-Che] Shou Univ, Coll Med, Kaohsiung 824005, Taiwan.
   [Kao Yang, Yea-Huei] Natl Cheng Kung Univ, Hlth Outcome Res Ctr, Tainan 701401, Taiwan.
C3 Kaohsiung Veterans General Hospital; National Cheng Kung University;
   Kaohsiung Veterans General Hospital; National Yang Ming Chiao Tung
   University; National Cheng Kung University; National Cheng Kung
   University Hospital; National Cheng Kung University; National Cheng Kung
   University Hospital; National Cheng Kung University
RP Cheng, CL; Yang, YHK (corresponding author), Natl Cheng Kung Univ, Inst Clin Pharm & Pharmaceut Sci, Sch Pharm, Coll Med, Tainan 701401, Taiwan.; Cheng, CL (corresponding author), Natl Cheng Kung Univ, Natl Cheng Kung Univ Hosp, Dept Pharm, Coll Med, Tainan 701006, Taiwan.; Yang, YHK (corresponding author), Natl Cheng Kung Univ, Hlth Outcome Res Ctr, Tainan 701401, Taiwan.
EM jia.love70@vghks.gov.tw; pauleoswu@vghks.gov.tw; chienchou.su@gmail.com;
   philips115@gmail.com; clcheng@mail.ncku.edu.tw; yhkao@mail.ncku.edu.tw
RI Su, Yichia/HJI-3668-2023
OI Cheng, Ching-lan/0000-0002-7201-8491; Kao Yang,
   Yea-Huei/0000-0003-4623-5561; Su, Chien-Chou/0000-0001-5046-125X; Wu,
   Chih-Chien/0000-0001-5791-4047; Su, Yi-Chia/0000-0002-9544-1153
FU Higher Education Sprout Project, Ministry of Education [D110-F2567];
   Kaohsiung Veterans General Hospital [KSVGH110-054]
FX This research was funded in part by the Higher Education Sprout Project,
   Ministry of Education to the Headquarters of University Advancement at
   National Cheng Kung University (grant number D110-F2567) and Kaohsiung
   Veterans General Hospital, grant number KSVGH110-054.
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Z9 4
U1 11
U2 22
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD MAY
PY 2022
VL 14
IS 9
AR 2118
DI 10.3390/cancers14092118
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 1E6LB
UT WOS:000794596500001
PM 35565247
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Yoshida, GJ
   Saya, H
AF Yoshida, Go J.
   Saya, Hideyuki
TI Molecular pathology underlying the robustness of cancer stem cells
SO REGENERATIVE THERAPY
LA English
DT Review
DE Cancer stem cell; CD44 variant; Epithelial-to-mesenchymal transition
   (EMT); Intratumoral heterogeneity; Niche; Plasticity
ID EPITHELIAL-MESENCHYMAL TRANSITION; HELICOBACTER-PYLORI CAGA; CIRCULATING
   TUMOR-CELLS; PROSTATE-CANCER; METASTATIC COLONIZATION; CD44 VARIANT;
   PROSPECTIVE IDENTIFICATION; COLORECTAL-CANCER; CLONOGENIC CELLS;
   DRUG-RESISTANCE
AB Intratumoral heterogeneity is tightly associated with the failure of anticancer treatment modalities including conventional chemotherapy, radiation therapy, and molecularly targeted therapy. Such heterogeneity is generated in an evolutionary manner not only as a result of genetic alterations but also by the presence of cancer stem cells (CSCs). CSCs are proposed to exist at the top of a tumor cell hierarchy and are undifferentiated tumor cells that manifest enhanced tumorigenic and metastatic potential, self-renewal capacity, and therapeutic resistance. Properties that contribute to the robustness of CSCs include the abilities to withstand redox stress, to rapidly repair damaged DNA, to adapt to a hyperinflammatory or hyponutritious tumor microenvironment, and to expel anticancer drugs by the action of ATP-binding cassette transporters as well as plasticity with regard to the transition between dormant CSC and transit-amplifying progenitor cell phenotypes. In addition, CSCs manifest the phenomenon of metabolic reprogramming, which is essential for maintenance of their self-renewal potential and their ability to adapt to changes in the tumor microenvironment. Elucidation of the molecular underpinnings of these biological features of CSCs is key to the development of novel anticancer therapies. In this review, we highlight the pathological relevance of CSCs in terms of their hallmarks and identification, the properties of their niched-both in primary tumors and at potential sites of metastasisd-and their resistance to oxidative stress dependent on system xc (-). (C) 2021, The Japanese Society for Regenerative Medicine. Production and hosting by Elsevier B.V.
C1 [Yoshida, Go J.; Saya, Hideyuki] Keio Univ, Inst Adv Med Res IAMR, Div Gene Regulat, Sch Med, Tokyo, Japan.
C3 Keio University
RP Saya, H (corresponding author), Keio Univ, Inst Adv Med Res IAMR, Div Gene Regulat, Sch Med,Shinjuku Ku, 35 Shinanomachi, Tokyo 1608582, Japan.
EM hsaya@a5.keio.jp
RI Saya, Hideyuki/J-4325-2013
OI Saya, Hideyuki/0000-0001-6610-1902; Yoshida, Go/0000-0002-1472-892X
FU KAKENHI grant from Japan Society for the Promotion of Science
   [20H00518]; Grants-in-Aid for Scientific Research [20H00518] Funding
   Source: KAKEN
FX This work was supported by a KAKENHI grant from Japan Society for the
   Promotion of Science (20H00518, to H.S.).
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NR 216
TC 22
Z9 24
U1 0
U2 11
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2352-3204
J9 REGEN THER
JI Regen. Ther.
PD JUN
PY 2021
VL 17
BP 38
EP 50
DI 10.1016/j.reth.2021.02.002
PG 13
WC Cell & Tissue Engineering; Engineering, Biomedical
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Engineering
GA UX5FX
UT WOS:000700870800006
PM 33869685
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Jin, K
   Li, T
   van Dam, H
   Zhou, FF
   Zhang, L
AF Jin, Ke
   Li, Tong
   van Dam, Hans
   Zhou, Fangfang
   Zhang, Long
TI Molecular insights into tumour metastasis: tracing the dominant events
SO JOURNAL OF PATHOLOGY
LA English
DT Review
DE tumour metastasis; epithelial-mesenchymal transition; transforming
   growth factor-; Wnt; Notch; circulating tumour cell; tissue tropism;
   signal transduction; mesenchymal-epithelial transition; targeted therapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; BREAST-CANCER CELLS; SUPPRESSES BRAIN
   METASTASIS; STEM-LIKE CELLS; TGF-BETA; COLORECTAL-CANCER; LUNG
   METASTASIS; RECEPTOR; GROWTH; PROMOTE
AB Metastasis of malignant cells to vital organs remains the major cause of mortality in many types of cancers. The tumour invasion-metastasis cascade is a stepwise and multistage process whereby tumour cells disseminate from primary sites and spread to colonize distant sites through the systemic haematogenous or lymphatic circulations. The general steps of metastasis may be similar in almost all tumour types, but metastasis to different tissues seems to require distinct sets of regulators and/or an educated' microenvironment which may facilitate the infiltration and colonization of tumour cells to specific tissues. Moreover, interactions of tumour cells with stromal cells, endothelial cells, and immune cells that they encounter will also aid them to gain survival advantages, evade immune surveillance, and adapt to the new host microenvironment. Due to the high correlation between tumour metastasis and survival rate of patients, a deeper understanding of the molecular participants and processes involved in metastasis could pave the way towards novel, more effective and targeted approaches to prevent and treat tumour metastasis. In this review, we provide an update on the regulation networks orchestrated by the dominant regulators of different stages throughout the metastatic process including, but not limited to, epithelial-mesenchymal transition in local invasion, resistance to anoikis during migration, and colonization of different distant sites. We also put forward some suggestions and problems concerning the treatment of tumour metastasis that should be solved and/or improved for better therapies in the near future. Copyright (c) 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
C1 [Jin, Ke; Zhang, Long] Zhejiang Univ, Inst Life Sci, 866 Yuhangtang Rd, Hangzhou 310058, Zhejiang, Peoples R China.
   [Jin, Ke; Zhang, Long] Zhejiang Univ, Innovat Ctr Cell Signaling Network, 866 Yuhangtang Rd, Hangzhou 310058, Zhejiang, Peoples R China.
   [Li, Tong] Zhejiang Univ, Inst Pharmacol & Toxicol, Coll Pharmaceut Sci, Hangzhou 310058, Zhejiang, Peoples R China.
   [van Dam, Hans; Zhou, Fangfang; Zhang, Long] Leiden Univ, Dept Mol Cell Biol, Canc Genom Ctr, Med Ctr, Postbus 9600, NL-2300 RC Leiden, Netherlands.
   [van Dam, Hans; Zhou, Fangfang; Zhang, Long] Leiden Univ, Ctr Biomed Genet, Med Ctr, Postbus 9600, NL-2300 RC Leiden, Netherlands.
   [Zhou, Fangfang] Soochow Univ, Inst Biol & Med Sci, Suzhou 215123, Peoples R China.
C3 Zhejiang University; Zhejiang University; Zhejiang University; Leiden
   University; Leiden University Medical Center (LUMC); Leiden University -
   Excl LUMC; Leiden University - Excl LUMC; Leiden University; Leiden
   University Medical Center (LUMC); Soochow University - China
RP Zhou, FF (corresponding author), Soochow Univ, Inst Biol & Med Sci, Suzhou 215123, Peoples R China.; Jin, K; Zhang, L (corresponding author), Inst Life Sci, Hangzhou 310058, Zhejiang, Peoples R China.; Jin, K; Zhang, L (corresponding author), Innovat Ctr Cell Signaling Network, Hangzhou 310058, Zhejiang, Peoples R China.
EM kejin@zju.edu.cn; zhoufangfang@suda.edu.cn; L_Zhang@zju.edu.cn
RI Zhang, Long/AAT-6571-2021; Jin, Ke/GQG-9869-2022
OI van Dam, Hans/0000-0002-8307-4325; Zhang, Long/0000-0001-8139-0474; Jin,
   Ke/0000-0001-5371-3440
FU National Natural Science Funds of China [31471315, 31571460, 31671457,
   K124924615, 81470851, L224903215]; Netherlands Organization for Health
   Research and Development (ZonMw) [8238-20864]; outstanding youth fund of
   Zhejiang province [R14C070002]; National Key Research and Development
   Program of China, Young Scientist project [2016YFA0502500]
FX This work was supported by the National Natural Science Funds of China
   (Grant No. 31471315, 31571460, 31671457, K124924615, 81470851, and
   L224903215), the Netherlands Organization for Health Research and
   Development (ZonMw Grant No. 8238-20864), the outstanding youth fund of
   Zhejiang province (Grant No. R14C070002), and the National Key Research
   and Development Program of China, Young Scientist project (Grant No.
   2016YFA0502500).
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NR 100
TC 43
Z9 49
U1 0
U2 53
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 APR
PY 2017
VL 241
IS 5
BP 567
EP 577
DI 10.1002/path.4871
PG 11
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA EP6CS
UT WOS:000397466300001
PM 28035672
DA 2025-01-04
ER

PT J
AU Hoang, T
   Kim, J
AF Hoang, Tung
   Kim, Jeongseon
TI Combining Correlated Outcomes and Surrogate Endpoints in a Network
   Meta-Analysis of Colorectal Cancer Treatments
SO CANCERS
LA English
DT Article
DE network meta-analysis; colorectal cancer; surrogate endpoints
ID RANDOMIZED PHASE-III; PROGRESSION-FREE SURVIVAL; UNRESECTABLE LIVER
   METASTASES; FLUOROURACIL PLUS LEUCOVORIN; 1ST-LINE TREATMENT; 2ND-LINE
   TREATMENT; IRINOTECAN FOLFIRI; OXALIPLATIN XELOX; CONTROLLED-TRIAL;
   OPEN-LABEL
AB Simple Summary Currently, cytotoxic agents and biological targeted agents are commonly combined for the treatment of advanced or metastatic colorectal cancer. However, questions of 'which chemotherapy or targeted therapy provides the higher efficacy and lower toxicity' or 'whether the addition of targeted therapy to chemotherapy not only increases the treatment effect but also reduces the adverse events' have been raised. In this study, we firstly calculated the treatment effect on overall survival, which has not been reached in several randomized controlled trials, based on treatment effects on overall response rate and/or progression-free survival. Then we performed the network meta-analysis to compare the efficacy and safety of 12 commonly used regimens. Finally, our analyses showed that FOLFOX+cetuximab and FOLFIRI+bevacizumab have high probabilities of being first-line and second-line treatments in terms of efficacy and safety, respectively. This study aimed to investigate the efficacy and safety of systemic therapies in the treatment of unresectable advanced or metastatic colorectal cancer. Predicted hazard ratios (HRs) and their 95% credible intervals (CrIs) for overall survival (OS) were calculated from the odds ratio (OR) for the overall response rate and/or HR for progression-free survival using multivariate random effects (MVRE) models. We performed a network meta-analysis (NMA) of 49 articles to compare the efficacy and safety of FOLFOX/FOLFIRI +/- bevacizumab (Bmab)/cetuximab (Cmab)/panitumumab (Pmab), and FOLFOXIRI/CAPEOX +/- Bmab. The NMA showed significant OS improvement with FOLFOX, FOLFOX+Cmab, and FOLFIRI+Cmab compared with that of FOLFIRI (HR = 0.84, 95% CrI = 0.73-0.98; HR = 0.76, 95% CrI = 0.62-0.94; HR = 0.80, 95% CrI = 0.66-0.96, respectively), as well as with FOLFOX+Cmab and FOLFIRI+Cmab compared with that of FOLFOXIRI (HR = 0.69, 95% CrI = 0.51-0.94 and HR = 0.73, 95% CrI = 0.54-0.97, respectively). The odds of adverse events grade >= 3 were significantly higher for FOLFOX+Cmab vs. FOLFIRI+Bmab (OR = 2.34, 95% CrI = 1.01-4.66). Higher odds of events were observed for FOLFIRI+Pmab in comparison with FOLFIRI (OR = 2.16, 95% CrI = 1.09-3.84) and FOLFIRI+Bmab (OR = 3.14, 95% CrI = 1.51-5.89). FOLFOX+Cmab and FOLFIRI+Bmab showed high probabilities of being first- and second-line treatments in terms of the efficacy and safety, respectively. The findings of the efficacy and safety comparisons may support the selection of appropriate treatments in clinical practice. PROSPERO registration: CRD42020153640.
C1 [Hoang, Tung; Kim, Jeongseon] Natl Canc Ctr, Grad Sch Canc Sci & Policy, Dept Canc Biomed Sci, Goyang 10408, South Korea.
C3 National Cancer Center - Korea (NCC)
RP Kim, J (corresponding author), Natl Canc Ctr, Grad Sch Canc Sci & Policy, Dept Canc Biomed Sci, Goyang 10408, South Korea.
EM 75256@ncc.re.kr; jskim@ncc.re.kr
RI KIM, JEONGSEON/AAA-4643-2022; Hoang, Tung/ABG-7027-2020
OI Hoang, Tung/0000-0001-6653-3406; KIM, JEONGSEON/0000-0002-0889-2686
FU National Cancer Center Korea [2010260, 1910330]
FX This study was supported by grants from the National Cancer Center Korea
   (Nos. 2010260 and 1910330).
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NR 82
TC 3
Z9 3
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 2020
VL 12
IS 9
AR 2663
DI 10.3390/cancers12092663
PG 22
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OD8DY
UT WOS:000580078600001
PM 32961943
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Jia, HT
   Shao, YF
   Zhou, XL
   Yang, G
   Huang, L
   Aikemu, B
   Li, SC
   Ding, CS
   Fan, XD
   Hong, HJ
   Zhang, S
   Pan, RJ
   Sun, J
AF Jia, Hong-tao
   Shao, Yan-fei
   Zhou, Xue-liang
   Yang, Guang
   Huang, Ling
   Aikemu, Batuer
   Li, Shu-chun
   Ding, Cheng-sheng
   Fan, Xiao-dong
   Hong, Hi-ju
   Zhang, Sen
   Pan, Rui-jun
   Sun, Jing
TI PKCδ promotes the invasion and migration of colorectal cancer through
   c-myc/NDRG1 pathway
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colorectal cancer; protein kinase C delta; N-myc downstream-regulated
   gene 1; metastasis; epithelial-mesenchymal transition
ID DEPENDENT PROTEIN-KINASE; METASTASIS SUPPRESSOR; CELL-MIGRATION;
   C-DELTA; NDRG1; ACTIVATION; MECHANISMS; INHIBITOR
AB Objective: Colorectal cancer (CRC) is the third cause of expected cancer deaths both in men and women in the U.S. and the third most commonly diagnosed cancer in China Targeted therapy has been proven to improve overall survival for unresectable metastatic CRC. But the location of the primary tumor or the presence of various core driver gene mutations that confer resistance may limit the utility of targeted therapy. Therefore, it is of great significance to further elucidate novel mechanisms of invasion and metastasis of CRC and find potential novel therapeutic targets. Protein Kinase C Delta (PKC delta) plays an important role in various diseases, including tumors. In CRC, the function of PKC delta on proliferation and differentiation is mostly studied but various research results were reported. Therefore, the role of PKC delta in CRC needs to be further studied, especially in tumor invasion and metastasis in CRC which few studies have looked into.Methods: The expression of PRKCD was analyzed by the Genotype-Tissue Expression (GTEx) and The Cancer Genome Atlas (TCGA) databases and Immunohistochemical (IHC). Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) enrichment analysis were used to explore the biological functions and pathways related to PRKCD. Lentivirus transfection was used to construct CRC cell lines with overexpression and knock-down of PKC delta or N-myc Downstream Regulated Gene 1 (NDRG1). Cell invasion and migration assay, wound healing assay were used to detect the function of PKC delta and NDRG1 in the invasion and migration of cells. Flow cytometry analysis was used to detect the influence of PKC delta on the CRC cell cycles .Immunofluorescence histochemistry ,Immunoprecipitation Assay and qPCR were used to detect the relationship of PKC delta and NDRG1. Xenograft model was used to verify the role of PKC delta in vivo.Results: PKC delta is overexpressed in CRC and could promote Epithelial-Mesenchymal Transition (EMT) and the invasion and migration of CRC in vitro. We confirmed that PKC delta and the tumor suppressor factor NDRG1 had a co-localization relationship in CRC. PKC delta inhibited NDRG1 transcription and protein expression. Overexpressing NDRG1 could inhibit the function of PKC delta in promoting tumor invasion and migration. PKC delta could regulate c-Myc, one transcription factor of NDRG1, to down-regulate NDRG1. In vivo, overexpressing PKC delta could promote xenograft growth and volume. Thus, our results showed that PKC delta reduced the expression of NDRG1 through c-Myc, promoting the invasion and migration of CRC through promoting EMT.Conclusion: The increased expression of PKC delta in CRC tumor tissue could promote the invasion and migration of tumor cells, and one of the mechanisms may be regulating c-Myc to inhibit the expression of NDRG1 and promote EMT.
C1 [Jia, Hong-tao; Shao, Yan-fei; Zhou, Xue-liang; Yang, Guang; Huang, Ling; Aikemu, Batuer; Li, Shu-chun; Ding, Cheng-sheng; Fan, Xiao-dong; Hong, Hi-ju; Zhang, Sen; Pan, Rui-jun; Sun, Jing] Shanghai Jiao Tong Univ, Ruijin Hosp, Dept Gen Surg, Sch Med, Shanghai, Peoples R China.
   [Jia, Hong-tao; Shao, Yan-fei; Zhou, Xue-liang; Yang, Guang; Huang, Ling; Aikemu, Batuer; Li, Shu-chun; Ding, Cheng-sheng; Fan, Xiao-dong; Hong, Hi-ju; Zhang, Sen; Pan, Rui-jun; Sun, Jing] Shanghai Jiao Tong Univ, Ruijin Hosp, Shanghai Minimally Invas Surg Ctr, Sch Med, Shanghai, Peoples R China.
   [Jia, Hong-tao; Shao, Yan-fei; Zhou, Xue-liang; Ding, Cheng-sheng; Fan, Xiao-dong] Shanghai Jiao Tong Univ, Ruijin Hosp, Shanghai Inst Digest Surg, Sch Med, Shanghai, Peoples R China.
C3 Shanghai Jiao Tong University; Shanghai Jiao Tong University; Shanghai
   Jiao Tong University
RP Zhang, S; Pan, RJ; Sun, J (corresponding author), Shanghai Jiao Tong Univ, Ruijin Hosp, Dept Gen Surg, Sch Med, Shanghai, Peoples R China.; Zhang, S; Pan, RJ; Sun, J (corresponding author), Shanghai Jiao Tong Univ, Ruijin Hosp, Shanghai Minimally Invas Surg Ctr, Sch Med, Shanghai, Peoples R China.
EM zhangsen6886@163.com; prj11522@rjh.com.cn; sj11788@rjh.com.cn
RI huang, ling/KLC-7916-2024; Fan, Xiaodong/JQV-7780-2023; yang,
   guang/AAV-2451-2021
OI Yang, Guang/0000-0001-6079-5093
FU National Nature Science Foundation of China (NSFC) [81871984, 82103207]
FX Funding This work is supported by National Nature Science Foundation of
   China (NSFC) (Grant No. 81871984, No. 82103207).
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NR 23
TC 2
Z9 3
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 FEB 2
PY 2023
VL 13
AR 1026561
DI 10.3389/fonc.2023.1026561
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 9F2WO
UT WOS:000937334500001
PM 36816970
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zheng, QM
   Wang, JH
   Li, WW
   Chen, XY
   Chen, SZ
   Chen, LH
AF Zheng, Qiaomei
   Wang, Jinhua
   Li, Wenwen
   Chen, Xiaoyun
   Chen, Shaozhan
   Chen, Lihong
TI Emodin Reverses the Epithelial-Mesenchymal Transition of Human
   Endometrial Stromal Cells by Inhibiting ILK/GSK-3β Pathway
SO DRUG DESIGN DEVELOPMENT AND THERAPY
LA English
DT Article
DE emodin; endometriosis; EMT; ILK; GSK-3 beta
ID INTEGRIN-LINKED KINASE; OVARIAN-CANCER CELLS; COLORECTAL-CANCER;
   BREAST-CANCER; BETA-CATENIN; IN-VITRO; MIGRATION; ILK; INVASION;
   PROLIFERATION
AB Purpose: To explore the exact mechanism through which emodin down-regulates the migration and invasion abilities of endometrial stromal cells. Moreover, to explore the theoretical basis of emodin in the treatment of endometriosis.
   Patients and Methods: Endometriosis endometrial stromal cells (EESs) were cultured from 15 women with endometriosis and control endometrial stromal cells (CESs) were cultured from 12 women without endometriosis. The levels of proteins were evaluated by Western blot. The migration and invasion abilities of cells were detected by transwell assays.
   Results: The abilities of migration and invasion of EESs were much stronger than those of CESs. After treated with emodin, the migration and invasion abilities of EESs and CESs were significantly down-regulated, and the levels of integrin-linked kinase (ILK) and p-GSK3 beta were statistically down-regulated in EESs. Besides that, the expression of keratin was upregulated while the expression of vimentin, beta-catenin and slug were all down-regulated by emodin in a dose- and time-dependent manner. Silencing of ILK gene in EESs also achieved the above effects, which were strengthened by emodin. Conversely, exogenous expression of ILK in CESs increased the expression of p-GSK-3 beta, which were abrogated by emodin. Furthermore, SB216763 increased migration and invasion abilities of CESs by facilitating the epithelial-mesenchymal transition (EMT) through up-regulating levels of p-GSK-3 beta, beta-catenin and slug, which were also abrogated by emodin.
   Conclusion: Emodin inhibits the migration and invasion abilities of human endometrial stromal cells by reversing the EMT via ILK/GSK-3 beta pathway. So, emodin may be considered as a promising targeted therapy for endometriosis.
C1 [Zheng, Qiaomei; Wang, Jinhua; Li, Wenwen; Chen, Xiaoyun; Chen, Shaozhan; Chen, Lihong] Fujian Med Univ, Affiliated Hosp 1, Dept Obstet & Gynecol, 20 Chazhong Rd, Fuzhou 350001, Fujian, Peoples R China.
C3 Fujian Medical University
RP Chen, LH (corresponding author), Fujian Med Univ, Affiliated Hosp 1, Dept Obstet & Gynecol, 20 Chazhong Rd, Fuzhou 350001, Fujian, Peoples R China.
EM chenlihong_0102@126.com
RI Zheng, Qiaomei/HPI-2128-2023; wang, wei/JYP-7819-2024
FU Startup Fund for Scientific Research, Fujian Medical University
   [2017XQ1056]; Natural Science Foundation of Fujian Province
   [2018J05126]; Joint Funds for the Innovation of Science and Technology,
   Fujian Province [2018Y9077]
FX This study was supported by grants from the Startup Fund for Scientific
   Research, Fujian Medical University (Grant number: 2017XQ1056), the
   Natural Science Foundation of Fujian Province (Grant number:
   2018J05126), and the Joint Funds for the Innovation of Science and
   Technology, Fujian Province (Grant number: 2018Y9077).
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NR 42
TC 7
Z9 7
U1 0
U2 6
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1177-8881
J9 DRUG DES DEV THER
JI Drug Des. Dev. Ther.
PY 2020
VL 14
BP 3663
EP 3672
DI 10.2147/DDDT.S262816
PG 10
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA NM9DF
UT WOS:000568390500001
PM 32982173
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ye, QL
   Liu, SX
   Lin, SQ
   Xie, W
AF Ye, Qianli
   Liu, Shixing
   Lin, Shiqiang
   Xie, Wen
TI Circular RNA circSEMA5A facilitates colorectal cancer development by
   regulating microRNA-195-5p to target CCNE1 axis
SO CELLULAR SIGNALLING
LA English
DT Article
DE circSEMA5A; miR-195-5p; CCNE1; Colorectal cancer; Diagnosis
ID BLADDER-CANCER; PROLIFERATION; PROGRESSION; RESISTANCE; STEMNESS
AB Colorectal cancer (CRC) is one of the most prevalent malignancies with a high mortality rate worldwide. Circular RNAs (circRNAs) have lately emerged as key molecules involved in cancer development and metastasis. CircSEMA5 is reported to be oncogenic in some cancers, yet its role in the pathogenesis of CRC remains unknown. Herein, we attempted to investigate the functional role and molecular mechanism of circSEMA5A underlying CRC progression. RT-qPCR and RNase R digestion assays were used to evaluate circSEMA5A expression characteristics in CRC cells. Loss-of-function assays were performed to clarify circSEMA5A role in CRC biological processes. Bioinformatics and mechanism experiments were conducted to assess the association of circSEMA5A or CCNE1 with miR-195-5p in CRC cells. Rescue assays were conducted to explore the regulatory function of circSEMA5A-miR-195-5p-CCNE1 in CRC cellular processes. Through bioinformatics and functional screening, we found that circSEMA5A was highly expressed in CRC cells and was mainly localized in the nucleus. CircSEMA5A promoted CRC proliferative, migratory, and invasive capabilities in cultured cells and facilitated the tumorigenic process in xenografts; however, circSEMA5A silencing repressed tumor metastasis in CRC cells. Mechanistically, circSEMA5A was competitively bound with miR-195-5p to upregulate CCNE1 expression. Moreover, the impact of circSEMA5A knockdown on CRC cell proliferative, migratory, and invasive capabilities was countervailed by miR-195-5p inhibitor or CCNE1 overexpression. To summarize, circSEMA5A is a novel circRNA that serves as an oncogene in CRC progression. CircSEMA5A facilitates CRC cell malignancy and tumor growth through sponging miR-195-5p to upregulate CCNE1, thus providing a new direction for CRC diagnosis and targeted therapy.
C1 [Ye, Qianli; Liu, Shixing; Lin, Shiqiang; Xie, Wen] Longyan Peoples Hosp, Dept External Med 2, 31 Denggao West Rd, Longyan 364000, Fujian, Peoples R China.
RP Liu, SX (corresponding author), Longyan Peoples Hosp, Dept External Med 2, 31 Denggao West Rd, Longyan 364000, Fujian, Peoples R China.
EM lsx111517@163.com
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NR 46
TC 3
Z9 3
U1 0
U2 1
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 JUL
PY 2023
VL 107
AR 110649
DI 10.1016/j.cellsig.2023.110649
EA MAY 2023
PG 11
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA I2SV0
UT WOS:001001341500001
PM 37164546
DA 2025-01-04
ER

PT J
AU Chen, ZY
   Chen, X
   Lu, BB
   Gu, Y
   Chen, QN
   Lei, TY
   Nie, FQ
   Gu, JY
   Huang, JL
   Wei, CC
   Sun, M
   Wang, Z
AF Chen, Zhenyao
   Chen, Xin
   Lu, Binbin
   Gu, Yu
   Chen, Qinnan
   Lei, Tianyao
   Nie, Fengqi
   Gu, Jingyao
   Huang, Jiali
   Wei, Chenchen
   Sun, Ming
   Wang, Zhaoxia
TI Up-regulated LINC01234 promotes non-small-cell lung cancer cell
   metastasis by activating VAV3 and repressing BTG2 expression
SO JOURNAL OF HEMATOLOGY & ONCOLOGY
LA English
DT Article
DE NSCLC; Metastasis; LINC01234; VAV3; BTG2
ID TARGETED THERAPY; GASTRIC-CANCER; INVASION; PROLIFERATION; PROGRESSION;
   INHIBITOR; APOPTOSIS; GENCODE; GROWTH
AB Background Long noncoding RNAs (lncRNAs) are known to regulate tumorigenesis and cancer progression, but their contributions to non-small-cell lung cancer (NSCLC) metastasis remain poorly understood. Our previous and other studies have revealed the involvement of upregulated LINC01234 in regulating gastric cancer and colon cancer cells proliferation, and we aimed to investigate whether LINC01234 overexpression also contribute to cancer cells metastasis in this study. Methods We collect the NSCLC tissues and adjacent non-tumor tissues and analyzed expression levels of LINC01234 by quantitative reverse-transcription PCR. LINC01234 were knocked down by using siRNAs or shRNAs, and overexpressed by transfection with overexpression vector; RNA levels of miRNA were downregulated or upregulated with inhibitors or mimics. Transwell assays were used to evaluate cell migration and invasive ability; in vivo metastasis experiments were performed to investigate the effect of LINC01234 on NSCLC cells metastasis. Luciferase reporter, RIP, and ChIP assays were used to determine the regulation of LINC01234 on its targets. Results LINC01234 expression is increased in NSCLC tissues, and its upregulation is associated with metastasis and shorter survival in NSCLC. Downregulation of LINC01234 impairs cell migration and invasion in vitro, and inhibits cells metastasis in vivo by acting as a competing endogenous RNA for the miR-340-5p and miR-27b-3p. LINC01234 also interacts with the RNA-binding proteins LSD1 and EZH2, leading to histone modification and transcriptional repression of the anti-proliferative genes BTG2. Conclusions Taken together, our findings identify two oncogenic regulatory axes in NSCLC centering on LINC01234: one involving miR-340-5p/miR-27b-3p in the cytoplasm and the second involving EZH2, LSD1, and BTG2 in the nucleus. Our study indicates that these genes may be targeted to reduce or prevent NSCLC metastasis.
C1 [Chen, Zhenyao; Chen, Xin; Lu, Binbin; Chen, Qinnan; Lei, Tianyao; Nie, Fengqi; Gu, Jingyao; Huang, Jiali; Wei, Chenchen; Wang, Zhaoxia] Nanjing Med Univ, Canc Med Ctr, Affiliated Hosp 2, Nanjing 210011, Jiangsu, Peoples R China.
   [Gu, Yu] Univ Waterloo, Fac Math, Waterloo, ON, Canada.
   [Sun, Ming] UT MD Anderson Canc Ctr, Dept Bioinformat & Computat Biol, Houston, TX 77030 USA.
C3 Nanjing Medical University; University of Waterloo; University of Texas
   System; UTMD Anderson Cancer Center
RP Wang, Z (corresponding author), Nanjing Med Univ, Canc Med Ctr, Affiliated Hosp 2, Nanjing 210011, Jiangsu, Peoples R China.; Sun, M (corresponding author), UT MD Anderson Canc Ctr, Dept Bioinformat & Computat Biol, Houston, TX 77030 USA.
EM msun7@mdanderson.org; zhaoxiawang66@126.com
RI sun, ming/AAS-5981-2020; YU, GU/AAQ-4509-2020
OI wang, zhaoxia/0000-0002-1893-371X
FU National Natural Science Foundation of China [81871871, 81902333,
   81602013, 81802275, 81703056]; Key Research and Development plan (Social
   development) of science and technology department of Jiangsu Province
   [BE2019760]; Medical Innovation Team Foundation of the Jiangsu
   Provincial Enhancement Health Project [CXTDA2017021]; Key young medical
   talents of Jiangsu Province [QNRC2016662]; Science and technology
   development fund of Nanjing Medical University [NMUB2018035];
   Postgraduate Research & Practice Innovation Program of Jiangsu Province
   [KYCX19_ 1170]
FX This work was supported by grants from the National Natural Science
   Foundation of China (grant numbers 81871871 to Z.W., 81902333 to X.C.,
   81602013 to F. N., 81802275 to Q.C. and 81703056 to C.W.); Key Research
   and Development plan (Social development) of science and technology
   department of Jiangsu Province(No. BE2019760 to Z.W); the Medical
   Innovation Team Foundation of the Jiangsu Provincial Enhancement Health
   Project (No. CXTDA2017021 to Z.W.); the Key young medical talents of
   Jiangsu Province (No. QNRC2016662 to B.L.); the Science and technology
   development fund of Nanjing Medical University (No.NMUB2018035 to X.C.);
   and Postgraduate Research & Practice Innovation Program of Jiangsu
   Province (No. KYCX19_ 1170 to Z.C.)
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NR 34
TC 84
Z9 87
U1 0
U2 35
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1756-8722
J9 J HEMATOL ONCOL
JI J. Hematol. Oncol.
PD JAN 20
PY 2020
VL 13
IS 1
AR 7
DI 10.1186/s13045-019-0842-2
PG 14
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA KK3KI
UT WOS:000512644800001
PM 31959200
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Murakami, T
   Singh, AS
   Kiyuna, T
   Dry, SM
   Li, YF
   James, AW
   Igarashi, K
   Kawaguchi, K
   DeLong, JC
   Zhang, Y
   Hiroshima, Y
   Russell, T
   Eckardt, MA
   Yanagawa, J
   Federman, N
   Matsuyama, R
   Chishima, T
   Tanaka, K
   Bouvet, M
   Endo, I
   Eilber, FC
   Hoffman, RM
AF Murakami, Takashi
   Singh, Arun S.
   Kiyuna, Tasuku
   Dry, Sarah M.
   Li, Yunfeng
   James, Aaron W.
   Igarashi, Kentaro
   Kawaguchi, Kei
   DeLong, Jonathan C.
   Zhang, Yong
   Hiroshima, Yukihiko
   Russell, Tara
   Eckardt, Mark A.
   Yanagawa, Jane
   Federman, Noah
   Matsuyama, Ryusei
   Chishima, Takashi
   Tanaka, Kuniya
   Bouvet, Michael
   Endo, Itaru
   Eilber, Fritz C.
   Hoffman, Robert M.
TI Effective molecular targeting of CDK4/6 and IGF-1R in a rare
   <i>FUS-ERG</i> fusion <i>CDKN2A</i>-deletion doxorubicin-resistant
   Ewing's sarcoma patient-derived orthotopic xenograft (PDOX) nude-mouse
   model
SO ONCOTARGET
LA English
DT Article
DE palbociclib; linsitinib; patient-derived orthotopic xenograft; PDOX;
   Ewing's sarcoma
ID SALMONELLA-TYPHIMURIUM A1-R; SOFT-TISSUE SARCOMA; HUMAN
   PANCREATIC-CANCER; HUMAN COLON-CANCER; ANTI-CEA ANTIBODY; INHIBITOR
   PD0332991; MYELOID-LEUKEMIA; INSULIN-RECEPTOR; GENE-EXPRESSION; THERAPY
AB Ew(i)ng's sarcoma is a rare and aggressive malignancy. In the present study, tumor from a patient with a Ewing's sarcoma with cyclin-dependent kinase inhibitor 2A/B (CDKN2A/B) loss and FUS-ERG fusion was implanted in the right chest wall of nude mice to establish a patient-derived orthotopic xenograft (PDOX) model. The aim of the present study was to determine efficacy of cyclin-dependent kinase 4/6 (CDK4/6) and insulin-like growth factor-1 receptor (IGF-1R) inhibitors on the Ewing's sarcoma PDOX. The PDOX models were randomized into the following groups when tumor volume reached 50 mm(3): G1, untreated control; G2, doxorubicin (DOX) (intraperitoneal (i.p.) injection, weekly, for 2 weeks); G3, CDK4/6 inhibitor (palbociclib, PD0332991, per oral (p.o.), daily, for 14 days); G4, IGF-1R inhibitor (linsitinib, OSI-906, p.o., daily, for 14 days). Tumor growth was significantly suppressed both in G3 (palbociclib) and in G4 (linsitinib) compared to G1 (untreated control) at all measured time points. In contrast, DOX did not inhibit tumor growth at any time point, which is consistent with the failure of DOX to control tumor growth in the patient. The results of the present study demonstrate the power of the PDOX model to identify effective targeted molecular therapy of a recalcitrant DOX-resistant Ewing's sarcoma with specific genetic alterations. The results of this study suggest the potential of PDOX models for individually-tailored, effective targeted therapy for recalcitrant cancer.
C1 [Murakami, Takashi; Kiyuna, Tasuku; Igarashi, Kentaro; Kawaguchi, Kei; Zhang, Yong; Hoffman, Robert M.] AntiCanc Inc, San Diego, CA 92111 USA.
   [Murakami, Takashi; DeLong, Jonathan C.; Bouvet, Michael; Hoffman, Robert M.] Univ Calif San Diego, Dept Surg, San Diego, CA 92103 USA.
   [Murakami, Takashi; Hiroshima, Yukihiko; Matsuyama, Ryusei; Chishima, Takashi; Tanaka, Kuniya; Endo, Itaru] Yokohama City Univ, Grad Sch Med, Dept Gastroenterol Surg, Yokohama, Kanagawa, Japan.
   [Singh, Arun S.] Univ Calif Los Angeles, Div Hematol Oncol, Los Angeles, CA USA.
   [Dry, Sarah M.; Li, Yunfeng; James, Aaron W.] Univ Calif Los Angeles, Dept Pathol, Los Angeles, CA 90024 USA.
   [Russell, Tara; Eckardt, Mark A.; Yanagawa, Jane; Eilber, Fritz C.] Univ Calif Los Angeles, Div Surg Oncol, Los Angeles, CA 90095 USA.
   [Eckardt, Mark A.] Yale Univ, Sch Med, Dept Surg, New Haven, CT 06510 USA.
   [Federman, Noah] Univ Calif Los Angeles, Dept Pediat, Los Angeles, CA 90024 USA.
   [Federman, Noah] Univ Calif Los Angeles, Dept Orthopaed, Los Angeles, CA USA.
   [Hoffman, Robert M.] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Sarcoma Program, Los Angeles, CA 90095 USA.
   [Hoffman, Robert M.] PDOX Inc, San Diego, CA 92111 USA.
C3 AntiCancer, Inc.; University of California System; University of
   California San Diego; Yokohama City University; University of California
   System; University of California Los Angeles; University of California
   System; University of California Los Angeles; University of California
   System; University of California Los Angeles; Yale University;
   University of California System; University of California Los Angeles;
   University of California System; University of California Los Angeles;
   UCLA Jonsson Comprehensive Cancer Center; University of California
   System; University of California Los Angeles
RP Hoffman, RM (corresponding author), AntiCanc Inc, San Diego, CA 92111 USA.; Hoffman, RM (corresponding author), Univ Calif San Diego, Dept Surg, San Diego, CA 92103 USA.; Eilber, FC (corresponding author), Univ Calif Los Angeles, Div Surg Oncol, Los Angeles, CA 90095 USA.; Hoffman, RM (corresponding author), Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Sarcoma Program, Los Angeles, CA 90095 USA.; Hoffman, RM (corresponding author), PDOX Inc, San Diego, CA 92111 USA.
EM fceilber@mednet.ucla.edu; all@anticancer.com
RI Li, Tengfei/AAI-5043-2020
OI Murakami, Takashi/0000-0002-9429-5705; Igarashi,
   Kentaro/0000-0003-2278-1736
FU Grants-in-Aid for Scientific Research [26462070] Funding Source: KAKEN
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NR 51
TC 76
Z9 79
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 JUL 26
PY 2016
VL 7
IS 30
BP 47556
EP 47564
DI 10.18632/oncotarget.9879
PG 9
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DY8WP
UT WOS:000385413000056
PM 27286459
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Guil-Luna, S
   Rivas-Crespo, A
   Navarrete-Sirvent, C
   Mantrana, A
   Pera, A
   Mena-Osuna, R
   Toledano-Fonseca, M
   García-Ortíza, MV
   Villar, C
   Sanchez-Montero, MT
   Krueger, J
   Medina-Fernandez, FJ
   Haba-Rodríguez, JDL
   Auxiliadora, E
   Aranda, E
   Rudd, CE
   Rodríguez-Ariza, A
AF Guil-Luna, Silvia
   Rivas-Crespo, Aurora
   Navarrete-Sirvent, Carmen
   Mantrana, Ana
   Pera, Alejandra
   Mena-Osuna, Rafael
   Toledano-Fonseca, Marta
   Garcia-Ortiza, Maria Victoria
   Villar, Carlos
   Sanchez-Montero, Maria Teresa
   Krueger, Janna
   Medina-Fernandez, Francisco Javier
   Haba-Rodriguez, Juan De La
   Gomez-Espana, Auxiliadora
   Aranda, Enrique
   Rudd, Christopher E.
   Rodriguez-Ariza, Antonio
TI Clinical significance of glycogen synthase kinase 3 (GSK-3) expression
   and tumor budding grade in colorectal cancer: Implications for targeted
   therapy
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Tumor budding; GSK-3; PD-L1; Humanized PDXs; Colorectal cancer
ID SMALL-MOLECULE INHIBITION; PD-L1 EXPRESSION; CELLS; GSK3-BETA;
   MICROENVIRONMENT; BLOCKADE; SURVIVAL
AB Introduction: Glycogen synthase kinase 3 (GSK-3) has been proposed as a novel cancer target due to its regulating role in both tumor and immune cells. However, the connection between GSK-3 and immunoevasive contexture, including tumor budding (TB) has not been previously examined.Methods: we investigated the expression levels of total GSK-3 as well as its isoforms (GSK-3 beta and GSK-3 alpha) and examined their potential correlation with TB grade and the programmed cell death-ligand 1 (PD-L1) in colorectal cancer (CRC) tumor samples. Additionally, we compared the efficacy of GSK-3-inhibition with PD-1/PD-L1 blockade in humanized patient-derived (PDXs) xenografts models of high-grade TB CRC.Results: we show that high-grade (BD3) TB CRC is associated with elevated expression levels of total GSK-3, specifically the GSK-3 beta isoform, along with increased expression of PD-L1 in tumor cells. Moreover, we define an improved risk stratification of CRC patients based on the presence of GSK-3+/PD-L1+/BD3 tumors, which are associated with a worse prognosis. Significantly, in contrast to the PD-L1/PD-1 blockade approach, the inhibition GSK-3 demonstrated a remarkable enhancement in the antitumor response. This was achieved through the reduction of tumor buds via necrosis and apoptosis pathways, along with a notable increase of activated tumor -infiltrating CD8+ T cells, NK cells, and CD4- CD8- T cells.Conclusions: our study provides compelling evidence for the clinical significance of GSK-3 expression and TB grade in risk stratification of CRC patients. Moreover, our findings strongly support GSK-3 inhibition as an effective therapy specifically targeting high-grade TB in CRC.
C1 [Guil-Luna, Silvia; Rivas-Crespo, Aurora; Navarrete-Sirvent, Carmen; Mantrana, Ana; Pera, Alejandra; Mena-Osuna, Rafael; Toledano-Fonseca, Marta; Garcia-Ortiza, Maria Victoria; Sanchez-Montero, Maria Teresa; Haba-Rodriguez, Juan De La; Gomez-Espana, Auxiliadora; Aranda, Enrique; Rodriguez-Ariza, Antonio] Maimonides Biomed Res Inst Cordoba IMIBIC, Cordoba, Spain.
   [Guil-Luna, Silvia; Rivas-Crespo, Aurora; Navarrete-Sirvent, Carmen; Mantrana, Ana; Mena-Osuna, Rafael; Toledano-Fonseca, Marta; Garcia-Ortiza, Maria Victoria; Sanchez-Montero, Maria Teresa; Haba-Rodriguez, Juan De La; Aranda, Enrique; Rodriguez-Ariza, Antonio] Canc Network Biomed Res Ctr CIBERONC, Madrid, Spain.
   [Guil-Luna, Silvia; Rivas-Crespo, Aurora; Navarrete-Sirvent, Carmen; Mantrana, Ana; Mena-Osuna, Rafael; Toledano-Fonseca, Marta; Garcia-Ortiza, Maria Victoria; Sanchez-Montero, Maria Teresa; Haba-Rodriguez, Juan De La; Gomez-Espana, Auxiliadora; Aranda, Enrique; Rodriguez-Ariza, Antonio] Andalusia ROCHE Network Mixed Alliance Precis Med, Madrid, Spain.
   [Haba-Rodriguez, Juan De La; Gomez-Espana, Auxiliadora; Aranda, Enrique] Univ Cordoba, Dept Med, Fac Med, Cordoba, Spain.
   [Pera, Alejandra] Univ Cordoba, Dept Cell Biol Physiol & Immunol, Cordoba, Spain.
   [Villar, Carlos] Reina Sofia Univ Hosp, Dept Pathol Anat, Cordoba, Spain.
   [Krueger, Janna] Maisonneuve Rosemont Hosp, Div Immunol, Oncol Res Ctr, Montreal, PQ, Canada.
   [Medina-Fernandez, Francisco Javier; Rudd, Christopher E.] Reina Sofia Univ Hosp, Gen & Digest Surg Dept, Cordoba, Spain.
   [Haba-Rodriguez, Juan De La; Gomez-Espana, Auxiliadora; Aranda, Enrique; Rodriguez-Ariza, Antonio] Reina Sofia Univ Hosp, Dept Med Oncol, Cordoba, Spain.
   [Rudd, Christopher E.] Univ Montreal, Fac Med, Montreal, PQ, Canada.
   [Guil-Luna, Silvia] Univ Cordoba, Dept Comparat Pathol, Fac Vet Med, Cordoba, Spain.
C3 Universidad de Cordoba; Universidad de Cordoba; Universite de Montreal;
   Hospital Universitario Reina Sofia - Cordoba; Universite de Montreal;
   Universidad de Cordoba
RP Guil-Luna, S (corresponding author), Maimonides Biomed Res Inst Cordoba IMIBIC, Cordoba, Spain.; Guil-Luna, S (corresponding author), Canc Network Biomed Res Ctr CIBERONC, Madrid, Spain.; Guil-Luna, S (corresponding author), Andalusia ROCHE Network Mixed Alliance Precis Med, Madrid, Spain.; Guil-Luna, S (corresponding author), Univ Cordoba, Dept Comparat Pathol, Fac Vet Med, Cordoba, Spain.
EM v22gulus@uco.es; z02ricra@uco.es; Carmen.navarretesirvent@imibic.org;
   b42masoa@uco.es; Alejandra.pera@imibic.org; b72meosr@uco.es;
   martatoledanofonseca@gmail.com; mvictoria.garcia@imibic.org;
   carlosm.villar.sspa@juntadeandalucia.es; maria.sanchez@imibic.org;
   krueger@web.de; mefef.dr@gmail.com; juahaba@gmail.com;
   auxiliadora.gomez.sspa@juntadeandalucia.es; earandaa@seom.org;
   christopher.e.rudd@umontreal.ca;
   Antonio.rodriguez.exts@juntadeandalucia.es
RI , Silvia/AAI-2005-2019; Rodriguez-Ariza, Antonio/JAO-0548-2023; Garcia
   Ortiz, Maria Victoria/L-1623-2014; Pera, Alejandra/J-1004-2018
OI Garcia Ortiz, Maria Victoria/0000-0001-6527-4908; Pera,
   Alejandra/0000-0003-1169-8996; Guil Luna, Silvia/0000-0001-7542-3903;
   Haba Rodriguez, Juan Rafael de la/0000-0001-5111-1702
FU University of Cordoba [PIP-0044-2020]; Consejeria de Salud de la Junta
   de Andalucia [UCO-FEDER 1260965, UCO-FEDER 1381156]; Junta de Andalucia
   [RH-0062-2020]; EMBO Scientific Exchange Grant [10229]; Canadian
   Institute of Health Foundation grant
FX This work was supported by funding from the Instituto de Salud Carlos
   III (CIBERONC, CB16/12/00349) , Consejeria de Salud de la Junta de
   Andalucia (PIP-0044-2020) , and University of Cordoba (UCO-FEDER 1260965
   and UCO-FEDER 1381156) . S.G.L. was funded with a researcher contract
   from Consejeria de Salud de la Junta de Andalucia (RH-0062-2020) and
   A.R.A. was funded with a researcher contract through the program
   "Nicolas Monardes" from Junta de Andalucia. A.R. C was supported by a
   EMBO Scientific Exchange Grant (10229) .C.E.R. was supported by the
   Canadian Institute of Health Foundation grant (159912).r de Andalucia
   (PIP-0044-2020) , and University of Cordoba (UCO-FEDER 1260965 and
   UCO-FEDER 1381156) . S.G.L. was funded with a researcher contract from
   Consejeria de Salud de la Junta de Andalucia (RH-0062-2020) and A.R.A.
   was funded with a researcher contract through the program "Nicol<acute
   accent>as Monardes" from Junta de Andalucia. A.R. C was supported by a
   EMBO Scientific Exchange Grant (10229) .C.E.R. was supported by the
   Canadian Institute of Health Foundation grant
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NR 50
TC 2
Z9 2
U1 0
U2 1
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 2023
VL 167
AR 115592
DI 10.1016/j.biopha.2023.115592
EA SEP 2023
PG 14
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA W0WA2
UT WOS:001088907200001
PM 37778272
OA gold
DA 2025-01-04
ER

PT J
AU Zhou, S
   Xia, HW
   Xu, HJ
   Tang, QL
   Nie, YZ
   Gong, QY
   Bi, F
AF Zhou, Sheng
   Xia, Hongwei
   Xu, Huanji
   Tang, Qiulin
   Nie, Yongzhan
   Gong, Qi Yong
   Bi, Feng
TI ERRα suppression enhances the cytotoxicity of the MEK inhibitor
   trametinib against colon cancer cells
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Article
DE Oestrogen-related receptor alpha (ERR alpha); Epidermal growth factor
   (EGF); Trametinib; Simvastatin
ID ESTROGEN-RELATED-RECEPTOR; PROLIFERATOR-ACTIVATED RECEPTOR;
   EPIDERMAL-GROWTH-FACTOR; COLORECTAL-CANCER; BREAST-CANCER;
   TRANSCRIPTIONAL REGULATOR; NUCLEAR RECEPTORS; EXPRESSION; GAMMA; KRAS
AB Background: ERR alpha, a constitutive transcription factor that regulates energy metabolism, plays an important role in the progression of various tumours. However, its role in cell survival and proliferation and its implication in targeted therapy in colon cancer remains elusive.
   Methods: The expression of ERR alpha in colon cancer tissues and cell lines was detected by using western blotting and immunohistochemistry. A wound healing assay and a transwell assay were performed to examine the migration and invasion of the colon cancer cells. A cell viability assay, clonogenic assay, western blot assay and the dual-luciferase reporter assay were employed to study the interaction between trametinib (inhibitor of MEK) and EGF treatment. Flow cytometry, western blotting, quantitative reverse-transcription polymerase chain reaction and xenograft studies were used to identify whether the combination of trametinib and simvastatin had a synergistic effect.
   Results: ERR alpha positively regulated the cell proliferation, migration and invasion of colon cancer cells, and the suppression of ERR alpha completely reduced the EGF treatment-induced proliferation of colon cancer cells. Further investigation showed that trametinib partially restrained the up-regulation of ERR alpha induced by the EGF treatment, and ERR alpha inhibition increased the sensitivity of colon cancer cells to trametinib. At last, we combined trametinib with simvastatin, a common clinically used drug with a new reported function of transcriptional activity inhibition of ERR alpha, and found that this combinatio n produced a synergistic effect in inhibiting the proliferation and survival of colon cancer cells in vitro as well as in vivo.
   Conclusions: The present data indicated that ERR alpha acted as an oncogene in colon cancer cells, and the combined targeting of ERR alpha and MEK might be a promising therapeutic strategy for colon cancer treatment.
C1 [Zhou, Sheng; Xu, Huanji; Bi, Feng] Sichuan Univ, West China Hosp, Canc Ctr, Dept Med Oncol, Chengdu, Sichuan, Peoples R China.
   [Zhou, Sheng; Xia, Hongwei; Xu, Huanji; Tang, Qiulin] Sichuan Univ, West China Hosp, State Key Lab Biotherapy & Canc Ctr, Lab Mol Targeted Therapy Oncol, Chengdu, Sichuan, Peoples R China.
   [Zhou, Sheng; Xia, Hongwei; Xu, Huanji; Tang, Qiulin] Sichuan Univ, West China Hosp, Canc Ctr, Chengdu, Sichuan, Peoples R China.
   [Zhou, Sheng; Xia, Hongwei; Xu, Huanji; Tang, Qiulin] Collaborat Innovat Ctr Biotherapy, Chengdu, Sichuan, Peoples R China.
   [Nie, Yongzhan] Fourth Mil Med Univ, State Key Lab Canc Biol, Xian, Shanxi, Peoples R China.
   [Nie, Yongzhan] Fourth Mil Med Univ, Xijing Hosp Digest Dis, Xian, Shanxi, Peoples R China.
   [Gong, Qi Yong] Sichuan Univ, West China Hosp, Dept Radiol, Chengdu, Sichuan, Peoples R China.
   [Bi, Feng] Sichuan Univ, West China Hosp, Dept Med Oncol, Lab Mol Targeted Therapy Oncol, Chengdu 610041, Sichuan, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University; Air Force
   Military Medical University; Air Force Military Medical University;
   Sichuan University; Sichuan University
RP Bi, F (corresponding author), Sichuan Univ, West China Hosp, Canc Ctr, Dept Med Oncol, Chengdu, Sichuan, Peoples R China.; Bi, F (corresponding author), Sichuan Univ, West China Hosp, Dept Med Oncol, Lab Mol Targeted Therapy Oncol, Chengdu 610041, Sichuan, Peoples R China.
EM bifeng@scu.edu.cn
RI Xu, Huanji/HZJ-6972-2023; Bi, Feng/J-7459-2015; Gong, Qiyong/W-3052-2019
OI Gong, Qiyong/0000-0002-5912-4871; Xu, Huanji/0000-0003-0314-5646
FU National Natural Science Foundation of China [81621003, 81572731];
   National key R&D Program of China [2016YFC1303200/2016YFC1303203]
FX National Natural Science Foundation of China (81621003); National key
   R&D Program of China (2016YFC1303200/2016YFC1303203); National Natural
   Science Foundation of China (81572731).
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NR 41
TC 24
Z9 26
U1 0
U2 13
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1756-9966
J9 J EXP CLIN CANC RES
JI J. Exp. Clin. Cancer Res.
PD SEP 5
PY 2018
VL 37
AR 218
DI 10.1186/s13046-018-0862-8
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GS8OT
UT WOS:000443972300002
PM 30185207
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Huemer, F
   Dunkl, C
   Rinnerthaler, G
   Schlick, K
   Heregger, R
   Emmanuel, K
   Neureiter, D
   Klieser, E
   Deutschmann, M
   Roeder, F
   Greil, R
   Weiss, L
AF Huemer, Florian
   Dunkl, Celine
   Rinnerthaler, Gabriel
   Schlick, Konstantin
   Heregger, Ronald
   Emmanuel, Klaus
   Neureiter, Daniel
   Klieser, Eckhard
   Deutschmann, Michael
   Roeder, Falk
   Greil, Richard
   Weiss, Lukas
TI Management of metastatic colorectal cancer in patients ≥70 years-a
   single center experience
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE elderly; age; ECOG performance score; colorectal cancer; sidedness;
   local ablative treatment; metastasectomy
ID FOLFOXIRI PLUS BEVACIZUMAB; OPEN-LABEL; ELDERLY-PATIENTS; OLDER
   PATIENTS; 1ST-LINE TREATMENT; LIVER METASTASES; PHASE-3; MULTICENTER;
   COMORBIDITY; SURVIVAL
AB BackgroundAge-standardized mortality rates for metastatic colorectal cancer (mCRC) are highest among elderly patients. In current clinical guidelines, treatment recommendations for this patient population are based on a limited number of clinical trials. Patients and methodsIn this monocentric, retrospective analysis we characterized patients aged & GE;70 years undergoing systemic therapy for mCRC and overall survival (OS) was investigated. ResultsWe included 117 unselected, consecutive mCRC patients aged & GE;70 years undergoing systemic therapy for mCRC between February 2009 and July 2022. Median OS was 25.6 months (95% CI: 21.8-29.4). The median age was 78 years (range: 70-90) and 21%, 48%, 26% and 5% had an ECOG performance score of 0, 1, 2, and 3, respectively. The median number of systemic therapy lines was 2 (range: 1-5). The choice of first-line chemotherapy backbone (doublet/triplet versus mono) did not impact OS (HR: 0.83, p=0.50) or the probability of receiving subsequent therapy (p=0.697). Metastasectomy and/or local ablative treatment in the liver, lung, peritoneum and/or other organs were applied in 26 patients (22%) with curative intent. First-line anti-EGFR-based therapy showed a trend towards longer OS compared to anti-VEGF-based therapy or chemotherapy alone in left-sided mCRC (anti-EGFR: 39.3 months versus anti-VEGF: 27.3 months versus chemotherapy alone: 13.8 months, p=0.105). In multivariable analysis, metastasectomy and/or local ablative treatment with curative intent (yes versus no, HR: 0.22, p<0.001), the ECOG performance score (2 versus 0, HR: 3.07, p=0.007; 3 versus 0, HR: 3.66, p=0.053) and the presence of liver metastases (yes versus no, HR: 1.79, p=0.049) were independently associated with OS. ConclusionsOur findings corroborate front-line monochemotherapy in combination with targeted therapy as the treatment of choice for elderly mCRC patients with palliative treatment intent. Metastasectomy and/or local ablative treatment with curative intent are feasible and may improve OS in selected elderly mCRC patients.
C1 [Huemer, Florian; Dunkl, Celine; Rinnerthaler, Gabriel; Schlick, Konstantin; Heregger, Ronald; Greil, Richard; Weiss, Lukas] Paracelsus Med Univ Salzburg, Salzburg Canc Res Inst, Ctr Clin Canc & Immunol Trials SCRI CCCIT, Dept Internal Med 3,Haematol Med Oncol Haemostaseo, Salzburg, Austria.
   [Rinnerthaler, Gabriel; Neureiter, Daniel; Greil, Richard; Weiss, Lukas] Canc Cluster Salzburg, Salzburg, Austria.
   [Emmanuel, Klaus] Paracelsus Med Univ Salzburg, Dept Surg, Salzburg, Austria.
   [Neureiter, Daniel; Klieser, Eckhard] Paracelsus Med Univ Salzburg, Inst Pathol, Salzburg, Austria.
   [Deutschmann, Michael] Paracelsus Med Univ Salzburg, Dept Radiol, Salzburg, Austria.
   [Roeder, Falk] Paracelsus Med Univ Salzburg, Dept Radiat Oncol, Salzburg, Austria.
   [Greil, Richard; Weiss, Lukas] Tumor Registry Prov Salzburg, Salzburg, Austria.
C3 Paracelsus Private Medical University; Paracelsus Private Medical
   University; Paracelsus Private Medical University; Paracelsus Private
   Medical University; Paracelsus Private Medical University
RP Weiss, L (corresponding author), Paracelsus Med Univ Salzburg, Salzburg Canc Res Inst, Ctr Clin Canc & Immunol Trials SCRI CCCIT, Dept Internal Med 3,Haematol Med Oncol Haemostaseo, Salzburg, Austria.; Weiss, L (corresponding author), Canc Cluster Salzburg, Salzburg, Austria.; Weiss, L (corresponding author), Tumor Registry Prov Salzburg, Salzburg, Austria.
EM lu.weiss@salk.at
RI Greil, Richard/C-7673-2017; Huemer, Florian/JWO-2337-2024; Rinnerthaler,
   Gabriel/GZM-5613-2022
FU Servier Austria GmbH
FX This work was supported by Servier Austria GmbH without any role in the
   design of the analysis, interpretation of data or influence on the
   content of the manuscript.
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NR 44
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 JUL 25
PY 2023
VL 13
AR 1222951
DI 10.3389/fonc.2023.1222951
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA O4RU7
UT WOS:001043710800001
PM 37560467
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wang, L
   Zeng, ZH
   Wu, ZQ
AF Wang, Lu
   Zeng, Zhaohao
   Wu, Zhiqiang
TI Case report: PRES associated with fruquintinib in a patient with
   metastatic colon cancer
SO NEUROLOGICAL SCIENCES
LA English
DT Article
DE Posterior reversible encephalopathy syndrome (PRES); Fruquintinib;
   Metastatic colon cancer
ID REVERSIBLE ENCEPHALOPATHY SYNDROME
AB Posterior reversible encephalopathy syndrome (PRES) is a rare, reversible neurological disease that is frequently associated with the use of targeted therapy agents. In this case study, we examine the development of posterior reversible encephalopathy syndrome (PRES) in a 44-year-old woman with metastatic colon cancer following 1 month of treatment with the vascular endothelial growth factor receptor (VEGFR) inhibitor, fruquintinib. The occurrence of PRES after 1 month of VEGFR inhibitor administration is a common phenomenon. However, it is noteworthy that this is the first reported case of PRES associated with fruquintinib. The patient's neurological function improved upon discontinuing the drug for a week, but worsening was observed following a lower-dose fruquintinib treatment. This patient's experience highlights the potential for neurological deterioration in those treated with fruquintinib, prompting physicians to consider the possibility of PRES. Notably, this may be the first reported case linking fruquintinib to the syndrome, underscoring the importance of recognizing the association between PRES and fruquintinib.
C1 [Wang, Lu; Wu, Zhiqiang] Wuhan Univ Sci & Technol, Dept Neurol, Xiaogan Hosp, Xiaogan, Hubei, Peoples R China.
   [Zeng, Zhaohao] Jinan Univ, Shenzhen Peoples Hosp, Dept Neurol, Clin Med Coll 2, Shenzhen, Peoples R China.
   [Zeng, Zhaohao] Southern Univ Sci & Technol, Affiliated Hosp 1, Shenzhen 518001, Guangdong, Peoples R China.
C3 Wuhan University of Science & Technology; Jinan University; Southern
   University of Science & Technology
RP Wu, ZQ (corresponding author), Wuhan Univ Sci & Technol, Dept Neurol, Xiaogan Hosp, Xiaogan, Hubei, Peoples R China.
EM 851487638@qq.com
RI Zeng, Zhaohao/JFJ-1579-2023
OI wang, lu/0000-0002-4392-4073
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NR 12
TC 1
Z9 1
U1 1
U2 2
PU SPRINGER-VERLAG ITALIA SRL
PI MILAN
PA VIA DECEMBRIO, 28, MILAN, 20137, ITALY
SN 1590-1874
EI 1590-3478
J9 NEUROL SCI
JI Neurol. Sci.
PD NOV
PY 2023
VL 44
IS 11
BP 4111
EP 4114
DI 10.1007/s10072-023-06991-7
EA AUG 2023
PG 4
WC Clinical Neurology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA U4ZR4
UT WOS:001049066000002
PM 37581770
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Cui, JZ
   Chew, ZH
   Lim, LHK
AF Cui, Jian-Zhou
   Chew, Zhi Huan
   Lim, Lina H. K.
TI New insights into nucleic acid sensor AIM2: The potential benefit in
   targeted therapy for cancer
SO PHARMACOLOGICAL RESEARCH
LA English
DT Article
DE AIM2 Inflammasome; Cytosolic DNA; Pyroptosis; Immunotherapy; DNA -RNA
   Hybrids; PD-L1
ID MELANOMA 2 INFLAMMASOME; DOUBLE-STRANDED DNA; RIG-I; CELL-DEATH;
   COLORECTAL-CANCER; STREPTOCOCCUS-PNEUMONIAE; NLRP3 INFLAMMASOMES;
   RNA-POLYMERASE; CYTOSOLIC DNA; CASPASE-1 ACTIVATION
AB The AIM2 inflammasome represents a multifaceted oligomeric protein complex within the innate immune system, with the capacity to perceive double-stranded DNA (dsDNA) and engage in diverse physiological reactions and disease contexts, including cancer. While originally conceived as a discerning DNA sensor, AIM2 has demonstrated its capability to discern various nucleic acid variations, encompassing RNA and DNA-RNA hybrids. Through its interaction with nucleic acids, AIM2 orchestrates the assembly of a complex involving multiple proteins, aptly named the AIM2 inflammasome, which facilitates the enzymatic cleavage of proinflammatory cytokines, namely pro-IL-1 beta and pro-IL-18. This process, in turn, underpins its pivotal biological role. In this review, we provide a systematic summary and discussion of the latest advancements in AIM2 sensing various types of nucleic acids. Additionally, we discuss the modulation of AIM2 activation, which can cause cell death, including pyroptosis, apoptosis, and autophagic cell death. Finally, we fully illustrate the evidence for the dual role of AIM2 in different cancer types, including both anti-tumorigenic and pro-tumorigenic functions. Considering the above information, we uncover the therapeutic promise of modulating the AIM2 inflammasome in cancer treatment.
C1 [Cui, Jian-Zhou; Chew, Zhi Huan; Lim, Lina H. K.] Natl Univ Singapore, Yong Loo Lin Sch Med, Translat Immunol Program, Singapore, Singapore.
   [Cui, Jian-Zhou; Chew, Zhi Huan; Lim, Lina H. K.] Natl Univ Singapore, Life Sci Inst, Immunol Program, Singapore, Singapore.
   [Cui, Jian-Zhou] Natl Univ Singapore, Life Sci Inst, Cambridge Immunophenotyping Ctr, Singapore, Singapore.
   [Chew, Zhi Huan; Lim, Lina H. K.] Natl Univ Singapore, NUS Grad Sch Integrat Sci & Engn, Singapore, Singapore.
   [Chew, Zhi Huan] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Microbiol, Singapore, Singapore.
   [Lim, Lina H. K.] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Physiol, Singapore, Singapore.
   [Lim, Lina H. K.] Natl Univ Singapore NUS, Yong Loo Lin Sch Med, Immunol Translat Res Program, 28 Med Dr,Life Sci Inst 03-06C & 03-06J, Singapore 117456, Singapore.
C3 National University of Singapore; National University of Singapore;
   National University of Singapore; National University of Singapore;
   National University of Singapore; National University of Singapore;
   National University of Singapore
RP Lim, LHK (corresponding author), Natl Univ Singapore NUS, Yong Loo Lin Sch Med, Immunol Translat Res Program, 28 Med Dr,Life Sci Inst 03-06C & 03-06J, Singapore 117456, Singapore.
EM jianzhou.cui@u.nus.edu; linalim@nus.edu.sg
RI Cui, Jianzhou/AAU-7765-2020
OI Cui, Jianzhou/0000-0003-1666-4082
FU Ministry of Education [MOE2014-T2-1-133, MOE2013-T2-2-032]; NUS Graduate
   School of Science and Technology
FX This work was financially supported by the Ministry of Education grants
   MOE2014-T2-1-133 and MOE2013-T2-2-032, awarded to LHKL. ZHC's endeavors
   were facilitated by an academic scholarship from the NUS Graduate School
   of Science and Technology. Our appreciation is directed towards Prof.
   Gene Yeo and his dedicated team at the Institute for Genomic Medicine,
   University of California, San Diego, La Jolla, CA, USA, for their
   indispensable assistance with the eClip data analysis. We recognize the
   vast body of significant work in the realm of nucleic acid sensor
   signaling and its application to cancer therapy. Regrettably, due to
   space constraints, we could not elaborate upon or reference several
   seminal contributions, and for that, we extend our apologies to the
   respective authors.
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NR 236
TC 4
Z9 4
U1 4
U2 7
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
EI 1096-1186
J9 PHARMACOL RES
JI Pharmacol. Res.
PD FEB
PY 2024
VL 200
AR 107079
DI 10.1016/j.phrs.2024.107079
EA JAN 2024
PG 17
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA JP1R6
UT WOS:001174283400001
PM 38272334
OA hybrid
DA 2025-01-04
ER

PT J
AU Xin, ZY
   Ma, Q
   Ren, SC
   Wang, GQ
   Li, F
AF Xin, Zhuoyuan
   Ma, Qin
   Ren, Shuangchun
   Wang, Guoqing
   Li, Fan
TI The understanding of circular RNAs as special triggers in carcinogenesis
SO BRIEFINGS IN FUNCTIONAL GENOMICS
LA English
DT Article
DE circular RNA; miRNA sponge; cancer; biomarker; targeted therapy
ID GROWTH-FACTOR RECEPTOR; HEPATITIS-DELTA-VIRUS; BREAST-CANCER CELLS;
   HUMAN COLORECTAL-CANCER; STEM-LIKE CELLS; MIR-7 EXPRESSION;
   GASTRIC-CANCER; LUNG-CANCER; IN-VIVO; EXON CIRCULARIZATION
AB Circular RNAs (circRNAs) are a large type of noncoding RNAs characterized by their circular shape resulting from covalently closed continuous loops. They are known to regulate gene expression in mammals. These tissue-specific transcripts are largely generated from exonic or intronic sequences of their host genes. Although several models of circRNA biogenesis have been proposed, the understanding of their origin is far from complete. Unlike other noncoding RNAs, circRNAs are widely expressed, highly conserved and stable in cytoplasm, which confer special functionalities to them. They are known to serve as microRNA (miRNA) sponges, regulators of alternative splicing, transcription factors and encode for proteins. The expression of circRNAs is associated with several pathological states and may potentially serve as novel diagnostic or predictive biomarkers. CircRNAs are known to regulate the expression of numerous cancer-related miRNAs. The circRNA-miRNA-mRNA axis is a known regulatory pattern of several cancer-associated pathways, with both agonist and antagonist effects on carcinogenesis. In consideration of their potential clinical relevance, circRNAs are at the center of ongoing research initiatives on cancer prevention and treatment. In this review, we discuss the current understanding of circRNAs and the prospects for their potential clinical application in the management of cancer patients.
C1 [Xin, Zhuoyuan; Ren, Shuangchun; Wang, Guoqing; Li, Fan] Jilin Univ, Minist Educ, Coll Basic Med Sci, Key Lab Bion Engn, Changchun, Peoples R China.
   [Ma, Qin] South Dakota State Univ, Bioinformat & computat Syst Biol, Brookings, SD USA.
C3 Jilin University; South Dakota State University
RP Wang, GQ; Li, F (corresponding author), Jilin Univ, Minist Educ, Coll Basic Med Sci, Key Lab Bion Engn, Changchun, Peoples R China.
EM qing@jlu.edu.cn; lifan@jlu.edu.cn
RI Fan, Li/AHA-6635-2022; Ma, Qin/V-7920-2019; Yuan, Xin/KCZ-2239-2024
FU National Natural Science Foundation of China [81320108025, 81271897,
   81472662]; Foundation of Jilin Province Science and Technology
   Department [20130522013JH, 20140414048GH]; Norman Bethune Program of
   Jilin University [2012219]; Jilin University-Xinjiang Medical University
FX This work was supported by the National Natural Science Foundation of
   China (81320108025, 81271897, 81472662); Foundation of Jilin Province
   Science and Technology Department (#20130522013JH and #20140414048GH),
   Norman Bethune Program of Jilin University (2012219); Jilin
   University-Xinjiang Medical University joint research project.
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NR 88
TC 59
Z9 62
U1 1
U2 32
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 2041-2649
EI 2041-2657
J9 BRIEF FUNCT GENOMICS
JI Brief. Funct. Genomics
PD MAR
PY 2017
VL 16
IS 2
BP 80
EP 86
DI 10.1093/bfgp/elw001
PG 7
WC Biotechnology & Applied Microbiology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA EP2IA
UT WOS:000397205400003
PM 26874353
OA hybrid
DA 2025-01-04
ER

PT J
AU Tu, JH
   Yu, YH
   Liu, W
   Chen, SP
AF Tu, Jinhua
   Yu, Yinghao
   Liu, Wei
   Chen, Shunping
TI Significance of human epidermal growth factor receptor 2 expression in
   colorectal cancer
SO EXPERIMENTAL AND THERAPEUTIC MEDICINE
LA English
DT Article
DE colorectal cancer; human epidermal growth factor receptor 2;
   immunohistochemistry; fluorescence in situ hybridization; herceptin
ID INDEPENDENT PROGNOSTIC-FACTOR; IN-SITU HYBRIDIZATION; HER2 GENE STATUS;
   BREAST-CANCER; HER-2/NEU OVEREXPRESSION; PROTEIN EXPRESSION;
   OVER-EXPRESSION; GASTRIC-CANCER; TISSUE; EGFR
AB The aim of the present study was to evaluate the protein expression level of human epidermal growth factor receptor 2 (HER-2) using immunohistochemistry (IHC), and assess the association with clinicopathological parameters and the prognosis of patients with colorectal cancer (CRC). In addition, the current study observed the consistency between the levels of HER-2 protein expression determined by IHC and HER-2 gene amplification determined by fluorescence in situ hybridization (FISH) in the CRC samples. Overexpression of HER-2 and gene amplification were examined with semiquantitative standardized IHC in 878 formalin-fixed paraffin-embedded CRC samples, while 102 of these cases were analyzed with FISH. A total of 102 cases (11.6%), out of the 878 cases, were determined by IHC to overexpress HER-2. Of these, 25 cases were strongly positive (IHC3+), while 77 cases revealed moderate staining (IHC2+). HER-2 overexpression was more frequent in early-stage cases compared with advanced-stage cases of CRC (P<0.001). However, there was no association observed between HER-2 overexpression and clinicopathological parameters. FISH analysis revealed that 64% (16/25) of the IHC3+ cases had HER-2 gene amplification. By contrast, only 6.5% (5/77) of the IHC2+ cases, and none of the 20 randomly selected IHC0 or 1+ cases, demonstrated HER-2 gene amplification. Furthermore, no associations were observed between HER-2 overexpression or gene amplification with the survival time. Thus, the present study observed that HER-2 overexpression does not correlate with other clinicopathological data or the survival rate, with the exception of clinical stages. However, IHC3+ and 2+ cases should be further analyzed by FISH to assess the status of the HER-2 gene in CRC. Patients with HER-2 gene amplification may constitute as potential candidates for targeted therapy with trastuzumab.
C1 [Tu, Jinhua] Xiamen Univ, Dept Pathol, Affiliated Hosp 1, Xiamen 361004, Fujian, Peoples R China.
   [Tu, Jinhua; Yu, Yinghao; Liu, Wei; Chen, Shunping] Fujian Med Univ, Dongfang Hosp, Dept Pathol, Fuzhou 350025, Fujian, Peoples R China.
C3 Xiamen University; Fujian Medical University
RP Yu, YH (corresponding author), Fujian Med Univ, Dongfang Hosp, Dept Pathol, 156 North Rd, Fuzhou 350025, Fujian, Peoples R China.
EM jinhuatu@163.com
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NR 49
TC 19
Z9 21
U1 0
U2 13
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-0981
EI 1792-1015
J9 EXP THER MED
JI Exp. Ther. Med.
PD JAN
PY 2015
VL 9
IS 1
BP 17
EP 24
DI 10.3892/etm.2014.2063
PG 8
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA AX1HS
UT WOS:000346699000003
PM 25452770
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Yu, YY
AF Yu, Yingyan
TI Molecular classification and precision therapy of cancer: immune
   checkpoint inhibitors
SO FRONTIERS OF MEDICINE
LA English
DT Article
DE molecular classification; precision medicine; pembrolizumab; PD-1/PD-L1;
   MSI-H
ID MISMATCH-REPAIR DEFICIENCY; MICROSATELLITE INSTABILITY; ANTI-PD-L1
   ANTIBODY; GASTRIC-CANCER; LYNCH SYNDROME; COLON-CANCER; PD-1;
   EXPRESSION; RESISTANCE; MUTATIONS
AB On May 23, 2017, the US Food and Drug Administration (FDA) approved a treatment for cancer patients with positive microsatellite instability-high (MSI-H) markers or mismatch repair deficient (dMMR) markers. This approach is the first approved tumor treatment using a common biomarker rather than specified tumor locations in the body. FDA previously approved Keytruda for treatment of several types of malignancies, such as metastatic melanoma, metastatic non-small-cell lung cancer, recurrent or metastatic head and neck cancer, refractory Hodgkin lymphoma, and urothelial carcinoma, all of which carry positive programmed death-1/programmed death-ligand 1 biomarkers. Therefore, indications of Keytruda significantly expanded. Several types of malignancies are disclosed by MSI-H status due to dMMR and characterized by increased neoantigen load, which elicits intense host immune response in tumor microenvironment, including portions of colorectal and gastric carcinomas. Currently, biomarker-based patient selection remains a challenge. Pathologists play important roles in evaluating histology and biomarker results and establishing detection methods. Taking gastric cancer as an example, its molecular classification is built on genome abnormalities, but it lacks acceptable clinical characteristics. Pathologists are expected to act as "genetic interpreters" or "genetic translators" and build a link between molecular subtypes with tumor histological features. Subsequently, by using their findings, oncologists will carry out targeted therapy based on molecular classification.
C1 [Yu, Yingyan] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Surg, Shanghai 200025, Peoples R China.
   [Yu, Yingyan] Shanghai Jiao Tong Univ, Sch Med, Shanghai Key Lab Gastr Neoplasms, Shanghai 200025, Peoples R China.
C3 Shanghai Jiao Tong University; Shanghai Jiao Tong University
RP Yu, YY (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Surg, Shanghai 200025, Peoples R China.; Yu, YY (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Shanghai Key Lab Gastr Neoplasms, Shanghai 200025, Peoples R China.
EM yingyan3y@sjtu.edu.cn
RI yu, yingying/GRR-7851-2022
OI Yu, Yingyan/0000-0002-3585-3252
FU Chinese National Key Program [2017YFC0908303, 2016YFC1303200]; National
   Natural Science Foundation of China [81772505, 81372644]; Innovation
   Foundation of Translational Medicine of Shanghai Jiao Tong University
   School of Medicine [15ZH1002, 15ZH4001, TM201617]
FX The author would like to thank the Chinese National Key Program (Nos.
   2017YFC0908303 and 2016YFC1303200), National Natural Science Foundation
   of China (Nos. 81772505 and 81372644), and Innovation Foundation of
   Translational Medicine of Shanghai Jiao Tong University School of
   Medicine (Nos. 15ZH1002, 15ZH4001, and TM201617) for supporting this
   study.
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NR 42
TC 44
Z9 46
U1 1
U2 22
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 2095-0217
EI 2095-0225
J9 FRONT MED-PRC
JI Front. Med.
PD APR
PY 2018
VL 12
IS 2
BP 229
EP 235
DI 10.1007/s11684-017-0581-0
PG 7
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA GC7EP
UT WOS:000429955900013
PM 29209918
DA 2025-01-04
ER

PT J
AU Lin, YL
   Tsai, NM
   Hsieh, CH
   Ho, SY
   Chang, J
   Wu, HY
   Hsu, MH
   Chang, CC
   Liao, KW
   Jackson, TLB
   Mold, DE
   Huang, RCC
AF Lin, Yu-Ling
   Tsai, Nu-Man
   Hsieh, Cheng-Hao
   Ho, Shu-Yi
   Chang, Jung
   Wu, Hsin-Yi
   Hsu, Ming-Hua
   Chang, Chia-Ching
   Liao, Kuang-Wen
   Jackson, Tiffany L. B.
   Mold, David E.
   Huang, Ru Chih C.
TI In vivo amelioration of endogenous antitumor autoantibodies via low-dose
   P<sub>4</sub>N through the LTA4H/activin A/BAFF pathway
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE endogenous antitumor autoantibody; P4N; B-cell proliferation; colorectal
   cancer; cancer immunotherapy
ID CLASS SWITCH RECOMBINATION; TUMOR-ASSOCIATED ANTIGENS; CELL-SURFACE
   GRP78; ACTIVIN-A; MONOCLONAL-ANTIBODY; MULTIPLE-MYELOMA; DENDRITIC
   CELLS; ATP SYNTHASE; CANCER; IMMUNOTHERAPY
AB Cancer progression is associated with the development of antitumor autoantibodies in patients' sera. Although passive treatment with antitumor antibodies has exhibited remarkable therapeutic efficacy, inhibitory effects on tumor progression by endogenous antitumor autoantibodies (EAAs) have been limited. In this study, we show that P4N, a derivative of the plant lignan nordihydroguaiaretic acid (NDGA), enhanced the production of EAAs and inhibited tumor growth at low noncytotoxic concentrations via its immunoregulatory activity. Intratumoral injection of P4N improved the quantity and quality of EAAs, and passive transfer of P4N-induced EAAs dramatically suppressed lung metastasis formation and prolonged the survival of mice inoculated with metastatic CT26 tumor cells. P4N-induced EAAs specifically recognized two surface antigens, 78-kDa glucose-regulated protein (GRP78) and F1F0 ATP synthase, on the plasma membrane of cancer cells. Additionally, P4N treatment led to B-cell proliferation, differentiation to plasma cells, and high titers of autoantibody production. By serial induction of autocrine and paracrine signals in monocytes, P4N increased B-cell proliferation and antibody production via the leukotriene A4 hydrolase (LTA4H)/activin A/B-cell activating factor (BAFF) pathway. This mechanism provides a useful platform for studying and seeking a novel immunomodulator that can be applied in targeting therapy by improving the quantity and quality of the EAAs.
C1 [Lin, Yu-Ling; Hsieh, Cheng-Hao; Ho, Shu-Yi; Chang, Jung; Chang, Chia-Ching; Liao, Kuang-Wen; Huang, Ru Chih C.] Natl Chiao Tung Univ, Dept Biol Sci & Technol, Hsinchu 30068, Taiwan.
   [Lin, Yu-Ling] Natl Chiao Tung Univ, Ctr Bioinformat Res, Hsinchu 30068, Taiwan.
   [Tsai, Nu-Man] Chung Shan Med Univ, Sch Med Lab & Biotechnol, Taichung 40201, Taiwan.
   [Tsai, Nu-Man] Chung Shan Med Univ Hosp, Clin Lab, Taichung 40201, Taiwan.
   [Wu, Hsin-Yi; Liao, Kuang-Wen] Natl Chiao Tung Univ, Inst Mol Med & Bioengn, Hsinchu 30068, Taiwan.
   [Hsu, Ming-Hua] Natl Tsing Hua Univ, Nucl Sci & Technol Dev Ctr, Hsinchu 30013, Taiwan.
   [Liao, Kuang-Wen] Kaohsiung Med Univ, Coll Med, Grad Inst Med, Kaohsiung 80708, Taiwan.
   [Jackson, Tiffany L. B.; Mold, David E.; Huang, Ru Chih C.] Johns Hopkins Univ, Dept Biol, Baltimore, MD 21218 USA.
C3 National Yang Ming Chiao Tung University; National Yang Ming Chiao Tung
   University; Chung Shan Medical University; Chung Shan Medical
   University; Chung Shan Medical University Hospital; National Yang Ming
   Chiao Tung University; National Tsing Hua University; Kaohsiung Medical
   University; Johns Hopkins University
RP Liao, KW; Huang, RCC (corresponding author), Natl Chiao Tung Univ, Dept Biol Sci & Technol, Hsinchu 30068, Taiwan.; Huang, RCC (corresponding author), Johns Hopkins Univ, Dept Biol, Baltimore, MD 21218 USA.
EM liaonms@mail.nctu.edu.tw; rhuang@jhu.edu
RI Chang, Chia-Ching/F-1247-2011
OI , Tiffany/0000-0002-0800-1484; Chang, Chia-Ching/0000-0002-3444-0894
FU Ministry of Science and Technology of Taiwan (MOST) [MOST
   104-2627-M-009-007, MOST 103-2112-M-009-011-MY3];  [NCTU 102W976]; 
   [NCTU 103W976]
FX We thank Prof. Jinn-Moon Yang for kind support in docking technology. We
   thank the core facility of the multiphoton and confocal microscope
   system and UPLC/HRMS/MS of the NCTU. This research was supported by
   Grants NCTU 102W976 and NCTU 103W976 (to R.C.C.H.) and Ministry of
   Science and Technology of Taiwan (MOST) Grants MOST 104-2627-M-009-007
   and MOST 103-2112-M-009-011-MY3 (to C.C.C.).
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NR 59
TC 9
Z9 10
U1 0
U2 10
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 29
PY 2016
VL 113
IS 48
BP E7798
EP E7807
DI 10.1073/pnas.1604752113
PG 10
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA ED4QR
UT WOS:000388835700017
PM 27856749
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Xie, B
   Hu, F
   Li, M
   Mo, L
   Xu, CS
   Xiao, Y
   Wang, XY
   Nie, J
   Yang, LX
   He, YH
AF Xie, Biao
   Hu, Fan
   Li, Mei
   Mo, Li
   Xu, Chongsi
   Xiao, You
   Wang, Xiaoyan
   Nie, Jing
   Yang, Lixia
   He, Yongheng
TI FLI-1 mediates tumor suppressor function via Klotho signaling in
   regulating CRC
SO CELL BIOLOGY INTERNATIONAL
LA English
DT Article
DE colorectal cancer; FLI-1; Klotho; methylation; shRNA
ID CANCER; GROWTH; APOPTOSIS; GENE
AB Colorectal cancer (CRC) is an aggressive malignancy with a high incidence and mortality rate. Although a targeting therapy has been developed, the 5-year survival rate is still very low in CRC patients with distant metastasis. Thus, the identification of new targets is still significant for improving CRC treatment. Klotho is a tumor suppressor, and its expression is aberrant in CRC. In this study, the roles of the FLI-1 gene in regulating Klotho gene expression and Klotho-associated signaling, as well as the effects of FLI-1 on colony formation, invasion, and apoptosis were investigated in CRC cell lines. The methylation of the FLI-1 gene was analyzed using a commercial methylation kit. Results showed that FLI-1 messenger RNA and protein expression were downregulated in six CRC cell lines when compared with the normal colon mucosal epithelial cell line, which negatively correlated with the level of DNA methylation. Silencing of FLI-1 gene expression decreased Klotho protein expression and phosphorylation of beta-catenin protein at Thr(41)/Ser(45), but increased Wnt3a and beta-catenin protein expression and IGF-1R phosphorylation in HT29 cells. In contrast to silencing FLI-1, overexpressing FLI-1 significantly increased Klotho protein expression and phosphorylation of beta-catenin protein at Thr(41)/Ser(45), but decreased Wnt3a and beta-catenin protein expression and IGF-1R phosphorylation in Caco-2 cells. Silencing of FLI-1 gene expression significantly increased colony formation and invasion, but decreased apoptosis in HT29 cells. In contrast, overexpressing the FLI-1 gene significantly decreased colony formation and invasion, but increased apoptosis in Caco-2 cells. These findings suggest that FLI-1 functions as a tumor suppressor in CRC cells and positively regulates Klotho signaling. Hypermethylation may be one of the causes of the loss of FLI-1 gene expression in CRC cells.
C1 [Xie, Biao; Hu, Fan; Li, Mei; Mo, Li; Xu, Chongsi; Xiao, You; Wang, Xiaoyan; He, Yongheng] Hunan Univ Chinese Med, Dept Anorectal Surg 1, Affiliated Hosp 2, Changsha 410005, Hunan, Peoples R China.
   [Nie, Jing] Hunan Slack King Lab Anim Co Ltd, Changsha 410125, Hunan, Peoples R China.
   [Yang, Lixia] Changsha Med Sch, Dept Canc, Affiliated Hosp 1, Changsha 410219, Hunan, Peoples R China.
C3 Hunan University of Chinese Medicine; Changsha Medical University
RP He, YH (corresponding author), Hunan Univ Chinese Med, Dept Anorectal Surg 1, Affiliated Hosp 2, Changsha 410005, Hunan, Peoples R China.
EM heyongheng1964@163.com
RI Yang, Lixia/AAB-7890-2022
FU Department of Education Key Project of Hunan Province [15A024];
   Postdoctoral Science Foundation of China [2016M602416]; National Natural
   Science Foundation of China [81704089]; Postdoctoral Science Fund
   Special Grant of China [2017T100603]; Natural Science Foundation of Huan
   Provence [2018JJ3400]; Changsha City Outstanding Innovation Youth
   Program [kq1707012]
FX This study was supported by the Department of Education Key Project of
   Hunan Province (15A024), the Postdoctoral Science Foundation of China
   (2016M602416), the National Natural Science Foundation of China
   (81704089), the Postdoctoral Science Fund Special Grant of China
   (2017T100603), the Natural Science Foundation of Huan Provence
   (2018JJ3400), and the Changsha City Outstanding Innovation Youth Program
   (kq1707012).
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NR 21
TC 6
Z9 7
U1 1
U2 9
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1065-6995
EI 1095-8355
J9 CELL BIOL INT
JI Cell Biol. Int.
PD JUL
PY 2020
VL 44
IS 7
BP 1514
EP 1522
DI 10.1002/cbin.11347
EA APR 2020
PG 9
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA LX9CD
UT WOS:000523622400001
PM 32196848
DA 2025-01-04
ER

PT J
AU Atanasova, VS
   Cardona, CD
   Hejret, V
   Tiefenbacher, A
   Mair, T
   Tran, L
   Pfneissl, J
   Draganic, K
   Binder, C
   Kabiljo, J
   Clement, J
   Woeran, K
   Neudert, B
   Wohlhaupter, S
   Haase, A
   Domazet, S
   Hengstschläger, M
   Mitterhauser, M
   Müllauer, L
   Tichy, B
   Bergmann, M
   Schweikert, G
   Hartl, M
   Dolznig, H
   Egger, G
AF Atanasova, Velina S.
   Cardona, Crhistian de Jesus
   Hejret, Vaclav
   Tiefenbacher, Andreas
   Mair, Theresia
   Tran, Loan
   Pfneissl, Janette
   Draganic, Kristina
   Binder, Carina
   Kabiljo, Julijan
   Clement, Janik
   Woeran, Katharina
   Neudert, Barbara
   Wohlhaupter, Sabrina
   Haase, Astrid
   Domazet, Sandra
   Hengstschlaeger, Markus
   Mitterhauser, Markus
   Muellauer, Leonhard
   Tichy, Boris
   Bergmann, Michael
   Schweikert, Gabriele
   Hartl, Markus
   Dolznig, Helmut
   Egger, Gerda
TI Mimicking Tumor Cell Heterogeneity of Colorectal Cancer in a
   Patient-derived Organoid-Fibroblast Model
SO CELLULAR AND MOLECULAR GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Cancer; Co-cultures; Colorectal Cancer; Fibroblasts; Organoids
ID GENE-EXPRESSION; STROMAL FIBROBLASTS; HUMAN BREAST; TARGETED THERAPY;
   QUALITY-CONTROL; HUMAN COLON; PROMOTES; CARCINOMA; PROGRESSION; INVASION
AB BACKGROUND & AIMS: Patient-derived organoid cancer models are generated from epithelial tumor cells and reflect tumor characteristics. However, they lack the complexity of the tumor microenvironment, which is a key driver of tumorigenesis and therapy response. Here, we developed a colorectal cancer organoid model that incorporates matched epithelial cells and stromal fibroblasts. METHODS: Primary fibroblasts and tumor cells were isolated from colorectal cancer specimens. Fibroblasts were character-ized for their proteome, secretome, and gene expression sig-natures. Fibroblast/organoid co-cultures were analyzed by immunohistochemistry and compared with their tissue of origin, as well as on gene expression levels compared with standard organoid models. Bioinformatics deconvolution was used to calculate cellular proportions of cell subsets in orga-noids based on single-cell RNA sequencing data. RESULTS: Normal primary fibroblasts, isolated from tumor adjacent tissue, and cancer associated fibroblasts retained their molecular characteristics in vitro, including higher motility of cancer associated compared with normal fibroblasts. Impor-tantly, both cancer-associated fibroblasts and normal fibro-blasts supported cancer cell proliferation in 3D co-cultures, without the addition of classical niche factors. Organoids grown together with fibroblasts displayed a larger cellular heteroge-neity of tumor cells compared with mono-cultures and closely resembled the in vivo tumor morphology. Additionally, we observed a mutual crosstalk between tumor cells and fibro-blasts in the co-cultures. This was manifested by considerably deregulated pathways such as cell-cell communication and extracellular matrix remodeling in the organoids. Thrombospondin-1 was identified as a critical factor for fibro-blast invasiveness. CONCLUSION: We developed a physiological tumor/stroma model, which will be vital as a personalized tumor model to study disease mechanisms and therapy response in colorectal cancer. (Cell Mol Gastroenterol Hepatol 2023;15:1391-1419; https://doi.org/10.1016/j.jcmgh.2023.02.014)
C1 [Mitterhauser, Markus; Bergmann, Michael; Egger, Gerda] Ludwig Boltzmann Inst Appl Diagnost, Vienna, Austria.
   [Cardona, Crhistian de Jesus] Eberhard Karls Univ Tubingen, Fac Math & Nat Sci, Tubingen, Germany.
   [Hejret, Vaclav; Tichy, Boris] Masaryk Univ, CEITEC Cent European Inst Technol, Brno, Czech Republic.
   [Muellauer, Leonhard; Egger, Gerda] Med Univ Vienna, Dept Pathol, Vienna, Austria.
   [Bergmann, Michael] Med Univ Vienna, Clin Gen Surg, Vienna, Austria.
   [Dolznig, Helmut] Med Univ Vienna, Inst Med Genet, Vienna, Austria.
   [Bergmann, Michael; Egger, Gerda] Med Univ Vienna, Comprehens Canc Ctr, Vienna, Austria.
   [Schweikert, Gabriele] Max Planck Inst Intelligent Syst, Tubingen, Germany.
   [Schweikert, Gabriele] Univ Dundee, Sch Life Sci, Div Computat Biol, Dundee, Scotland.
   [Hartl, Markus] Univ Vienna, Dept Biochem & Cell Biol, Vienna BioCtr VBC, Max Perutz Labs, Vienna, Austria.
   [Hartl, Markus] Univ Vienna, Mass Spectrometry Facil, Max Perutz Labs, Vienna BioCtr, Vienna, Austria.
C3 Eberhard Karls University of Tubingen; Masaryk University Brno; Medical
   University of Vienna; Medical University of Vienna; Medical University
   of Vienna; Medical University of Vienna; Max Planck Society; University
   of Dundee; Medical University of Vienna; University of Vienna; Vienna
   Biocenter (VBC); Max F. Perutz Laboratories (MFPL); Medical University
   of Vienna; University of Vienna; Vienna Biocenter (VBC); Max F. Perutz
   Laboratories (MFPL)
RP Egger, G (corresponding author), Med Univ Vienna, Dept Pathol, Waehringer Guertel 18-20, A-1090 Vienna, Austria.; Dolznig, H (corresponding author), Med Univ Vienna, Inst Med Genet, Waehringer Str 10, A-1090 Vienna, Austria.
EM helmut.dolznig@meduniwien.ac.at; gerda.egger@meduniwien.ac.at
RI Müllauer, Leonhard/GSN-9884-2022; Bergmann, Michael/GZK-7700-2022;
   Egger, Gerda/B-7177-2013; Tichy, Boris/GQZ-2278-2022; Tiefenbacher,
   Andreas/KIK-4990-2024; Hartl, Markus/F-2866-2010
OI Tiefenbacher, Andreas/0000-0001-7410-6164; Kabiljo,
   Julijan/0000-0002-6778-6648; Egger, Gerda/0000-0003-2489-155X; Hartl,
   Markus/0000-0002-4970-7336; Draganic, Kristina/0000-0002-3351-242X
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NR 119
TC 17
Z9 17
U1 9
U2 46
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.
PY 2023
VL 15
IS 6
BP 1391
EP 1419
DI 10.1016/j.jcmgh.2023.02.014
EA APR 2023
PG 29
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA M5LA4
UT WOS:001030618700001
PM 36868311
OA Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Leers, MPG
AF Leers, Math P. G.
TI Circulating tumor DNA and their added value in molecular oncology
SO CLINICAL CHEMISTRY AND LABORATORY MEDICINE
LA English
DT Review
DE cell-free DNA; circulating tumor DNA; liquid biopsy; somatic mutations;
   tumor heterogeneity
ID CELL-FREE DNA; ACQUIRED-RESISTANCE; CANCER-PATIENTS; LUNG-CANCER;
   COLORECTAL-CANCER; EGFR BLOCKADE; BLOOD-PLASMA; MUTATIONS; EVOLUTION;
   THERAPY
AB New methods for molecular diagnosis are now available in oncology thanks to the discovery of circulating tumor DNA molecules in the plasma of cancer patients. By utilizing blood samples, rather than traditional tissue sampling, clinical practice is on the verge of new discoveries from the analysis of cell-free DNA (cfDNA). The method, known as a "liquid biopsy", consists of analyzing therapeutic targets and drug-resistant conferring gene mutations in circulating tumor cells (CTC) and cell-free circulating tumor DNA (ctDNA). These are subsequently released from primary tumors and metastatic deposits into the peripheral blood. The advantages of the method can be observed in the diagnosis, but also in the choice of treatment for solid tumors (e.g. non-small cell lung carcinomas [NSCLC]). In order to interpret the results, an understanding of the biological characteristics of circulating tumor DNA is required. Currently there is no consensus as to how a liquid biopsy should be conducted. In this review, we will assess the pros of ctDNA as analytes in peripheral blood samples and its impact on clinical applications in solid tumors and hematological malignancies. We will also address practical issues facing clinical implementation, such as pre-analytical factors. Moreover, we will emphasize the open questions that remain when considering the current state of personalized medicine and targeted therapy.
C1 [Leers, Math P. G.] Zuyderland Med Ctr Sittard Geleen, Dept Clin Chem & Hematol, Dr H Van der Hoffpl 1,POB 5500, NL-6130 MB Sittard, Netherlands.
RP Leers, MPG (corresponding author), Zuyderland Med Ctr Sittard Geleen, Dept Clin Chem & Hematol, Dr H Van der Hoffpl 1,POB 5500, NL-6130 MB Sittard, Netherlands.
EM mat.leers@zuyderland.nl
RI Leers, Mathie/AFV-8239-2022
OI Leers, Mathie/0000-0001-5186-5600
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NR 78
TC 10
Z9 10
U1 0
U2 20
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1434-6621
EI 1437-4331
J9 CLIN CHEM LAB MED
JI Clin. Chem. Lab. Med.
PD FEB
PY 2020
VL 58
IS 2
BP 152
EP 161
DI 10.1515/cclm-2019-0436
PG 10
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA JZ3QV
UT WOS:000505017300011
PM 31490771
OA Bronze
DA 2025-01-04
ER

PT J
AU Xing, HT
   Wang, PY
   Liu, SJ
   Jing, SY
   Lin, JX
   Yang, JP
   Zhu, YY
   Yu, M
AF Xing, Haotian
   Wang, Pinying
   Liu, Shuangjie
   Jing, Siyang
   Lin, Jiaxing
   Yang, Jieping
   Zhu, Yuyan
   Yu, Meng
TI A global integrated analysis of UNC5C down-regulation in cancers:
   insights from mechanism and combined treatment strategy
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE UNC5C; Tumor suppressor gene; Pan-cancer analysis; TCGA; Multi-omics;
   Epigenetic regulation
AB As the transmembrane receptor of Netrin-1, the tumor suppressor gene Unc-5 Netrin Receptor C (UNC5C) can trigger apoptosis. Although its tumor suppressor effects have been demonstrated in solid tumors such as colon cancer, there is still a lack of systematic research on its expression regulation mechanism. To address this need, we analyzed datasets from The Cancer Genome Atlas (TCGA) database, including multi-omics data for 32 types of cancers and 10,967 cases. Analysis of these data revealed a trend of significantly decreased UNC5C expression in 16 types of solid tumors. Additionally, low UNC5C expression is related to poor prognosis of five types of tumors and restoring the expression of UNC5C can effectively inhibit the proliferation potential of renal cancer cells. Promoter DNA methylation, chromatin remodeling-mediated epigenetic regulation, transcriptional inhibition, RNA-binding protein and miRNA-mediated post-transcriptional inhibition, genetic changes caused by deep deletion and truncated mutations, and ubiquitinating enzyme-mediated protein degradation can synergistically cause the down-regulation of UNC5C expression in solid tumors. This study is the first to analyze the comprehensive molecular mechanism of down-regulation of the tumor suppressor gene UNC5C from multiple dimensions using pan-cancer data. Our results suggest that analyses of gene expression regulation relying on computational biological methods may help guide the targeted therapy of tumor suppressor gene reactivation.
C1 [Xing, Haotian; Liu, Shuangjie; Lin, Jiaxing; Yang, Jieping; Zhu, Yuyan] China Med Univ, Hosp 1, Dept Urol, Shenyang 110001, Liaoning, Peoples R China.
   [Wang, Pinying] China Med Univ, Hosp 1, Dept Pain Med, Shenyang 110001, Liaoning, Peoples R China.
   [Jing, Siyang; Yu, Meng] China Med Univ, Dept Lab Anim Sci, 77 Puhe Rd, Shenyang 110122, Liaoning, Peoples R China.
   [Jing, Siyang; Yu, Meng] China Med Univ, Key Lab Transgenet Anim Res, 77 Puhe Rd, Shenyang 110122, Liaoning, Peoples R China.
C3 China Medical University; China Medical University; China Medical
   University; China Medical University
RP Zhu, YY (corresponding author), China Med Univ, Hosp 1, Dept Urol, Shenyang 110001, Liaoning, Peoples R China.; Yu, M (corresponding author), China Med Univ, Dept Lab Anim Sci, 77 Puhe Rd, Shenyang 110122, Liaoning, Peoples R China.
EM yyzhu@cmu.edu.cn; yumeng@cmu.cn
RI Liu, Shuangjie/HMP-1023-2023; Lin, Jiaxing/Q-3555-2018; Zhu,
   Yuyan/ABE-4176-2021
OI Zhu, Yuyan/0000-0003-0479-3151
FU National Natural Science Foundation of China [81672523, 81472404,
   81472403, 81272834, 31000572]; 2018 Support Plan for innovative talents
   in Colleges and Universities of Liaoning Province (China); 2018 "million
   talents Project" Project of Liaoning Province (China); 2019 Key Research
   and Development Projects of Shenyang (China)
FX This work was supported in part by the National Natural Science
   Foundation of China (grants 81672523, 81472404, 81472403, 81272834, and
   31000572), the 2018 Support Plan for innovative talents in Colleges and
   Universities of Liaoning Province (China), the 2018 "million talents
   Project" funded Project of Liaoning Province (China), and the 2019 Key
   Research and Development Projects of Shenyang (China).
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NR 42
TC 8
Z9 9
U1 1
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 JUN
PY 2021
VL 138
AR 111355
DI 10.1016/j.biopha.2021.111355
EA MAR 2021
PG 9
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA RO9WS
UT WOS:000641389900005
PM 33706130
OA gold
DA 2025-01-04
ER

PT J
AU Villalba, M
   Evans, SR
   Vidal-Vanaclocha, F
   Calvo, A
AF Villalba, Maria
   Evans, Stephanie R.
   Vidal-Vanaclocha, Fernando
   Calvo, Alfonso
TI Role of TGF-β in metastatic colon cancer: it is finally time for
   targeted therapy
SO CELL AND TISSUE RESEARCH
LA English
DT Review
DE Colon cancer; Metastasis; TGF-beta; Cancer stem cells; Epithelial to
   mesenchymal transition
ID LIVER METASTASIS; COLORECTAL-CANCER; TUMOR SUPPRESSION; I-RECEPTOR;
   GROWTH; INHIBITOR; SMAD4; MAMMARY; PATHWAY; MICE
AB Colorectal cancer (CRC) is one of the most frequent tumor types in Western countries. Approximately 20% of patients show metastasis at the time of diagnosis, with the liver being one of the most affected organs. Transforming growth factor-beta (TGF-beta) plays a regulatory role not only in the physiology of the normal colon but also in the development of CRC and its metastatic process. In this review, we analyze the molecular mechanisms leading to TGF-beta dysregulation in tumor and stroma cells and the modification of the microenvironment that fosters CRC metastasis. Recent genomic studies have identified a CRC subtype with a mesenchymal and aggressive phenotype having TGF-beta as a hub gene of this signature. Consistent with these findings, the inhibition of TGF-beta signaling has been shown to impair experimental CRC metastasis to the liver. Based on these and other results conducted in various tumor types, the pharmaceutical industry has developed a variety of strategies to target TGF-beta. We provide up-to-date information of these therapies, which are currently in preclinical or clinical trials.
C1 [Villalba, Maria; Evans, Stephanie R.; Calvo, Alfonso] Univ Navarra, CIBERONC, IDISNA, Navarra 31008, Spain.
   [Villalba, Maria; Evans, Stephanie R.; Calvo, Alfonso] Univ Navarra, Program Solid Tumors & Biomarkers, Ctr Appl Med Res CIMA, Navarra 31008, Spain.
   [Villalba, Maria; Calvo, Alfonso] Univ Navarra, Dept Histol & Pathol, Sch Med, Navarra 31008, Spain.
   [Vidal-Vanaclocha, Fernando] Catholic Univ, IVP, Valencia Sch Med & Odontol, Valencia, Spain.
   [Calvo, Alfonso] Ctr Appl Med Res CIMA, Program Solid Tumors & Biomarkers, Lab 2 03, Calle Pio 12 55, Pamplona 31008, Spain.
C3 CIBER - Centro de Investigacion Biomedica en Red; CIBERONC; University
   of Navarra; University of Navarra; University of Navarra; Universidad
   Catolica de Valencia San Vicente Martir; University of Navarra
RP Calvo, A (corresponding author), Univ Navarra, CIBERONC, IDISNA, Navarra 31008, Spain.; Calvo, A (corresponding author), Univ Navarra, Program Solid Tumors & Biomarkers, Ctr Appl Med Res CIMA, Navarra 31008, Spain.; Calvo, A (corresponding author), Univ Navarra, Dept Histol & Pathol, Sch Med, Navarra 31008, Spain.; Calvo, A (corresponding author), Ctr Appl Med Res CIMA, Program Solid Tumors & Biomarkers, Lab 2 03, Calle Pio 12 55, Pamplona 31008, Spain.
EM acalvo@unav.es
RI Villalba, María/AAG-4022-2021; Calvo, Alfonso/V-7945-2017
OI Villalba Esparza, Maria/0000-0002-9183-0610; Calvo,
   Alfonso/0000-0003-4074-4242
FU CIBERONC; FEDER; RTICC [RD12/0036/0040]; FIS [PI13/00093, PI16/01352];
   MINECO [BIO2013-50458-EXP]; AECC Scientific Foundation [GCB14-2170]; FPU
   [FPU-14/03247]
FX This work was supported by CIBERONC (co-funded with FEDER), RTICC
   (RD12/0036/0040), FIS (PI13/00093 and PI16/01352), MINECO
   (BIO2013-50458-EXP) and the AECC Scientific Foundation (GCB14-2170, to
   A.C.). Maria Villalba was supported by a FPU fellowship (FPU-14/03247).
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NR 72
TC 84
Z9 91
U1 0
U2 23
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0302-766X
EI 1432-0878
J9 CELL TISSUE RES
JI Cell Tissue Res.
PD OCT
PY 2017
VL 370
IS 1
BP 29
EP 39
DI 10.1007/s00441-017-2633-9
PG 11
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA FH9CE
UT WOS:000411503400003
PM 28560691
DA 2025-01-04
ER

PT J
AU Chen, PJ
   Yeh, YS
   Tsai, HL
   Huang, CW
   Yang, SF
   Wang, JY
AF Chen, Po-Jung
   Yeh, Yung-Sung
   Tsai, Hsiang-Lin
   Huang, Ching-Wen
   Yang, Sheau-Fang
   Wang, Jaw-Yuan
TI Deficient mismatch repair and <i>BRAF-V600E</i>-mutated metastatic
   colorectal cancer responds to nivolumab therapy after progression under
   bevacizumab plus FOLFIRI
SO JOURNAL OF CANCER RESEARCH AND THERAPEUTICS
LA English
DT Article
DE BRAF-V600E mutation; deficient mismatch repair (dMMR); metastatic
   colorectal cancer; nivolumab
ID OPEN-LABEL; SUBGROUP ANALYSES; SURVIVAL
AB Nivolumab, a PD-1 immune checkpoint inhibitor, has been demonstrated to be clinically effective in patients with deficient mismatch repair (dMMR) and BRAF-V600E-mutated metastatic colorectal cancer (mCRC). We present the case of an 81-year-old Taiwanese woman with mCRC who responded favorably to nivolumab for 20 months after the failure of bevacizumab plus FOLFIRI (5-fluorouracil, folinic acid, and irinotecan) treatment. The woman visited our institute and received a diagnosis of ascending colon cancer in December 2019. She underwent right hemicolectomy; the pathologic stage was T3N1bM0, stage IIIb. After 7 months, multiple liver metastases had developed and bevacizumab plus FOLFIRI were administered. However, the disease progressed even after targeted therapy plus chemotherapy. Since February 2021, she has received 3 mg/kg nivolumab biweekly and the best objective response has been found to be partial response as per the response evaluation criteria in solid tumors criteria. No severe adverse events have occurred. The patient has received 33 cycles of nivolumab over 20 months without exhibiting eventual tumor progression. Nivolumab could be considered for dMMR and BRAF-V600E-mutated mCRC that has progressed despite treatment with bevacizumab plus FOLFIRI.
C1 [Chen, Po-Jung; Tsai, Hsiang-Lin; Huang, Ching-Wen; Wang, Jaw-Yuan] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Colorectal Surg, Kaohsiung, Taiwan.
   [Chen, Po-Jung; Wang, Jaw-Yuan] Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, Kaohsiung, Taiwan.
   [Yeh, Yung-Sung] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Div Trauma & Surg Crit Care, Dept Surg, Kaohsiung, Taiwan.
   [Yeh, Yung-Sung] Kaohsiung Med Univ, Coll Med, Fac Postbaccalaureate Med, Dept Emergency Med, Kaohsiung, Taiwan.
   [Yeh, Yung-Sung] Taipei Med Univ, Grad Inst Injury Prevent & Control, Coll Publ Hlth, Taipei, Taiwan.
   [Tsai, Hsiang-Lin; Huang, Ching-Wen; Wang, Jaw-Yuan] Kaohsiung Med Univ, Coll Med, Fac Med, Dept Surg, Kaohsiung, Taiwan.
   [Yang, Sheau-Fang] Kaohsiung Med Univ, Dept Pathol, Kaohsiung Med Univ Hosp, Kaohsiung, Taiwan.
   [Yang, Sheau-Fang] Kaohsiung Med Univ, Coll Med, Fac Med, Dept Pathol, Kaohsiung, Taiwan.
   [Wang, Jaw-Yuan] Kaohsiung Med Univ, Grad Inst Med, Coll Med, Kaohsiung, Taiwan.
   [Wang, Jaw-Yuan] Kaohsiung Med Univ, Ctr Canc Res, Kaohsiung, Taiwan.
   [Wang, Jaw-Yuan] Pingtung Hosp, Minist Hlth & Welf, Pingtung, Taiwan.
RP Wang, JY (corresponding author), 100 Tzyou 1st Rd, Kaohsiung 80708, Taiwan.
EM cy614112@ms14.hinet.net
FU Ministry of Science and Technology [MOST 109-2314-B-037-046-MY3, MOST
   111-2314-B-037-070-MY3, MOST 111-2314-B-037-049]; Ministry of Health and
   Welfare [12D1-IVMOHW02]; health and welfare surcharge of on tobacco
   products; Kaohsiung Medical University Hospital [KMUH111-1R31,
   KMUH111-1R32, KMUH111-1M28, KMUH111-1M29, KMUH111-1M31]; Kaohsiung
   Medical University Research Center Grant [KMU-TC112A04]; Grant of Taiwan
   Precision Medicine Initiative; Taiwan Biobank, Academia Sinica, Taiwan,
   R.O.C.
FX This work was supported by grants through funding from the Ministry of
   Science and Technology (MOST 109-2314-B-037-046-MY3, MOST
   111-2314-B-037-070-MY3, MOST 111-2314-B-037-049) and the Ministry of
   Health and Welfare (12D1-IVMOHW02) and funded by the health and welfare
   surcharge of on tobacco products, and the Kaohsiung Medical University
   Hospital (KMUH111-1R31, KMUH111-1R32, KMUH111-1M28, KMUH111-1M29,
   KMUH111-1M31) and Kaohsiung Medical University Research Center Grant
   (KMU-TC112A04). In addition, this study was supported by the Grant of
   Taiwan Precision Medicine Initiative and Taiwan Biobank, Academia
   Sinica, Taiwan, R.O.C.
CR Caputo F, 2019, INT J MOL SCI, V20, DOI 10.3390/ijms20215369
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NR 12
TC 0
Z9 0
U1 0
U2 0
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, Maharashtra, INDIA
SN 0973-1482
EI 1998-4138
J9 J CANCER RES THER
JI J. Canc. Res. Ther.
PD OCT-DEC
PY 2024
VL 20
IS 6
BP 1878
EP 1881
DI 10.4103/jcrt.jcrt_2164_22
PG 4
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA Q0K0P
UT WOS:001381671900040
DA 2025-01-04
ER

PT J
AU Maus, MKH
   Hanna, DL
   Stephens, CL
   Astrow, SH
   Yang, D
   Grimminger, PP
   Loupakis, F
   Hsiang, JH
   Zeger, G
   Wakatsuki, T
   Barzi, A
   Lenz, HJ
AF Maus, M. K. H.
   Hanna, D. L.
   Stephens, C. L.
   Astrow, S. H.
   Yang, D.
   Grimminger, P. P.
   Loupakis, F.
   Hsiang, J. H.
   Zeger, G.
   Wakatsuki, T.
   Barzi, A.
   Lenz, H-J
TI Distinct gene expression profiles of proximal and distal colorectal
   cancer: implications for cytotoxic and targeted therapy
SO PHARMACOGENOMICS JOURNAL
LA English
DT Article
ID THYMIDYLATE SYNTHASE EXPRESSION; SIDED COLON-CANCER; ISLAND METHYLATOR
   PHENOTYPE; K-RAS MUTATIONS; PHASE-III TRIAL; MICROSATELLITE-INSTABILITY;
   1ST-LINE TREATMENT; BRAF MUTATION; DIHYDROPYRIMIDINE DEHYDROGENASE;
   ADJUVANT CHEMOTHERAPY
AB Colorectal cancer (CRC) is a heterogeneous disease with genetic profiles and clinical outcomes dependent on the anatomic location of the primary tumor. How location has an impact on the molecular makeup of a tumor and how prognostic and predictive biomarkers differ between proximal versus distal colon cancers is not well established. We investigated the associations between tumor location, KRAS and BRAF mutation status, and the messenger RNA (mRNA) expression of proteins involved in major signaling pathways, including tumor growth (epidermal growth factor receptor (EGFR)), angiogenesis (vascular endothelial growth factor receptor 2 (VEGFR2)), DNA repair (excision repair cross complement group 1 (ERCC1)) and fluoropyrimidine metabolism (thymidylate synthase (TS)). Formalin-fixed paraffin-embedded tumor specimens from 431 advanced CRC patients were analyzed. The presence of seven different KRAS base substitutions and the BRAF V600E mutation was determined. ERCC1, TS, EGFR and VEGFR2 mRNA expression levels were detected by reverse transcriptase-PCR. BRAF mutations were significantly more common in the proximal colon (P < 0.001), whereas KRAS mutations occurred at similar frequencies throughout the colorectum. Rectal cancers had significantly higher ERCC1 and VEGFR2 mRNA levels compared with distal and proximal colon tumors (P = 0.001), and increased TS levels compared with distal colon cancers (P = 0.02). Mutant KRAS status was associated with lower ERCC1, TS, EGFR and VEGFR2 gene expression in multivariate analysis. In a subgroup analysis, this association remained significant for all genes in the proximal colon and for VEGFR2 expression in rectal cancers. The mRNA expression patterns of predictive and prognostic biomarkers, as well as associations with KRAS and BRAF mutation status depend on primary tumor location. Prospective studies are warranted to confirm these findings and determine the underlying mechanisms.
C1 [Maus, M. K. H.; Grimminger, P. P.] Univ Cologne, Dept Gen Visceral & Tumor Surg, D-50931 Cologne, Germany.
   [Maus, M. K. H.; Stephens, C. L.; Astrow, S. H.; Hsiang, J. H.; Zeger, G.] Response Genet Inc, Los Angeles, CA USA.
   [Hanna, D. L.; Yang, D.; Loupakis, F.; Wakatsuki, T.; Barzi, A.; Lenz, H-J] Univ So Calif, Norris Comprehens Canc Ctr, Div Med Oncol, Los Angeles, CA 90033 USA.
   [Loupakis, F.] Univ Pisana, Inst Toscano, Azienda Osped, Oncol Med, Tumori, Italy.
   [Zeger, G.] Univ So Calif, Keck Sch Med, Dept Pathol, Los Angeles, CA 90033 USA.
C3 University of Cologne; University of Southern California; University of
   Pisa; Azienda Ospedaliero Universitaria Pisana; University of Southern
   California
RP Lenz, HJ (corresponding author), Univ So Calif, Norris Comprehens Canc Ctr, Div Med Oncol, 1441 Eastlake Ave,Suite 3456, Los Angeles, CA 90033 USA.
EM lenz@med.usc.edu
RI Yang, Dongyun/M-2579-2019; Grimminger, Peter/AFM-2285-2022; Loupakis,
   Fotios/I-7243-2012
OI Loupakis, Fotios/0000-0001-9651-0395; Grimminger,
   Peter/0000-0002-1859-9213; Yang, Dongyun/0000-0003-0736-4977
FU Dhont Foundation [P30CA014089-27S1]; Wunderglo Foundation
FX This study was funded by P30CA014089-27S1 and supported by the Dhont
   Foundation, Wunderglo Foundation.
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NR 76
TC 36
Z9 37
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1470-269X
EI 1473-1150
J9 PHARMACOGENOMICS J
JI Pharmacogenomics J.
PD AUG
PY 2015
VL 15
IS 4
BP 354
EP 362
DI 10.1038/tpj.2014.73
PG 9
WC Genetics & Heredity; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity; Pharmacology & Pharmacy
GA CN5CY
UT WOS:000358448500010
PM 25532759
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Fleitas-Kanonnikoff, T
   Martinez-Ciarpaglini, C
   Ayala, J
   Gauna, C
   Denis, R
   Yoffe, I
   Sforza, S
   Martínez, MT
   Pomata, A
   Ibarrola-Villava, M
   Arevshatyan, S
   Burriel, V
   Boscá, D
   Pastor, O
   Ferrer-Martinez, A
   Carrasco, F
   Mongort, C
   Navarro, S
   Ribas, G
   Cervantes, A
AF Fleitas-Kanonnikoff, Tania
   Martinez-Ciarpaglini, Carolina
   Ayala, Josefina
   Gauna, Cinthia
   Denis, Rita
   Yoffe, Ita
   Sforza, Silvia
   Teresa Martinez, Maria
   Pomata, Alicia
   Ibarrola-Villava, Maider
   Arevshatyan, Sipan
   Burriel, Veronica
   Bosca, Diego
   Pastor, Oscar
   Ferrer-Martinez, Ana
   Carrasco, Francisca
   Mongort, Cristina
   Navarro, Samuel
   Ribas, Gloria
   Cervantes, Andres
TI Molecular profile in Paraguayan colorectal cancer patients, towards to a
   precision medicine strategy
SO CANCER MEDICINE
LA English
DT Article
DE colorectal cancer; microsatellite instability; mutational profile;
   Oncocarta; precision medicine
ID SOMATIC ONCOGENIC MUTATIONS; FOLFIRI PLUS BEVACIZUMAB; MICROSATELLITE
   INSTABILITY; 1ST-LINE TREATMENT; TARGETED THERAPY; BRAF MUTATION;
   OPEN-LABEL; PHASE-III; SOLID TUMORS; SURVIVAL
AB Somatic mutation analysis and evaluation of microsatellite instability (MSI) have become mandatory for selecting personalized therapy strategies for advanced colorectal cancer and are not available as routine methods in Paraguay. The aims of this study were to analyze the molecular profile as well as the microsatellite status in a series of advanced colorectal patients from two public hospitals from Paraguay, to introduce these methodologies in the routine practice to guide the therapeutic decisions. Thirty-six patients diagnosed with advanced colorectal cancer from two referent public hospitals from Paraguay were recruited from May 2017 to February 2018. Sequenom Mass spectrometry, Oncocarta Panel V.1 was applied to analyze the mutational profile from formalin-fixed paraffin-embedded samples. The microsatellite status was tested by immunohistochemistry (IHC). The mean age of the patients was 52 years with a range from 20 to 74 years. Eighty-three percent of the patients included in the study have advanced-stage tumors at the moment of the diagnosis. Sixteen patients (44.4%) were wild-type for all the oncogene regions analyzed with the Oncocarta panel. Thirty-two hot-spot pathogenic variants on seven oncogenes, among 20 patients (55.6%), were identified, including KRAS, NRAS, BRAF, PI3KCA, FGFR, epidermal growth factor receptor, and PDGFRA. Moreover, 14 (38.8%) of these patients presented pathogenic variants in KRAS/NRAS or BRAF genes that have implications in the clinical practice decisions. Five patients (14%) presented MSI. The IHC study for microsatellite status and the molecular profile analysis through Sequenom mass spectrometry are feasible and useful methods, due to identify those patient candidates for targeted therapies and for the budgetary calculations of the National Health Plans.
C1 [Fleitas-Kanonnikoff, Tania; Ibarrola-Villava, Maider; Ferrer-Martinez, Ana; Carrasco, Francisca; Ribas, Gloria; Cervantes, Andres] Univ Valencia, Biomed Res Inst INCLIVA, CIBERONC, Dept Med Oncol, Ave Blasco Ibanez 17, Valencia 46010, Spain.
   [Martinez-Ciarpaglini, Carolina; Mongort, Cristina; Navarro, Samuel] Univ Valencia, Biomed Res Inst INCLIVA, CIBERONC, Dept Pathol, Valencia, Spain.
   [Ayala, Josefina; Gauna, Cinthia; Sforza, Silvia] Inst Nacl Canc INCAN, Dept Med Oncol, Capiata, Paraguay.
   [Denis, Rita; Yoffe, Ita] Univ Nacl Asuncion, Dept Med Oncol, Hosp Clin, San Lorenzo, Paraguay.
   [Teresa Martinez, Maria] Labs Curie SA, Asuncion, Paraguay.
   [Pomata, Alicia] Inst Nacl Canc INCAN, Dept Pathol, Capiata, Paraguay.
   [Arevshatyan, Sipan; Burriel, Veronica; Pastor, Oscar] Univ Politecn Valencia, Gembiosoft, Valencia, Spain.
   [Bosca, Diego] Veratech, Valencia, Spain.
C3 University of Valencia; CIBER - Centro de Investigacion Biomedica en
   Red; CIBERONC; University of Valencia; CIBER - Centro de Investigacion
   Biomedica en Red; CIBERONC; Universidad Nacional de Asuncion;
   Universitat Politecnica de Valencia
RP Ribas, G; Cervantes, A (corresponding author), Univ Valencia, Biomed Res Inst INCLIVA, CIBERONC, Dept Med Oncol, Ave Blasco Ibanez 17, Valencia 46010, Spain.
EM gribas@incliva.es; andres.cervantes@uv.es
RI PASTOR, OSCAR/HSD-6372-2023; Navarro, Samuel/AAD-2021-2020;
   Ribas-Despuig, Gloria/M-6190-2017; Pastor Lopez, Oscar/S-4216-2016;
   Cervantes, Andres/J-8713-2013; Ribas, Gloria/K-3379-2013
OI Fleitas-Kanonnikoff, Tania/0000-0002-2789-9082; Pomata,
   Alicia/0000-0001-6085-3783; Pastor Lopez, Oscar/0000-0002-1320-8471;
   Ibarrola-Villava, Maider/0000-0003-0946-8075; Cervantes,
   Andres/0000-0003-3806-3691; Gauna, Cinthia Viviana/0009-0001-5669-8431;
   Mongort, Cristina/0009-0009-7921-7862; Ribas,
   Gloria/0000-0001-6883-4130; ayala leon, silvia
   josefina/0000-0003-4223-8378; Martinez Ciarpaglini,
   Carolina/0000-0002-8797-2114
FU CONACYT Paraguay [PINV-156/2015]; INSTITUTO CARLOS III [17/00026,
   CD15/00153]; FONDOS FEDER
FX CONACYT Paraguay, Grant/Award Number: PINV-156/2015; INSTITUTO CARLOS
   III, Grant/Award Number: 17/00026 and CD15/00153; FONDOS FEDER; Bankia
CR [Anonymous], MOD PATHOL
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NR 43
TC 1
Z9 3
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD JUN
PY 2019
VL 8
IS 6
BP 3120
EP 3130
DI 10.1002/cam4.2191
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IH1YO
UT WOS:000474292100041
PM 31059199
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Froelich, MF
   Petersen, EL
   Heinemann, V
   Nörenberg, D
   Hesse, N
   Gesenhues, AB
   Modest, DP
   Sommer, WH
   Hofmann, FO
   Stintzing, S
   Holch, JW
AF Froelich, Matthias F.
   Petersen, Elina L.
   Heinemann, Volker
   Noerenberg, Dominik
   Hesse, Nina
   Gesenhues, Alena B.
   Modest, Dominik P.
   Sommer, Wieland H.
   Hofmann, Felix O.
   Stintzing, Sebastian
   Holch, Julian W.
TI Impact of Size and Location of Metastases on Early Tumor Shrinkage and
   Depth of Response in Patients With Metastatic Colorectal Cancer:
   Subgroup Findings of the Randomized, Open-Label Phase 3 Trial FIRE-3/AIO
   KRK-0306
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE Bevacizumab; Cetuximab; Surrogate end point; Survival prediction;
   Targeted therapy
ID FOLFIRI PLUS CETUXIMAB; PROGRESSION-FREE SURVIVAL; LIVER METASTASES;
   BEVACIZUMAB; STATISTICS; MUTATIONS; DYNAMICS; THERAPY; PATTERN; TRENDS
AB Early tumor shrinkage (ETS) and depth of response (DpR) were proposed as promising outcome parameters in metastatic colorectal cancer. However, further characterization is necessary toward their implementation in clinical practice. In 395 patients of the FIRE-3 trial, we identified influencing factors on ETS and DpR, namely size and location of metastases. Considering these associations might help increase the predictive accuracy of ETS and DpR.
   Background: The Response Evaluation Criteria in Solid Tumors (RECIST) are used to define degrees of response to chemotherapy. For accelerated response evaluation, early tumor shrinkage (ETS) of >= 20% has been suggested as a predictor for outcome in metastatic colorectal cancer (mCRC). Together with depth of response (DpR), new alternative metrics have been provided, yielding promising outcome parameters. In this analysis, we aimed to further characterize ETS and DpR. Patients and Methods: This analysis was based on FIRE-3, a randomized phase 3 trial comparing first-line FOLFIRI plus either cetuximab or bevacizumab in KRAS exon 2 wild-type mCRC. ETS and DpR were determined on the basis of RECIST 1.1 in a blinded radiologic review. ETS was evaluated as a categorized (>= 20% shrinkage) and continuous parameter. The impact of baseline location and size of metastases on ETS and DpR were evaluated by univariate and multivariate analyses. Results: Of 592 patients, 395 (66.7%) had data available for radiologic review. Median continuous ETS for lung, liver, and suspected lymph node metastases was 20%, 23%, and 30%, respectively. The median DpR was -32%, -44%, and -50%, respectively (all P < .01). In multivariate analysis, lung metastases were significantly associated with inferior DpR (P = .021), whereas hepatic metastases led to higher DpR (P = .024). Large metastases were associated with favorable ETS, whereas small metastases were correlated with higher DpR (P < .001). Conclusion: ETS and DpR depend on the location and size of metastases in mCRC. These associations may establish the basis for further research to optimize the predictive accuracy of both parameters. This may help basing treatment decisions on ETS and DpR. (C) 2020 Elsevier Inc. All rights reserved.
C1 [Froelich, Matthias F.; Petersen, Elina L.; Noerenberg, Dominik; Hesse, Nina; Gesenhues, Alena B.; Sommer, Wieland H.; Hofmann, Felix O.] Ludwig Maximilians Univ Munchen, Dept Radiol, Univ Hosp, Munich, Germany.
   [Petersen, Elina L.] Ludwig Maximilians Univ Munchen, Inst Med Informat Biometry & Epidemiol, Munich, Germany.
   [Heinemann, Volker; Holch, Julian W.] Ludwig Maximilians Univ Munchen, Dept Med 3, Univ Hosp, Munich, Germany.
   [Hofmann, Felix O.] Ludwig Maximilians Univ Munchen, Dept Gen Vasc & Thorac Surg, Univ Hosp, Munich, Germany.
   [Froelich, Matthias F.; Noerenberg, Dominik] Univ Med Ctr Mannheim, Dept Clin Radiol & Nucl Med, Mannheim, Germany.
   [Heinemann, Volker; Holch, Julian W.] Comprehens Canc Ctr Munich, Munich, Germany.
   [Heinemann, Volker; Holch, Julian W.] German Canc Consortium DKTK, Partner Site Munich, Heidelberg, Germany.
   [Heinemann, Volker; Holch, Julian W.] German Canc Res Ctr, Heidelberg, Germany.
   [Modest, Dominik P.; Stintzing, Sebastian] Charite Univ Med Berlin, Dept Med, Div Hematol Oncol & Tumor Immunol CCM, Berlin, Germany.
C3 University of Munich; University of Munich; University of Munich;
   University of Munich; Ruprecht Karls University Heidelberg; 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
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 Froelich, Matthias/AAG-9109-2020; Modest, Dominik Paul/AAW-9756-2021;
   Stintzing, Sebastian/I-4538-2016; Petersen, Elina Larissa/GRY-4362-2022
OI Froelich, Matthias/0000-0001-8501-2147; Stintzing,
   Sebastian/0000-0002-3297-5801; Baumann, Alena/0000-0002-2067-1616;
   Petersen, Elina Larissa/0000-0002-1235-5066
FU Merck KGaA; Pfizer
FX The authors thank all patients and families for their participation in
   the studies, along with medical colleagues and nursing staff at the
   participating FIRE-3 study centers. The FIRE-3 trial was funded by Merck
   KGaA and Pfizer. Merck KGaA and Pfizer reviewed the document before
   submission. The funding sources had no role in the design,
   interpretation, or conduct of the study; the writing of the report; or
   the decision to submit or publish the data.
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NR 36
TC 10
Z9 9
U1 2
U2 4
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 291
EP +
DI 10.1016/j.clcc.2020.06.005
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OW6AP
UT WOS:000592967200027
PM 32917529
DA 2025-01-04
ER

PT J
AU Pothuganti, MK
   Mitra, S
   Iyer, P
   Gowda, N
AF Pothuganti, Manoj Kumar
   Mitra, Sayan
   Iyer, Pravin
   Gowda, Nagaraj
TI Recent Developments, Challenges and Opportunities in Targeting the KRAS
   Pathway
SO LETTERS IN DRUG DESIGN & DISCOVERY
LA English
DT Review
DE KRAS; SOS1; SHP2; KRAS G12C; sotorasib; adagrasib; tri-complex
   inhibitors; resistance; combination therapy
ID CELL LUNG-CANCER; GUANINE-NUCLEOTIDE EXCHANGE; KRYSTAL-1 ACTIVITY;
   ADAGRASIB MRTX849; RATIONAL DESIGN; SOLID TUMORS; RAS; INHIBITION; SHP2;
   ACTIVATION
AB KRAS is a highly mutated gene among cancers, especially in the lung, pancreatic and colorectal cancers (CRC). Despite extensive efforts in the past three decades, KRAS remains undruggable. But lately, inhibitors selectively binding to cysteine mutant at 12(th) position (G12C) are in clinical trials as a single agent and in combination with other drugs. FDA approved LUMAKRAS (Sotorasib, AMG510) for metastatic NSCLC, while Adagrasib (MRTX849) is under clinical trials, and it is showing good safety and efficacy in pancreatic and GI tumors. Both these molecules demonstrated better response in NSCLC but have less efficacy in colorectal and other solid cancers. Among non-G12C KRAS mutant cancers, promising data are emerging from G12D inhibition. This review covers the status of KRAS G12C, non-G12C inhibitors, and discusses different nodal proteins in the RAS signaling pathway, mechanism of resistance in targeted therapy and combination approaches. Ongoing clinical trials with G12C inhibitors have promising results. However, a combination of KRAS inhibition with other inhibitors of signaling components in vertical axis (SHP2, SOS1, MEK, PI3K/AKT and EGFR inhibitors) might be beneficial for durable clinical response. Sotorasib in combination with MEK inhibitor showed promising results in preclinical xenograft and PDx models of KRAS mutated cancers. Although at a preclinical stage, other approaches like Tri complex inhibitor, KRAS (ON) inhibitors, and non-G12C inhibitors are of significant interest in KRAS drug discovery. Multiple targeted approaches are being explored based on tumor specific gene expression profiles considering dynamic nature of KRAS activity and heterogeneity of hard to treat tumors.
C1 [Pothuganti, Manoj Kumar; Mitra, Sayan; Iyer, Pravin; Gowda, Nagaraj] MIDC, Glenmark Res Ctr, Navi Mumbai 421204, Maharashtra, India.
RP Gowda, N (corresponding author), MIDC, Glenmark Res Ctr, Navi Mumbai 421204, Maharashtra, India.
EM Nagaraj.Gowda@Glenmarkpharma.com
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NR 63
TC 0
Z9 0
U1 1
U2 15
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1570-1808
EI 1875-628X
J9 LETT DRUG DES DISCOV
JI Lett. Drug Des. Discov.
PY 2023
VL 20
IS 8
BP 992
EP 1004
DI 10.2174/1570180819666220704104028
PG 13
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA L0SQ1
UT WOS:001020443200002
DA 2025-01-04
ER

PT J
AU Philibert, R
   Dawes, K
   Philibert, W
   Andersen, AM
   Hoffman, EA
AF Philibert, Robert
   Dawes, Kelsey
   Philibert, Willem
   Andersen, Allan M.
   Hoffman, Eric A.
TI Alcohol Use Intensity Decreases in Response to Successful Smoking
   Cessation Therapy
SO GENES
LA English
DT Article
DE smoking; alcohol dependence; DNA methylation; smoking cessation;
   epigenetics
ID COLON-CANCER; CONSUMPTION; DRINKING; RISK
AB Smokers frequently drink heavily. However, the effectiveness of smoking cessation therapy for those with comorbid alcohol abuse is unclear, and the content of smoking cessation programs often does not address comorbid alcohol consumption. In order to achieve a better understanding of the relationship between changes in rate of smoking to the change in intensity of alcohol consumption, and the necessity for alcohol-specific programming for dual users, we quantified cigarette and alcohol consumption in 39 subjects undergoing a 3-month contingency management smoking cessation program using recently developed DNA methylation tools. Intake alcohol consumption, as quantified by the Alcohol T Score (ATS), was highly correlated with cg05575921 smoking intensity (adjusted R-2 = 0.49) with 19 of the 39 subjects having ATS scores indicative of Heavy Alcohol Consumption. After 90 days of smoking cessation therapy, ATS values decreased with the change in ATS score being highly correlated with change in cg05575921 smoking intensity (adjusted R-2 = 0.60), regardless of whether or not the subject managed to completely quit smoking. We conclude that alcohol consumption significantly decreases in response to successful smoking cessation. Further studies to determine whether targeted therapy focused on comorbid alcohol use increases the success of smoking cessation in those with dual use should be explored.
C1 [Philibert, Robert; Dawes, Kelsey; Philibert, Willem; Andersen, Allan M.] Univ Iowa, Dept Psychiat, Iowa City, IA 52242 USA.
   [Philibert, Robert] Behav Diagnost LLC, Coralville, IA 52241 USA.
   [Philibert, Robert; Hoffman, Eric A.] Univ Iowa, Dept Biomed Engn, Iowa City, IA 52242 USA.
   [Hoffman, Eric A.] Univ Iowa, Dept Radiol, Iowa City, IA 52242 USA.
C3 University of Iowa; University of Iowa; University of Iowa
RP Philibert, R (corresponding author), Univ Iowa, Dept Psychiat, Iowa City, IA 52242 USA.; Philibert, R (corresponding author), Behav Diagnost LLC, Coralville, IA 52241 USA.; Philibert, R (corresponding author), Univ Iowa, Dept Biomed Engn, Iowa City, IA 52242 USA.
EM robert-philibert@uiowa.edu; kelsey-dawes@uiowa.edu;
   willem-philibert@uiowa.edu; allan-andersen@uiowa.edu;
   eric-hoffman@uiowa.edu
RI Nybo Andersen, Anne-Marie/E-4993-2013
OI Philibert, Robert/0000-0001-7822-4977; Andersen,
   Allan/0000-0001-7006-7639; Hoffman, Eric/0000-0001-8456-9437; Dawes,
   Kelsey/0000-0003-4112-2760
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NR 28
TC 3
Z9 4
U1 0
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4425
J9 GENES-BASEL
JI Genes
PD JAN
PY 2022
VL 13
IS 1
AR 2
DI 10.3390/genes13010002
PG 8
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA YO3CW
UT WOS:000747822300001
PM 35052343
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yang, P
   Li, B
   Yin, QF
   Wang, YJ
AF Yang, Peng
   Li, Bing
   Yin, Qi-Feng
   Wang, Yu-Juan
TI Carboxymethyl chitosan nanoparticles coupled with CD59-specific ligand
   peptide for targeted delivery of C-phycocyanin to HeLa cells
SO TUMOR BIOLOGY
LA English
DT Article
DE Cancer therapy; drug delivery; C-phycocyanin; carboxymethyl chitosan;
   nanoparticles
ID IN-VITRO; COLON-CANCER; GROWTH; VIVO; MECHANISM; ACID
AB The combination of nanotechnology and medicine will be the next generation of vehicles for targeted drug delivery. Carboxymethyl chitosan loaded with the anticancer drug C-phycocyanin and the CD59-specific ligand peptide for cancer cell targeting were used to create C-phycocyanin/carboxymethyl chitosan-CD59-specific ligand peptide nanoparticles using the ionic-gelation method. Optimal synthesis conditions, selected by response surface methodology, comprised the ratio carboxymethyl chitosan: C-phycocyanin = 3: 1, and carboxymethyl chitosan and CaCl2 concentrations of 2.0 and 1.0 mg/mL, respectively. The resulting nanoparticles were spherical, with diameters of approximately 200 nm; the entrapment efficient was about 65%; and the drug loading was about 20%. The release of C-phycocyanin from C-phycocyanin/carboxymethyl chitosan nanoparticles was pH sensitive and had a sustainable effect in vitro. Guided by the CD59-specific ligand peptide, the nanoparticles efficiently targeted the surface of HeLa cells and had an obvious inhibitory effect on HeLa cell proliferation as determined by methyl thiazolyl tetrazolium assays. The nanoparticles were hemocompatible and induced apoptosis by upregulation of cleaved caspase-3 and cleaved polyADP-ribose polymerase proteins, and downregulation of Bcl-2 proteins. Our study provides a novel approach to the research and development of marine drugs, and support for targeted therapy using anticancer drugs.
C1 [Yang, Peng; Li, Bing; Yin, Qi-Feng; Wang, Yu-Juan] Qingdao Univ, Med Coll, Dept Biol, 38 Dengzhou Rd, Qingdao 266021, Peoples R China.
C3 Qingdao University
RP Li, B (corresponding author), Qingdao Univ, Med Coll, Dept Biol, 38 Dengzhou Rd, Qingdao 266021, Peoples R China.
EM libing_516619@163.com
OI Li, Bing/0000-0002-5545-9674
FU National Natural Science Foundation of China [81471546, 81001346,
   81273206]
FX This work was supported by grants from the National Natural Science
   Foundation of China (81471546, 81001346, and 81273206).
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NR 20
TC 12
Z9 16
U1 2
U2 47
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1010-4283
EI 1423-0380
J9 TUMOR BIOL
JI Tumor Biol.
PD MAR
PY 2017
VL 39
IS 3
AR 692267
DI 10.1177/1010428317692267
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ET4OS
UT WOS:000400263700027
PM 28347253
OA gold
DA 2025-01-04
ER

PT J
AU Krishnan, KA
   Valavi, SG
   Joy, A
AF Krishnan, K. Amrutha
   Valavi, Sudha George
   Joy, Amitha
TI Identification of Novel EGFR Inhibitors for the Targeted Therapy of
   Colorectal Cancer Using Pharmacophore Modelling, Docking, Molecular
   Dynamic Simulation and Biological Activity Prediction
SO ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
LA English
DT Article
DE Computer-aided drug discovery; virtual hits; hit optimization; ADME
   properties; toxicity studies; QSAR analysis
ID PREVIOUSLY TREATED PATIENTS; PHASE-II; DRUG DISCOVERY; OPEN BABEL;
   GEFITINIB; MUTATIONS; OXALIPLATIN; TUMORS; LEUCOVORIN; VALIDATION
AB Background Colorectal cancer (CRC) is considered the second deadliest cancer in the world. One of the reasons for the occurrence of this cancer is the deregulation of the Epidermal Growth Factor Receptor (EGFR), which plays a critical role in regulating cell division, persistence, differentiation, and migration. The overexpression of the EGFR protein leads to its dysregulation and causes CRC.Objectives Hence, this work aims to identify and validate novel EGFR inhibitors for the treatment of colorectal cancer employing various computer aided techniques such as pharmacophore modeling, docking, molecular dynamic simulation and Quantitative Structure-Activity Relationship (QSAR) analysis.Methods In this work, a shared-featured ligand-based pharmacophore model was generated using the known inhibitors of EGFR. The best model was validated and screened against ZincPharmer and Maybridge databases, and 143 hits were obtained. Pharmacokinetic and toxicological properties of these hits were studied, and the acceptable ligands were docked against EGFR. The best five protein-ligand complexes with binding energy less than -5 kcal/mol were selected. The molecular dynamic simulation studies of these complexes were conducted for 100 nanoseconds (ns), and the results were analyzed. The biological activity of this ligand was calculated using QSAR analysis.Results The best complex with Root Mean Square Deviation (RMSD) 3.429 angstrom and Radius of Gyration (RoG) 20.181 angstrom was selected. The Root Mean Square Fluctuations (RMSF) results were also found to be satisfactory. The biological activity of this ligand was found to be 1.38 mu M.Conclusion This work hereby proposes the ligand 2-((1,6-dimethyl-4-oxo-1,4-dihydropyridin-3-yl)oxy)-N-(1H-indol-4-yl)acetamide as a potential EGFR inhibitor for the treatment of colorectal cancer. The wet lab analysis must be conducted, however, to confirm this hypothesis.
C1 [Krishnan, K. Amrutha; Valavi, Sudha George] APJ Abdul Kalam Technol Univ, Sahrdaya Coll Engn & Technol, Dept Appl Sci & Humanities, Trichur, Kerala, India.
   [Joy, Amitha] APJ Abdul Kalam Technol Univ, Sahrdaya Coll Engn & Technol, Dept Biotechnol, Trichur, Kerala, India.
RP Krishnan, KA (corresponding author), APJ Abdul Kalam Technol Univ, Sahrdaya Coll Engn & Technol, Dept Appl Sci & Humanities, Trichur, Kerala, India.
EM krishnamrutha18@gmail.com
OI joy, amitha/0000-0001-7535-4944; George Valavi,
   Sudha/0009-0008-4472-7937; Krishnan K, Amrutha/0009-0009-6491-3283
FU CERD (Centre for Engineering Research and Development) PhD Research
   Fellowship Programme of the APJ Abdul Kalam Technological University;
   Government of Kerala, India
FX The authors express their genuine gratitude towards Prof. Paola
   Gramatica, Senior Professor of University of Insubria, for the
   permission to use QSARINS software. The authors also extend their
   sincere gratitude to CERD (Centre for Engineering Research and
   Development) PhD Research Fellowship Programme of the APJ Abdul Kalam
   Technological University, established by Government of Kerala, India.
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NR 62
TC 0
Z9 0
U1 2
U2 6
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 2024
VL 24
IS 4
BP 263
EP 279
DI 10.2174/0118715206275566231206094645
PG 17
WC Oncology; Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA ML9U4
UT WOS:001193902400003
PM 38173208
DA 2025-01-04
ER

PT J
AU Liang, YH
   Shi, JB
   He, QS
   Sun, GR
   Gao, L
   Ye, JH
   Tang, XL
   Qu, H
AF Liang, Yahang
   Shi, Jingbo
   He, Qingsi
   Sun, Guorui
   Gao, Lei
   Ye, Jianhong
   Tang, Xiaolong
   Qu, Hui
TI Hsa_circ_0026416 promotes proliferation and migration in colorectal
   cancer via miR-346/NFIB axis
SO CANCER CELL INTERNATIONAL
LA English
DT Article
DE hsa_circ_0026416; miR-346; NFIB; Colorectal cancer; Target therapy;
   Biomarker
ID CIRCULAR RNA; CELL-PROLIFERATION; PROGRESSION; METASTASIS; BIOMARKERS;
   INVASION; GROWTH
AB BackgroundColorectal cancer (CRC) is one of the most common cancers worldwide. Circular RNAs (circRNAs), a novel class of non-coding RNAs, have been confirmed to be key regulators of many diseases. With many scholars devoted to studying the biological function and mechanism of circRNAs, their mysterious veil is gradually being revealed. In our research, we explored a new circRNA, hsa_circ_0026416, which was identified as upregulated in CRC with the largest fold change (logFC=3.70) of the evaluated circRNAs via analysing expression profiling data by high throughput sequencing of members of the GEO dataset (GSE77661) to explore the molecular mechanisms of CRC.MethodsqRT-PCR and western blot analysis were utilized to assess the expression of hsa_circ_0026416, miR-346 and Nuclear Factor I/B (NFIB). CCK-8 and transwell assays were utilized to examine cell proliferation, migration and invasion in vitro, respectively. A luciferase reporter assay was used to verify the combination of hsa_circ_0026416, miR-346 and NFIB. A nude mouse xenograft model was also utilized to determine the role of hsa_circ_0026416 in CRC cell growth in vivo.ResultsHsa_circ_0026416 was markedly upregulated in CRC patient tissues and plasma and was a poor prognosis in CRC patients. In addition, the area under the curve (AUC) of hsa_circ_0026416 (0.767) was greater than the AUC of CEA (0.670), CA19-9 (0.592) and CA72-4 (0.575). Functionally, hsa_circ_0026416 promotes cell proliferation, migration and invasion both in vitro and in vivo. Mechanistically, hsa_circ_0026416 may function as a ceRNA via competitively absorbing miR-346 to upregulate the expression of NFIB.ConclusionsIn summary, our findings demonstrate that hsa_circ_0026416 is an oncogene in CRC. Hsa_circ_0026416 promotes the progression of CRC via the miR-346/NFIB axis and may represent a potential biomarker for diagnosis and therapy in CRC.
C1 [Liang, Yahang; Shi, Jingbo; He, Qingsi; Sun, Guorui; Gao, Lei; Ye, Jianhong; Tang, Xiaolong; Qu, Hui] Shandong Univ, Qilu Hosp, Dept Gen Surg, Cheeloo Coll Med, 107 West Wenhua St, Jinan 250012, Peoples R China.
C3 Shandong University
RP Tang, XL; Qu, H (corresponding author), Shandong Univ, Qilu Hosp, Dept Gen Surg, Cheeloo Coll Med, 107 West Wenhua St, Jinan 250012, Peoples R China.
EM tangxl666@foxmail.com; quhuidoctor@163.com
RI Shi, Jingbo/AAJ-3866-2020; Xiaolong, Tang/HJB-4028-2022; Gao,
   Lei/I-4159-2013; Ye, Jianhong/A-6331-2011
OI Qu, Hui/0000-0003-4809-570X
FU China Postdoctoral Science Foundation [2019M652393]; Science Foundation
   of Qilu Hospital of Shandong University [2017QLQN16]
FX This study was supported by grants from the China Postdoctoral Science
   Foundation [No. 2019M652393] and the Science Foundation of Qilu Hospital
   of Shandong University [No. 2017QLQN16]. The funding body had no role in
   the design of the study and collection, analysis, and interpretation of
   data and in writing of this manuscript.
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NR 43
TC 29
Z9 30
U1 0
U2 5
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1475-2867
J9 CANCER CELL INT
JI Cancer Cell Int.
PD OCT 12
PY 2020
VL 20
IS 1
AR 494
DI 10.1186/s12935-020-01593-1
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OI3AE
UT WOS:000583155000001
PM 33061846
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Rahman, S
   Garrel, S
   Gerber, M
   Maitra, R
   Goel, S
AF Rahman, Shafia
   Garrel, Shimon
   Gerber, Michael
   Maitra, Radhashree
   Goel, Sanjay
TI Therapeutic Targets of KRAS in Colorectal Cancer
SO CANCERS
LA English
DT Review
DE colorectal cancer; KRAS mutation; targeted therapy
ID TYROSINE PHOSPHATASE SHP-2; SIGNAL-REGULATED KINASE; MUTANT KRAS;
   ANTITUMOR-ACTIVITY; TUMOR-GROWTH; G-QUADRUPLEX; RAS; INHIBITOR;
   ACTIVATION; MUTATIONS
AB Simple Summary Colorectal cancer is among the most common cancers in the United States. The advancement in treatment and early diagnosis have enabled a reduction in mortality from the disease among the patients with early and localized disease; however, the survival continues to be dismal in the metastatic colorectal cancers. Understanding the biological and genetic factors is crucial is making the therapeutic strategy and improving survival outcomes. One of such critical steps is the understanding of the mechanism and development of therapeutic targets against metastatic colorectal cancers bearing the KRAS mutation. Patients with metastatic colorectal cancer have a 5-year overall survival of less than 10%. Approximately 45% of patients with metastatic colorectal cancer harbor KRAS mutations. These mutations not only carry a predictive role for the absence of response to anti-EGFR therapy, but also have a negative prognostic impact on the overall survival. There is a growing unmet need for a personalized therapy approach for patients with KRAS-mutant colorectal cancer. In this article, we focus on the therapeutic strategies targeting KRAS- mutant CRC, while reviewing and elaborating on the discovery and physiology of KRAS.
C1 [Rahman, Shafia; Maitra, Radhashree; Goel, Sanjay] Montefiore Med Ctr, Albert Einstein Coll Med, Dept Med Oncol, 1695 Eastchester Rd Bronx, New York, NY 10461 USA.
   [Garrel, Shimon] Lander Coll Men, Dept Biol, 75-31 150th St, New York, NY 11367 USA.
   [Gerber, Michael; Maitra, Radhashree] Yeshiva Univ, Dept Biol, 500 West 185th St, New York, NY 10033 USA.
C3 Montefiore Medical Center; Yeshiva University; Yeshiva University
RP Goel, S (corresponding author), Montefiore Med Ctr, Albert Einstein Coll Med, Dept Med Oncol, 1695 Eastchester Rd Bronx, New York, NY 10461 USA.
EM sgarrel@student.touro.edu
RI Rahman, Shafia/AAS-9418-2021; Garrel, Shimon/JRX-3429-2023
OI Maitra, Radhashree/0000-0002-5365-5890; GOEL,
   SANJAY/0000-0002-2798-7568; Gerber, Michael/0000-0001-9662-4085
FU NIH R 21 [AG058027 02]; Yeshiva University Office of the Provost
   [252869-252929];  [2A4108]
FX This research was funded from NIH R 21 # AG058027 02 (NIA) and the
   start-up fund #2A4108 (received by Sanjay Goel), as well as from an
   Alexander Fund 252869-252929 provided by the Yeshiva University Office
   of the Provost to Radhashree Maitra.
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NR 95
TC 7
Z9 8
U1 2
U2 34
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD DEC
PY 2021
VL 13
IS 24
AR 6233
DI 10.3390/cancers13246233
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA XX3AQ
UT WOS:000736173500001
PM 34944853
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Maurya, NS
   Mani, A
AF Maurya, Neha Shree
   Mani, Ashutosh
TI Navigating Molecular Pathways: An Update on Drugs in Colorectal Cancer
   Treatment
SO CURRENT TOPICS IN MEDICINAL CHEMISTRY
LA English
DT Review
DE Colorectal cancer; Signaling pathways; Mutation; Drug targets; Drug
   repurposing; Neoplasm; Predominantly
ID NOTCH SIGNALING PATHWAY; CELL-CYCLE ARREST; GROWTH-FACTOR BETA-1;
   COLON-CANCER; TGF-BETA; MESENCHYMAL TRANSITION; WNT/BETA-CATENIN;
   STEM-CELLS; COMBINATION CHEMOTHERAPY; PROGENITOR CELLS
AB Colorectal cancer (CRC) is a multifaceted and heterogeneous ailment that affects the colon or rectum of the digestive system. It is the second most commonly occurring form of cancer and ranks third in terms of mortality rate. The progression of CRC does not occur due to a single mutational event; rather, it is the result of the sequential and cumulative accumulation of mutations in key driver genes of signaling pathways. The most significant signaling pathways, which have oncogenic potential due to their deregulation, include Wnt/beta-catenin, Notch, TGF-beta, EGFR/MAPK, and PI3K/AKT pathways. Numerous drug target therapies have been developed to treat CRC using small molecule inhibitors, antibodies, or peptides. Although drug-targeted therapy is effective in most cases, the development of resistance mechanisms in CRC has raised questions about their efficacy. To overcome this issue, a novel approach to drug repurposing has come to light, which utilizes already FDA-approved drugs to treat CRC. This approach has shown some promising experimental results, making it a crucial avenue of research in the treatment of CRC.
C1 [Maurya, Neha Shree; Mani, Ashutosh] Motilal Nehru Natl Inst Technol Allahabad, Dept Biotechnol, Prayagraj 211004, India.
C3 National Institute of Technology (NIT System); Motilal Nehru National
   Institute of Technology
RP Mani, A (corresponding author), Motilal Nehru Natl Inst Technol Allahabad, Dept Biotechnol, Prayagraj 211004, India.
EM amani@mnnit.ac.in
OI Maurya, Neha/0000-0001-5275-2288
FU The authors acknowledge the Department of Biotechnology, MNNIT,
   Allahabad, for providing the necessary support for conducting the study
   smoothly. AM and NM have written the manuscript.; Department of
   Biotechnology, MNNIT
FX The authors acknowledge the Department of Biotechnology, MNNIT,
   Allahabad, for providing the necessary support for conducting the study
   smoothly. AM and NM have written the manuscript.
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NR 192
TC 2
Z9 2
U1 1
U2 4
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1568-0266
EI 1873-4294
J9 CURR TOP MED CHEM
JI Curr. Top. Med. Chem.
PY 2023
VL 23
IS 30
BP 2821
EP 2843
DI 10.2174/1568026623666230614165548
EA JUL 2023
PG 23
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DT6K2
UT WOS:001096426700001
PM 37317918
DA 2025-01-04
ER

PT J
AU Bao, XX
   Li, W
   Jia, RX
   Meng, DD
   Zhang, HR
   Xia, L
AF Bao, Xingxun
   Li, Wei
   Jia, Ruixue
   Meng, Dandan
   Zhang, Hairong
   Xia, Lei
TI Molecular mechanism of ferulic acid and its derivatives in tumor
   progression
SO PHARMACOLOGICAL REPORTS
LA English
DT Review
DE Ferulic acid; Tumor; Derivative; Nanoliposome; Mechanism of action
ID COLORECTAL-CANCER CELLS; ANTITUMOR-ACTIVITY; PROLIFERATION; COMBINATION;
   RESISTANCE; INHIBITION; MIGRATION; APOPTOSIS; MELANOMA; PATHWAY
AB Cancer is a significant disease that poses a major threat to human health. The main therapeutic methods for cancer include traditional surgery, radiotherapy, chemotherapy, and new therapeutic methods such as targeted therapy and immunotherapy, which have been developed rapidly in recent years. Recently, the tumor antitumor effects of the active ingredients of natural plants have attracted extensive attention. Ferulic acid (FA), (3-methoxy-4-hydroxyl cinnamic), with the molecular formula is C10H10O4, is a phenolic organic compound found in ferulic, angelica, jujube kernel, and other Chinese medicinal plants but is also, abundant in rice bran, wheat bran, and other food raw materials. FA has anti-inflammatory, analgesic, anti-radiation, and immune-enhancing effects and also shows anticancer activity, as it can inhibit the occurrence and development of various malignant tumors, such as liver cancer, lung cancer, colon cancer, and breast cancer. FA can cause mitochondrial apoptosis by inducing the generation of intracellular reactive oxygen species (ROS). FA can also interfere with the cell cycle of cancer cells, arrest most cancer cells in G(0)/G(1) phase, and exert an antitumor effect by inducing autophagy; inhibiting cell migration, invasion, and angiogenesis; and synergistically improving the efficacy of chemotherapy drugs and reducing adverse reactions. FA acts on a series of intracellular and extracellular targets and is involved in the regulation of tumor cell signaling pathways, including the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT), B-cell lymphoma-2 (Bcl-2), and tumor protein 53 (P53) pathways and other signaling pathways. In addition, FA derivatives and nanoliposomes, as platforms for drug delivery, have an important regulatory effect on tumor resistance. This paper reviews the effects and mechanisms of antitumor therapies to provide new theoretical support and insight for clinical antitumor therapy.
C1 [Bao, Xingxun; Jia, Ruixue; Meng, Dandan] Shandong Univ Tradit Chinese Med, Sch Chinese Med, Jinan 250355, Peoples R China.
   [Li, Wei] Linyi Third Peoples Hosp, Dept Obstet & Gynecol, Linyi, Peoples R China.
   [Zhang, Hairong] Shandong Prov Third Hosp, Dept Obstet & Gynecol, Jinan 250031, Peoples R China.
   [Xia, Lei] Shandong Univ Tradit Chinese Med, Dept Pathol, Jinan 250355, Peoples R China.
C3 Shandong University of Traditional Chinese Medicine; Shandong University
   of Traditional Chinese Medicine
RP Zhang, HR (corresponding author), Shandong Prov Third Hosp, Dept Obstet & Gynecol, Jinan 250031, Peoples R China.; Xia, L (corresponding author), Shandong Univ Tradit Chinese Med, Dept Pathol, Jinan 250355, Peoples R China.
EM bxx0722@163.com; jiangyongjun721203@163.com; sdzhhr7211@163.com;
   pathology001@sina.com
RI Xia, Lei/GYD-8772-2022; Zhang, Hairong/LDF-6073-2024
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NR 118
TC 23
Z9 23
U1 5
U2 39
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1734-1140
EI 2299-5684
J9 PHARMACOL REP
JI Pharmacol. Rep.
PD AUG
PY 2023
VL 75
IS 4
BP 891
EP 906
DI 10.1007/s43440-023-00494-0
EA MAY 2023
PG 16
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA M9PH9
UT WOS:000990451900001
PM 37202657
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Takada, R
   Fujiwara, M
   Maki, M
   Takahashi, Y
   Tamura, K
AF Takada, Ryo
   Fujiwara, Miki
   Maki, Masatoshi
   Takahashi, Yoko
   Tamura, Koji
TI Risk factors for thromboembolism during first-line treatment of patients
   with unresectable advanced or recurrent colorectal cancer: a
   retrospective short study
SO JOURNAL OF PHARMACEUTICAL HEALTH CARE AND SCIENCES
LA English
DT Article
DE Colorectal cancer; Epidermal growth factor receptor inhibitors;
   Thromboembolism; Vascular endothelial growth factor inhibitors
ID EPIDERMAL-GROWTH-FACTOR; VENOUS THROMBOEMBOLISM; JAPANESE-SOCIETY;
   RECEPTOR; ANGIOGENESIS; MECHANISMS; THERAPY; CELLS; VEGF; PROTEIN
AB BackgroundWhile cancer is a risk factor for developing thromboembolism, so is the use of molecularly targeted therapies. This study aimed to determine whether thromboembolism incidence differed between vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFR) inhibitor use in patients with unresectable advanced or recurrent colorectal cancer, and to compare the risk of thromboembolism caused by cancer and the use of molecular targeted therapy drugs.Main bodyWe retrospectively evaluated patients with unresectable advanced or recurrent colorectal cancer who were treated with a cytotoxic anticancer drug and a VEGF or EGFR inhibitor combination between April 2016 and October 2021. Patients were compared in terms of the regimen administered, thromboembolism occurrence during the first-line treatment period, patient background, and clinical laboratory values. Of the 179 included patients, 12 of 134 (8.9%) in the VEGF-inhibitor group and 8 of 45 (17.8%) in the EGFR-inhibitor group developed thromboembolism, with no significant difference between the groups (P = 0.11). There was no significant difference in time to thromboembolism between patients in the VEGF- inhibitor group and patients in the EGFR-inhibitor group (P = 0.206). The cutoff value determined by a receiver operating characteristic analysis for the occurrence of thromboembolism was one point. Multivariate analysis using the occurrence of thromboembolism as the response variable identified at least one risk factor for thromboembolism (odds ratio = 4.17, P = 0.006, 95% confidence interval = 1.51-11.50). Molecular targeted therapies were not identified as a risk factor.ConclusionsAlthough the small sample size, there was no difference in the incidence of thromboembolism between the two molecular-targeted therapies in first-line treatment of patients with unresectable advanced or recurrent colorectal cancer. Our results suggest that risk factors for thromboembolism may be more strongly influenced by cancer itself than by the use of molecularly targeted therapies.
C1 [Takada, Ryo; Fujiwara, Miki; Maki, Masatoshi; Takahashi, Yoko; Tamura, Koji] Natl Hosp Org Fukuyama Med Ctr, Dept Hosp Pharm, 4-14-17 Okinogami Cho, Fukuyama, Hiroshima 7208520, Japan.
RP Takada, R (corresponding author), Natl Hosp Org Fukuyama Med Ctr, Dept Hosp Pharm, 4-14-17 Okinogami Cho, Fukuyama, Hiroshima 7208520, Japan.
EM takada.ryo.nw@mail.hosp.go.jp
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NR 19
TC 0
Z9 0
U1 1
U2 1
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2055-0294
J9 J PHARM HEALTH CARE
JI J. PHARM. HEALTH CARE SCI.
PD JUL 3
PY 2023
VL 9
IS 1
AR 22
DI 10.1186/s40780-023-00291-0
PG 7
WC Pharmacology & Pharmacy
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA K8HZ2
UT WOS:001018806200001
PM 37394446
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Rütter, M
   Milosevic, N
   Ventura, Y
   Feinshtein, V
   David, A
AF Rutter, Marie
   Milosevic, Nenad
   Ventura, Yvonne
   Feinshtein, Valeria
   David, Ayelet
TI E-selectin-targeted polymer-doxorubicin conjugate induces regression of
   established colorectal liver metastases and improves mice survival
SO NANO TODAY
LA English
DT Article
DE Biomedical polymers; Colorectal cancer; E-selectin; Metastasis;
   Nanomedicines; Polymer-drug conjugate; Targeted therapy
ID CANCER; INHIBITION; ADHESION; CELLS
AB Liver metastases arising from colorectal cancer (CRC) are a major challenge for cancer treatment, as they often emerge as unresectable and resistant to therapy. Novel treatments targeting the specific metastatic tumor microenvironment (TME) may improve the therapeutic outcome. One relevant receptor at the TME in the liver is the endothelial-expressed cell adhesion molecule E-selectin.
   In this study, we showed in a mouse model of aggressive CT26-derived liver metastasis, that the delivery of otherwise non-effective Doxorubicin via an E-selectin-targeted polymer-peptide-drug conjugate reduced tumor burden of liver metastases and significantly prolonged survival, with similar to 50% of mice being tumor-free. In contrast to B16-derived lung metastases, which can successfully be prevented by a "drug-free" E-selectin-blocking copolymer, neither E-selectin-blocking pre-treatment nor the combination with targeted Doxorubicin-delivery proved beneficial against CT26 liver metastasis. In-depth inquiry revealed that E-selectin-blockade by the "drug-free" copolymer reduced E-selectin expression in metastatic livers, but did not prevent CT26 liver colonization, and increased the prevalence of B-cells, possibly indicating an ambiguous role of these cells. However, it did not significantly alter leukocyte migration into the malignant tissue.
   Overall, targeting E-selectin with nanomedicines is a highly efficient strategy to treat established liver metastases, while the benefit of E-selectin blockade by itself may depend on tumor type and TME-specific factors.
C1 [Rutter, Marie; Milosevic, Nenad; Ventura, Yvonne; Feinshtein, Valeria; David, Ayelet] Ben Gurion Univ Negev, Fac Hlth Sci, Dept Clin Biochem & Pharmacol, IL-84105 Beer Sheva, Israel.
C3 Ben Gurion University
RP David, A (corresponding author), Ben Gurion Univ Negev, Fac Hlth Sci, Dept Clin Biochem & Pharmacol, IL-84105 Beer Sheva, Israel.
EM ayeletda@bgu.ac.il
OI David, Ayelet/0000-0002-8929-5700; Ruetter, Marie/0009-0001-5343-7252
FU Israel Science Foundation (ISF) [1115/19]; Minerva Foundation; Vaxil
   Biotherapeutics LTD.
FX This project was supported by funds from Israel Science Foundation (ISF
   grant #1115/19) and Vaxil Biotherapeutics LTD. The authors wish to thank
   the Minerva Foundation for funding M.R. scholarship throughout her PhD
   studies.
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NR 35
TC 0
Z9 0
U1 2
U2 7
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 1748-0132
EI 1878-044X
J9 NANO TODAY
JI Nano Today
PD APR
PY 2024
VL 55
AR 102182
DI 10.1016/j.nantod.2024.102182
EA FEB 2024
PG 11
WC Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials
   Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA LD5H7
UT WOS:001184849800001
DA 2025-01-04
ER

PT J
AU Ye, Y
   Wang, M
   Wang , B
   Li, Y
   Yang, XM
   Chen, ZN
AF Ye, Ying
   Wang, Miao
   Wang, Bin
   Li, Yu
   Yang, Xiang-Min
   Chen, Zhi-Nan
TI CD98, a potential diagnostic cancer-related biomarker, and its
   prognostic impact in colorectal cancer patients
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
LA English
DT Article
DE CD98; cancer-associated biomarker; colorectal cancer; poor prognosis
ID ACID TRANSPORTER 1; TONGUE CANCER; EXPRESSION; ADENOMA; MARKER; TUMORS;
   ASCT2; LAT1; GENE
AB Background: Successive discoveries in recent years suggested CD98 played an extensive and significant role due to its high levels in human diseased or normal tissues. The current study concentrated on exploring CD98 expression in different cancer and its potential application in diverse clinical settings including risk assessment, detection and localization as a cancer-associated biomarker. Methods: We evaluated the protein expression levels of CD98 in 15 TMAs and 100 samples of histologically confirmed CRC tissues and analyzed the relationships between their expression levels, clinicopathological parameters and their prognostic significance. Results: On immunohistochemical analysis of 15 TMAs with 713 samples of carcinoma tissues and 260 samples of normal or cancer adjacent normal tissues, CD98 was expressed in carcinoma with an overall positivity rate of 74%, which was significantly higher than that in adjacent normal or normal tissues (41%, P < 0.0001). In addition, a retrospective study of pathological sections of 100 matched pairs of normal and tumor tissues from patients confirmed diagnoses of CRC demonstrated CD98 expression had clinicopathological significance, and the differential expression in colorectal carcinoma and adjacent normal tissues was also found at the mRNA level (P < 0.001). CD98 expression level significantly correlated with tumor size, clinical stage, tumor grading, T factor, N factor, distant metastasis (all P < 0.05). Univariate analysis confirmed that tumor size, clinical stage, tumor grading, T factor, N factor, distant metastasis and CD98 expression level (all P < 0.05). Cox regression analysis indicated CD98 was an independent prognostic factor for OS (HR= 0.307, 95% CI= 0.168-0.560, P < 0.001) in CRC. Conclusions: CD98 was significantly expressed in various cancers and appears to have prognostic significance, suggesting it a possible cancer-associated biomarker for pathological diagnosis, prognostic evaluation and targeted therapy of a broad range of cancer types. In addition, CD98 expression was positively correlated with poor prognosis and was an independent prognostic factor in colorectal cancer patients. CD98 may be a potential target for improving treatments for CRC.
C1 [Ye, Ying; Wang, Miao; Wang, Bin; Li, Yu; Yang, Xiang-Min; Chen, Zhi-Nan] Fourth Mil Med Univ, Natl Translat Sci Ctr Mol Med, State Key Lab Canc Biol, Dept Cell Biol,Cell Engn Res Ctr, 169 Changle West Rd, Xian 710032, Peoples R China.
C3 Air Force Military Medical University
RP Yang, XM; Chen, ZN (corresponding author), Fourth Mil Med Univ, Natl Translat Sci Ctr Mol Med, State Key Lab Canc Biol, Dept Cell Biol,Cell Engn Res Ctr, 169 Changle West Rd, Xian 710032, Peoples R China.
EM yxiangmind@163.com; zhinanchen@fmmu.edu
RI liu, yuanyuan/IQS-2755-2023; chen, zhihao/GXM-3816-2022
OI Chen, Zhi-Nan/0000-0001-5512-4623
FU National Basic Research Program of China [2015CB553701]; National
   Natural Science Foundation of China [30801058, 31371405]; National High
   Technology Research and Development Program of China [2014AA020506]
FX This study was funded by the National Basic Research Program of China
   (2015CB553701), the National Natural Science Foundation of China
   (30801058, 31371405), and the National High Technology Research and
   Development Program of China (2014AA020506).
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NR 20
TC 10
Z9 11
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 2017
VL 10
IS 5
BP 5418
EP 5429
PG 12
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA EW1UG
UT WOS:000402279600047
DA 2025-01-04
ER

PT J
AU Ruan, YJ
   Lu, GR
   Yu, YJ
   Luo, Y
   Wu, H
   Shen, YT
   Gao, ZJ
   Shen, Y
   Cai, ZZ
   Li, LY
AF Ruan, Yejiao
   Lu, Guangrong
   Yu, Yaojun
   Luo, Yue
   Wu, Hao
   Shen, Yating
   Gao, Zejun
   Shen, Yao
   Cai, Zhenzhai
   Li, Liyi
TI PF-04449913 Inhibits Proliferation and Metastasis of Colorectal Cancer
   Cells by Down-regulating MMP9 Expression through the ERK/p65 Pathway
SO CURRENT MOLECULAR PHARMACOLOGY
LA English
DT Article
DE PF-04449913; Proliferation; Metastasis; Colorectal cancer; MMP9
   expression; ERK/p65 pathway.
ID ACUTE MYELOID-LEUKEMIA; SIGNALING PATHWAYS; TARGETED THERAPY; HEDGEHOG;
   PROGRESSION; MIGRATION; GROWTH
AB Introduction: Colorectal cancer remains a life-threatening malignancy with increasing morbidity and mortality worldwide. Therefore, new and effective anticolorectal cancer therapeutics are urgently needed. Methods: In this study, we have studied the anti-tumor properties and potential mechanisms of PF-04449913. Colorectal cancer cell viability was reduced by PF-04449913 in a dose-dependent manner. The migration and invasion ability of malignant colon cells were attenuated by the drug, as demonstrated by the Transwell test. Moreover, PF-04449913 repressed the phosphorylation levels of ERK and other proteins, and the expression levels of MMP9. The anti- tumor effects of the drug in vivo were demonstrated in BALB/c-nude mice models, and PF-04449913 inhibited the malignant phenotype of colorectal cancer cells, including reduction of tumor size and promotion of apoptosis. At the molecular level, PF-04449913 induced a significant decrease in ERK and p65 protein phosphorylation levels and inhibited MMP9 protein expression. Results: Both in vivo and in vitro results showed PF-04449913 to demonstrate antitumor effects, which have been proposed to be mediated through blockade of the ERK/p65 signaling pathway, and subsequent repression of MMP9 expression. Conclusion: Our study provides a new perspective on the potential clinical application of PF-04449913 in the treatment of colorectal cancer.
C1 [Ruan, Yejiao; Lu, Guangrong; Yu, Yaojun; Luo, Yue; Wu, Hao; Shen, Yating; Gao, Zejun; Shen, Yao; Cai, Zhenzhai; Li, Liyi] Wenzhou Med Univ, Affiliated Hosp 2, 109 Xueyuan West Rd, Wenzhou 325027, Zhejiang, Peoples R China.
   [Ruan, Yejiao; Lu, Guangrong; Yu, Yaojun; Luo, Yue; Wu, Hao; Shen, Yating; Gao, Zejun; Shen, Yao; Cai, Zhenzhai; Li, Liyi] Wenzhou Med Univ, Yuying Childrens Hosp, 109 Xueyuan West Rd, Wenzhou 325027, Zhejiang, Peoples R China.
C3 Wenzhou Medical University; Wenzhou Medical University
RP Cai, ZZ; Li, LY (corresponding author), Wenzhou Med Univ, Affiliated Hosp 2, 109 Xueyuan West Rd, Wenzhou 325027, Zhejiang, Peoples R China.; Cai, ZZ; Li, LY (corresponding author), Wenzhou Med Univ, Yuying Childrens Hosp, 109 Xueyuan West Rd, Wenzhou 325027, Zhejiang, Peoples R China.
EM caizhenzhai@wmu.edu.cn; liliyi@wmu.edu.cn
RI Yang, Xiyu/KBC-4381-2024
FU Natural Science Foundation of Zhejiang Province [LY18H030009,
   LTGD23H160005]; Academician Helin new Medical Research Fund [19331104];
   Scientific research project of Wenzhou Science & Technology Bureau
   [Y20210920]; Major Project of Wenzhou Science & Technology Bureau
   [2018ZY004]; Public Welfare Research Project of Science Technology
   Department of Zhejiang Province [LGF20H160019]
FX This work was supported by the Natural Science Foundation of Zhejiang
   Province (No. LY18H030009 and No. LTGD23H160005), Academician Helin new
   Medical Research Fund (No. 19331104), the Scientific research project of
   Wenzhou Science & Technology Bureau (No. Y20210920), the Major Project
   of Wenzhou Science & Technology Bureau (No. 2018ZY004), and the Public
   Welfare Research Project of Science Technology Department of Zhejiang
   Province (No. LGF20H160019).
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   Yu Y, 2021, FRONT ONCOL, V11, DOI 10.3389/fonc.2021.650360
   Zhang HC, 2023, GENES-BASEL, V14, DOI 10.3390/genes14051024
   Zhang WD, 2014, TOXICOL LETT, V229, P118, DOI 10.1016/j.toxlet.2014.06.004
NR 44
TC 0
Z9 0
U1 2
U2 3
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1874-4672
EI 1874-4702
J9 CURR MOL PHARMACOL
JI Curr. Molec. Pharmacol.
PY 2024
VL 17
DI 10.2174/1874467217666230915125622
PG 13
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA IC3J2
UT WOS:001164081900012
PM 37724680
OA hybrid
DA 2025-01-04
ER

PT J
AU Weng, ML
   Li, T
   Zhao, J
   Guo, MM
   Zhao, WL
   Gu, WC
   Sun, CH
   Yue, Y
   Zhong, ZW
   Nan, K
   Liao, QW
   Sun, ML
   Zhou, D
   Miao, CH
AF Weng, Meilin
   Li, Ting
   Zhao, Jing
   Guo, Miaomiao
   Zhao, Wenling
   Gu, Wenchao
   Sun, Caihong
   Yue, Ying
   Zhong, Ziwen
   Nan, Ke
   Liao, Qingwu
   Sun, Minli
   Zhou, Di
   Miao, Changhong
TI mRNAsi-related metabolic risk score model identifies poor prognosis,
   immunoevasive contexture, and low chemotherapy response in colorectal
   cancer patients through machine learning
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE colorectal cancer; mRNAsi; stemness; risk score model; immunotherapy;
   metabolism; immune evasion; Machine learning
ID COLON-CANCER; CELL INFILTRATION; TARGETED THERAPY; IMMUNE CELLS; R
   PACKAGE; EXPRESSION; MICROENVIRONMENT; HETEROGENEITY; RESISTANCE;
   STEMNESS
AB Colorectal cancer (CRC) is one of the most fatal cancers of the digestive system. Although cancer stem cells and metabolic reprogramming have an important effect on tumor progression and drug resistance, their combined effect on CRC prognosis remains unclear. Therefore, we generated a 21-gene mRNA stemness index-related metabolic risk score model, which was examined in The Cancer Genome Atlas and Gene Expression Omnibus databases (1323 patients) and validated using the Zhongshan Hospital cohort (200 patients). The high-risk group showed more immune infiltrations; higher levels of immunosuppressive checkpoints, such as CD274, tumor mutation burden, and resistance to chemotherapeutics; potentially better response to immune therapy; worse prognosis; and advanced stage of tumor node metastasis than the low-risk group. The combination of risk score and clinical characteristics was effective in predicting overall survival. Zhongshan cohort validated that high-risk score group correlated with malignant progression, worse prognosis, inferior adjuvant chemotherapy responsiveness of CRC, and shaped an immunoevasive contexture. This tool may provide a more accurate risk stratification in CRC and screening of patients with CRC responsive to immunotherapy.
C1 [Weng, Meilin; Li, Ting; Guo, Miaomiao; Zhao, Wenling; Sun, Caihong; Yue, Ying; Zhong, Ziwen; Nan, Ke; Liao, Qingwu; Sun, Minli; Zhou, Di; Miao, Changhong] Fudan Univ, Zhongshan Hosp, Dept Anesthesiol, Shanghai, Peoples R China.
   [Weng, Meilin; Li, Ting; Guo, Miaomiao; Zhao, Wenling; Sun, Caihong; Yue, Ying; Zhong, Ziwen; Nan, Ke; Liao, Qingwu; Sun, Minli; Zhou, Di; Miao, Changhong] Fudan Univ, Zhongshan Hosp, Shanghai Key Lab Perioperat Stress & Protect, Shanghai, Peoples R China.
   [Zhao, Jing] Fudan Univ, Obstet & Gynecol Hosp, Dept Pathol, Shanghai, Peoples R China.
   [Gu, Wenchao] Univ Tsukuba, Dept Diagnost & Intervent Radiol, Tsukuba, Ibaraki, Japan.
   [Gu, Wenchao] Gunma Univ, Grad Sch Med, Dept Diagnost Radiol & Nucl Med, Maebashi, Japan.
C3 Fudan University; Fudan University; Fudan University; University of
   Tsukuba; Gunma University
RP Sun, ML; Zhou, D; Miao, CH (corresponding author), Fudan Univ, Zhongshan Hosp, Dept Anesthesiol, Shanghai, Peoples R China.; Sun, ML; Zhou, D; Miao, CH (corresponding author), Fudan Univ, Zhongshan Hosp, Shanghai Key Lab Perioperat Stress & Protect, Shanghai, Peoples R China.
EM sunminli@sina.com; judy612542@163.com; 15111230032@fudan.edu.cn
RI Yue, Ying/ABY-8206-2022
OI Li, Ting/0009-0009-2967-3237
FU National Natural Science Foundation of China; Shanghai Pujiang Talent
   Plan; Clinical Research Plan of SHDC; National Key Research and
   Development Program of China;  [82002538];  [82072213];  [2020PJD013]; 
   [SHDC2020CR1005A];  [2020YFC2008400]
FX Funding Our study was supported by the National Natural Science
   Foundation of China (No.82002538, 82072213); Shanghai Pujiang Talent
   Plan (No. 2020PJD013); Clinical Research Plan of SHDC (No.
   SHDC2020CR1005A); and National Key Research and Development Program of
   China (No. 2020YFC2008400).
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NR 62
TC 5
Z9 6
U1 0
U2 15
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 AUG 23
PY 2022
VL 13
AR 950782
DI 10.3389/fimmu.2022.950782
PG 19
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 4H9PT
UT WOS:000850210300001
PM 36081499
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Lou, EM
   Xiu, J
   Baca, Y
   Nelson, AC
   Weinberg, BA
   Beg, MS
   Salem, ME
   Lenz, HJ
   Philip, P
   El-Deiry, WS
   Korn, WM
AF Lou, Emil
   Xiu, Joanne
   Baca, Yasmine
   Nelson, Andrew C.
   Weinberg, Benjamin A.
   Beg, Muhammad Shaalan
   Salem, Mohamed E.
   Lenz, Heinz-Josef
   Philip, Philip
   El-Deiry, Wafik S.
   Korn, W. Michael
TI Expression of Immuno-Oncologic Biomarkers Is Enriched in Colorectal
   Cancers and Other Solid Tumors Harboring the A59T Variant of <i>KRAS</i>
SO CELLS
LA English
DT Article
DE colon cancer; colorectal cancer; molecular oncology; oncogene; KRAS;
   A59T; immuno-oncology; predictive biomarkers
ID RAS MUTATIONS; ASSOCIATION; IRINOTECAN; CETUXIMAB; BURDEN; PD-L1
AB The molecular heterogeneity of KRAS is well established, with a pool of variants comprising >75% of all known mutations; this pool includes mutations in classic codons 12, 13, and 61, as well as 146 and 117. In addition, there are rare variants that are more frequently encountered clinically due to the advances in next-generation sequencing and more widespread implementation of All-RAS sequencing over the past five years. We have previously identified a missense variant of KRAS, A59T, in a patient with CRC that was associated with a response to an epidermal growth factor inhibitor when added to chemotherapy, supporting the hypothesis that distinct biochemical impacts of different KRAS mutations may produce varied responses to targeted therapy. In this study, we explored a large genomic database comprising 17,909 cases of CRC to determine the prevalence of the A59T mutation and characterized the concurrent genomic alterations associated with this variant in more detail, particularly in relation to the expanding set of potential predictive immuno-oncologic biomarkers. We identified 14 cases of A59 mutations in this dataset (0.08% prevalence). We evaluated the prevalence of high tumor mutation burden (TMB), positive PD-L1 expression, and microsatellite instability-high/mismatch repair-deficiency (MSI-H/dMMR) using both next generation sequencing (NGS) and immunohistochemistry (IHC). The genomic features of pertinent signaling pathways were also described, including RAS pathway, chromatin remodeling, DDR, hedgehog signaling, PI3K, receptor tyrosine kinases, signal transduction, TGF-beta, TP53, and WNT. We uncovered a high level of association of predictive markers of responsiveness to checkpoint inhibition and potentially other forms of immunotherapy, with nearly half of all cases harboring microsatellite instability as assessed using NGS. A59T was also detected in 11 additional cancer types, most prominently in cases of gynecologic or other gastrointestinal sites of origin. This study provides supportive evidence that A59T, and possibly other similarly rare KRAS variants, co-occur with predictive biomarkers of response to immunotherapy.
C1 [Lou, Emil] Univ Minnesota, Dept Med, Div Hematol Oncol & Transplantat, Minneapolis, MN 55455 USA.
   [Xiu, Joanne; Baca, Yasmine; Korn, W. Michael] Caris Life Sci, Phoenix, AZ 85040 USA.
   [Nelson, Andrew C.] Univ Minnesota, Lab Med & Pathol, Minneapolis, MN 55455 USA.
   [Weinberg, Benjamin A.] Lombardi Comprehens Canc Ctr, Ruesch Ctr Cure Gastrointestinal Canc, Washington, DC 20007 USA.
   [Beg, Muhammad Shaalan] Univ Texas Southwestern Med Ctr Dallas, Simmons Comprehens Canc Ctr, Dallas, TX 75390 USA.
   [Salem, Mohamed E.] Levine Canc Inst, Dept Med Oncol, Charlotte, NC 28204 USA.
   [Lenz, Heinz-Josef] Univ Southern Calif, Norris Comprehens Canc Ctr, Med, Los Angeles, CA 90033 USA.
   [Philip, Philip] Wayne State Univ, Sch Med, Dept Oncol, Detroit, MI 48202 USA.
   [El-Deiry, Wafik S.] Brown Univ, Lifespan Canc Inst, Dept Pathol & Lab Med, Div Hematol Oncol,Warren Alpert Med Sch, Providence, RI 02903 USA.
C3 University of Minnesota System; University of Minnesota Twin Cities;
   University of Minnesota System; University of Minnesota Twin Cities;
   University of Texas System; University of Texas Southwestern Medical
   Center Dallas; University of Southern California; Wayne State
   University; Brown University; Lifespan Health Rhode Island
RP Lou, EM (corresponding author), Univ Minnesota, Dept Med, Div Hematol Oncol & Transplantat, Minneapolis, MN 55455 USA.
EM emil-lou@umn.edu; jxiu@carisls.com; ybaca@carisls.com; nels2055@umn.edu;
   Benjamin.A.Weinberg@gunet.georgetown.edu;
   muhammad.beg@utsouthwestern.edu; Mohamed.Salem@atriumhealth.org;
   lenz@med.usc.edu; philipp@karmanos.org; wafik_el-deiry@brown.edu;
   wmkorn@carisls.com
OI Nelson, Andrew/0000-0002-4741-0010; Lou, Emil/0000-0002-1607-1386; Baca,
   Yasmine/0000-0003-2130-0611
FU American Association for Cancer Research; Minnesota Ovarian Cancer
   Alliance; Celgene; Novocure; Intima Biosciences; NCI
FX E. Lou reports research grants from the American Association for Cancer
   Research (2019 AACR-Novocure Tumor-Treating Fields Research Grant) and
   the Minnesota Ovarian Cancer Alliance (2019-20; 2021-22); honorarium and
   travel expenses for a research talk at GlaxoSmithKline (2016); honoraria
   and travel expenses for lab-based research talks and equipment for
   laboratory-based research from Novocure (2018-21); consultant, Nomocan
   Pharmaceuticals (unpaid); scientific advisory board member, Minnetronix,
   LLC (2018-present; unpaid); consultant and speaker honorarium, Boston
   Scientific US (2019); institutional principal investigator for clinical
   trials sponsored by Celgene, Novocure, Intima Biosciences, and the NCI;
   and University of Minnesota membership in the Caris Life Sciences
   Precision Oncology Alliance (unpaid).
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NR 37
TC 5
Z9 5
U1 0
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD JUN
PY 2021
VL 10
IS 6
AR 1275
DI 10.3390/cells10061275
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA SZ7FJ
UT WOS:000666726000001
PM 34063999
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Liu, RT
   Wang, GR
   Liu, C
   Qiu, J
   Yan, LK
   Li, XJ
   Wang, XQ
AF Liu, Rui-Ting
   Wang, Guo-Rong
   Liu, Chang
   Qiu, Jian
   Yan, Li-Kun
   Li, Xiao-Jun
   Wang, Xiao-Qiang
TI RNAi-mediated downregulation of DNA binding protein A inhibits
   tumorigenesis in colorectal cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
LA English
DT Article
DE DNA binding protein A; lentivirus-mediated shRNA; colorectal cancer;
   proliferation; apoptosis
ID PROGRAMMED CELL-DEATH; COLD-SHOCK DOMAIN; HEPATOCELLULAR-CARCINOMA;
   PREDICTIVE BIOMARKERS; TARGETED THERAPY; UP-REGULATION; APOPTOSIS; DBPA;
   EXPRESSION; PROLIFERATION
AB DNA binding protein A (dbpA) belongs to the Y-box binding protein family and has been reported to play an important role in carcinogenesis. Our previous study demonstrated that the knockdown of dbpA in gastric cancer cells inhibited cell proliferation by modulating the cell cycle. However, the role of dbpA in human colorectal cancer (CRC) remains unclear. In this study, immunohistochemical (IHC) staining and clinicopathological parameter analysis were employed to detect dbpA expression in 44 paired CRC samples and 7 CRC cell lines. Lentivirus-mediated short hairpin RNA (shRNA) was used to silence dbpA, and the effects of dbpA knockdown on cell proliferation were determined by MTT assay, colony formation assay and flow cytometry. Furthermore, a xenograft model was established to observe tumor growth in vivo. Functional analysis indicated that dbpA was overexpressed in the CRC tissues and cell lines, and a high dbpA expression was associated with the depth of invasion (p<0.001), the degree of differentiation (p<0.001), lymphatic metastasis (p<0.001) and vessel invasion (p<0.001). The suppression of dbpA expression resulted in decreased cell proliferation in vitro and tumor growth in vivo, and it induced cell cycle arrest and promoted the apoptosis of the CRC cells. As a whole, our findings illustrate the crucial role of dbpA in colorectal tumorigenesis. Thus, dbpA may be used as a novel and potent therapeutic target in CRC.
C1 [Liu, Rui-Ting; Liu, Chang] Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Hepatobiliary Surg, Coll Med, 277 West Yanta Rd, Xian 710061, Shaanxi, Peoples R China.
   [Liu, Rui-Ting; Wang, Guo-Rong; Qiu, Jian; Yan, Li-Kun; Li, Xiao-Jun; Wang, Xiao-Qiang] Xi An Jiao Tong Univ, Affiliated Hosp 3, Dept Gen Surg, Coll Med, Xian 710068, Shaanxi, Peoples R China.
C3 Xi'an Jiaotong University; Xi'an Jiaotong University
RP Liu, C (corresponding author), Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Hepatobiliary Surg, Coll Med, 277 West Yanta Rd, Xian 710061, Shaanxi, Peoples R China.
EM eyrechang@126.com
RI liu, chang/HCI-5413-2022
OI Liu, Ruiting/0000-0002-2423-2338
FU National Natural Science Foundation of China [81172363/H1617]; Natural
   Science Foundation of Shaanxi Province [2014JM4089]
FX The present study was funded by grants from the National Natural Science
   Foundation of China (no. 81172363/H1617) and the Natural Science
   Foundation of Shaanxi Province (2014JM4089).
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NR 31
TC 5
Z9 5
U1 0
U2 8
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 2016
VL 38
IS 3
BP 703
EP 712
DI 10.3892/ijmm.2016.2662
PG 10
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA DU8EA
UT WOS:000382444900003
PM 27430286
OA Green Published, hybrid, Green Submitted
DA 2025-01-04
ER

PT J
AU Papierska, K
   Judasz, E
   Toninska, W
   Kubicki, M
   Krajka-Kuzniak, V
AF Papierska, Katarzyna
   Judasz, Eliza
   Toninska, Wiktoria
   Kubicki, Maciej
   Krajka-Kuzniak, Violetta
TI Modulatory Effects of Chalcone Thio-Derivatives on NF-κB and STAT3
   Signaling Pathways in Hepatocellular Carcinoma Cells: A Study on
   Selected Active Compounds
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE anakoinosis; apoptosis; p53; TNF-alpha; STAT3; NF-kappa B; thio-chalcone
   derivatives; hepatocellular carcinoma cells
ID INFLAMMATION; APOPTOSIS; FIBROSIS; ENZYMES
AB Our previous studies demonstrated the modulatory effects of new synthetic thio-chalcone derivatives in dishes on the Nrf2, NF-kappa B, and STAT3 signaling pathways in colon cancer cells. This study aimed to evaluate the effect of four selected active chalcone thio-derivatives on the NF-kappa B and STAT3 signaling pathways involved in inflammatory processes and cell proliferation in human liver cancer cells. Cell survival was assessed for cancer (HepG2) and normal (THLE-2) cell lines. Activation of NF-kappa B and STAT3 signaling pathways and the expression of proteins controlled by these pathways were estimated by Western blot, and qRT-PCR assessed the expression of NF-kappa B and STAT3 target genes. We also evaluated the impact on the selected kinases responsible for the phosphorylation of the studied transcription factors by MagneticBead-Based Multiplex Immunoassay. Among the thio-derivatives tested, especially derivatives 1 and 5, there was an impact on cell viability, cell cycle, apoptosis, and activation of NF-kappa B and STAT3 pathways in hepatocellular carcinoma (HCC), which confirms the possibilities of using them in combinatorial molecular targeted therapy of HCC. The tested synthetic thio-chalcones exhibit anticancer activity by initiating proapoptotic processes in HCC while showing low toxicity to non-cancerous cells. These findings confirm the possibility of using chalcone thio-derivatives in molecularly targeted combination therapy for HCC.
C1 [Papierska, Katarzyna; Judasz, Eliza; Toninska, Wiktoria; Krajka-Kuzniak, Violetta] Poznan Univ Med Sci, Dept Pharmaceut Biochem, Rokietnicka 3, PL-60806 Poznan, Poland.
   [Kubicki, Maciej] Adam Mickiewicz Univ, Fac Chem, Uniwersytetu Poznanskiego 8, PL-61712 Poznan, Poland.
C3 Poznan University of Medical Sciences; Adam Mickiewicz University
RP Papierska, K (corresponding author), Poznan Univ Med Sci, Dept Pharmaceut Biochem, Rokietnicka 3, PL-60806 Poznan, Poland.
EM kpapierska@ump.edu.pl; judasz.eliza@gmail.com;
   wiktoria.toninska99@gmail.com; maciej.kubicki@amu.edu.pl;
   vkrajka@ump.edu.pl
FU National Science Centre, Poland;  [2021/05/X/NZ3/01519]
FX This research was funded by grant number 2021/05/X/NZ3/01519 from the
   National Science Centre, Poland.
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NR 41
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 OCT
PY 2024
VL 25
IS 19
AR 10739
DI 10.3390/ijms251910739
PG 20
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA I7Z1M
UT WOS:001332392100001
PM 39409068
OA gold
DA 2025-01-04
ER

PT J
AU Liu, B
   Ding, JF
   Luo, J
   Lu, L
   Yang, F
   Tan, XD
AF Liu, Bei
   Ding, Jin-feng
   Luo, Jian
   Lu, Li
   Yang, Fen
   Tan, Xiao-dong
TI Seven protective miRNA signatures for prognosis of cervical cancer
SO ONCOTARGET
LA English
DT Article
DE cervical cancer; survival analysis; Cox's model; GO enrichment; pathway
   analysis
ID TUMOR-GROWTH; COLON-CANCER; PROLIFERATION; INFORMATION; MIR-142-3P;
   EXPRESSION; BIOMARKER; SURVIVAL; INVASION; MIR-150
AB Cervical cancer is the second cause of cancer death in females in their 20s and 30s, but there were limited studies about its prognosis. This study aims to identify miRNA related to prognosis and study their functions. TCGA data of patients with cervical cancer were used to build univariate Cox's model with single clinical parameter or miRNA expression level. Multivariate Cox's model was built using both clinical information and miRNA expression levels. At last, STRING was used to enrich gene ontology or pathway for validated targets of significant miRNAs, and visualize the interactions among them. Using univariate Cox's model with clinical parameters, we found that two clinical parameters, tobacco use and clinical stage, and seven miRNAs were highly correlated with the survival status. Only using the expression level of miRNA signatures, the model could separate patients into high-risk and low-risk groups successfully. An optimal feature-selected model was proposed based on two clinical parameters and seven miRNAs. Functional analysis of these seven miRNAs showed they were associated to various pathways related to cancer, including MAPK, VEGF and P53 pathways. These results helped the research of identifying targets for targeted therapy which could potentially allow tailoring of treatment for cervical cancer patients.
C1 [Liu, Bei; Tan, Xiao-dong] Wuhan Univ, Sch Publ Hlth, Wuhan 430071, Peoples R China.
   [Ding, Jin-feng] Taizhou Hosp, Dept Anesthesiol, Taizhou 317000, Peoples R China.
   [Luo, Jian] Huazhong Univ Sci & Technol, Tongji Hosp, Dept Geriatr Med, Wuhan 430030, Peoples R China.
   [Lu, Li] Chinese Univ Hong Kong, Sir YK Pao Ctr Canc, Dept Clin Oncol, Canc Epigenet Lab, Hong Kong 999077, Hong Kong, Peoples R China.
   [Lu, Li] Chinese Univ Hong Kong, Li Ka Shing Inst Hlth Sci, Hong Kong 999077, Hong Kong, Peoples R China.
   [Yang, Fen] Hubei Univ Chinese Med, Dept Nursing, Wuhan 430063, Peoples R China.
C3 Wuhan University; Huazhong University of Science & Technology; Chinese
   University of Hong Kong; Chinese University of Hong Kong; Hubei
   University of Chinese Medicine
RP Tan, XD (corresponding author), Wuhan Univ, Sch Publ Hlth, Wuhan 430071, Peoples R China.
EM tanxiaodong_1@163.com
RI Yang, Fen/JKI-6754-2023
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NR 28
TC 22
Z9 22
U1 0
U2 12
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 30
PY 2016
VL 7
IS 35
BP 56690
EP 56698
DI 10.18632/oncotarget.10678
PG 9
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EA8TL
UT WOS:000386911600060
PM 27447860
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Fujita, T
   Chiwaki, F
   Takahashi, RU
   Aoyagi, K
   Yanagihara, K
   Nishimura, T
   Tamaoki, M
   Komatsu, M
   Komatsuzaki, R
   Matsusaki, K
   Ichikawa, H
   Sakamoto, H
   Yamada, Y
   Fukagawa, T
   Katai, H
   Konno, H
   Ochiya, T
   Yoshida, T
   Sasaki, H
AF Fujita, Takeshi
   Chiwaki, Fumiko
   Takahashi, Ryou-u
   Aoyagi, Kazuhiko
   Yanagihara, Kazuyoshi
   Nishimura, Takao
   Tamaoki, Masashi
   Komatsu, Masayuki
   Komatsuzaki, Rie
   Matsusaki, Keisuke
   Ichikawa, Hitoshi
   Sakamoto, Hiromi
   Yamada, Yasuhide
   Fukagawa, Takeo
   Katai, Hitoshi
   Konno, Hiroyuki
   Ochiya, Takahiro
   Yoshida, Teruhiko
   Sasaki, Hiroki
TI Identification and Characterization of CXCR4-Positive Gastric Cancer
   Stem Cells
SO PLOS ONE
LA English
DT Article
ID ACUTE MYELOID-LEUKEMIA; INITIATING CELLS; TGF-BETA; TUMOR HETEROGENEITY;
   SCIRRHOUS CARCINOMA; COLORECTAL-CANCER; METASTASIS; SURVIVAL; STOMACH;
   GROWTH
AB Diffuse-type solid tumors are often composed of a high proportion of rarely proliferating (i.e., dormant) cancer cells, strongly indicating the involvement of cancer stem cells (CSCs) Although diffuse-type gastric cancer (GC) patients have a poor prognosis due to high-frequent development of peritoneal dissemination (PD), it is limited knowledge that the PD-associated CSCs and efficacy of CSC-targeting therapy in diffuse-type GC. In this study, we established highly metastatic GC cell lines by in vivo selection designed for the enrichment of PD-associated GC cells. By microarray analysis, we found C-X-C chemokine receptor type 4 (CXCR4) can be a novel marker for highly metastatic CSCs, since CXCR4-positive cells can grow anchorage-independently, initiate tumors in mice, be resistant to cytotoxic drug, and produce differentiated daughter cells. In clinical samples, these CXCR4-positive cells were found from not only late metastasis stage (accumulated ascites) but also earlier stage (peritoneal washings). Moreover, treatment with transforming growth factor-beta enhanced the anti-cancer effect of docetaxel via induction of cell differentiation/asymmetric cell division of the CXCR4-positive gastric CSCs even in a dormant state. Therefore, differentiation inducers hold promise for obtaining the maximum therapeutic outcome from currently available anti-cancer drugs through re-cycling of CSCs.
C1 [Fujita, Takeshi; Chiwaki, Fumiko; Aoyagi, Kazuhiko; Nishimura, Takao; Tamaoki, Masashi; Komatsu, Masayuki; Komatsuzaki, Rie; Sasaki, Hiroki] Natl Canc Ctr, Dept Translat Oncol, Tokyo, Japan.
   [Takahashi, Ryou-u; Ochiya, Takahiro] Natl Canc Ctr, Div Mol & Cellular Med, Tokyo, Japan.
   [Ichikawa, Hitoshi] Natl Canc Ctr, Dept Clin Genom, Tokyo, Japan.
   [Ichikawa, Hitoshi; Sakamoto, Hiromi; Yoshida, Teruhiko] Natl Canc Ctr, Dept Translat Oncol, Tokyo, Japan.
   [Yamada, Yasuhide] Natl Canc Ctr, Gastrointestinal Med Oncol, Tokyo, Japan.
   [Fukagawa, Takeo; Katai, Hitoshi] Natl Canc Ctr, Gastr Surg Div, Tokyo, Japan.
   [Yanagihara, Kazuyoshi] Natl Canc Ctr, Exploratory Oncol Res & Clin Trial Ctr, Div Translat Res, Chiba, Japan.
   [Matsusaki, Keisuke] Kanamecho Hosp, Tokyo, Japan.
   [Konno, Hiroyuki] Hamamatsu Univ, Sch Med, Dept Surg 2, Shizuoka, Japan.
C3 National Cancer Center - Japan; National Cancer Center - Japan; National
   Cancer Center - Japan; National Cancer Center - Japan; National Cancer
   Center - Japan; National Cancer Center - Japan; National Cancer Center -
   Japan; Hamamatsu University School of Medicine
RP Sasaki, H (corresponding author), Natl Canc Ctr, Dept Translat Oncol, Tokyo, Japan.
EM hksasaki@ncc.go.jp
RI Yamada, Yasuhide/AAH-9124-2020; Ochiya, Takahiro/AAH-7585-2019; Yoshida,
   Teruhiko/JGM-7448-2023
FU National Institute of Biomedical Innovation [ID10-41]; Ministry of
   Health, Labour and Welfare of Japan [H22-007]; National Cancer Center
   Research and Development Fund [25-A-6, 26-A-3]; Foundation for Promotion
   of Cancer Research in Japan; Grants-in-Aid for Scientific Research
   [26870877, 15K14389] Funding Source: KAKEN
FX This work was supported in part by the National Institute of Biomedical
   Innovation (for the Advanced Research for Medical Products Mining
   Programme ID10-41), the Ministry of Health, Labour and Welfare of Japan
   (for the Third Comprehensive 10-Year Strategy for Cancer Control
   H22-007), National Cancer Center Research and Development Fund (25-A-6,
   26-A-3). Drs T Fujita, M Tamaoki and T Nishimura are the recipients of a
   Research Resident Fellowship from the Foundation for Promotion of Cancer
   Research in Japan.
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NR 50
TC 34
Z9 35
U1 0
U2 8
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 JUN 25
PY 2015
VL 10
IS 6
AR e0130808
DI 10.1371/journal.pone.0130808
PG 19
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA CL4OY
UT WOS:000356933800087
PM 26110809
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhang, YW
   Zhang, YJ
   Song, JJ
   Cheng, XF
   Zhou, CL
   Huang, S
   Zhao, WT
   Zong, Z
   Yang, LL
AF Zhang, Yiwei
   Zhang, Yujun
   Song, Jingjing
   Cheng, Xifu
   Zhou, Chulin
   Huang, Shuo
   Zhao, Wentao
   Zong, Zhen
   Yang, Lingling
TI Targeting the "tumor microenvironment": RNA-binding proteins in the
   spotlight in colorectal cancer therapy
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Review
DE RNA-binding proteins; Colorectal cancer; Tumor microenvironment;
   Mechanistic function; Molecular targeted therapy
ID ANTI-ANGIOGENIC ISOFORMS; MESSENGER-RNA; COLON-CANCER;
   EXTRACELLULAR-MATRIX; BREAST-CANCER; GROWTH-FACTOR; INVADOPODIA
   FORMATION; CELL-PROLIFERATION; MOLECULAR-ORIGINS; STABILITY FACTOR
AB Colorectal cancer (CRC) is the third most common cancer and has the second highest mortality rate among cancers. The development of CRC involves both genetic and epigenetic abnormalities, and recent research has focused on exploring the ex-transcriptome, particularly post -transcriptional modifications. RNA -binding proteins (RBPs) are emerging epigenetic regulators that play crucial roles in post -transcriptional events. Dysregulation of RBPs can result in aberrant expression of downstream target genes, thereby affecting the progression of colorectal tumors and the prognosis of patients. Recent studies have shown that RBPs can influence CRC pathogenesis and progression by regulating various components of the tumor microenvironment (TME). Although previous research on RBPs has primarily focused on their direct regulation of colorectal tumor development, their involvement in the remodeling of the TME has not been systematically reported. This review aims to highlight the significant role of RBPs in the intricate interactions within the CRC tumor microenvironment, including tumor immune microenvironment, inflammatory microenvironment, extracellular matrix, tumor vasculature, and CRC cancer stem cells. We also highlight several compounds under investigation for RBP-TME-based treatment of CRC, including small molecule inhibitors such as antisense oligonucleotides (ASOs), siRNAs, agonists, gene manipulation, and tumor vaccines. The insights gained from this review may lead to the development of RBP-based targeted novel therapeutic strategies aimed at modulating the TME, potentially inhibiting the progression and metastasis of CRC.
C1 [Zhang, Yiwei; Zhang, Yujun; Song, Jingjing; Zong, Zhen] Nanchang Univ, Affiliated Hosp 2, Dept Gastrointestinal Surg, 1 MinDe Rd, Nanchang 330006, Peoples R China.
   [Zhang, Yiwei; Zhang, Yujun; Song, Jingjing; Yang, Lingling] Nanchang Univ, Affiliated Hosp 2, Dept Gastroenterol, 1 Mingde Rd, Nanchang 330006, Jiangxi, Peoples R China.
   [Zhang, Yiwei] Nanchang Univ, Queen Mary Sch, Nanchang 330006, Peoples R China.
   [Song, Jingjing; Cheng, Xifu] Optometry Nanchang Univ, Sch Ophthalmol, Nanchang, Peoples R China.
   [Zhou, Chulin; Huang, Shuo] Nanchang Univ, Clin Med Coll 2, Nanchang 330006, Peoples R China.
   [Zhao, Wentao] China Med Univ, Clin Dept 3, Dept Med Genet, Shenyang, Peoples R China.
C3 Nanchang University; Nanchang University; Nanchang University; Nanchang
   University; China Medical University
RP Zong, Z (corresponding author), Nanchang Univ, Affiliated Hosp 2, Dept Gastrointestinal Surg, 1 MinDe Rd, Nanchang 330006, Peoples R China.; Yang, LL (corresponding author), Nanchang Univ, Affiliated Hosp 2, Dept Gastroenterol, 1 Mingde Rd, Nanchang 330006, Jiangxi, Peoples R China.
EM zongzhenmd@126.com; eleanyang2008@163.com
RI Song, Jing/HRC-8045-2023; Cheng, Xifu/JBS-1163-2023
OI Cheng, Xifu/0009-0009-6262-308X
FU China Postdoctoral Science Foundation [2023M741523]; National Natural
   Science Foundation of China [82060453, 82103645, 82260596, 82103655];
   Training Plan for Academic and Technical Young Leaders of Major
   Disciplines in Jiangxi Province [20204BCJ23021]; Interdisciplinary
   innovation fund of Nanchang University [9167-28220007-YB2108]
FX This research was financially supported by "The China Postdoctoral
   Science Foundation" (Grant Number: 2023M741523) , "the National Natural
   Science Foundation of China" (Grant Number: 82060453 and 82103645 and
   82260596 and 82103655) , "Training Plan for Academic and Technical Young
   Leaders of Major Disciplines in Jiangxi Province" (Grant Number:
   20204BCJ23021) , and "Interdisciplinary innovation fund of Nanchang
   University" (Grant Number: 9167-28220007-YB2108) .
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NR 289
TC 5
Z9 5
U1 6
U2 7
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD APR 20
PY 2024
VL 131
AR 111876
DI 10.1016/j.intimp.2024.111876
EA MAR 2024
PG 21
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA OQ2E0
UT WOS:001208666500001
PM 38493688
DA 2025-01-04
ER

PT J
AU Liu, HF
   Zhou, DD
   Liu, DQ
   Xu, X
   Zhang, K
   Hu, RX
   Xiong, P
   Wang, CX
   Zeng, XF
   Wang, LF
   Zhang, SY
AF Liu, Hongfu
   Zhou, Dongdong
   Liu, Dongqin
   Xu, Xi
   Zhang, Kai
   Hu, Ruxia
   Xiong, Peng
   Wang, Changxin
   Zeng, Xiangfu
   Wang, Liefeng
   Zhang, Shuyong
TI Synergistic antitumor activity between HER2 antibody-drug conjugate and
   chemotherapy for treating advanced colorectal cancer
SO CELL DEATH & DISEASE
LA English
DT Article
ID GEMCITABINE RESISTANCE; TRASTUZUMAB DERUXTECAN; AURISTATIN-E; BREAST;
   TRIAL; CISPLATIN; THERAPY; MULTICENTER; MECHANISMS; EMTANSINE
AB Colorectal cancer (CRC) is the third most common cancer associated with a poor prognosis. Effective targeted therapy alone or in combination for treating advanced CRC remains to be a major clinical challenge. Here, we propose the therapeutic efficacy and molecular mechanism underlying RC48, a FDA-approved anti-HER2 antibody conjugate via a cleavable linker to the microtubule inhibitor monomethyl auristatin E (MMAE), either alone or in combination with gemcitabine (GEM) in various models of HER2-positive advanced CRC. Our findings demonstrated that HER2 was widely expressed and located on the plasma membrane of CRC patient specimens, PDX xenograft tumors and cell lines. It confirmed that RC48 alone significantly targeted and eradicated HER2 positive CRC tumor in these models. Moreover, we screened a panel of FDA-approved first-line chemotherapy drugs in vitro. We found that GEM exhibited stronger antiproliferative activity compared to the other first-line anti-cancer agents. Furthermore, combination therapy of RC48 and GEM significantly showed synergetic antitumor activity in vitro and in vivo. To gain further mechanistic insights into the combination therapy, we performed RNA-seq analysis. The results revealed that combination treatment of RC48 and GEM regulated multiple signaling pathways, such as PI3K-AKT, MAPK, p53, Foxo, apoptosis, cell cycle and cell senescence, etc., to exert its antitumor activity in CRC cells. Collectively, these preclinical findings demonstrated that RC48 alone or combinational therapy exerted promising antitumor activity, and meriting the preclinical framework for combinational therapy of anti-HER2 drug conjugate drug and chemotherapy drugs for HER2-positive patients with advanced CRC.
C1 [Liu, Hongfu; Liu, Dongqin; Wang, Changxin; Zeng, Xiangfu] Gannan Med Univ, Affiliated Hosp 1, Dept Gen Surg, Ganzhou 341000, Peoples R China.
   [Liu, Hongfu; Zhou, Dongdong; Liu, Dongqin; Xu, Xi; Zhang, Kai; Hu, Ruxia; Xiong, Peng; Wang, Changxin; Zeng, Xiangfu; Wang, Liefeng; Zhang, Shuyong] Gannan Med Univ, Key Lab Prevent & Treatment Cardiovasc & Cerebrova, Minist Educ, Ganzhou 341000, Peoples R China.
   [Zhou, Dongdong; Xu, Xi; Zhang, Kai; Hu, Ruxia; Xiong, Peng; Wang, Liefeng; Zhang, Shuyong] Gannan Med Univ, Sch Basic Med, Ganzhou 341000, Peoples R China.
C3 Gannan Medical University; Gannan Medical University; Gannan Medical
   University
RP Zeng, XF (corresponding author), Gannan Med Univ, Affiliated Hosp 1, Dept Gen Surg, Ganzhou 341000, Peoples R China.; Zeng, XF; Wang, LF; Zhang, SY (corresponding author), Gannan Med Univ, Key Lab Prevent & Treatment Cardiovasc & Cerebrova, Minist Educ, Ganzhou 341000, Peoples R China.; Wang, LF; Zhang, SY (corresponding author), Gannan Med Univ, Sch Basic Med, Ganzhou 341000, Peoples R China.
EM 643001901@qq.com; 469730795@qq.com; zsy206@163.com
RI Wang, Changxin/AAX-4575-2020; Liu, Hong-Fu/U-9348-2019
OI Zhang, Shuyong/0000-0002-9739-2682
FU National Natural Science Foundation of China (National Science
   Foundation of China) [82260720]; National Natural Science Foundation of
   China [20224ACB206033]; Natural Science Foundation of Jiangxi Province
FX This work was supported in part by National Natural Science Foundation
   of China (82260720) and Natural Science Foundation of Jiangxi Province
   (20224ACB206033). We gratefully acknowledge the technical support
   provided by scientists at Novogene Co., Ltd. (Tianjin, China).
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NR 53
TC 2
Z9 2
U1 3
U2 12
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 MAR 5
PY 2024
VL 15
IS 3
AR 187
DI 10.1038/s41419-024-06572-2
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA KM1P6
UT WOS:001180295000005
PM 38443386
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Huang, T
   Peng, LS
   Han, YY
   Wang, D
   He, XY
   Wang, JP
   Ou, CL
AF Huang, Tao
   Peng, Lushan
   Han, Yingying
   Wang, Dan
   He, Xiaoyun
   Wang, Junpu
   Ou, Chunlin
TI Lipid nanoparticle-based mRNA vaccines in cancers: Current advances and
   future prospects
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE mRNA vaccine; nanocarrier; therapeutic target; delivery system; cancer
   therapy
ID CELL LUNG-CANCER; CYTOTOXIC T-LYMPHOCYTES; IN-VIVO; DRUG-DELIVERY;
   MEDIATED DELIVERY; COLORECTAL-CANCER; GENE-EXPRESSION; DENDRITIC CELLS;
   RABIES VACCINE; POLY(A) TAIL
AB Messenger RNA (mRNA) vaccines constitute an emerging therapeutic method with the advantages of high safety and efficiency as well as easy synthesis; thus, they have been widely used in various human diseases, especially in malignant cancers. However, the mRNA vaccine technology has some limitations, such as instability and low transitive efficiency in vivo, which greatly restrict its application. The development of nanotechnology in the biomedical field offers new strategies and prospects for the early diagnosis and treatment of human cancers. Recent studies have demonstrated that Lipid nanoparticle (LNP)-based mRNA vaccines can address the poor preservation and targeted inaccuracy of mRNA vaccines. As an emerging cancer therapy, mRNA vaccines potentially have broad future applications. Unlike other treatments, cancer mRNA vaccines provide specific, safe, and tolerable treatments. Preclinical studies have used personalized vaccines to demonstrate the anti-tumor effect of mRNA vaccines in the treatment of various solid tumors, including colorectal and lung cancer, using these in a new era of therapeutic cancer vaccines. In this review, we have summarized the latest applications and progress of LNP-based mRNA vaccines in cancers, and discussed the prospects and limitations of these fields, thereby providing novel strategies for the targeted therapy of cancers.
C1 [Huang, Tao; Peng, Lushan; Han, Yingying; Wang, Dan; Wang, Junpu; Ou, Chunlin] Cent South Univ, Xiangya Hosp, Dept Pathol, Changsha, Peoples R China.
   [He, Xiaoyun] Cent South Univ, Xiangya Hosp, Dept Ultrasound Imaging, Changsha, Peoples R China.
   [Wang, Junpu] Cent South Univ, Sch Basic Med, Dept Pathol, Changsha, Peoples R China.
   [Wang, Junpu] Cent South Univ, Xiangya Hosp, Key Lab Hunan Prov Neurodegenerat Disorders, Changsha, Peoples R China.
   [Ou, Chunlin] Cent South Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, Changsha, Peoples R China.
C3 Central South University; Central South University; Central South
   University; Central South University; Central South University
RP Wang, JP; Ou, CL (corresponding author), Cent South Univ, Xiangya Hosp, Dept Pathol, Changsha, Peoples R China.; He, XY (corresponding author), Cent South Univ, Xiangya Hosp, Dept Ultrasound Imaging, Changsha, Peoples R China.; Wang, JP (corresponding author), Cent South Univ, Sch Basic Med, Dept Pathol, Changsha, Peoples R China.; Wang, JP (corresponding author), Cent South Univ, Xiangya Hosp, Key Lab Hunan Prov Neurodegenerat Disorders, Changsha, Peoples R China.; Ou, CL (corresponding author), Cent South Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, Changsha, Peoples R China.
EM hexiaoyun@csu.edu.cn; wang-jp2013@csu.edu.cn; ouchunlin@csu.edu.cn
RI Huang, Tao/GPK-7568-2022; He, Xiaoyun/GOP-3600-2022
OI Ou, Chunlin/0000-0003-2313-4186
FU National Natural Science Foundation of China; China Postdoctoral Science
   Foundation; Outstanding Youth Foundation of Hunan Provincial Natural
   Science Foundation of China; Hunan Provincial Natural Science Foundation
   of China; Science and Technology Program Foundation of Changsha City;
   Youth Fund of Xiangya Hospital;  [81602167];  [81903032]; 
   [2020M672520];  [2022JJ20098];  [2021JJ31100];  [2021JJ41013]; 
   [kq2004085];  [2018Q011]
FX Funding This work was supported by the National Natural Science
   Foundation of China (No. 81602167 and 81903032), the China Postdoctoral
   Science Foundation (No. 2020M672520), the Outstanding Youth Foundation
   of Hunan Provincial Natural Science Foundation of China (No.
   2022JJ20098), the Hunan Provincial Natural Science Foundation of China
   (No. 2021JJ31100 and 2021JJ41013), the Science and Technology Program
   Foundation of Changsha City (No. kq2004085) and the Youth Fund of
   Xiangya Hospital (No. 2018Q011).
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NR 134
TC 40
Z9 41
U1 8
U2 125
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 AUG 26
PY 2022
VL 13
AR 922301
DI 10.3389/fimmu.2022.922301
PG 14
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 4K8AP
UT WOS:000852165600001
PM 36090974
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wallner, M
   Köck-Hódi, S
   Booze, S
   White, KJ
   Mayer, H
AF Wallner, Martin
   Koeck-Hodi, Sabine
   Booze, Shaina
   White, Kathryn J.
   Mayer, Hanna
TI Nursing Management of Cutaneous Toxicities From Epidermal Growth Factor
   Receptor Inhibitors
SO CLINICAL JOURNAL OF ONCOLOGY NURSING
LA English
DT Article
DE targeted therapy; epidermal growth factor receptor; cutaneous
   toxicities; adherence; patient education; quality of life
ID METASTATIC COLORECTAL-CANCER; QUALITY-OF-LIFE; DERMATOLOGICAL
   TOXICITIES; TARGETED THERAPIES; SKIN RASH; EGFR INHIBITORS; ADVERSE
   EVENTS; CETUXIMAB; IMPACT; RECOMMENDATIONS
AB Background: Personalized targeted therapies have become an emerging paradigm in cancer treatment. Although generally more tolerable than other chemotherapeutic agents, one therapy, epidermal growth factor receptor inhibitors (EGFRIs), commonly results in the formation of cutaneous toxicities, which can negatively affect patients' treatment adherence and quality of life.
   Objectives: The aim of this article is to review nursing management strategies for EGFRI-related cutaneous toxicities.
   Methods: A systematic literature review was performed, including database searches in PubMed/MEDLINE (R), CINAHL (R), Cochrane Library, PsycINFO (R), and Web of Science.
   Findings: Nurses are essential to the management of EGFRI-related cutaneous toxicities and are in an ideal position to provide supportive care throughout the course of the EGFRI treatment. The aim of nursing management is to maintain patients' treatment adherence and quality of life by employing a preemptive and proactive approach. Patient education is the most frequently reported management strategy. However, treatment options and management strategies are largely anecdotal and based on individual reports and expert opinions. Although no evidence-based management strategies exist, nurses can rely on existing assessment tools and guidelines to provide patients with symptom management and supportive care.
C1 [Wallner, Martin; Koeck-Hodi, Sabine] Univ Vienna, Dept Nursing Sci, A-1010 Vienna, Austria.
   [Booze, Shaina] Georgia Southern Univ, Sch Nursing, Statesboro, GA USA.
   [White, Kathryn J.] Univ Sydney, Nursing Res Unit, Sydney, NSW 2006, Australia.
   [White, Kathryn J.] Univ Sydney, Sydney Nursing Sch, Sydney, NSW 2006, Australia.
   [Mayer, Hanna] Univ Vienna, Dept Nursing Sci, A-1010 Vienna, Austria.
C3 University of Vienna; University System of Georgia; Georgia Southern
   University; University of Sydney; University of Sydney; University of
   Vienna
RP Wallner, M (corresponding author), Univ Vienna, Dept Nursing Sci, A-1010 Vienna, Austria.
EM martin.wallner@univie.ac.at
RI White, Kate/H-1061-2011
OI White, Kathryn/0000-0003-4763-1734; Wallner, Martin/0000-0001-6819-2916
FU National Institute on Minority Health and Health Disparities, National
   Institutes of Health
FX Martin Wallner, RN, BSc, MA, and Sabine Kock-Hodi, Mag., are both
   research associates in the Department of Nursing Science at the
   University of Vienna in Austria; Shaina Booze, RN, BSN, is a 2012
   Minority Health and Health Disparities International Research Training
   fellow in the School of Nursing at Georgia Southern University in
   Statesboro; Kathryn J. White, RN, PhD, is a professor in the Nursing
   Research Unit and Sydney Nursing School at the University of Sydney in
   New South Wales, Australia; and Hanna Mayer, RN, PhD, is a professor in
   the Department of Nursing Science at the University of Vienna. The
   authors take full responsibility for the content of the article. Booze
   was supported by a scholarship from the National Institute on Minority
   Health and Health Disparities, National Institutes of Health (Kathryn
   Hoehn Anderson, PhD, ARNP, LMFT, principal investigator). The content is
   solely the responsibility of the authors and does not necessarily
   represent the official views of the National Institutes of Health. The
   content of this article has been reviewed by independent peer reviewers
   to ensure that it is balanced, objective, and free from commercial bias.
   No financial relationships relevant to the content of this article have
   been disclosed by the independent peer reviewers or editorial staff.
   Mention of specific products and opinions related to those products do
   not indicate or imply endorsement by the Clinical Journal of Oncology
   Nursing or the Oncology Nursing Society. Wallner can be reached at
   martin. wallner@univie.ac.at, with copy to editor at CJONEditor@ons.org.
   (Submitted February 2015. Revision submitted December 2015. Accepted for
   publication January 25, 2016.)
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NR 50
TC 3
Z9 4
U1 0
U2 10
PU ONCOLOGY NURSING SOC
PI PITTSBURGH
PA 125 ENTERPRISE DR, PITTSBURGH, PA 15275 USA
SN 1092-1095
EI 1538-067X
J9 CLIN J ONCOL NURS
JI Clin. J. Oncol. Nurs.
PD OCT
PY 2016
VL 20
IS 5
BP 529
EP 536
DI 10.1188/16.CJON.529-536
PG 8
WC Oncology; Nursing
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Oncology; Nursing
GA DX7BL
UT WOS:000384540800010
PM 27668373
DA 2025-01-04
ER

PT J
AU He, YT
   Yu, X
   Zhang, MG
   Guo, WZ
AF He, Yuting
   Yu, Xiao
   Zhang, Menggang
   Guo, Wenzhi
TI Pan-cancer analysis of m<SUP>5</SUP>C regulator genes reveals consistent
   epigenetic landscape changes in multiple cancers
SO WORLD JOURNAL OF SURGICAL ONCOLOGY
LA English
DT Article
DE m(5)C regulatory genes; Frequent network mining; Pan-cancer analysis;
   Survival; 5-Methylcytosine
ID ABERRANT DNA METHYLATION; COPY NUMBER VARIATIONS; COLORECTAL-CANCER;
   TARGETED THERAPY; RNA; METHYLTRANSFERASE; IDENTIFICATION; ASSOCIATION;
   PREDICTION; PROGNOSIS
AB Background 5-Methylcytosine (m(5)C) is a reversible modification to both DNA and various cellular RNAs. However, its roles in developing human cancers are poorly understood, including the effects of mutant m(5)C regulators and the outcomes of modified nucleobases in RNAs. Methods Based on The Cancer Genome Atlas (TCGA) database, we uncovered that mutations and copy number variations (CNVs) of m(5)C regulatory genes were significantly correlated across many cancer types. We then assessed the correlation between the expression of individual m(5)C regulators and the activity of related hallmark pathways of cancers. Results After validating m(5)C regulators' expression based on their contributions to cancer development and progression, we observed their upregulation within tumor-specific processes. Notably, our research connected aberrant alterations to m(5)C regulatory genes with poor clinical outcomes among various tumors that may drive cancer pathogenesis and/or survival. Conclusion Our results offered strong evidence and clinical implications for the involvement of m(5)C regulators.
C1 [He, Yuting; Yu, Xiao; Zhang, Menggang; Guo, Wenzhi] Zhengzhou Univ, Affiliated Hosp 1, Dept Hepatobiliary & Pancreat Surg, 1 Jianshe Rd, Zhengzhou 450052, Peoples R China.
   [He, Yuting; Yu, Xiao; Zhang, Menggang; Guo, Wenzhi] Zhengzhou Univ, Affiliated Hosp 1, Key Lab Hepatobiliary & Pancreat Surg & Digest Or, Zhengzhou 450052, Peoples R China.
   [He, Yuting; Yu, Xiao; Zhang, Menggang; Guo, Wenzhi] Open & Key Lab Hepato biliary & Pancreat Surg & D, Zhengzhou 450052, Peoples R China.
   [He, Yuting; Yu, Xiao; Zhang, Menggang; Guo, Wenzhi] Henan Key Lab Digest Organ Transplantat, Zhengzhou 450052, Peoples R China.
C3 Zhengzhou University; Zhengzhou University
RP He, YT; Guo, WZ (corresponding author), Zhengzhou Univ, Affiliated Hosp 1, Dept Hepatobiliary & Pancreat Surg, 1 Jianshe Rd, Zhengzhou 450052, Peoples R China.
EM fccheyt1@zzu.edu.cn; fccguowz@zzu.edu.cn
RI he, yuting/HLX-6751-2023
OI he, yuting/0000-0002-9779-6863
FU National Natural Science Foundation of China [81902832]; Youth Talent
   Lifting Project of Henan Province [2021HYTP059]
FX This work was supported by the National Natural Science Foundation of
   China (81902832) and the Youth Talent Lifting Project of Henan Province
   (2021HYTP059).
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NR 64
TC 16
Z9 16
U1 1
U2 11
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1477-7819
J9 WORLD J SURG ONCOL
JI World J. Surg. Oncol.
PD JUL 29
PY 2021
VL 19
IS 1
AR 224
DI 10.1186/s12957-021-02342-y
PG 12
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA TU3AK
UT WOS:000680912100001
PM 34325709
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Wang, HL
   Li, YM
   Shi, G
   Wang, Y
   Lin, Y
   Wang, Q
   Zhang, YJ
   Yang, QM
   Dai, L
   Cheng, L
   Su, XL
   Yang, Y
   Zhang, S
   Li, Z
   Li, J
   Wei, YQ
   Yu, DC
   Deng, HX
AF Wang, Huiling
   Li, Yiming
   Shi, Gang
   Wang, Yuan
   Lin, Yi
   Wang, Qin
   Zhang, Yujing
   Yang, Qianmei
   Dai, Lei
   Cheng, Lin
   Su, Xiaolan
   Yang, Yang
   Zhang, Shuang
   Li, Zhi
   Li, Jia
   Wei, Yuquan
   Yu, Dechao
   Deng, Hongxin
TI A Novel Antitumor Strategy: Simultaneously Inhibiting Angiogenesis and
   Complement by Targeting VEGFA/PIGF and C3b/C4b
SO MOLECULAR THERAPY-ONCOLYTICS
LA English
DT Article
ID ANTIANGIOGENIC THERAPY; CANCER; GROWTH; CELLS; RESISTANCE; ESCAPE;
   INTERRUPTION; INFLAMMATION; PROGRESSION; METASTASIS
AB Therapeutic antibodies targeting vascular endothelial growth factor (VEGF) have become a critical regimen for tumor therapy, but the efficacy of monotherapy is usually limited by drug resistance and multiple angiogenic mechanisms. Complement proteins are becoming potential candidates for cancer-targeted therapy based on their role in promoting cancer progression and angiogenesis. However, the antitumor abilities of simultaneous VEGF and complement blockade were unknown. We generated a humanized soluble VEGFR-Fc fusion protein (VID) binding VEGFA/PIGF and a CR1-Fc fusion protein (CID) targeting C3b/C4b. Both VID and CID had good affinities to their ligands and showed effective bioactivities. In vitro, angiogenesis effects induced by VEGF and hemolysis induced by complement were inhibited by VID and CID, respectively. Further, VID and CID confer a synergetic therapeutic effect in a colitis-associated colorectal cancer (CAC) model and an orthotopic 4T1 breast cancer model. Mechanically, combination therapy inhibited tumor angiogenesis, cell proliferation, and MDSC infiltration in the tumor microenvironment and promoted tumor cell apoptosis. Our study offers a novel therapeutic strategy for anti-VEGF-resistant tumors and chronic-inflammation-associated tumors.
C1 [Wang, Huiling; Li, Yiming; Shi, Gang; Wang, Yuan; Lin, Yi; Wang, Qin; Zhang, Yujing; Yang, Qianmei; Dai, Lei; Cheng, Lin; Su, Xiaolan; Yang, Yang; Wei, Yuquan; Yu, Dechao; Deng, Hongxin] Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Ke Yuan Rd 4,1,Gao Peng St, Chengdu 610041, Sichuan, Peoples R China.
   [Wang, Huiling; Li, Yiming; Shi, Gang; Wang, Yuan; Lin, Yi; Wang, Qin; Zhang, Yujing; Yang, Qianmei; Dai, Lei; Cheng, Lin; Su, Xiaolan; Yang, Yang; Wei, Yuquan; Yu, Dechao; Deng, Hongxin] Sichuan Univ, West China Hosp, Canc Ctr, Collaborat Innovat Ctr Biotherapy, Ke Yuan Rd 4,1,Gao Peng St, Chengdu 610041, Sichuan, Peoples R China.
   [Zhang, Shuang; Wei, Yuquan; Yu, Dechao] Sichuan Univ, West China Hosp, Canc Ctr, Dept Biotherapy, Chengdu 610041, Sichuan, Peoples R China.
   [Li, Yiming; Li, Zhi; Li, Jia] Innovent Biol Suzhou Co Ltd, Suzhou 215000, Jiangsu, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University
RP Deng, HX (corresponding author), Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Ke Yuan Rd 4,1,Gao Peng St, Chengdu 610041, Sichuan, Peoples R China.; Deng, HX (corresponding author), Sichuan Univ, West China Hosp, Canc Ctr, Collaborat Innovat Ctr Biotherapy, Ke Yuan Rd 4,1,Gao Peng St, Chengdu 610041, Sichuan, Peoples R China.; Yu, DC (corresponding author), Innovent Biol Suzhou Co Ltd, Suzhou 215000, Jiangsu, Peoples R China.
EM michael.yu@innoventbio.com; denghongx@scu.edu.cn
RI Wang, He/JCO-3900-2023; wang, lili/HDL-7210-2022; Li, Yi
   ming/JWA-3152-2024
OI Deng, Hongxin/0000-0001-5094-1376
FU National Natural Science Foundation of China [81372445]
FX We thank Andy Tsun for article revision and Zhangyi Huang for assistance
   with statistical analysis. This work was supported by the National
   Natural Science Foundation of China (81372445).
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NR 51
TC 15
Z9 16
U1 4
U2 19
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
SN 2372-7705
J9 MOL THER-ONCOLYTICS
JI Mol. Ther.-Oncolytics
PD MAR 27
PY 2020
VL 16
BP 20
EP 29
DI 10.1016/j.omto.2019.12.004
PG 10
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA KY6KN
UT WOS:000522681900003
PM 31909182
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Guo, ZY
   Lloyd, RV
AF Guo, Zhenying
   Lloyd, Ricardo V.
TI Use of monoclonal antibodies to detect specific mutations in
   formalin-fixed, paraffin-embedded tissue sections
SO HUMAN PATHOLOGY
LA English
DT Article
DE Mutation-specific antibodies; Gene sequencing; BRAF; EGFR; SDHB;
   Immunohistochemistry
ID GROWTH-FACTOR RECEPTOR; BRAF V600E MUTATION; GENE COPY NUMBER; CELL
   LUNG-CANCER; GASTROINTESTINAL STROMAL TUMORS; METASTATIC
   COLORECTAL-CANCER; PAPILLARY THYROID-CARCINOMA; ACTIVATING EGFR
   MUTATIONS; SUCCINATE-DEHYDROGENASE; BRAF(V600E) MUTATION
AB Treatment options for cancer patients have changed considerably in recent years with the introduction of variable gene mutation and targeted therapy. Although molecular testing for gene mutations remains the gold standard in assessing biopsy tissues for specific mutations and for subsequent therapy, recent developments have led to the use of highly specific monoclonal antibodies to detect mutated genes in tissue sections. Some of the early developments included antibodies against EGFR, but have expanded to include antibodies detecting mutated RAS, BRAF, and SDHx. Immunohistochemical detection of gene mutations using mutation-specific antibodies has the advantage of allowing the detailed visualization of protein distributions in situ and provides direct visualization of the heterogeneity in the distribution of targeted proteins. This review will discuss the use of selected mainly monoclonal antibodies targeting specific mutated molecules and indicate how the detection of these proteins can be used for chemotherapeutic purposes in targeting mutated genes. (C) 2016 Elsevier Inc. All rights reserved.
C1 [Guo, Zhenying] Zhejiang Canc Hosp, Hangzhou 310022, Zhejiang, Peoples R China.
   [Guo, Zhenying; Lloyd, Ricardo V.] Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI 53726 USA.
C3 Zhejiang Cancer Hospital; University of Wisconsin System; University of
   Wisconsin Madison
RP Lloyd, RV (corresponding author), Univ Wisconsin, Dept Pathol & Lab Med, Madison, WI 53706 USA.
EM rvlloyd@wisc.edu
FU Zhejiang Provincial Natural Science Foundation of China [LY16H160036];
   National Natural Science Foundation of China [81300236]
FX We thank Dr. Zhenjie Liu for critical reading of the manuscript and
   Debbie Lloyd for technical and grammatical assistance. Z. Guo was
   supported by Zhejiang Provincial Natural Science Foundation of China
   LY16H160036 and National Natural Science Foundation of China
   (No.81300236).
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NR 91
TC 7
Z9 8
U1 0
U2 6
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 2016
VL 53
BP 168
EP 177
DI 10.1016/j.humpath.2016.03.013
PG 10
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA DP7GW
UT WOS:000378668200022
PM 27083401
DA 2025-01-04
ER

PT J
AU Geng, HF
   Zheng, FY
   Sun, WT
   Huang, SQ
   Wang, ZY
   Yang, KS
   Wang, CK
   Tian, CZ
   Xu, C
   Zhai, GC
   Zhao, MY
   Hou, SB
   Song, AG
   Zhang, YS
   Zhao, QC
AF Geng, Hefeng
   Zheng, Fangyuan
   Sun, Wentao
   Huang, Shuoqi
   Wang, Zhiya
   Yang, Kaisi
   Wang, Chengkang
   Tian, Caizhi
   Xu, Chang
   Zhai, Guanchao
   Zhao, Mingyi
   Hou, Shanbo
   Song, Aigang
   Zhang, Yingshi
   Zhao, Qingchun
TI Effect and mechanism of novel HDAC inhibitor ZDLT-1 in colorectal cancer
   by regulating apoptosis and inflammation
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Article
DE Colorectal cancer; HDAC inhibitor; Dehydroharmine derivative ZDLT-1;
   Apoptosis; Inflammation
ID PATHWAY
AB Background: Histone deacetylase (HDAC) is a potential target for Colorectal Cancer (CRC) molecular target therapy, dehydroharmine derivative ZDLT-1 was designed to inhibit CRC cell proliferation by inhibiting HDAC target. This study aimed to explore the effect of ZDLT-1 could induce apoptosis in CRC in vitro and in vivo, and determine the mechanism of ZDLT-1. Methods: First, MTT assay, colony formation, wound healing, Transwell assay, Hoechst33342 staining and Annexin V-FITC/PI double staining assay were used to investigate the in vitro effect of ZDLT-1. Second, the toxicity and the anti-tumor effect of ZDLT-1 by subcutaneous tumorigenesis assay were used to determine the in vivo effect of ZDLT-1. In terms of mechanism, we evaluated the effect of ZDLT-1 on HDAC downstream proteins such as HIF-1 alpha, NF-kappa B, Cleaved-Caspase-3/9, GSDMD and acetylated histone by immunofluorescence and Western blot assessments. Results: This study confirmed that ZDLT-1 had anti-tumor activity by inhibiting cell proliferation in vitro and solid tumor growth in vivo. Furthermore, ZDLT-1 can inhibit CRC cell invasion, migration and apoptosis in vitro. Moreover, ZDLT-1 can promote the expression of apoptosis proteins in HIF-1 alpha/Caspase-3/Caspase-9 pathway and inhibit the expression of tumor-related immune proteins mainly in NF-kappa B/GSDMD/GSDME pathway. Conclusion: ZDLT-1 as HDAC inhibitor could suppresses CRC cell growth in vivo and in vitro by triggering HIF-1 alpha/ Caspase-3/Caspase-9 pathway in promoting apoptosis, and triggering NF-kappa B/GSDMD/GSDME pathway in inhibiting tumor inflammation. Our results propose dehydroharmine derivative ZDLT-1 as a promising therapeutic small molecular agent for CRC.
C1 [Geng, Hefeng; Zheng, Fangyuan; Wang, Zhiya; Yang, Kaisi; Wang, Chengkang; Xu, Chang; Zhang, Yingshi; Zhao, Qingchun] Shenyang Pharmaceut Univ, Gen Hosp Northern Theater Command, Teaching Hosp, Shenyang 100016, Liaoning, Peoples R China.
   [Geng, Hefeng; Zheng, Fangyuan; Sun, Wentao; Huang, Shuoqi; Wang, Zhiya; Yang, Kaisi; Wang, Chengkang; Tian, Caizhi; Xu, Chang; Zhai, Guanchao; Zhao, Mingyi; Zhang, Yingshi; Zhao, Qingchun] Shenyang Pharmaceut Univ, Dept Clin Pharm, Shenyang, Liaoning, Peoples R China.
   [Huang, Shuoqi] Tianjin Hosp, Pharm Dept, Tianjin, Peoples R China.
   [Hou, Shanbo; Song, Aigang] Luoxin Pharmaceut Grp Stock Co Ltd, Linyi, Peoples R China.
C3 Shenyang Pharmaceutical University; Shenyang Pharmaceutical University
RP Zhang, YS; Zhao, QC (corresponding author), Shenyang Pharmaceut Univ, Gen Hosp Northern Theater Command, Teaching Hosp, Shenyang 100016, Liaoning, Peoples R China.
EM x876892517@163.com; zhengfangyuanzxq@163.com; s17824267658@163.com;
   hsq199696@163.com; 15091190776@163.com; syphuyks100@163.com;
   W1877816073@outlook.com; syphu_tiancaizhi@163.com;
   Charlottexu1996@163.com; z1098319369@163.com; zmy_dl@126.com;
   shanbohou@luoxin.cn; aigangsong@luoxin.cn; zhangyingshi@syphu.edu.cn;
   zhaoqingchun1967@163.com
RI Wang, Chengkang/AAE-7957-2019; Wang, Zhiya/LSK-2012-2024
FU Science and Technology Projects in Liaoning Province
   [2022JH2/101300093]; National Col-lege Students Innovation and
   Entrepreneurship Training Program of Shenyang Pharmaceutical University
   [202410163048]
FX This research was supported Science and Technology Projects in Liaoning
   Province (grant no. 2022JH2/101300093) and National Col-lege Students
   Innovation and Entrepreneurship Training Program of Shenyang
   Pharmaceutical University (grant no. 202410163048) .
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NR 44
TC 0
Z9 0
U1 5
U2 5
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD DEC 25
PY 2024
VL 143
AR 113333
DI 10.1016/j.intimp.2024.113333
EA OCT 2024
PN 1
PG 11
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA I9I6M
UT WOS:001333320500001
PM 39383785
DA 2025-01-04
ER

PT J
AU Parikh, P
   Bahl, A
   Sharma, G
   Pramanik, R
   Wadhwa, J
   Bajpai, P
   Jandyal, S
   Dubey, AP
   Sarin, A
   Dadhich, SC
   Saklani, AP
   Kumar, A
   Chandra, A
   Rawat, S
   Selvasekar, C
   Aggarwal, S
AF Parikh, Purvish
   Bahl, Ankur
   Sharma, Gopal
   Pramanik, Raja
   Wadhwa, Jyoti
   Bajpai, Peush
   Jandyal, Sunny
   Dubey, A. P.
   Sarin, Aditya
   Dadhich, Subash Chandra
   Saklani, Avinash P.
   Kumar, Ashok
   Chandra, Abhijit
   Rawat, Saumitra
   Selvasekar, C.
   Aggarwal, Shyam
TI Management of Metastatic Colorectal Cancer (mCRC): Real-World
   Recommendations
SO SOUTH ASIAN JOURNAL OF CANCER
LA English
DT Article; Early Access
DE aggressive cancer; overall survival; personalized oncology; systemic
   therapy
ID RAS WILD-TYPE; QUALITY-OF-LIFE; 1ST-LINE TREATMENT; OPEN-LABEL; LIVER
   METASTASES; HEPATIC RESECTION; SUBGROUP ANALYSES; RANDOMIZED-TRIAL; PLUS
   IRINOTECAN; BRAF-MUTATION
AB Introduction Metastatic CRC is considered as a heterogenous disease. Its management is therefore complex and dynamic. In order the give a ready reference to community oncologists, we developed this real world recommendations. Methods A group of experts with academic background and real world experience in mCRC got together. We reviewed the current literature and the insights gained from our real world experience. Based on the same we put together these recommendations. Recommendations (Results) Molecular testing should be done wherever possible. Most of these patients will be treated with a palliative approach. Doublet chemotherapy is a long-standing standard of care. Triplet therapy may be offered where a more aggressive approach is indicated. Combination with anti -vascular endothelial growth factor antibodies and/or anti EGFR antibodies is also considered standard. In the first-line setting, pembrolizumab can be used for patients with mCRC and microsatellite instability-high or deficient mismatch repair tumours; Left and right sided tumours are distinct entities. Combination of chemotherapy and targeted therapy is used as per individual patient and tumour characteristics. Oligometastatic disease can be approached with potentially curative intent. Cytoreductive surgery plus chemotherapy can be offered to selected patients with peritoneal only metastases. Stereotactic body radiation therapy can be used as local therapy for patients with oligometastatic liver only disease who cannot be taken up for surgery. New strategies include induction-maintenance chemotherapy and perioperative chemotherapy. All drugs/ regimen included as standard of care in the first line can also be used in subsequent lines. Specific targetable driver mutation tumours can be treated accordingly with their complementary biological therapy. Conclusion Multidisciplinary team management and shared decision making are possible when patient and caregivers choose to become active participants.
C1 [Parikh, Purvish] Mahatma Gandhi Univ Med Sci & Technol, Sri Ram Canc Ctr, Dept Clin Hematol, Jaipur 302022, Rajasthan, India.
   [Bahl, Ankur] Fortis Hosp, Dept Med Oncol, Gurugram, Haryana, India.
   [Sharma, Gopal] Max Healthcare Hosp, Dept Med Oncol, New Delhi, India.
   [Pramanik, Raja] All India Inst Med Sci AIIMS, Dept Med Oncol, New Delhi, India.
   [Wadhwa, Jyoti] Tata Mem Hosp, Dept Med Oncol, Mumbai, Maharashtra, India.
   [Bajpai, Peush] Manipal Hosp, Dept Med Oncol, New Delhi, India.
   [Jandyal, Sunny] Act Balajee Canc Hosp, Dept Med Oncol, New Delhi, India.
   [Dubey, A. P.] Delhi Heart & Lung Inst, Dept Med Oncol, New Delhi, India.
   [Sarin, Aditya] Sir Ganga Ram Hosp, Dept Med Oncol, New Delhi, India.
   [Dadhich, Subash Chandra] Arogya Hosp, Dept Laparoscop Surg, Vizag, Andhra Pradesh, India.
   [Saklani, Avinash P.] Tata Mem Hosp, Dept Surg Gastroenterol, Mumbai, Maharashtra, India.
   [Kumar, Ashok] Sanjay Gandhi Post Grad Inst Med Sci SGPGI, Dept Surg Gastroenterol, Lucknow, Uttar Pradesh, India.
   [Chandra, Abhijit] King George Med Univ, Dept Surg Gastroenterol, Lucknow, Uttar Pradesh, India.
   [Rawat, Saumitra] Sir Ganga Ram Hosp, Dept Surg Gastroenterol, New Delhi, India.
   [Selvasekar, C.] Christie NHS Fdn Trust, Clin Serv & Specialist Surg, Manchester, Lancs, England.
   [Aggarwal, Shyam] Sir Ganga Ram Hosp, Dept Med Oncol, New Delhi, India.
C3 All India Institute of Medical Sciences (AIIMS) New Delhi; Tata Memorial
   Centre (TMC); Tata Memorial Hospital; Tata Memorial Centre (TMC); Tata
   Memorial Hospital; Sanjay Gandhi Postgraduate Institute of Medical
   Sciences; King George's Medical University; Christie NHS Foundation
   Trust
RP Parikh, P (corresponding author), Mahatma Gandhi Univ Med Sci & Technol, Sri Ram Canc Ctr, Dept Clin Hematol, Jaipur 302022, Rajasthan, India.
EM purvish1@gmail.com
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NR 75
TC 0
Z9 0
U1 0
U2 0
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 2278-330X
EI 2278-4306
J9 SOUTH ASIAN J CANCER
JI South Asian J. Cancer
PD 2024 DEC 11
PY 2024
DI 10.1055/s-0044-1791689
EA DEC 2024
PG 9
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA P1P3B
UT WOS:001375710800001
DA 2025-01-04
ER

PT J
AU Kubecek, O
   Laco, J
   Spacek, J
   Kubecková, A
   Petera, J
   Krulichová, IS
   Bezrouk, A
   Filip, S
   Kopecky, J
AF Kubecek, Ondrej
   Laco, Jan
   Spacek, Jiri
   Kubeckova, Alena
   Petera, Jiri
   Krulichova, Iva Selke
   Bezrouk, Ales
   Filip, Stanislav
   Kopecky, Jindrich
TI Clinicopathological Characteristics and Prognostic Factors in Ovarian
   Metastases from Right- and Left-Sided Colorectal Cancer
SO CURRENT ONCOLOGY
LA English
DT Article
DE colorectal cancer; metastasis; ovarian metastases; prognostic factors
ID CLINICAL CHARACTERISTICS; PROPHYLACTIC OOPHORECTOMY; SURGICAL-TREATMENT;
   COLON-CANCER; TUMORS; DIAGNOSIS; SECONDARY; ORIGIN; ADENOCARCINOMA;
   MANAGEMENT
AB Background: Secondary tumors of the ovary (STOs) account for 10-25% of all ovarian malignancies, including metastases from primary gynecological tumors. Colorectal cancer (CRC) has been recognized as one of the most common causes of STOs in Western countries. Despite it being well-known that CRC originating from the right versus left side of the colon/rectum differ substantially, there is a paucity of information regarding the effect of the primary tumor sidedness on the clinicopathological characteristics of STOs. Methods: This retrospective, observational chart review study included patients with histologically confirmed STOs of CRC origin diagnosed between January 2000 and December 2019. The clinicopathological characteristics of STOs originating from left-sided and right-sided CRC were compared. Univariable and multivariable analyses employing elastic net Cox proportional hazard models were used to evaluate potential prognostic factors. Further, the role of imaging methods in STOs diagnostics was evaluated. Results: Fifty-one patients with STOs of colorectal origin were identified. The primary tumor originated in the right and left colon/rectum in 39% and 61% of the cases, respectively. STOs originating from right-sided primary tumors were more frequently bilateral, associated with peritoneal carcinomatosis, had the ovarian surface affected by the tumor, and contained a mucinous component. The independent prognostic factors for overall survival in the whole cohort included: the presence of macroscopic residual disease after cytoreductive surgery, menopausal status, the application of systemic therapy, and the application of targeted therapy. In 54% of cases, the imaging methods failed to determine the laterality of the STOs correctly as compared to pathological reports and/or intraoperative findings. Conclusion: STOs originating from left-sided and right-sided CRC show distinct clinicopathological characteristics. Moreover, different metastatic pathways might be employed according to the primary tumor sidedness. Considering the discrepancies between radiological assessment and histopathological findings regarding the laterality of STOs, bilateral adnexectomy should be advised whenever feasible.
C1 [Kubecek, Ondrej; Petera, Jiri; Filip, Stanislav; Kopecky, Jindrich] Charles Univ Prague, Fac Med, Dept Oncol & Radiotherapy, Sokolska 581, Hradec Kralove 50005, Czech Republic.
   [Kubecek, Ondrej; Laco, Jan; Spacek, Jiri; Petera, Jiri; Filip, Stanislav; Kopecky, Jindrich] Charles Univ Prague, Univ Hosp Hradec Kralove, Sokolska 581, Hradec Kralove 50005, Czech Republic.
   [Laco, Jan] Charles Univ Prague, Fac Med, Fingerland Dept Pathol, Sokolska 581, Hradec Kralove 50005, Czech Republic.
   [Spacek, Jiri] Charles Univ Prague, Fac Med, Dept Obstet & Gynecol, Sokolska 581, Hradec Kralove 50005, Czech Republic.
   [Kubeckova, Alena] First Private Surg Ctr Ltd, Dept Gynecol, Labska Kotlina I-1220, Hradec Kralove 50002, Czech Republic.
   [Krulichova, Iva Selke; Bezrouk, Ales] Charles Univ Prague, Fac Med Hradec Kralove, Dept Med Biophys, Simkova 870, Hradec Kralove 50003, Czech Republic.
C3 University Hospital Hradec Kralove; Charles University Prague;
   University Hospital Hradec Kralove; Charles University Prague; Charles
   University Prague; University Hospital Hradec Kralove; University
   Hospital Hradec Kralove; Charles University Prague; Charles University
   Prague; University Hospital Hradec Kralove
RP Kopecky, J (corresponding author), Charles Univ Prague, Fac Med, Dept Oncol & Radiotherapy, Sokolska 581, Hradec Kralove 50005, Czech Republic.; Kopecky, J (corresponding author), Charles Univ Prague, Univ Hosp Hradec Kralove, Sokolska 581, Hradec Kralove 50005, Czech Republic.
EM okubec@gmail.com; jan.laco@fnhk.cz; jiri.spacek@fnhk.cz;
   gynekolog.hk@gmail.com; jiri.petera@fnhk.cz; krulich@lfhk.cuni.cz;
   BezroukA@lfhk.cuni.cz; stanislav.filip@fnhk.cz; jindrich.kopecky@fnhk.cz
RI Kopecky, Jindrich/IQV-8052-2023; Kubeček, Ondřej/S-3542-2016;
   Krulichova, Iva/E-9944-2017; Filip, Stanislav/AAU-9160-2020; Filip,
   Stanislav/D-4908-2017; Laco, Jan/L-9715-2017; Bezrouk, Ales/A-6654-2017
OI Kopecky, Jindrich/0000-0002-4126-0410; Filip,
   Stanislav/0000-0002-8567-0745; Kubecek, Ondrej/0000-0003-2105-625X;
   Laco, Jan/0000-0002-9602-7501; Bezrouk, Ales/0000-0002-2397-3847
FU Charles University Faculty of Medicine in Hradec Kralove grant [Progres
   Q40/06, Progres Q40/09, Progres Q40/11]
FX This work was supported by the Charles University Faculty of Medicine in
   Hradec Kralove grant Progress Q40/06, Q40/09, and Q40/11.
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NR 53
TC 1
Z9 1
U1 0
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1198-0052
EI 1718-7729
J9 CURR ONCOL
JI Curr. Oncol.
PD AUG
PY 2021
VL 28
IS 4
BP 2914
EP 2927
DI 10.3390/curroncol28040255
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UI9PD
UT WOS:000690928400001
PM 34436021
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ma, CX
   Guan, X
   Wei, R
   Wang, S
   Quan, JC
   Zhao, ZX
   Chen, HP
   Liu, Z
   Jiang, Z
   Wang, XS
AF Ma, Chen-xi
   Guan, Xu
   Wei, Ran
   Wang, Song
   Quan, Ji-chuan
   Zhao, Zhi-xun
   Chen, Hai-peng
   Liu, Zheng
   Jiang, Zheng
   Wang, Xi-shan
TI The Distinction of Clinicopathological Characteristics, Treatment
   Strategy and Outcome in Colorectal Cancer Patients With Synchronous vs.
   Metachronous Bone Metastasis
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colorectal cancer; bone metastasis; synchronous; metachronous; cancer
   specific survival; prognostic factor
ID PRIMARY TUMOR RESECTION; QUALITY-OF-LIFE; COLON-CANCER; SPINAL
   METASTASES; SURVIVAL; LUNG; BISPHOSPHONATES; PREDICT; BREAST; TRIALS
AB Background:The impact of the timing of bone metastasis (BM) diagnosis on colorectal cancer (CRC) patients is unclear. Our study aimed to explore the differences in clinicopathological characteristics, treatments and prognosis between synchronous BM (SBM) and metachronous BM (MBM) from CRC. Methods:We retrospectively investigated clinical data of CRC patients with SBM or MBM from 2008 to 2017 at Chinese National Cancer Center. Cancer specific survival (CSS) after BM diagnosis was estimated using the Kaplan-Meier method. The multivariable COX regression model identified the prognostic factors of CSS. Results:Finally, 63 CRC patients with SBM and 138 CRC patients with MBM were identified. Compared to SBM from CRC, MBM significantly was more involving multiple bone lesions (63.0 vs. 7.9%;p< 0.001), and more frequently originated from rectal cancer (60.9 vs. 41.3%;p= 0.033). The therapeutic strategies in SBM and MBM group were contrasted including systemic treatment, bisphosphonates, radiotherapy and metastasectomy for BM. 85.5% of patients in MBM group and 25.4% of patients in SBM group underwent primary tumor resection at initial diagnosis (p< 0.001). The median CSS was 11 months in both SBM and MBM group (p= 0.556), yet MBM patients developed from CRC in early AJCC stage presented obviously longer survival than those from advanced stage. Furthermore, patients could have improved CSS from primary tumor resection while there might be no survival benefit from targeted therapy in both SBM and MBM groups. Bisphosphonates was associated with a better CSS for patients with SBM, while radiotherapy for BM was related to a better CSS for patients with MBM. Conclusion:The CRC patients in SBM and MBM group represented different clinicopathological characteristics and treatment modalities, which affected the prognosis in different ways. Distinct consideration for CRC patients with SBM and MBM in clinical decision making is required.
C1 [Ma, Chen-xi; Guan, Xu; Wei, Ran; Quan, Ji-chuan; Zhao, Zhi-xun; Chen, Hai-peng; Liu, Zheng; Jiang, Zheng; Wang, Xi-shan] Chinese Acad Med Sci & Peking Union Med Coll, Natl Clin Res Ctr Canc, Dept Colorectal Surg, Natl Canc Ctr,Canc Hosp, Beijing, Peoples R China.
   [Wang, Song] Harbin Med Univ, Dept Colorectal Surg, Affiliated Hosp 2, Harbin, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Peking Union Medical College; Cancer Institute & Hospital - CAMS; Harbin
   Medical University
RP Guan, X; Jiang, Z; Wang, XS (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Natl Clin Res Ctr Canc, Dept Colorectal Surg, Natl Canc Ctr,Canc Hosp, Beijing, Peoples R China.
EM drguanxu@163.com; 812818858@qq.com; wxshan_1208@126.com
FU CAMS Innovation Fund for Medical Sciences (CIFMS) [2016-I2M-1-001];
   Beijing Science and Technology Program [D17110002617004]
FX This work was supported by CAMS Innovation Fund for Medical Sciences
   (CIFMS) (2016-I2M-1-001) and Beijing Science and Technology Program
   (D17110002617004).
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NR 30
TC 6
Z9 7
U1 0
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 JUN 19
PY 2020
VL 10
AR 974
DI 10.3389/fonc.2020.00974
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA MJ9IG
UT WOS:000548398900001
PM 32637357
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Lee, KH
   Kim, JS
   Kim, JY
AF Lee, Kyung Ha
   Kim, Jin Soo
   Kim, Ji Yeon
TI Necessity of Genetic Evaluation of Metachronous Metastases of Colorectal
   Cancer: Quantitative Analysis of Genetic Discordance Between
   Metachronous Metastases and Radically Resected Primary Colorectal
   Cancers Using Next-Generation Sequencing
SO DISEASES OF THE COLON & RECTUM
LA English
DT Article
DE Biological therapy; Colorectal neoplasms; Deoxyribonucleic acid
   mutational analysis; Neoplasm metastasis
ID PIK3CA MUTATIONS; PRIMARY TUMORS; KRAS STATUS; HETEROGENEITY; EVOLUTION;
   THERAPY; BRAF
AB BACKGROUND: Mutation analyses provide the basis of selecting an appropriate target agent for the treatment of metastatic colorectal cancer. However, metachronous metastases developed after the treatment of primary tumor could create significant opportunities for different genetic profiles relative to the primary tumors. OBJECTIVE: The purpose of this study was to assess the necessity of genetic evaluation of metachronous metastases; we performed a quantitative analysis of genetic discordance between metachronous metastases and radically resected primary colorectal cancers using next-generation sequencing. DESIGN: This was a retrospective study. SETTINGS: Patients from a single-institution tertiary care center were studied. PATIENTS: We enrolled 33 patients who underwent resection of metachronous metastases between January 2014 and December 2016, >= 6 months after radical resection of primary colorectal cancer and whose tissue was available for analysis. MAIN OUTCOME MEASURES: Tumor samples were analyzed by next-generation sequencing. The mutant allele frequency was analyzed to evaluate the proportion of mutations in the tumor tissue. RESULTS: The mutant allele frequency of KRAS in metachronous metastases was higher in 6 cases (mean difference =% 25.5% (range, 9.5%-58.0%)) and lower in 3 cases (mean difference = 9.3% (range, 8.0-10.0%) compared with each of their primary tumors. In 1 case, the KRAS mutant-type (mutant allele frequency = 22.6%) metachronous metastasis had developed from the KRAS wild-type primary tumor. LIMITATIONS: Tumor sample may not represent perfectly the whole tumor of the patient because of heterogeneity. CONCLUSIONS: Genetic discordance can exist between metachronous metastases and radically resected primary colorectal cancers. For appropriate target therapy, genetic evaluation of metachronous metastases needs to be considered when possible. See Video Abstract at .
C1 [Lee, Kyung Ha; Kim, Jin Soo; Kim, Ji Yeon] Chungnam Natl Univ Hosp, Dept Surg, 282 Munwharo, Daejeon 301721, South Korea.
C3 Chungnam National University; Chungnam National University Hospital
RP Kim, JS (corresponding author), Chungnam Natl Univ Hosp, Dept Surg, 282 Munwharo, Daejeon 301721, South Korea.
EM jkim@cnu.ac.kr
RI Kim, Jong/I-3135-2019; lee, sangwoo/KUD-1906-2024
CR [Anonymous], COL CANC VERS 2 2017
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NR 19
TC 1
Z9 1
U1 0
U2 1
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 JUL
PY 2019
VL 62
IS 7
BP 832
EP 839
DI 10.1097/DCR.0000000000001386
PG 8
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA ID4VU
UT WOS:000471675200011
PM 31188184
DA 2025-01-04
ER

PT J
AU Nan, H
   Guo, PK
   Fan, JN
   Zeng, W
   Hu, CH
   Zheng, C
   Pan, BJ
   Cao, Y
   Ge, YW
   Xue, XY
   Li, WS
   Lin, KZ
AF Nan, Han
   Guo, Pengkun
   Fan, Jianing
   Zeng, Wen
   Hu, Chonghan
   Zheng, Can
   Pan, Bujian
   Cao, Yu
   Ge, Yiwen
   Xue, Xiangyang
   Li, Wenshu
   Lin, Kezhi
TI Comprehensive analysis of the prognosis, tumor microenvironment, and
   immunotherapy response of SDHs in colon adenocarcinoma
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE succinate dehydrogenase (SDH); colorectal cancer; colon adenocarcinoma
   (COAD); prognostic; immune infiltration; immune treatment
ID SUCCINATE-DEHYDROGENASE SUBUNIT; IMMUNE CHECKPOINT INHIBITORS; STROMAL
   TUMORS; COLORECTAL-CANCER; CARBOXYLASE 1; GENE; MUTATIONS; METABOLISM;
   EXPRESSION; THERAPY
AB BackgroundSuccinate dehydrogenase (SDH), one of the key enzymes in the tricarboxylic acid cycle, is mainly found in the mitochondria. SDH consists of four subunits encoding SDHA, SDHB, SDHC, and SDHD. The biological function of SDH is significantly related to cancer progression. Colorectal cancer (CRC) is one of the most common malignant tumors globally, whose most common histological subtype is colon adenocarcinoma (COAD). However, the correlation between SDH factors and COAD remains unclear. MethodsThe data on pan-cancer was obtained from The Cancer Genome Atlas (TCGA) database. Kaplan-Meier survival analysis showed the prognostic ability of SDHs. The cBioPortal database reflected genetic variations of SDHs. The correlation analysis was conducted between SDHs and mitochondrial energy metabolism genes (MMGs) and the protein-protein interaction (PPI) network was built. Consequently, Univariate and Multivariate Cox Regression Analysis on SDHs and other clinical characteristics were conducted. A nomogram was established. The ssGSEA analysis visualized the association between SDHs and immune infiltration. Immunophenoscore (IPS) explored the correlation between SDHs and immunotherapy, and the correlation between SDHs and targeted therapy was investigated through Genomics of Drug Sensitivity in Cancer. Finally, qPCR and immunohistochemistry detected SDHs' expression. ResultsAfter assessing SDHs differential expression in pan-cancer, we found that SDHB, SDHC, and SDHD benefit COAD patients. The cBioPortal database demonstrated that SDHA was the top gene in mutation frequency rank. Correlation analysis mirrored a strong link between SDHs and MMGs. We formulated a nomogram and found that SDHB, SDHC, SDHD, and clinical characteristics correlated with COAD patients' survival. For T helper cells, Th2 cells, and Tem, SDHA, SDHB, SDHC, and SDHD were significantly enriched in the high expression group. Moreover, COAD patients with high SDHA expression were more suitable for immunotherapy. And COAD patients with different SDHs' expression have different sensitivity to targeted drugs. Further verifying the gene and protein expression levels of SDHs, we found that the tissues were consistent with the bioinformatics analysis. ConclusionsOur study analyzed the expression and prognostic value of SDHs in COAD, explored the pathway mechanisms involved, and the immune cell correlations, indicating that SDHs might be biomarkers for COAD patients.
C1 [Nan, Han; Cao, Yu] Wenzhou Med Univ, Sch & Hosp Stomatol, Wenzhou, Zhejiang, Peoples R China.
   [Guo, Pengkun; Zeng, Wen; Hu, Chonghan] Wenzhou Med Univ, Sch Basic Med Sci, Wenzhou, Zhejiang, Peoples R China.
   [Fan, Jianing; Ge, Yiwen] Wenzhou Med Univ, Sch Clin Med 2, Wenzhou, Zhejiang, Peoples R China.
   [Zheng, Can] Wenzhou Med Univ, Sch Med 1, Sch Informat & Engn, Wenzhou, Peoples R China.
   [Pan, Bujian] Wenzhou Med Univ, Wenzhou Cent Hosp, Dept Hepatobiliary Surg, Dingli Clin Inst, Wenzhou, Peoples R China.
   [Xue, Xiangyang; Lin, Kezhi] Wenzhou Med Univ, Experiemtial Ctr Basic Med, Sch Basic Med Sci, Wenzhou Key Lab Canc Related Pathogens & Immun,Wen, Wenzhou, Peoples R China.
   [Xue, Xiangyang] Wenzhou Med Univ, Affiliated Hosp 2, Dept Gen Surg, Wenzhou, Peoples R China.
   [Xue, Xiangyang] Wenzhou Med Univ, Yuying Childrens Hosp, Wenzhou, Peoples R China.
   [Li, Wenshu] Wenzhou Med Univ, Inst Mol Virol & Immunol, Sch Basic Med Sci, Wenzhou, Zhejiang, Peoples R China.
C3 Wenzhou Medical University; Wenzhou Medical University; Wenzhou Medical
   University; Wenzhou Medical University; Wenzhou Medical University;
   Wenzhou Medical University; Wenzhou Medical University; Wenzhou Medical
   University; Wenzhou Medical University
RP Xue, XY; Lin, KZ (corresponding author), Wenzhou Med Univ, Experiemtial Ctr Basic Med, Sch Basic Med Sci, Wenzhou Key Lab Canc Related Pathogens & Immun,Wen, Wenzhou, Peoples R China.; Xue, XY (corresponding author), Wenzhou Med Univ, Affiliated Hosp 2, Dept Gen Surg, Wenzhou, Peoples R China.; Xue, XY (corresponding author), Wenzhou Med Univ, Yuying Childrens Hosp, Wenzhou, Peoples R China.; Li, WS (corresponding author), Wenzhou Med Univ, Inst Mol Virol & Immunol, Sch Basic Med Sci, Wenzhou, Zhejiang, Peoples R China.
EM wzxxy001@163.com; lws161@163.com; lkz@wmu.edu.cn
RI lin, ke/GZM-8300-2022; CAO, Yu/A-7073-2019
FU Key R&D program of Science Technology Department of Zhejiang Province
   [2020C03029]; Wenzhou Basic Scientific Research Project [Y20220172];
   National Innovation and Entrepreneurship Training Program for College
   Students [202210343053]; Research Grant for Students of Wenzhou Medical
   University [wyx2021101149]; Basic study on public projects of Zhejiang
   Province [LGF18H030011]
FX This work was supported by Key R&D program of Science Technology
   Department of Zhejiang Province (2020C03029), Wenzhou Basic Scientific
   Research Project (Y20220172), National Innovation and Entrepreneurship
   Training Program for College Students (202210343053), Research Grant for
   Students of Wenzhou Medical University (wyx2021101149), and Basic study
   on public projects of Zhejiang Province (No. LGF18H030011).
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NR 80
TC 1
Z9 1
U1 2
U2 13
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 MAR 6
PY 2023
VL 14
AR 1093974
DI 10.3389/fimmu.2023.1093974
PG 17
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA A1VL8
UT WOS:000953076800001
PM 36949947
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Li, C
   Wiseman, L
   Okoh, E
   Lind, M
   Roy, R
   Beavis, AW
   Pires, IM
AF Li, Chun
   Wiseman, Lucy
   Okoh, Ene
   Lind, Michael
   Roy, Rajarshi
   Beavis, Andrew W.
   Pires, Isabel M.
TI Exploring hypoxic biology to improve radiotherapy outcomes
SO EXPERT REVIEWS IN MOLECULAR MEDICINE
LA English
DT Review
DE DNA damage response; HAPs; HIF; hypoxia; radioresistance; radiotherapy;
   targeted therapy
ID SQUAMOUS-CELL CARCINOMA; PHASE-I TRIAL; PROTEASE INHIBITOR NELFINAVIR;
   ANTI-PD-1 ANTIBODY SHR-1210; TRANS-SODIUM CROCETINATE; ADVANCED
   RECTAL-CANCER; RADIATION-THERAPY RT; DOUBLE-STRAND BREAKS; LUNG-CANCER;
   DNA-DAMAGE
AB Ionising radiotherapy is a well-established, effective cancer treatment modality, whose efficacy has improved with the application of newer technological modalities. However, patient outcomes are governed and potentially limited by aspects of tumour biology that are associated with radioresistance. Patients also still endure treatment-associated toxicities owed to the action of ionising radiation in normoxic tissue adjacent to the tumour mass. Tumour hypoxia is recognised as a key component of the tumour microenvironment and is well established as leading to therapy resistance and poor prognosis. In this review, we outline the current understanding of hypoxia-mediated radiotherapy resistance, before exploring targeting tumour hypoxia for radiotherapy sensitisation to improve treatment outcomes and increase the therapeutic window. This includes increasing oxygen availability in solid tumours, the use of hypoxia-activated prodrugs, targeting of hypoxia-regulated or associated signalling pathways, as well as the use of high-LET radiotherapy modalities. Ultimately, targeting hypoxic radiobiology combined with precise radiotherapy delivery modalities and modelling should be associated with improvement to patient outcomes.
C1 [Li, Chun; Wiseman, Lucy; Okoh, Ene; Pires, Isabel M.] Univ Hull, Fac Hlth Sci, Dept Biomed Sci, Hypoxia & Tumour Microenvironm Lab, Kingston Upon Hull, N Humberside, England.
   [Lind, Michael; Roy, Rajarshi] Castle Hill Hosp, Queens Ctr Oncol & Haematol, Castle Rd, Cottingham HU16 5JQ, England.
   [Lind, Michael; Beavis, Andrew W.] Univ Hull, Fac Hlth Sci, Cottingham Rd, Kingston Upon Hull HU16 7RX, N Humberside, England.
   [Beavis, Andrew W.] Hull Univ Teaching Hosp NHS Trust, Queens Ctr Oncol, Dept Med Phys, Cottingham HU16 5JQ, England.
   [Beavis, Andrew W.] Sheffield Hallam Univ, Fac Hlth & Well Being, Sheffield S10 2BP, S Yorkshire, England.
C3 University of Hull; University of Hull; University of Hull; Sheffield
   Hallam University
RP Pires, IM (corresponding author), Univ Hull, Fac Hlth Sci, Dept Biomed Sci, Hypoxia & Tumour Microenvironm Lab, Kingston Upon Hull, N Humberside, England.
EM i.pires@hull.ac.uk
OI beavis, andrew/0000-0002-2519-0205; Monteiro dos Santos Pires,
   Isabel/0000-0002-0417-2710; Roy, Rajarshi/0000-0003-3718-7967
FU University of Hull, Adaptive Radiotherapy PhD cluster; NHS Trust; Bowel
   Research UK PhD studentship [000100009]
FX CL and IMP are funded by a University of Hull studentship part of the
   Adaptive Radiotherapy PhD cluster, which is a collaborative project with
   the NHS Trust, led by IMP (University of Hull) and AWB (Hull University
   Teaching Hospitals NHS Trust). IMP, LWand RR are funded by a Bowel
   Research UK PhD studentship (reference 000100009).
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NR 288
TC 8
Z9 8
U1 2
U2 20
PU CAMBRIDGE UNIV PRESS
PI CAMBRIDGE
PA EDINBURGH BLDG, SHAFTESBURY RD, CB2 8RU CAMBRIDGE, ENGLAND
SN 1462-3994
J9 EXPERT REV MOL MED
JI Expert Rev. Mol. Med.
PD APR 27
PY 2022
VL 24
AR e21
DI 10.1017/erm.2022.14
PG 18
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine
GA 1I7UV
UT WOS:000797433800001
PM 35586915
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Wu, LJ
   Chen, LQ
AF Wu, Lingjuan
   Chen, Liqun
TI Characteristics of Nur77 and its ligands as potential anticancer
   compounds
SO MOLECULAR MEDICINE REPORTS
LA English
DT Review
DE nuclear receptor; Nur77; cancer; compounds; target therapy
ID NUCLEAR RECEPTOR NUR77; COLON-CANCER CELLS; ORPHAN-RECEPTOR;
   BREAST-CANCER; NGFI-B; TUMOR-GROWTH; TRANSCRIPTIONAL REGULATORS;
   COACTIVATOR RECRUITMENT; NEGATIVE REGULATION; PROAPOPTOTIC GENES
AB Nuclear receptor subfamily 4 group A member 1 (NR4A1; also termed Nur77/TR3/NGFIB), a member of the nuclear receptor superfamily, is expressed as an early response gene to regulate the expression of multiple target genes. Nur77 has the typical structure of a nuclear receptor, including an N-terminal domain, a DNA binding domain, and a ligand-binding domain. The expression and localization of Nur77 are closely associated with its roles in cell proliferation and apoptosis. Nur77 was first identified as an orphan receptor, the endogenous ligand of which has not yet been identified; however, an increasing number of compounds targeting Nur77 have been reported to have beneficial effects in the treatment of cancer and other diseases. This review provides a brief overview of the identification, structure, expression and localization, transcriptional role and non-genomic function of Nur77, and summarizes the ligands that have been shown to interact with Nur77, including cytosporone B, cisplatin, TMPA, PDNPA, CCE9, THPN, Z-ligustilide, celastrol and bisindole methane compounds, which may potentially be used to treat cancer in humans.
C1 [Wu, Lingjuan; Chen, Liqun] Fuzhou Univ, Coll Biol Sci & Engn, 2 Xueyuan Rd, Fuzhou 350108, Fujian, Peoples R China.
C3 Fuzhou University
RP Chen, LQ (corresponding author), Fuzhou Univ, Coll Biol Sci & Engn, 2 Xueyuan Rd, Fuzhou 350108, Fujian, Peoples R China.
EM lqchen@fzu.edu.cn
FU National Natural Science Foundation [31500616]; Natural Science
   Foundation of Fujian Province [2017J01445]
FX This study was supported by grants from the National Natural Science
   Foundation (grant no. 31500616) and the Natural Science Foundation of
   Fujian Province (grant no. 2017J01445).
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NR 96
TC 59
Z9 66
U1 3
U2 66
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1791-2997
EI 1791-3004
J9 MOL MED REP
JI Mol. Med. Rep.
PD DEC
PY 2018
VL 18
IS 6
BP 4793
EP 4801
DI 10.3892/mmr.2018.9515
PG 9
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA HA7DE
UT WOS:000450440600003
PM 30272297
OA Green Published, Green Submitted, hybrid
DA 2025-01-04
ER

PT J
AU Cao, H
   Liu, XY
   Chen, YX
   Yang, P
   Huang, TX
   Song, LL
   Xu, RL
AF Cao, Hua
   Liu, Xinyi
   Chen, Yixin
   Yang, Pan
   Huang, Tanxiao
   Song, Lele
   Xu, Ruilian
TI Circulating Tumor DNA Is Capable of Monitoring the Therapeutic Response
   and Resistance in Advanced Colorectal Cancer Patients Undergoing
   Combined Target and Chemotherapy
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colorectal cancer; ctDNA; NGS; sequencing; bevacizumab; cetuximab;
   monitoring; resistance
AB Colorectal cancer (CRC) is a highly lethal disease worldwide. The majority of patients receiving targeted therapy or chemotherapy develop drug resistance, while its molecular mechanism remains to be elucidated. The plasma circulating tumor DNA (ctDNA) exhibited the potential in identifying gene variations and monitoring drug resistance in CRC treatment. In this study, we monitored the ctDNA mutational changes in advanced CRC patients underwent first-line therapy with bevacizumab and cetuximab combined with chemotherapy. The mutation spectrum of 43 patients was established by a 605-gene next-generation sequencing (NGS) panel. The baseline measurement shows that genes with the highest mutation frequency were TP53 (74%), APC (58%), KRAS (40%), SYNE1 (33%), LRP1B (23%), TOP1 (23%), and PIK3CA (21%). Mutations in TP53, APC, and KRAS were detected in 29 paired plasma and tissue samples with the consistency of 81, 67, and 42%, respectively. Clinically targetable gene mutations, such as APC, RNF43, SMAD4, BRAD1, KRAS, RAF1, and TP53, were also identified in ctDNA. The overall consistency between ctDNA and tissue samples was 54.6%. Alleviation of mutational burden in BRAF, KRAS, AMER1, and other major driving genes was observed following the first-line therapy. Patients with KRAS and TP53 mutations in tissues appeared to benefit more than the wild-type counterpart. The dynamic change of plasma mutation status was consistent with the tissue tumor burden and was closely correlated with disease progression. In conclusion, ctDNA monitoring is a useful method for molecular genotyping of colorectal cancer patients. Dynamic changes in resistance can be sensitively monitored by gene variation status, which potentially helps to develop treatment strategy.
C1 [Cao, Hua; Chen, Yixin; Xu, Ruilian] Southern Univ Sci & Technol, Dept Oncol, Shenzhen Peoples Hosp, Sch Clin Med 2,Jinan Univ,Affiliated Hosp 1, Shenzhen, Peoples R China.
   [Liu, Xinyi; Yang, Pan; Huang, Tanxiao; Song, Lele] HaploX Biotechnol Co Ltd, Shenzhen, Peoples R China.
C3 Southern University of Science & Technology; Jinan University
RP Xu, RL (corresponding author), Southern Univ Sci & Technol, Dept Oncol, Shenzhen Peoples Hosp, Sch Clin Med 2,Jinan Univ,Affiliated Hosp 1, Shenzhen, Peoples R China.
EM xuruilian@126.com
RI liu, xinyi/GWZ-8739-2022
FU Sanming project of Shenzhen People's Hospital [SYLY201725]; project
   Monitoring the efficacy of chemotherapy and evaluation of drug
   resistance in digestive tract tumors based on liquid biopsy; project
   Head-to-head comparison of apatinib mesylate combined with chemotherapy:
   a randomized study of bevacizumab combined with chemotherapy as
   second-line therapy for advanced intestinal cancer patients
FX This study was supported by the project Monitoring the efficacy of
   chemotherapy and evaluation of drug resistance in digestive tract tumors
   based on liquid biopsy and project Head-to-head comparison of apatinib
   mesylate combined with chemotherapy: a randomized study of bevacizumab
   combined with chemotherapy as second-line therapy for advanced
   intestinal cancer patients (SYLY201725), supported by Sanming project of
   Shenzhen People's Hospital.
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NR 24
TC 21
Z9 22
U1 0
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 APR 7
PY 2020
VL 10
AR 466
DI 10.3389/fonc.2020.00466
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LH7YJ
UT WOS:000529000100001
PM 32318348
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ricci, V
   Ronzoni, M
   Fabozzi, T
AF Ricci, Vincenzo
   Ronzoni, Monica
   Fabozzi, Teresa
TI Aflibercept a new target therapy in cancer treatment: a review
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE Angiogenesis; Antiangiogenic agent; Aflibercept; Placental growth
   factor; VEGF-A; VEGF-B
ID ENDOTHELIAL GROWTH-FACTOR; I DOSE-ESCALATION; POTENT VEGF BLOCKADE;
   PHASE-II; FACTOR-TRAP; INTRAVENOUS AFLIBERCEPT; OVARIAN-CANCER;
   DOUBLE-BLIND; TUMOR ANGIOGENESIS; COLORECTAL-CANCER
AB Angiogenesis is the process through which new blood vessels are formed from pre-existing vessels and is essential for the growth of all solid tumors. Vascular endothelial growth factor (VEGF) is a regulator of angiogenesis, which is crucial for tumor growth and metastasis. Its inhibition with antiangiogenic drugs is thought to improve delivery of chemotherapy through vascular normalization and disruption of tumor vasculature. Aflibercept is a recombinant fusion protein of the VEGF receptor (VEGFR)1 and VEGFR2 extracellular domains that binds to VEGF-A, VEGF-B, placental growth factor (P1GF) 1 and 2. Aflibercept has demonstrated preclinical efficacy in different tumor types and exerts its antiangiogenic effects through regression of tumor vasculature, remolding of vasculature, and inhibition of new tumor vessel growth. This review examines the effects of aflibercept on tumor vasculature and on different types of solid tumors, and explores the preclinical and clinical benefits of inclusion aflibercept into anticancer treatment strategies. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
C1 [Ricci, Vincenzo; Ronzoni, Monica] San Raffaele Inst, Dept Oncol, I-20132 Milan, Italy.
   [Fabozzi, Teresa] San Raffaele Inst, I-20132 Milan, Italy.
C3 Vita-Salute San Raffaele University; IRCCS Ospedale San Raffaele;
   Vita-Salute San Raffaele University; IRCCS Ospedale San Raffaele
RP Ricci, V (corresponding author), Ist Sci San Raffaele, Dept Med Oncol, Via Olgettina 60, I-20132 Milan, Italy.
OI Ronzoni, Monica/0000-0002-2845-275X; Ricci, Vincenzo/0000-0002-8779-4792
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NR 80
TC 21
Z9 24
U1 0
U2 15
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1040-8428
EI 1879-0461
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD DEC
PY 2015
VL 96
IS 3
BP 569
EP 576
DI 10.1016/j.critrevonc.2015.07.001
PG 8
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA CY6RP
UT WOS:000366536800017
PM 26224565
DA 2025-01-04
ER

PT J
AU Weng, WH
   Leung, WH
   Pang, YJ
   Hsu, HH
AF Weng, Wen-Hui
   Leung, Wai-Hung
   Pang, Yeu-Jye
   Hsu, Hsi-Hsien
TI Laurie acid can improve the sensitization of Cetuximab in KRAS/BRAF
   mutated colorectal cancer cells by retrievable microRNA-378 expression
SO ONCOLOGY REPORTS
LA English
DT Article
DE lauric acid; colorectal cancer cells; KRAS; BRAF; miR-378; Cetuximab
ID TUMOR-GROWTH; FATTY-ACIDS; KRAS; PANITUMUMAB; MUTATIONS; APOPTOSIS;
   INVASION; MIR-378; BRAF
AB EGFR-inhibitor (Cetuximab) is one of the main targeted drugs used for metastatic colorectal carcinoma (CRC). The benefit from Cetuximab appears to be limited to a subtype of patients, not for the patients with tumors harboring mutated BRAF or KRAS genes; unfortunately, it accounts for similar to 40-50% of CRC cases. Previous studies have connected higher expression levels of miR-378 to be commonly presented in patients without BRAF or KRAS mutants than in mutated CRCs. The microRNA-378 (miR-378) is coexpressed with PGC-1 beta and can be easily induced by fatty acid, for example lauric acid. Therefore, we hypothesized that elevation of miR-378 expression in mutated CRCs may stimulate the cell response to Cetuximab. Herein, seven CRC cell lines with confirmed mutation status were involved in two parallel experiments; directly in vitro transfected miR-378 mimics, and using lauric acid to indirectly induce the level of miR-378 in cells. After the increase of miR-378 in cells by either direct or indirect approaches, sensitivity to Cetuximab was restored in all BRAF mutants (p-value <0.0001-0.0003), and half of KRAS mutants CRC (p-value 0.039-0.007). Further evidence was gained by decreasing expression of MEK and ERK2 proteins after transfection with miR-378; it was similar to the indirect induction by lauric acid approach. In conclusion, the present study demonstrated that lauric acid may efficiently induce miR-378 expression in CRC mutants, and both BRAF and a subtype of KRAS mutants presented significantly improved sensitivity to Cetuximab. Notably, BRAF mutants could even be inhibited in cell proliferation after elevated concentration of miR-378 in cells without combining with targeted therapy. This new approach may shed new light on BRAF or KRAS mutation in CRC patients for clinical trial, since lauric acid may easily be obtain from natural food, and it is supposed to be harmless to the cardiovascular system.
C1 [Weng, Wen-Hui; Leung, Wai-Hung] Natl Taipei Univ Technol, Dept Chem Engn & Biotechnol, Taipei 106, Taiwan.
   [Weng, Wen-Hui; Leung, Wai-Hung] Natl Taipei Univ Technol, Grad Inst Biochem & Biomed Engn, Taipei 106, Taiwan.
   [Leung, Wai-Hung; Hsu, Hsi-Hsien] Mackay Mem Hosp, Dept Surg, Div Colorectal Surg, Taipei 104, Taiwan.
   [Pang, Yeu-Jye] Hull York Med Sch, York YO10 5DD, N Yorkshire, England.
C3 National Taipei University of Technology; National Taipei University of
   Technology; Mackay Memorial Hospital; University of York - UK;
   University of Hull
RP Weng, WH (corresponding author), Natl Taipei Univ Technol, Dept Chem Engn & Biotechnol, 1 Sect 3,Zhongxiao E Road, Taipei 106, Taiwan.
EM wwhlab@gmail.com
RI Weng, Wen/AAV-7260-2021
FU  [NTUT-MMH-104-7]
FX The authors would like to thank the grant NTUT-MMH-104-7 support, Miss
   Jing-Jung Chen, Mr. Yu-Wen Wu and Mr. Cheng-Chi Wang (National Taipei
   University of Technology, Taiwan) for their instructions of statistical
   analysis and excellent assistance with laboratory work.
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NR 35
TC 25
Z9 27
U1 0
U2 11
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 JAN
PY 2016
VL 35
IS 1
BP 107
EP 116
DI 10.3892/or.2015.4336
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CY0BZ
UT WOS:000366072500013
PM 26496897
OA Bronze
DA 2025-01-04
ER

PT J
AU Qin, YF
   Li, GM
   Wang, G
   Kone, DJ
   Wang, HD
   Zhao, YM
   Hao, JP
   Qin, H
   Sun, DQ
   Wang, H
AF Qin, Ya-Fei
   Li, Guang-Ming
   Wang, Grace
   Kone, De-Jun
   Wang, Hong-Da
   Zhao, Yi-Ming
   Hao, Jing-Peng
   Qin, Hong
   Sun, Da-Qing
   Wang, Hao
TI Identification of Hub Gene TIMP1 and Relative ceRNAs Regulatory Network
   in Colorectal Cancer
SO THERAPEUTICS AND CLINICAL RISK MANAGEMENT
LA English
DT Article
DE circRNAs; colorectal cancer; ceRNAs; TIMP1; bioinformatic analysis
ID TISSUE INHIBITOR; BREAST-CANCER; MESENCHYMAL TRANSITION; CELLS;
   METASTASIS; EXPRESSION; BIOINFORMATICS; PROMOTES; RNA; OVEREXPRESSION
AB Objective: This study aimed to discover the ceRNAs network in the pathophysiological development of human colorectal cancer (CRC) and to screen biomarkers for target therapy and prognosis by using integrated bioinformatics analysis. Methods: Data on gene expressions of mRNAs, miRNAs, and circRNAs and clinical information were downloaded from The Cancer Genome Atlas and Gene Expression Omnibus databases, respectively. Differentially expressed mRNAs (DEmRNAs) were identified by using the DESeq2 package of R software. Functional enrichment analysis was conducted using the ClusterProfiler package of R software. The protein-protein interaction (PPI) network was shown by the STRING website. Survival analysis of hub genes was performed using the survival package in R software. Interactions among hub genes, differentially expressed miRNAs (DEmiRNAs), and differentially expressed circRNAs (DEcircRNAs) were used to construct the ceRNAs network. Results: A total of 412 DEmRNAs including 82 upregulated and 330 downregulated genes were screened out between 473 CRC and 41 normal samples. Two hundred and sixty DEcircRNAs including 253 upregulated and 7 downregulated genes were altered between 23 CRC and 23 normal samples. One hundred and ninety DEmiRNAs including 82 upregulated and 108 down regulated genes were obtained between 450 CRC and 8 normal samples. A ceRNAs and PPI network were successfully constructed, and TIMP1 associated with prognosis was employed. Conclusion: The present study identified a novel circRNAs-miRNAs-mRNA ceRNAs network, which implied that TIMP1 and related miRNAs, circRNAs were potential biomarkers underlying the development of CRC, providing new insights for survival predictions and therapeutic targets.
C1 [Qin, Ya-Fei; Li, Guang-Ming; Kone, De-Jun; Wang, Hong-Da; Zhao, Yi-Ming; Qin, Hong; Wang, Hao] Tianjin Med Univ, Dept Gen Surg, Gen Hosp, Tianjin, Peoples R China.
   [Qin, Ya-Fei; Li, Guang-Ming; Kone, De-Jun; Wang, Hong-Da; Zhao, Yi-Ming; Qin, Hong; Wang, Hao] Tianjin Med Univ, Tianjin Gen Surg Inst, Gen Hosp, Tianjin, Peoples R China.
   [Wang, Grace] Univ Toronto, Fac Med, Toronto, ON, Canada.
   [Hao, Jing-Peng] Tianjin Med Univ, Hosp 2, Dept Anorectal Surg, Tianjin, Peoples R China.
   [Sun, Da-Qing] Tianjin Med Univ, Dept Pediat Surg, Tianjin, Peoples R China.
C3 Tianjin Medical University; Tianjin Medical University; University of
   Toronto; Tianjin Medical University; Tianjin Medical University
RP Wang, H (corresponding author), Tianjin Med Univ, Dept Gen Surg, Gen Hosp, Tianjin, Peoples R China.; Wang, H (corresponding author), Tianjin Med Univ, Tianjin Gen Surg Inst, Gen Hosp, Tianjin, Peoples R China.; Sun, DQ (corresponding author), Tianjin Med Univ, Dept Pediat Surg, Tianjin, Peoples R China.
EM sdqchris2019@hotmail.com; hwangca272@hotmail.com
RI Kong, Dejun/KBB-2178-2024; Qin, Yafei/LSJ-0652-2024
OI Kong, Dejun/0000-0002-6878-9293
FU National Natural Science Foundation of China [82071802]; Tianjin
   Application Basis and Cutting-Edge Technology Research Grant
   [14JCZDJC35700]; Li Jieshou Intestinal Barrier Research Special Fund
   [LJS_201412]; Natural Science Foundation of Tianjin [18JCZDJC35800];
   Tianjin Medical University Talent Fund; Tianjin Research Innovation
   Project for postgraduate students [2019YJSS184]
FX This work was supported by grants to Hao Wang from the National Natural
   Science Foundation of China (No. 82071802) , Tianjin Application Basis
   and Cutting-Edge Technology Research Grant (No. 14JCZDJC35700) , Li
   Jieshou Intestinal Barrier Research Special Fund (No. LJS_201412) ,
   Natural Science Foundation of Tianjin (No. 18JCZDJC35800) , and Tianjin
   Medical University Talent Fund; by a grant to Dejun Kong from Tianjin
   Research Innovation Project for postgraduate students (No. 2019YJSS184)
   .
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NR 67
TC 0
Z9 0
U1 0
U2 17
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
EI 1178-203X
J9 THER CLIN RISK MANAG
JI Therap. Clin. Risk Manag.
PY 2021
VL 17
BP 889
EP 901
DI 10.2147/TCRM.S321101
PG 13
WC Health Care Sciences & Services
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Health Care Sciences & Services
GA UJ3OI
UT WOS:000691198500001
PM 34475758
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Cruz-Duarte, R
   de Almeida, CR
   Negrao, M
   Fernandes, A
   Borralho, P
   Sobral, D
   Gallego-Paez, LM
   Machado, D
   Gramaça, J
   Vílchez, J
   Xavier, AT
   Ferreira, MG
   Miranda, AR
   Mansinho, H
   Brito, MJ
   Pacheco, TR
   Abreu, C
   Lucia-Costa, A
   Mansinho, A
   Fior, R
   Costa, L
   Martins, M
AF Cruz-Duarte, Raquel
   de Almeida, Catia Rebelo
   Negrao, Magda
   Fernandes, Afonso
   Borralho, Paula
   Sobral, Daniel
   Gallego-Paez, Lina M.
   Machado, Daniel
   Gramaca, Joao
   Vilchez, Jose
   Xavier, Ana T.
   Ferreira, Miguel Godinho
   Miranda, Ana R.
   Mansinho, Helder
   Brito, Maria J.
   Pacheco, Teresa R.
   Abreu, Catarina
   Lucia-Costa, Ana
   Mansinho, Andre
   Fior, Rita
   Costa, Luis
   Martins, Marta
TI Predictive and Therapeutic Implications of a Novel PLCγ1/SHP2-Driven
   Mechanism of Cetuximab Resistance in Metastatic Colorectal Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; PHOSPHOLIPASE-C-GAMMA; 1ST-LINE TREATMENT; PLCG1
   MUTATIONS; RAS MUTATIONS; CELLS; EXPRESSION; C-GAMMA-1; BENEFIT;
   FLUOROURACIL
AB Purpose Cetuximab is an EGFR-targeted therapy approved for the treatment of RAS wild-type (WT) metastatic colorectal cancer (mCRC). However, about 60% of these patients show innate resistance to cetuximab. To increase cetuximab efficacy, it is crucial to successfully identify responder patients, as well as to develop new therapeutic approaches to overcome cetuximab resistance.
   Experimental Design: We evaluated the value of EGFR effector phospholipase C gamma 1 (PLC gamma 1) in predicting cetuximab responses, by analyzing progression-free survival (PFS) of a multicentric retrospective cohort of 94 treated patients with mCRC (log-rank test and Cox regression model). Furthermore, we used in vitro and zebrafish xenotransplant models to identify and target the mechanism behind PLC gamma 1-mediated resistance to cetuximab.
   Results: In this study, levels of PLC gamma 1 were found increased in RAS WT tumors and were able to predict cetuximab responses in clinical samples and in vitro and in vivo models. Mechanistically, PLC gamma 1 expression was found to bypass cetuximab-dependent EGFR inhibition by activating ERK and AKT pathways. This novel resistance mechanism involves a noncatalytic role of PLC gamma 1 SH2 tandem domains in the propagation of downstream signaling via SH2-containing protein tyrosine phosphatase 2 (SHP2). Accordingly, SHP2 inhibition sensitizes PLC gamma 1-resistant cells to cetuximab.
   Conclusions: Our discoveries reveal the potential of PLC gamma 1 as a predictive biomarker for cetuximab responses and suggest an alternative therapeutic approach to circumvent PLC gamma 1-mediated resistance to cetuximab in patients with RAS WT mCRC. In this way, this work contributes to the development of novel strategies in the medical management and treatment of patients with mCRC.
C1 [Cruz-Duarte, Raquel; Fernandes, Afonso; Pacheco, Teresa R.; Mansinho, Andre; Costa, Luis; Martins, Marta] Univ Lisbon, Fac Med, Inst Med Mol Joao Lobo Antunes, P-1649028 Lisbon, Portugal.
   [de Almeida, Catia Rebelo; Negrao, Magda; Ferreira, Miguel Godinho; Fior, Rita] Champalimaud Fdn, Champalimaud Ctr Unknown, Lisbon, Portugal.
   [Borralho, Paula] Univ Lisbon, Fac Med, Inst Pathol, Lisbon, Portugal.
   [Sobral, Daniel] Univ Nova Lisboa, UCIBIO, Fac Ciencias & Tecnol, Dept Ciencias Vida, Caparica, Portugal.
   [Gallego-Paez, Lina M.] BioMed X Inst GmbH, Neuenheimer Feld 583, Heidelberg, Germany.
   [Machado, Daniel; Gramaca, Joao; Vilchez, Jose; Xavier, Ana T.] Ctr Hosp Barreiro Montijo, Oncol Div, Barreiro, Portugal.
   [Ferreira, Miguel Godinho] Univ Cote dAzur, Inst Res Canc & Aging Nice IRCAN, UMR7284 U1081 UNS, Nice, France.
   [Miranda, Ana R.; Mansinho, Helder] Hosp Garcia Orta, Hematooncol Div, Almada, Portugal.
   [Brito, Maria J.] Hosp Garcia Orta, Pathol Div, Almada, Portugal.
   [Pacheco, Teresa R.; Abreu, Catarina; Lucia-Costa, Ana; Mansinho, Andre; Costa, Luis] Hosp Santa Maria, Ctr Hosp Lisboa Norte, Oncol Div, Lisbon, Portugal.
C3 Universidade de Lisboa; Fundacao Champalimaud; Universidade de Lisboa;
   Universidade Nova de Lisboa; Universite Cote d'Azur; Hospital Garcia de
   Orta; Hospital Garcia de Orta; Universidade de Lisboa; Hospital Santa
   Maria
RP Costa, L (corresponding author), Univ Lisbon, Fac Med, Inst Med Mol Joao Lobo Antunes, P-1649028 Lisbon, Portugal.; Martins, M (corresponding author), Inst Med Mol Joao Lobo Antunes, Translat Oncol, P-1649028 Lisbon, Portugal.
EM luiscosta.oncology@gmail.com; marta.martins@medicina.ulisboa.pt
RI Martins, Marta/A-9905-2013; Sobral, Daniel/K-3097-2019; Brito,
   Maria/K-4813-2019; Costa, Luis/E-5117-2015; Godinho Ferreira,
   Miguel/F-9290-2012; Sobral, Daniel/B-4786-2014
OI Fior, Rita/0000-0001-5550-2428; Costa, Luis/0000-0002-4782-7318;
   Borralho Nunes, Paula/0000-0002-8556-2090; Martins,
   Marta/0000-0003-0429-9380; Godinho Ferreira, Miguel/0000-0002-8363-7183;
   Sobral, Daniel/0000-0003-3955-0117
FU Liga Portuguesa Contra o Cancro (LPCC): Terry Fox Fundation;
   Investigador FCT Fundacao para a Ciencia e Technologia [IF/00409/2014];
   IMM Bridge grant; Fundacao para a Ciencia e Technologia
   [SFRH/BD/139138/2018]; LPCC-IMM BIOBANK; Champalimaud Foundation; Merck
   Serono; Fundação para a Ciência e a Tecnologia [SFRH/BD/139138/2018]
   Funding Source: FCT
FX We acknowledge the help of Carla Sousa and Genomed for assessing RAS
   mutations on tumor samples, the help of Dr. Vasco Rodrigues, and Dr. Rui
   Marques for their contribution at the Hospital Santa Maria Pharmacy and
   Champalimaud Fish Platform (C. Certal and J. Monteiro) for excellent
   animal care. Wethank Tom Bunney and Matilda Katan for helpful advice on
   this project and contribution with PLCg1 plasmids. The authors thank
   Champalimaud Foundation and M. Godinho Ferreira for the initial support
   of this project. M. Martins' research was supported by Liga Portuguesa
   Contra o Cancro (LPCC): Terry Fox Fundation; Investigador FCTFundacao
   para a Ciencia e Technologia (IF/00409/2014) and IMM Bridge grant; RC-D
   research was supported by Fundaao para a Ciencia e Technologia
   (SFRH/BD/139138/2018). A. Fernandes was supported by LPCC-IMM BIOBANK;
   R. Fior was supported by Champalimaud Foundation and L. Costa was
   supported by Merck Serono.
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NR 50
TC 8
Z9 9
U1 0
U2 0
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 MAR 15
PY 2022
VL 28
IS 6
BP 1203
EP 1216
DI 10.1158/1078-0432.CCR-21-1992
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZX9IS
UT WOS:000772207100001
PM 34980600
OA Green Submitted, Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Ruiz-Bañobre, J
   Kandimalla, R
   Goel, A
AF Ruiz-Banobre, Juan
   Kandimalla, Raju
   Goel, Ajay
TI Predictive Biomarkers in Metastatic Colorectal Cancer: A Systematic
   Review
SO JCO PRECISION ONCOLOGY
LA English
DT Review
ID SYNTHASE PROTEIN EXPRESSION; THYMIDYLATE SYNTHASE; RAS MUTATIONS;
   CLINICAL-RESPONSE; TARGETED THERAPY; GENETIC-VARIANTS; PLUS CETUXIMAB;
   SOLID TUMORS; OPEN-LABEL; PHASE-II
AB PURPOSE The development and use of predictive biomarkers to guide treatment decisions are paramount not only for improving survival in patients with metastatic colorectal cancer (mCRC), but also for sparing them from unnecessary toxicity and reducing the economic burden of expensive treatments. We conducted a systematic review of published studies and evaluated the predictive biomarker landscape in the mCRC setting from a molecular and clinical viewpoint.
   METHODS Studies analyzing predictive biomarkers for approved therapies in patients with mCRC were identified systematically using electronic databases. Preclinical studies and those providing no relevant information were excluded.
   RESULTS A total of 173 studies comprising 148 biomarkers were selected for final analysis. Of all the biomarkers analyzed, 1.4% (two of 148) were explored in a prospective manner, whereas 98.6% (146 of 148) were evaluated in retrospective studies. Of the latter group, 78.8% (115 of 146) were not tested in subsequent phases, 9.6% (14 of 146) were tested in other retrospective cohorts, 8.9% (13 of 146) were retrospectively tested in at least one or more randomized cohorts, and only 2.7% (four of 146) were prospectively tested in a clinical trial. Finally, only 1.4% (two of 148) were validated sufficiently and are recognized as biomarkers for guiding treatment decision making in patients with mCRC. These markers were RAS mutational status for anti-EGFR antibodies and microsatellite instability status for anti-programmed cell death-1 drugs.
   CONCLUSION Despite notable efforts to identify predictive biomarkers for various therapies used in the mCRC setting, because of a lack of data beyond retrospective studies and successful biomarker-driven approaches, only two molecular biomarkers have thus far found their translation into the clinic, highlighting the imperative need for implementing novel strategies and additional research in this clinically important field. (C) 2019 by American Society of Clinical Oncology
C1 [Ruiz-Banobre, Juan] Arquitecto Marcide Univ Hosp, Ferrol, Spain.
   [Ruiz-Banobre, Juan; Kandimalla, Raju; Goel, Ajay] Baylor Univ, Med Ctr, Dallas, TX USA.
   [Ruiz-Banobre, Juan] Univ Clin Hosp Santiago de Compostela, ONCOMET, CIBERONC, Santiago De Compostela, Spain.
C3 Baylor University Medical Center; Baylor University; CIBER - Centro de
   Investigacion Biomedica en Red; CIBERONC; Complexo Hospitalario
   Universitario de Santiago de Compostela
RP Goel, A (corresponding author), Baylor Univ, Med Ctr, Oncol Baylor Scott & White Res Inst, Ctr Gastrointestinal Res,Ctr Translat Genom & Onc, 3410 Worth St,Suite 610, Dallas, TX 75246 USA.
EM ajay.goel@bswhealth.org
RI Goel, Ajay/ADO-9623-2022; Kandimalla, Raju/C-1400-2016
OI Kandimalla, Raju/0000-0002-0342-5229; Ruiz-Banobre,
   Juan/0000-0003-0755-4295
FU National Cancer Institute, National Institutes of Health [CA181572,
   CA184792, CA187956, CA214254]; Cancer Prevention Research Institute of
   Texas [RP140784]; Baylor Foundation; Baylor Scott & White Research
   Institute, Dallas, TX
FX Supported by Grant Nos. CA181572, CA184792, CA187956, and CA214254 from
   the National Cancer Institute, National Institutes of Health; by Grant
   No. RP140784 from the Cancer Prevention Research Institute of Texas; and
   by grants from the Baylor Foundation and Baylor Scott & White Research
   Institute, Dallas, TX.
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NR 100
TC 16
Z9 17
U1 0
U2 7
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 MAR 28
PY 2019
VL 3
DI 10.1200/PO.18.00260
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HQ8HI
UT WOS:000462664700001
PM 32914007
OA Green Published
DA 2025-01-04
ER

PT J
AU Thonhauser, R
   Poglitsch, M
   Jonas, JP
   Dong, YW
   Tschögl, M
   Gramberger, M
   Salem, M
   Santol, J
   Brandl, I
   Klimpfinger, M
   Vierziger, C
   Gruenberger, T
AF Thonhauser, Rebecca
   Poglitsch, Marcus
   Jonas, Jan Philipp
   Dong, Yawen
   Tschoegl, Madita
   Gramberger, Mariel
   Salem, Mohamed
   Santol, Jonas
   Brandl, Irmgard
   Klimpfinger, Martin
   Vierziger, Constantin
   Gruenberger, Thomas
TI The Effect of Induction Chemotherapy with VEGF Inhibition on Tumor
   Response in Synchronously Metastasized Potentially Resectable Colorectal
   Cancer
SO CANCERS
LA English
DT Article
DE colorectal cancer; synchronous liver metastases; targeted therapy; tumor
   regression grading
ID UNRESECTABLE LIVER METASTASES; FOLFIRI PLUS BEVACIZUMAB; PATHOLOGICAL
   RESPONSE; NEOADJUVANT CHEMOTHERAPY; HEPATIC RESECTION; OPEN-LABEL;
   CETUXIMAB; FOLFOXIRI; SURVIVAL; OXALIPLATIN
AB (1) Background: The pathological tumor response of the primary tumor to induction chemotherapy in synchronously metastasized colorectal cancer (mCRC) patients has not been investigated. The aim of this study was to compare patients treated with induction chemotherapy combined with vascular endothelial growth factor (VEGF) or with epidermal growth factor receptor (EGFR) antibodies. (2) Methods: We present a retrospective analysis, where we included 60 consecutive patients with potentially resectable synchronous mCRC who received induction chemotherapy combined with either VEGF or EGFR antibodies. The primary endpoint of this study was the regression of the primary tumor, which was assessed by the application of the histological regression score according to Rodel. The secondary endpoints were recurrence-free survival (RFS) and overall survival (OS). (3) Results: A significantly better pathological response and a longer RFS for patients treated with the VEGF antibody therapy compared to those treated with the EGFR antibodies was demonstrated (p = 0.005 for the primary tumor and log-rank = 0.047 for RFS). The overall survival did not differ. The trial was registered with clinicaltrial.gov, number NCT05172635. (4) Conclusion: Induction chemotherapy combined with a VEGF antibody revealed a better pathological response of the primary tumor, leading to a better RFS compared to that with EGFR therapy; this has clinical relevance in patients with potentially resectable synchronously mCRC.
C1 [Thonhauser, Rebecca; Poglitsch, Marcus; Jonas, Jan Philipp; Dong, Yawen; Tschoegl, Madita; Gramberger, Mariel; Salem, Mohamed; Santol, Jonas; Gruenberger, Thomas] Clin Favoriten, HPB Ctr, Dept Surg, A-1100 Vienna, Austria.
   [Brandl, Irmgard; Klimpfinger, Martin] Clin Favoriten, Inst Pathol & Bacteriol, A-1100 Vienna, Austria.
   [Vierziger, Constantin] Clin Favoriten, Inst Diagnost & Intervent Radiol, A-1100 Vienna, Austria.
RP Thonhauser, R; Gruenberger, T (corresponding author), Clin Favoriten, HPB Ctr, Dept Surg, A-1100 Vienna, Austria.
EM thonhauser.rebecca@gmail.com; tellsantol@gmail.com;
   tgruenberger@icloud.com
RI Gruenberger, Thomas/ABA-1661-2020
OI Santol, Jonas/0000-0002-8097-9735; Gruenberger,
   Thomas/0000-0002-2671-0540
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NR 32
TC 2
Z9 2
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PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD MAY 24
PY 2023
VL 15
IS 11
AR 2900
DI 10.3390/cancers15112900
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA I9ME0
UT WOS:001005940100001
PM 37296862
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Cantor, DI
   Cheruku, HR
   Westacott, J
   Shin, JS
   Mohamedali, A
   Ahn, SB
AF Cantor, David I.
   Cheruku, Harish R.
   Westacott, Jack
   Shin, Joo-Shik
   Mohamedali, Abidali
   Ahn, Seong Boem
TI Proteomic investigations into resistance in colorectal cancer
SO EXPERT REVIEW OF PROTEOMICS
LA English
DT Review
DE Chemotherapy; colorectal cancer; cytotoxicity; proteomics; resistance
ID THYMIDYLATE SYNTHASE EXPRESSION; MACHINE LEARNING APPLICATIONS;
   COLON-CANCER; PROTEOGENOMIC CHARACTERIZATION; THYMIDINE PHOSPHORYLASE;
   MASS-SPECTROMETRY; CELL-LINE; TOF MS; 5-FLUOROURACIL; CHEMOTHERAPY
AB Introduction: Despite advances in screening and treatment options, colorectal cancer (CRC) remains one of the most prevalent and lethal cancer subtypes. Resistance to cytotoxic or targeted therapy has remained a constant challenge to the treatment and long-term management of patients, attracting intense worldwide investigation since the 1950s. Through extensive investigations into the proteomic mechanisms and functions that convey resistance to therapy/s, researchers have become able to implicate alterations in several signaling pathways that provide and sustain resistance to treatment. Areas covered: In this review, we summarize how protein alterations are associated with resistance to therapy, with particular emphasis on CRC. An overview of the mechanisms of therapeutic resistance is described, highlighting recent studies which endeavor to elucidate the proteomic changes that are associated with the acquisition and promulgation of therapeutic resistance. Expert opinion: While cancers such as CRC have been intensively studied for decades, unresponsiveness and the resistance to therapy remain critical obstacles in the treatment of patients. Due to the inherent biological and clinical heterogeneity of individual CRCs, proteomic methods stand to become powerful tools to provide biological insights that may guide therapeutic strategies with the ultimate goal of refining emergent immunotherapeutic treatments.
C1 [Cantor, David I.] Macquarie Univ, Australian Proteome Anal Facil, Rm 437,Bldg 4WW, Sydney, NSW 2109, Australia.
   [Cheruku, Harish R.] PRA Hlth Sci, Sydney, NSW, Australia.
   [Westacott, Jack; Mohamedali, Abidali] Macquarie Univ, Fac Sci & Engn, Sydney, NSW, Australia.
   [Shin, Joo-Shik] Univ Sydney, Royal Prince Alfred Hosp, Tissue Pathol & Diagnost Oncol, Sydney, NSW, Australia.
   [Shin, Joo-Shik] Univ Sydney, Fac Med, Sydney, NSW, Australia.
   [Ahn, Seong Boem] Macquarie Univ, Fac Hlth & Med Sci, Sydney, NSW, Australia.
C3 Macquarie University; Macquarie University; University of Sydney; NSW
   Health; Royal Prince Alfred Hospital; University of Sydney; Macquarie
   University
RP Cantor, DI (corresponding author), Macquarie Univ, Australian Proteome Anal Facil, Rm 437,Bldg 4WW, Sydney, NSW 2109, Australia.
EM david.cantor@mq.edu.au
RI Mohamedali, Abidali/AGZ-8179-2022
OI Ahn, Seong Beom/0000-0001-5907-3544; Mohamedali,
   Abidali/0000-0001-5627-4105
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NR 117
TC 11
Z9 11
U1 0
U2 22
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1478-9450
EI 1744-8387
J9 EXPERT REV PROTEOMIC
JI Expert Rev. Proteomics
PD JAN 2
PY 2020
VL 17
IS 1
BP 49
EP 65
DI 10.1080/14789450.2020.1713103
EA JAN 2020
PG 17
WC Biochemical Research Methods
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA KH0FX
UT WOS:000507813900001
PM 31914823
DA 2025-01-04
ER

PT J
AU Siraj, AK
   Parvathareddy, SK
   Annaiyappanaidu, P
   Haqawi, W
   Al-Rasheed, M
   AlManea, HM
   AlHussaini, HF
   Al-Dayel, F
   Al-Kuraya, KS
AF Siraj, Abdul K.
   Parvathareddy, Sandeep Kumar
   Annaiyappanaidu, Padmanaban
   Haqawi, Wael
   Al-Rasheed, Maha
   AlManea, Hadeel M.
   AlHussaini, Hussah F.
   Al-Dayel, Fouad
   Al-Kuraya, Khawla S.
TI PD-L1 Expression Is Associated with Deficient Mismatch Repair and Poor
   Prognosis in Middle Eastern Colorectal Cancers
SO JOURNAL OF PERSONALIZED MEDICINE
LA English
DT Article
DE PD-L1; colorectal cancer; mismatch repair; prognosis
ID DEATH-LIGAND 1; TUMOR-INFILTRATING LYMPHOCYTES; PAPILLARY
   THYROID-CANCER; MICROSATELLITE INSTABILITY; SAUDI-ARABIA; IMPACT;
   PREVALENCE; MUTATIONS; NIVOLUMAB; BLOCKADE
AB Several clinical trials are investigating the use of immune-targeted therapy with Programmed death ligand-1 (PD-L1) inhibitors for colorectal cancer (CRC), with promising results for patients with mismatch repair (MMR) deficiency or metastatic CRC. However, the prognostic significance of PD-L1 expression in CRC is controversial and such data are lacking in CRC from Middle Eastern ethnicity. We carried out this large retrospective study to investigate the prognostic and clinico-pathological impact of PD-L1 expression in Middle Eastern CRC using immunohistochemistry. A total of 1148 CRC were analyzed for PD-L1 expression. High PD-L1 expression was noted in 37.3% (428/1148) cases and was correlated with aggressive clinico-pathological features such as high malignancy grade (p < 0.0001), larger tumor size (p = 0.0007) and mucinous histology (p = 0.0005). Interestingly, PD-L1 expression was significantly higher in patients exhibiting MMR deficiency (p = 0.0169) and BRAF mutation (p = 0.0008). Furthermore, the expression of PD-L1 was found to be an independent marker for overall survival (HR = 1.45; 95% CI = 1.06-1.99; p = 0.0200). In conclusion, the results of this study indicate that PD-L1 expression could be a valid biomarker for poor prognosis in Middle Eastern CRC patients. This information can help in decision-making for anti-PD-L1 therapy in Middle Eastern CRC, especially for patients with MMR deficient tumors.
C1 [Siraj, Abdul K.; Parvathareddy, Sandeep Kumar; Annaiyappanaidu, Padmanaban; Haqawi, Wael; Al-Rasheed, Maha; Al-Kuraya, Khawla S.] King Faisal Specialist Hosp & Res Ctr, Res Ctr, Human Canc Genom Res, POB 3354, Riyadh 11211, Saudi Arabia.
   [AlManea, Hadeel M.; AlHussaini, Hussah F.; Al-Dayel, Fouad] King Faisal Specialist Hosp & Res Ctr, Dept Pathol, POB 3354, Riyadh 11211, Saudi Arabia.
C3 King Faisal Specialist Hospital & Research Center; King Faisal
   Specialist Hospital & Research Center
RP Al-Kuraya, KS (corresponding author), King Faisal Specialist Hosp & Res Ctr, Res Ctr, Human Canc Genom Res, POB 3354, Riyadh 11211, Saudi Arabia.
EM asiraj@kfshrc.edu.sa; psandeepkumar@kfshrc.edu.sa;
   pannaiyappanaidu97@kfshrc.edu.sa; whaqawi@kfshrc.edu.sa;
   mrasheed@kfshrc.edu.sa; halmanea@kfshrc.edu.sa;
   halhussaini@kfshrc.edu.sa; dayelf@kfshrc.edu.sa; kkuraya@kfshrc.edu.sa
RI Parvathareddy, Sandeep Kumar/JBI-9330-2023; Siraj, Abdul/IQW-1179-2023;
   Alrasheed, Maha/AGZ-9897-2022; Alkuraya, Khawla/AFQ-7946-2022
OI Alkuraya, Khawla/0000-0002-4126-3419; Al Dayel,
   Fouad/0000-0001-6175-9051
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NR 52
TC 9
Z9 9
U1 2
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4426
J9 J PERS MED
JI J. Pers. Med.
PD FEB
PY 2021
VL 11
IS 2
AR 73
DI 10.3390/jpm11020073
PG 10
WC Health Care Sciences & Services; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Health Care Sciences & Services; General & Internal Medicine
GA QN8JU
UT WOS:000622699300001
PM 33530623
OA gold, Green Published
DA 2025-01-04
ER

PT S
AU Goulet, CR
   Pouliot, F
AF Goulet, Cassandra Ringuette
   Pouliot, Frederic
BE Birbrair, A
TI TGFβ Signaling in the Tumor Microenvironment
SO TUMOR MICROENVIRONMENT: SIGNALING PATHWAYS, PT B
SE Advances in Experimental Medicine and Biology
LA English
DT Article; Book Chapter
DE TGF beta; TGF beta R; Tumor; Microenvironment; Epithelial-mesenchymal
   transition; Invasion; Metastasis; Metastatic niche; Angiogenesis;
   Cancer-associated fibroblast; Immune cells; Extracellular matrix; Matrix
   remodeling; Targeted therapy; TGF beta pathway inhibitors
ID TRANSFORMING-GROWTH-FACTOR; CANCER-ASSOCIATED FIBROBLASTS;
   EPITHELIAL-MESENCHYMAL TRANSITION; I KINASE INHIBITOR; SQUAMOUS-CELL
   CARCINOMA; RECEPTOR-TYPE-II; BREAST-CANCER; THERAPEUTIC TARGET;
   COLORECTAL-CANCER; MYOFIBROBLAST DIFFERENTIATION
AB Transforming growth factor beta (TGF beta) is a pleiotropic growth factor. Under normal physiological conditions, TGF beta maintains homeostasis in mammalian tissues by restraining the growth of cells and stimulating apoptosis. However, the role of TGF beta signaling in the carcinogenesis is complex. TGF beta acts as a tumor suppressor in the early stages of disease and as a tumor promoter in its later stages where cancer cells have been relieved from TGF beta growth controls. Overproduction of TGF beta by cancer cells lead to a local fibrotic and immune-suppressive microenvironment that fosters tumor growth and correlates with invasive and metastatic behavior of the cancer cells. Here, we present an overview of the complex biology of the TGF beta family, and we discuss the roles of TGF beta signaling in carcinogenesis and how this knowledge is being leveraged to develop TGF beta inhibition therapies against the tumor.
C1 [Goulet, Cassandra Ringuette; Pouliot, Frederic] CHU Quebec Res Ctr, Div Oncol, Quebec City, PQ, Canada.
   [Goulet, Cassandra Ringuette; Pouliot, Frederic] Laval Univ, Fac Med, Dept Surg, Quebec City, PQ, Canada.
   [Pouliot, Frederic] Laval Univ, CHU Quebec Res Ctr, Dept Surg, Quebec City, PQ, Canada.
C3 Laval University; Laval University
RP Pouliot, F (corresponding author), CHU Quebec Res Ctr, Div Oncol, Quebec City, PQ, Canada.; Pouliot, F (corresponding author), Laval Univ, Fac Med, Dept Surg, Quebec City, PQ, Canada.; Pouliot, F (corresponding author), Laval Univ, CHU Quebec Res Ctr, Dept Surg, Quebec City, PQ, Canada.
EM frederic.pouliot@crchudequebec.ulaval.ca
OI Pouliot, Frederic/0000-0002-6651-1079
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NR 180
TC 13
Z9 14
U1 1
U2 31
PU SPRINGER INTERNATIONAL PUBLISHING AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 0065-2598
EI 2214-8019
BN 978-3-030-47189-7; 978-3-030-47188-0
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 2021
VL 1270
BP 89
EP 105
DI 10.1007/978-3-030-47189-7_6
D2 10.1007/978-3-030-47189-7
PG 17
WC Biochemistry & Molecular Biology; Oncology
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA BQ5AB
UT WOS:000595857200007
PM 33123995
DA 2025-01-04
ER

PT J
AU Torresano, L
   Nuevo-Tapioles, C
   Santacatterina, F
   Cuezva, JM
AF Torresano, Laura
   Nuevo-Tapioles, Cristina
   Santacatterina, Fulvio
   Cuezva, Jose M.
TI Metabolic reprogramming and disease progression in cancer patients
SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
LA English
DT Review
DE ATP synthase; ATPase inhibitory factor 1; Enzyme biomarkers; Metabolism;
   Mitochondria patients' survival; Reverse phase protein arrays
ID ATPASE INHIBITORY FACTOR-1; BETA-F1-ATPASE MESSENGER-RNA;
   EPITHELIAL-MESENCHYMAL TRANSITION; PREDICTS POOR-PROGNOSIS; AGGRESSIVE
   CLINICOPATHOLOGICAL FEATURES; PROMOTES TUMOR PROGRESSION;
   PYRUVATE-KINASE M2; OXIDATIVE-PHOSPHORYLATION; COLORECTAL-CANCER;
   BREAST-CANCER
AB Genomics has contributed to the treatment of a fraction of cancer patients. However, there is a need to profile the proteins that define the phenotype of cancer and its pathogenesis. The reprogramming of metabolism is a major trait of the cancer phenotype with great potential for prognosis and targeted therapy. This review overviews the major changes reported in the steady-state levels of proteins of metabolism in primary carcinomas, paying attention to those enzymes that correlate with patients' survival. The upregulation of enzymes of glycolysis, pentose phosphate pathway, lipogenesis, glutaminolysis and the antioxidant defense is concurrent with the downregulation of mitochondrial proteins involved in oxidative phosphorylation, emphasizing the potential of mitochondrial metabolism as a promising therapeutic target in cancer. We stress that high-throughput quantitative expression profiling of differentially expressed proteins in large cohorts of carcinomas paired with normal tissues will accelerate translation of metabolism to a successful personalized medicine in cancer.
C1 [Torresano, Laura; Nuevo-Tapioles, Cristina; Santacatterina, Fulvio; Cuezva, Jose M.] CSIC UAM, Ctr Biol Mol Severo Ochoa, Dept Biol Mol, Madrid, Spain.
   [Torresano, Laura; Nuevo-Tapioles, Cristina; Santacatterina, Fulvio; Cuezva, Jose M.] ISCIII, CIBERER, Madrid 28049, Spain.
   [Torresano, Laura; Nuevo-Tapioles, Cristina; Santacatterina, Fulvio; Cuezva, Jose M.] Univ Autonoma Madrid, Inst Invest Hosp 12 Octubre, Madrid 28049, Spain.
C3 Consejo Superior de Investigaciones Cientificas (CSIC); CSIC - Centro de
   Biologia Molecular Severo Ochoa (CBM); CIBER - Centro de Investigacion
   Biomedica en Red; CIBERER; Instituto de Salud Carlos III; Hospital
   Universitario 12 de Octubre; Autonomous University of Madrid
RP Cuezva, JM (corresponding author), Univ Autonoma Madrid, Ctr Biol Mol Severo Ochoa, E-28049 Madrid, Spain.
EM jmcuezva@cbm.csic.es
RI Cuezva, Jose/AAR-5392-2020; Nuevo-Tapioles, Cristina/AAT-5772-2021;
   Santacatterina, Fulvio/F-5722-2016
OI Nuevo-Tapioles, Cristina/0000-0001-5809-2030
FU FPI-MINECO; Fondo Social Europeo; MINECO [SAF2016-75916-R]; Fundacion
   Ramon Areces, Spain; CIBERER-ISCIII [CB06/07/0017]
FX We thank Mrs. A. Gray for proofreading and English editing. LT and CNT
   were supported by predoctoral fellowships from FPI-MINECO and Fondo
   Social Europeo, respectively. The work was supported by grants from
   MINECO (SAF2016-75916-R), CIBERER-ISCIII (CB06/07/0017) and Fundacion
   Ramon Areces, Spain.
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NR 260
TC 48
Z9 50
U1 1
U2 29
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0925-4439
EI 1879-260X
J9 BBA-MOL BASIS DIS
JI Biochim. Biophys. Acta-Mol. Basis Dis.
PD MAY 1
PY 2020
VL 1866
IS 5
AR 165721
DI 10.1016/j.bbadis.2020.165721
PG 16
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA LG2PL
UT WOS:000527949200021
PM 32057942
OA Bronze
DA 2025-01-04
ER

PT J
AU Xu, JJ
   Huang, LY
   Sha, Y
   Mo, C
   Gong, WW
   Tian, XY
   Hou, XL
   Chen, W
   Ou, ML
AF Xu, Jiajun
   Huang, Lingyu
   Sha, Yu
   Mo, Chune
   Gong, Weiwei
   Tian, Xiayu
   Hou, Xianliang
   Chen, Wei
   Ou, Minglin
TI High-throughput sequencing reveals crebanine inhibits colorectal cancer
   by modulating Tregs immune prognostic target genes
SO ONCOLOGIE
LA English
DT Article
DE crebanine; regulatory T cells; colorectal cancer; high-throughput
   sequencing; prognosis
ID O-METHYLBULBOCAPNINE; GROWTH
AB Objectives: Crebanine, an alkaloid exhibiting sedative, anti-inflammatory, and anticancer properties, remains unexplored in terms of its anticancer potential against colorectal cancer (CRC). This study aims to bridge this knowledge gap, specifically investigating whether crebanine can suppress CRC and elucidating its underlying molecular mechanism.
   Methods: We employed the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) assay, cell scratch assay, and flow cytometry to observe the effects of crebanine on the growth, migration, and apoptosis of CRC SW480 cells, respectively. High-throughput sequencing was employed to detect differentially expressed genes (DEGs) in SW480 cells treated with crebanine. Enriched pathways of these DEGs were identified through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Genes exhibiting the highest correlation in the enriched pathway were further analyzed using clinical data from The Cancer Genome Atlas Program (TCGA) public database, utilizing R software.
   Results: Crebanine effectively inhibited the proliferation, migration, and invasion of SW480 cells, with concentrations of >= 15 mu g/mL promoting apoptosis. Analysis revealed that the function of DEGs linked to the most enriched pathways was associated with immune infiltration by regulatory T cells (Tregs). When analyzed in conjunction with clinical data, the genes exhibiting the highest correlation in the enrichment pathway were found to be directly associated with clinical prognostic survival.
   Conclusions: Our study demonstrates that crebanine inhibits colorectal cancer by regulating prognostic target genes related to Tregs. This finding offers a novel approach for pharmacological inhibition and Tregs-targeted therapy in CRC.
C1 [Xu, Jiajun; Huang, Lingyu; Sha, Yu; Mo, Chune; Gong, Weiwei; Tian, Xiayu; Hou, Xianliang; Ou, Minglin] Guilin Med Univ, Affiliated Hosp 2, Lab Ctr, Guangxi Hlth Commiss,Key Lab Glucose & Lipid Meta, Guilin, Peoples R China.
   [Xu, Jiajun; Huang, Lingyu; Sha, Yu; Mo, Chune; Gong, Weiwei; Tian, Xiayu; Hou, Xianliang; Ou, Minglin] Guilin Med Univ, Guangxi Key Lab Metab Reprogramming & Intelligent, Guilin, Peoples R China.
   [Chen, Wei] Guilin Med Univ, Dept Gastrointestinal Surg, Affiliated Hosp 2, Guilin, Peoples R China.
C3 Guilin Medical University; Guilin Medical University; Guilin Medical
   University
RP Ou, ML (corresponding author), Guilin Med Univ, Affiliated Hosp 2, Lab Ctr, Guangxi Hlth Commiss,Key Lab Glucose & Lipid Meta, Guilin, Peoples R China.; Ou, ML (corresponding author), Guilin Med Univ, Guangxi Key Lab Metab Reprogramming & Intelligent, Guilin, Peoples R China.
EM minglinou@glmc.edu.cn
RI zhu, yujie/KBC-4009-2024; Hou, Xianliang/IXN-8243-2023; Liu,
   Yuling/HGV-1868-2022; Li, Yingrui/K-1064-2015; Sha, Yu/KOC-3542-2024
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NR 50
TC 1
Z9 1
U1 3
U2 3
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1292-3818
EI 1765-2839
J9 ONCOLOGIE
JI Oncologie
PD AUG 2
PY 2024
VL 26
IS 4
BP 643
EP 656
DI 10.1515/oncologie-2024-0073
EA MAY 2024
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA A5Z1A
UT WOS:001221882900001
OA hybrid
DA 2025-01-04
ER

PT J
AU Matsuoka, T
   Yashiro, M
AF Matsuoka, Tasuku
   Yashiro, Masakazu
TI The Role of the Transforming Growth Factor-β Signaling Pathway in
   Gastrointestinal Cancers
SO BIOMOLECULES
LA English
DT Review
DE transforming growth factor-beta; smad; gastrointestinal cancers;
   epithelial-mesenchymal transition; tumor microenvironment; immune
   evasion; targeted therapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; TARGETING TGF-BETA;
   HEPATOCELLULAR-CARCINOMA; NONCODING RNA; DOWN-REGULATION; STEM-CELLS;
   CARDIOVASCULAR TOXICITY; TUMOR MICROENVIRONMENT; PROMOTES PROLIFERATION;
   COLORECTAL-CANCER
AB Transforming growth factor-beta (TGF-beta) has attracted attention as a tumor suppressor because of its potent growth-suppressive effect on epithelial cells. Dysregulation of the TGF-beta signaling pathway is considered to be one of the key factors in carcinogenesis, and genetic alterations affecting TGF-beta signaling are extraordinarily common in cancers of the gastrointestinal system, such as hereditary nonpolyposis colon cancer and pancreatic cancer. Accumulating evidence suggests that TGF-beta is produced from various types of cells in the tumor microenvironment and mediates extracellular matrix deposition, tumor angiogenesis, the formation of CAFs, and suppression of the anti-tumor immune reaction. It is also being considered as a factor that promotes the malignant transformation of cancer, particularly the invasion and metastasis of cancer cells, including epithelial-mesenchymal transition. Therefore, elucidating the role of TGF-beta signaling in carcinogenesis, cancer invasion, and metastasis will provide novel basic insight for diagnosis and prognosis and the development of new molecularly targeted therapies for gastrointestinal cancers. In this review, we outline an overview of the complex mechanisms and functions of TGF-beta signaling. Furthermore, we discuss the therapeutic potentials of targeting the TGF-beta signaling pathway for gastrointestinal cancer treatment and discuss the remaining challenges and future perspectives on targeting this pathway.
C1 [Matsuoka, Tasuku; Yashiro, Masakazu] Osaka Metropolitan Univ, Grad Sch Med, Mol Oncol & Therapeut, Osaka, Osaka 5458585, Japan.
C3 Osaka Metropolitan University
RP Yashiro, M (corresponding author), Osaka Metropolitan Univ, Grad Sch Med, Mol Oncol & Therapeut, Osaka, Osaka 5458585, Japan.
EM t22738q@omu.ac.jp; i21496f@omu.ac.jp
OI Matsuoka, Tasuku/0000-0001-5019-8519
FU KAKENHI [18H02883]
FX This research was funded by the KAKENHI (Grant-in-Aid for Scientific
   Research),No. 18H02883.
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NR 204
TC 6
Z9 6
U1 0
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2218-273X
J9 BIOMOLECULES
JI Biomolecules
PD OCT
PY 2023
VL 13
IS 10
AR 1551
DI 10.3390/biom13101551
PG 26
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA X4QP2
UT WOS:001098316200001
PM 37892233
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ramos, H
   Soares, MIL
   Silva, J
   Raimundo, L
   Calheiros, J
   Gomes, C
   Reis, F
   Monteiro, FA
   Nunes, C
   Reis, S
   Bosco, B
   Piazza, S
   Domingues, L
   Chlapek, P
   Vlcek, P
   Fabian, P
   Rajado, AT
   Carvalho, ATP
   Veselska, R
   Inga, A
   Melo, TMVDPE
   Saraiva, L
AF Ramos, Helena
   Soares, Maria I. L.
   Silva, Joana
   Raimundo, Liliana
   Calheiros, Juliana
   Gomes, Celia
   Reis, Flavio
   Monteiro, Filipe A.
   Nunes, Claudia
   Reis, Salette
   Bosco, Bartolomeo
   Piazza, Silvano
   Domingues, Lucilia
   Chlapek, Petr
   Vlcek, Petr
   Fabian, Pavel
   Rajado, Ana Teresa
   Carvalho, A. T. P.
   Veselska, Renata
   Inga, Alberto
   Melo, Teresa M. V. D. Pinho E.
   Saraiva, Lucilia
TI A selective p53 activator and anticancer agent to improve colorectal
   cancer therapy
SO CELL REPORTS
LA English
DT Article
ID GAIN-OF-FUNCTION; MUTANT P53; IN-VITRO; HUMAN-COLON; IMAGE;
   PATHOGENESIS; REACTIVATION; VALIDATION; SOLUBILITY; REPRESSION
AB Impairment of the p53 pathway is a critical event in cancer. Therefore, reestablishing p53 activity has become one of the most appealing anticancer therapeutic strategies. Here, we disclose the p53-activating anticancer drug (3S)-6,7-bis(hydroxymethyl)-5-methyl-3-phenyl-1H,3H-pyrrolo[1,2-c]thiazole (MANIO). MANIO demonstrates a notable selectivity to the p53 pathway, activating wild-type (WT)p53 and restoring WT-like function to mutant (mut)p53 in human cancer cells. MANIO directly binds to the WT/mutp53 DNA-binding domain, enhancing the protein thermal stability, DNA-binding ability, and transcriptional activity. The high efficacy of MANIO as an anticancer agent toward cancers harboring WT/mutp53 is further demonstrated in patient-derived cells and xenograft mouse models of colorectal cancer (CRC), with no signs of undesirable side effects. MANIO synergizes with conventional chemotherapeutic drugs, and in vitro and in vivo studies predict its adequate drug-likeness and pharmacokinetic properties for a clinical candidate. As a single agent or in combination, MANIO will advance anticancer-targeted therapy, particularly benefiting CRC patients harboring distinct p53 status.
C1 [Ramos, Helena; Raimundo, Liliana; Calheiros, Juliana; Saraiva, Lucilia] Univ Porto, Fac Farm, Dept Ciencias Biol, Lab Microbiol,LAQV REQUIMTE, Porto, Portugal.
   [Soares, Maria I. L.; Melo, Teresa M. V. D. Pinho E.] Univ Coimbra, Coimbra Chem Ctr, P-3004535 Coimbra, Portugal.
   [Soares, Maria I. L.; Melo, Teresa M. V. D. Pinho E.] Univ Coimbra, Dept Chem, P-3004535 Coimbra, Portugal.
   [Silva, Joana; Domingues, Lucilia] Univ Minho, CEB Ctr Biol Engn, Campus Gualtar, P-4710057 Braga, Portugal.
   [Gomes, Celia; Reis, Flavio] Univ Coimbra, Coimbra Inst Clin & Biomed Res iCBR, Fac Med, Coimbra, Portugal.
   [Gomes, Celia; Reis, Flavio] Univ Porto, Ctr Innovat Biomed & Biotechnol CIBB, Coimbra, Portugal.
   [Gomes, Celia; Reis, Flavio] Clin Acad Ctr Coimbra CACC, Coimbra, Portugal.
   [Monteiro, Filipe A.] Univ Porto, Fac Med, Unidade Biol Expt, Dept Biomed,FMUP, P-4200319 Porto, Portugal.
   [Monteiro, Filipe A.] IBMC Inst Biol Celular & Mol, Pain Res Grp, P-4150180 Porto, Portugal.
   [Monteiro, Filipe A.] Univ Porto, i3S Inst Invest & Inovacao Saude, P-4150180 Porto, Portugal.
   [Nunes, Claudia; Reis, Salette] Univ Porto, Fac Farm, Dept Ciencias Quim, Lab Quim Aplicada,LAQV REQUIMTE, Porto, Portugal.
   [Bosco, Bartolomeo; Piazza, Silvano; Inga, Alberto] Univ Trento, Lab Transcript Networks, Dept CIBIO, Via Sommar 9, I-38123 Trento, Italy.
   [Chlapek, Petr; Veselska, Renata] Masaryk Univ, Dept Expt Biol, Lab Tumor Biol, Brno, Czech Republic.
   [Chlapek, Petr; Veselska, Renata] St Annes Univ Hosp, Int Clin Res Ctr, Brno, Czech Republic.
   [Vlcek, Petr] St Annes Univ Hosp, Dept Surg 1, Brno, Czech Republic.
   [Fabian, Pavel] Masaryk Mem Canc Inst, Dept Ontol & Expt Pathol, Brno, Czech Republic.
   [Rajado, Ana Teresa; Carvalho, A. T. P.] Univ Coimbra, CNC Ctr Neurosci & Cell Biol, P-3004504 Coimbra, Portugal.
C3 Universidade do Porto; Universidade de Coimbra; Universidade de Coimbra;
   Universidade do Minho; Universidade de Coimbra; Universidade de Coimbra;
   Universidade do Porto; Universidade de Coimbra; Universidade do Porto;
   Universidade do Porto; i3S - Instituto de Investigacao e Inovacao em
   Saude, Universidade do Porto; Universidade do Porto; University of
   Trento; Masaryk University Brno; St. Anne's University Hospital Brno
   (FNUSA); St. Anne's University Hospital Brno (FNUSA-ICRC); St. Anne's
   University Hospital Brno (FNUSA); Masaryk Memorial Cancer Institute;
   Universidade de Coimbra
RP Saraiva, L (corresponding author), Univ Porto, Fac Farm, Dept Ciencias Biol, Lab Microbiol,LAQV REQUIMTE, Porto, Portugal.; Melo, TMVDPE (corresponding author), Univ Coimbra, Coimbra Chem Ctr, P-3004535 Coimbra, Portugal.; Melo, TMVDPE (corresponding author), Univ Coimbra, Dept Chem, P-3004535 Coimbra, Portugal.
EM tmelo@ci.uc.pt; lucilia.saraiva@ff.up.pt
RI Chlapek, Petr/AAD-2657-2022; Raimundo, Liliana/AAN-9892-2020; Piazza,
   Silvano/LOS-0977-2024; Inga, Alberto/AAC-3815-2022; Saraiva,
   Lucília/D-4897-2013; Veselska, Renata/L-7661-2016; Reis,
   Flávio/E-7077-2016; Monteiro, Filipe/N-8479-2018; Calheiros,
   Juliana/AAG-9714-2019; Gomes, Celia/HZK-6179-2023; Nunes,
   Claudia/A-9173-2013; Pinho e Melo, Teresa/N-3325-2015; Domingues,
   Lucilia/B-2191-2010; Reis, Salette/A-9613-2013; Soares,
   Maria/C-6746-2011
OI Monteiro, Filipe/0000-0003-0670-3658; Reis, Flavio/0000-0003-3401-9554;
   Chlapek, Petr/0000-0002-7274-897X; Calheiros,
   Juliana/0000-0001-5895-6951; Gomes, Celia/0000-0002-7497-4129; Bosco,
   Bartolomeo/0000-0002-3069-714X; Nunes, Claudia/0000-0002-1502-3710;
   Pinho e Melo, Teresa/0000-0003-3256-4954; Rajado, Ana
   Teresa/0000-0002-3669-3780; Silva, Joana/0000-0001-6796-7070; Domingues,
   Lucilia/0000-0003-1089-7627; Veselska, Renata/0000-0002-0048-9913; Reis,
   Salette/0000-0002-0736-2835; Ramos, Helena/0000-0001-5546-9998; Saraiva,
   Lucilia/0000-0002-9531-4939; Soares, Maria/0000-0001-8860-0470; Piazza,
   Silvano/0000-0002-7156-5434
FU PT national funds (FCT/MCTES, Fundacao para a Ciencia e a Tecnologia,
   and Ministerio da Ciencia, Tecnologia e Ensino Superior)
   [UIDB/50006/2020, UID/BIO/04469/2019, UIDB/04539/2020, UIDP/04539/2020];
   European Regional Development Fund under the Norte2020 -Programa
   Operacional Regional do Norte [NORTE-01-0145-FEDER000004,
   Norte-01-0145-FEDER-000008]; Masaryk University [MUNI/A/1127/2019];
   Ministry of Education, Youth and Sports of the Czech Republic [LQ1605,
   LM2018125]; FCT [SFRH/BD/119144/2016, SFRH/BD/117949/2016]; Fondazione
   AIRC [18985]; Programa Operacional Potencial Humano (POCH); PT National
   Funds (FCT/MCTES, Fundacao para a Ciencia e Tecnologia, and Ministerio
   da Ciencia, Tecnologia e Ensino Superior) [UIDB/50006/2020,
   UIDB/00313/2020, UIDP/00313/2020]; COMPETE2020-UE; BiotechHealth
   Programme (Doctoral Programme on Cellular and Molecular Biotechnology
   Applied to Health Sciences) [PD/00016/2012]; Fundação para a Ciência e a
   Tecnologia [SFRH/BD/117949/2016, SFRH/BD/119144/2016,
   UID/BIO/04469/2019] Funding Source: FCT
FX We thank PT national funds (FCT/MCTES, Fundacao para a Ciencia e a
   Tecnologia, and Ministerio da Ciencia, Tecnologia e Ensino Superior)
   through grants UIDB/50006/2020, UID/BIO/04469/2019, UIDB/04539/2020, and
   UIDP/04539/2020 (CIBB); BioTecNorte operation
   (NORTE-01-0145-FEDER000004) and Porto Neurosciences and Neurologic
   Disease Research Initiative at I3S (Norte-01-0145-FEDER-000008) funded
   by the European Regional Development Fund under the scope of Norte2020
   -Programa Operacional Regional do Norte; Masaryk University (Project
   MUNI/A/1127/2019) and Ministry of Education, Youth and Sports of the
   Czech Republic (project nos. LQ1605 and LM2018125); FCT financial
   support through the fellowships SFRH/BD/119144/2016 (H.R.) and
   SFRH/BD/117949/2016 (L.R.); Fondazione AIRC (IG#18985, A.I.); and the
   Programa Operacional Potencial Humano (POCH), specifically the
   BiotechHealth Programme (Doctoral Programme on Cellular and Molecular
   Biotechnology Applied to Health Sciences, PD/00016/2012). We thank Dario
   Rizzotto for assistance in preparing the libraries for RNA sequencing.
   Funding: This work was supported by PT National Funds (FCT/MCTES,
   Fundacao para a Ciencia e Tecnologia, and Ministerio da Ciencia,
   Tecnologia e Ensino Superior) via the projects UIDB/50006/2020
   (LAQV/REQUIMTE), UIDB/00313/2020, and UIDP/00313/2020, co-funded by
   COMPETE2020-UE.
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NR 71
TC 27
Z9 30
U1 0
U2 21
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD APR 13
PY 2021
VL 35
IS 2
AR 108982
DI 10.1016/j.celrep.2021.108982
EA APR 2021
PG 24
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA RN1PW
UT WOS:000640127100021
PM 33852837
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Lee, SJ
   Lee, J
   Park, SH
   Park, JO
   Lim, HY
   Kang, WK
   Park, YS
   Kim, ST
AF Lee, Su Jin
   Lee, Jeeyun
   Park, Se Hoon
   Park, Joon Oh
   Lim, Ho Yeong
   Kang, Won Ki
   Park, Young Suk
   Kim, Seung Tae
TI c-MET Overexpression in Colorectal Cancer: A Poor Prognostic Factor for
   Survival
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE c-MET; Colorectal cancer; Immunohistochemistry; Prognosis
ID GENE AMPLIFICATION; RECEPTOR; EXPRESSION; ANGIOGENESIS; CHEMOTHERAPY;
   BEVACIZUMAB; METASTASIS; INHIBITORS; MUTATIONS; CETUXIMAB
AB Mesenchymal-epithelial transition factor gene (c-MET) overexpression might be an important biomarker in colorectal cancer (CRC). We evaluated the incidence of c-MET overexpression and its prognostic significance in 255 patients with metastatic CRC. We found that 15.3% had c-MET overexpression and c-MET overexpression was associated with shorter survival.
   Introduction: Increased mesenchymal-epithelial transition factor gene (c-MET) expression in several human malignancies is related to increased tumor progression and is a new potential drug target for several types of cancers. In the present study, we investigated the incidence of c-MET overexpression and its prognostic significance in patients with colorectal cancer (CRC). Patients and Methods: We retrospectively reviewed the data from 255 stage IV CRC patients who had results from a c-MET immunohistochemical test at Samsung Medical Center. We explored the relationships between c-MET overexpression and clinicopathological features and survival. Results: Primary tumor sites were 67 right-sided colon, 98 left-sided colon, and 90 rectum. Forty-two patients (16.7%) had poorly differentiated or mucinous carcinoma. Among the 255 patients, 39 (15.3%) exhibited c-MET overexpression. There was no significant difference in the prevalence of c-MET overexpression according to primary site, histologic differentiation, molecular markers, or metastatic sites. In a comparison of the tumor response to first-line chemotherapy according to the level of c-MET expression, we found no significant difference in either partial response or disease control rate. In the survival analysis, patients with c-MET overexpression had significantly shorter overall survival (39 vs. 27 months; P=.018) and progression-free survival (PFS) during bevacizumab treatment (10 vs. 7 months; P=.024). Conclusion: c-MET overexpression, which was detected in 39 CRC patients (15.3%) irrespective of primary sites or molecular markers, indicated a poor survival prognosis and predicted shorter PFS during bevacizumab treatment in patients with CRC. Further studies are warranted to elucidate the value of ceMET-targeted therapy in CRC patients. (C) 2018 The Authors. Published by Elsevier Inc.
C1 [Lee, Su Jin; Lee, Jeeyun; Park, Se Hoon; Park, Joon Oh; Lim, Ho Yeong; Kang, Won Ki; Park, Young Suk; Kim, Seung Tae] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Div Hematol Oncol,Dept Med, 81 Irwon Ro, Seoul 06351, 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 shty1@skku.edu
RI Lee, Su Hwan/R-6161-2019; kim, st/O-5928-2014; Lee, Jee/C-9646-2011;
   Park, Se Hoon/GMX-1199-2022; Lim, Ho Yeong/KBA-8868-2024; Park,
   Susan/JRY-5671-2023; Kim, Kyunga/LCL-2839-2024
OI Lee, Su Jin/0000-0003-3405-9935
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NR 31
TC 61
Z9 64
U1 0
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 SEP
PY 2018
VL 17
IS 3
BP 165
EP 169
DI 10.1016/j.clcc.2018.02.013
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GR5KI
UT WOS:000442669400018
PM 29576428
OA hybrid
DA 2025-01-04
ER

PT J
AU Wong, XY
   Lim, AQJ
   Shen, QY
   Chia, JWK
   Chew, MH
   Tan, WS
   Wee, HL
AF Wong, Xin Yi
   Lim, Andrew Qi Jun
   Shen, Qianyu
   Chia, John Whay Kuang
   Chew, Min Hoe
   Tan, Wah Siew
   Wee, Hwee-Lin
TI Patient preferences and predicted relative uptake for targeted therapies
   in metastatic colorectal cancer: a discrete choice experiment
SO CURRENT MEDICAL RESEARCH AND OPINION
LA English
DT Article
DE Targeted therapy; metastatic colorectal cancer; discrete choice
   experiment; patient preferences; relative uptake
ID CONJOINT-ANALYSIS; COLON-CANCER; HEALTH; CHEMOTHERAPY; LUNG
AB Objective Ras wild-type metastatic colorectal cancers (mCRC) may be treated with anti-vascular endothelial growth factor (VEGF) or anti-epidermal growth factor receptor (EGFR) agents. We aim to estimate patients' preferences for mCRC treatment and relative importance of cost, efficacy improvement, avoidance of side effects and therapy convenience, and relative uptake between profiles that resemble Bevacizumab (anti-VEGF) and Cetuximab (anti-EGFR), two commonly prescribed mCRC targeted therapies. Methods Discrete choice experiment (DCE) was administered to English- or Chinese-speaking Stage 2 or 3 colon cancer patients at the National Cancer Centre Singapore. DCE attributes comprise progression-free survival (PFS), severity of acne-like skin rashes, severity of bleeding, out-of-pocket cost per month and frequency of drug administration. Mixed logit model was used to calculate preference weights for all attribute levels. Subgroup analyses were conducted by interacting attribute levels with selected respondent characteristics. Relative uptake rates for various medication scenarios were studied. Results 169 respondents aged 61.5 +/- 10.5 years completed the survey. They placed the greatest weight on cost, followed by bleeding and skin rashes, then PFS and finally frequency of drug administration. This was similarly observed in the subgroup analyses. A scenario with shorter PFS but less severe side effects has a slightly higher relative uptake at 55%. One quarter of respondents reported that they would not take the treatment they preferred in the choice task. Conclusion Patients were willing to trade off some degree of efficacy to avoid certain severity of side effects. It is therefore crucial for patients and physicians to discuss patients' preferences and circumstances to understand which attributes are more important, as well as patients' views on the trade-offs between treatment benefits and risks.
C1 [Wong, Xin Yi; Shen, Qianyu; Wee, Hwee-Lin] Natl Univ Singapore, Fac Sci, Dept Pharm, Singapore, Singapore.
   [Lim, Andrew Qi Jun] Hwa Chong Inst, Coll Sect, NUS Sci Res Programme, Singapore, Singapore.
   [Chia, John Whay Kuang] Natl Canc Ctr Singapore, Div Med Oncol, Singapore, Singapore.
   [Chew, Min Hoe; Tan, Wah Siew] Singapore Gen Hosp, Dept Colorectal Surg, Singapore, Singapore.
   [Wee, Hwee-Lin] Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Tahir Fdn Bldg,12 Sci Dr 2,09-01U, Singapore 117549, Singapore.
C3 National University of Singapore; National Cancer Centre Singapore
   (NCCS); Singapore General Hospital; National University of Singapore
RP Wee, HL (corresponding author), Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Tahir Fdn Bldg,12 Sci Dr 2,09-01U, Singapore 117549, Singapore.
EM weehweelin@nus.edu.sg
RI ; Wee, Hwee Lin/D-4126-2012
OI Wong, Xin Yi/0000-0002-5232-1864; SHEN, QIANYU/0000-0002-7098-8144; Wee,
   Hwee Lin/0000-0002-7150-1801
FU Health Preferences of Colorectal Patients in Singapore
FX We thank A/Prof Lita Chew (Department of Pharmacy, National Cancer
   Centre Singapore [NCCS]) for providing valuable insights and direction
   during the study conception phase. We thank the attending physicians and
   clinic staff at NCCS Clinic D for their kind assistance during study
   recruitment. We also thank Dr Swee Sung Soon, Mr Keegan Lin and Ms Janie
   Lim for their contribution in research administration and Phase 1 data
   collection (funded by "Health Preferences of Colorectal Patients in
   Singapore") and Ms Joy Yau and Ms Isy Yu for their assistance in patient
   screening and data collection in Phase 3. They were funded by indirect
   research costs (cumulative from various grants awarded to Dr Hwee-Lin
   Wee).
CR [Anonymous], 2006, CANC THER EV PROGR T
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NR 38
TC 11
Z9 11
U1 3
U2 15
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0300-7995
EI 1473-4877
J9 CURR MED RES OPIN
JI Curr. Med. Res. Opin.
PD OCT 2
PY 2020
VL 36
IS 10
BP 1677
EP 1686
DI 10.1080/03007995.2020.1790348
EA AUG 2020
PG 10
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA NX8ES
UT WOS:000555241900001
PM 32609014
DA 2025-01-04
ER

PT J
AU Schmitz, K
   Schatz, C
   Knabl, L
AF Schmitz, Katja
   Schatz, Christoph
   Knabl, Ludwig
TI KRAS (Kirsten rat sarcoma) in modern oncology-The molecular pathological
   point of view
SO MEMO-MAGAZINE OF EUROPEAN MEDICAL ONCOLOGY
LA English
DT Review
DE RAS; KRAS; PanRAS; Molecular biology; NGS; Liquid biopsy; Targeted
   therapy
ID COLORECTAL-CANCER; MUTATIONS; BRAF
AB The Rat sarcoma protein (RAS) was the first proto-oncogene to be discovered and is one of the best researched tumor drivers today. The RAS protein family includes the underlying genes KRAS, HRAS (Harvey rat sarcoma), and NRAS (Neuroblastoma rat sarcoma), with the majority of mutations affecting the KRAS gene. Mutations and other genetic alteration promote cell division, cell survival and proliferation. As a result of ever-improving diagnostics and the growing understanding of the role of RAS in tumor development and progression, numerous therapies have been developed in recent years that target either KRAS itself or a protein upstream or downstream in the KRAS pathway. PanRAS inhibitors are promising subjects in clinical trials. There have also been significant improvements in the field of diagnostics due to the emergence of new technologies that allow the genomic material of tumor samples to be decoded quickly and cost-effectively. The correct pathological and clinical understanding of molecular reports generated is essential. Nevertheless, in their current clinical role, KRAS mutations still represent a major challenge for medicine, and intensive research is still needed to optimize the treatment of KRAS mutated tumors.
C1 [Schmitz, Katja; Schatz, Christoph; Knabl, Ludwig] Tyrolpath Obrist Brunhuber GmbH, Zams, Austria.
   [Schmitz, Katja; Knabl, Ludwig] St Vinzenz Hosp, Zams, Austria.
   [Schmitz, Katja] Klostergasse 1, A-6511 Zams, Tyrol, Austria.
RP Schmitz, K (corresponding author), Tyrolpath Obrist Brunhuber GmbH, Zams, Austria.; Schmitz, K (corresponding author), St Vinzenz Hosp, Zams, Austria.; Schmitz, K (corresponding author), Klostergasse 1, A-6511 Zams, Tyrol, Austria.
EM katja.schmitz@tyrolpath.at
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NR 31
TC 0
Z9 0
U1 1
U2 1
PU SPRINGER WIEN
PI Vienna
PA Prinz-Eugen-Strasse 8-10, A-1040 Vienna, AUSTRIA
SN 1865-5041
EI 1865-5076
J9 MEMO-MAG EUR MED ONC
JI Memo-Mag. Eur. Med. Oncol.
PD DEC
PY 2024
VL 17
IS 4
BP 287
EP 291
DI 10.1007/s12254-024-00986-6
EA AUG 2024
PG 5
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA O0A7N
UT WOS:001295750700001
DA 2025-01-04
ER

PT J
AU Jiang, X
   Yu, M
   Wang, WK
   Zhu, LY
   Wang, X
   Jin, HC
   Feng, LF
AF Jiang, Xin
   Yu, Min
   Wang, Wei-kai
   Zhu, Li-yuan
   Wang, Xian
   Jin, Hong-chuan
   Feng, Li-feng
TI The regulation and function of Nrf2 signaling in ferroptosis-activated
   cancer therapy
SO ACTA PHARMACOLOGICA SINICA
LA English
DT Review
DE ferroptosis; nuclear factor E2 related factor 2 (Nrf2); cancer therapy;
   drug resistance; iron metabolism; antioxidant system
ID TRANSCRIPTION FACTOR NRF2; COLORECTAL-CANCER; CELL-DEATH; PATHWAY;
   PROMOTES; IRON; ANTIOXIDANT; RESISTANCE; PHOSPHORYLATION; INACTIVATION
AB Ferroptosis is an iron-dependent programmed cell death process that involves lipid oxidation via the Fenton reaction to produce lipid peroxides, causing disruption of the lipid bilayer, which is essential for cellular survival. Ferroptosis has been implicated in the occurrence and treatment response of various types of cancer, and targeting ferroptosis has emerged as a promising strategy for cancer therapy. However, cancer cells can escape cellular ferroptosis by activating or remodeling various signaling pathways, including oxidative stress pathways, thereby limiting the efficacy of ferroptosis-activating targeted therapy. The key anti-oxidative transcription factor, nuclear factor E2 related factor 2 (Nrf2 or NFE2L2), plays a dominant role in defense machinery by reprogramming the iron, intermediate, and glutathione peroxidase 4 (GPX4)-related network and the antioxidant system to attenuate ferroptosis. In this review, we summarize the recent advances in the regulation and function of Nrf2 signaling in ferroptosis-activated cancer therapy and explore the prospect of combining Nrf2 inhibitors and ferroptosis inducers as a promising cancer treatment strategy.
C1 [Jiang, Xin; Wang, Wei-kai; Zhu, Li-yuan; Wang, Xian; Jin, Hong-chuan; Feng, Li-feng] Zhejiang Univ, Dept Med Oncol, Canc Ctr,Sir Run Run Shaw Hosp,Sch Med, Zhejiang Key Lab Multiprecis Diag & Treatment Live, Hangzhou 310016, Peoples R China.
   [Yu, Min] Zhejiang Univ, Affiliated Jinhua Hosp, Sch Med, Dept Hepatobiliary & Pancreat Surg, Jinhua 321000, Peoples R China.
C3 Zhejiang University; Zhejiang University
RP Jin, HC; Feng, LF (corresponding author), Zhejiang Univ, Dept Med Oncol, Canc Ctr,Sir Run Run Shaw Hosp,Sch Med, Zhejiang Key Lab Multiprecis Diag & Treatment Live, Hangzhou 310016, Peoples R China.
EM jinhc@zju.edu.cn; lffeng@zju.edu.cn
FU National Natural Science Foundation of China [82273092]; Natural Science
   Foundation in Zhejiang province [LD22H160003]
FX This work was supported by the National Natural Science Foundation of
   China (82273092) to LFF and Natural Science Foundation in Zhejiang
   province (LD22H160003) to XW.
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NR 135
TC 2
Z9 2
U1 17
U2 17
PU NATURE PUBL GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1671-4083
EI 1745-7254
J9 ACTA PHARMACOL SIN
JI Acta Pharmacol. Sin.
PD NOV
PY 2024
VL 45
IS 11
BP 2229
EP 2240
DI 10.1038/s41401-024-01336-2
EA JUL 2024
PG 12
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA J2U0Q
UT WOS:001270470300001
PM 39020084
DA 2025-01-04
ER

PT J
AU Carrasco, J
   Gizzi, M
   Pairet, G
   Lannoy, V
   Lefesvre, P
   Gigot, JF
   Hubert, C
   Jouret-Mourin, A
   Humblet, Y
   Canon, JL
   Sempoux, C
   Chapaux, X
   Danse, E
   Tinton, N
   Navez, B
   Van den Eynde, M
AF Carrasco, J.
   Gizzi, M.
   Pairet, G.
   Lannoy, V.
   Lefesvre, P.
   Gigot, J-F
   Hubert, C.
   Jouret-Mourin, A.
   Humblet, Y.
   Canon, J-L
   Sempoux, C.
   Chapaux, X.
   Danse, E.
   Tinton, N.
   Navez, B.
   Van den Eynde, M.
TI Pathological responses after angiogenesis or EGFR inhibitors in
   metastatic colorectal cancer depend on the chemotherapy backbone
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE pathological response; colorectal cancer; targeted therapy; liver
   metastases; surgical resection
ID RESECTABLE LIVER METASTASES; NEOADJUVANT CHEMOTHERAPY; HISTOLOGICAL
   RESPONSE; PHASE-3 TRIAL; BEVACIZUMAB; RESECTION; SURGERY; CETUXIMAB;
   FOLFOX4; TUMORS
AB Background: Optimal preoperative treatment before colorectal cancer metastases (CRCM) resection remains unclear. This study evaluated pathological responses (pR) in CRCM resected after chemotherapy alone or combined with angiogenesis or epidermal growth factor receptor (EGFR) inhibitors.
   Methods: Pathological response was retrospectively evaluated on 264 resected metastases from 99 patients. The proportion of responding metastases after different preoperative treatments was reported and compared. Patient's progression-free survival (PFS) and overall survival (OS) were compared based on pR.
   Results: The combination of anti-angiogenics with oxaliplatin-based chemotherapy resulted in more pR than when they were combined with irinotecan-based chemotherapy (80% vs 50%; P<0.001). Inversely, the combination of EGFR inhibitors with oxaliplatin-based chemotherapy seemed to induce fewer pR than when they were combined with irinotecan-based treatment (53% vs 72%; P = 0.049). Overall survival at 5 years was improved for patients with a pR in all resected metastases compared with those who did not achieve a pR (68.5% vs 32.6%; P = 0.023) and this response was the only factor predicting OS in a multivariate analysis.
   Conclusion: The chemotherapy partner combined with angiogenesis or EGFR inhibitors influenced pR in resected CRCM. In our exploratory analysis anti-angiogenic/oxaliplatin-based regimens and anti-EGFR/irinotecan-based regimens were associated with the highest pR. Prospective randomised trials should be performed to validate these observations.
C1 [Carrasco, J.; Gizzi, M.; Canon, J-L] GHdC, Dept Med Oncol, B-6000 Charleroi, Belgium.
   [Pairet, G.; Jouret-Mourin, A.; Sempoux, C.] Catholic Univ Louvain, Clin Univ St Luc, Dept Pathol, B-1200 Brussels, Belgium.
   [Lannoy, V.; Humblet, Y.; Van den Eynde, M.] Catholic Univ Louvain, Clin Univ St Luc, Dept Med Oncol, B-1200 Brussels, Belgium.
   [Lefesvre, P.] IPG, Dept Mol Pathol, B-6041 Gosselies, Belgium.
   [Gigot, J-F; Hubert, C.; Navez, B.] Catholic Univ Louvain, Clin Univ St Luc, Dept Abdominal Surg & Transplantat, B-1200 Brussels, Belgium.
   [Chapaux, X.] GHdC, Dept Radiol, B-6000 Charleroi, Belgium.
   [Danse, E.] Catholic Univ Louvain, Clin Univ St Luc, Dept Radiol, B-1200 Brussels, Belgium.
   [Tinton, N.] GHdC, Dept Abdominal Surg, B-6000 Charleroi, Belgium.
C3 Grand Hopital De Charleroi; Universite Catholique Louvain; Cliniques
   Universitaires Saint-Luc; Universite Catholique Louvain; Cliniques
   Universitaires Saint-Luc; Universite Catholique Louvain; Cliniques
   Universitaires Saint-Luc; Grand Hopital De Charleroi; Universite Libre
   de Bruxelles; Universite Catholique Louvain; Cliniques Universitaires
   Saint-Luc; Grand Hopital De Charleroi
RP Carrasco, J (corresponding author), GHdC, Dept Med Oncol, Grand Rue 3, B-6000 Charleroi, Belgium.
EM javier.carrasco@ghdc.be
RI GIGOT, Jean-François/AAB-7144-2019
OI Hubert, Catherine/0000-0001-6837-2511; Sempoux,
   Christine/0000-0003-1375-3979
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NR 22
TC 16
Z9 17
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD NOV 3
PY 2015
VL 113
IS 9
BP 1298
EP 1304
DI 10.1038/bjc.2015.321
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CV8HV
UT WOS:000364524400007
PM 26461062
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Lei, XX
   Hu, XG
   Lu, QL
   Fu, W
   Sun, W
   Ma, QC
   Huang, DS
   Xu, QR
AF Lei, Xiangxiang
   Hu, Xiaoge
   Lu, Qiliang
   Fu, Wen
   Sun, Wen
   Ma, Qiancheng
   Huang, Dongsheng
   Xu, Qiuran
TI Ubiquitin-conjugating enzymes as potential biomarkers and therapeutic
   targets for digestive system cancers (Review)
SO ONCOLOGY REPORTS
LA English
DT Review
DE ubiquitin-conjugating enzymes; digestive system cancers; ubiquitination;
   oncogene; target
ID PROMOTES GASTRIC-CANCER; HEPATOCELLULAR-CARCINOMA; POOR-PROGNOSIS;
   CELL-PROLIFERATION; UP-REGULATION; IN-VITRO; UBCH10 EXPRESSION; E2
   ENZYMES; UBE2C; MIGRATION
AB Digestive system cancers are the leading cause of cancer-related death worldwide due to their high morbidity and mortality rates. The current treatment methods include surgical treatment, chemotherapy, radiotherapy and endoscopic treatment, and the precisely targeted therapy of digestive system cancers requires to be further studied. The ubiquitin-proteasome system is the main pathway for protein degradation in cells and the ubiquitin-conjugating enzymes (E2s) have a decisive role in the specific selection of target proteins for degradation. The E2s have an important physiological role in digestive system cancers, which is related to the clinical tumor stage, differentiation degree and poor prognosis. Furthermore, they are involved in the physiological processes of digestive system tumor cell proliferation, migration, invasion, stemness, drug resistance and autophagy. In the present article, the progress and achievements of the E2s in gastric cancer, hepatocellular carcinoma, pancreatic cancer, colorectal cancer, intrahepatic cholangiocarcinoma, gallbladder cancer and esophageal squamous cell carcinoma were reviewed, which may provide early screening indicators and reliable therapeutic targets for digestive system cancers.
C1 [Lei, Xiangxiang] Hangzhou Med Coll, Inst Basic Med Sci & Forens Med, Hangzhou 310053, Zhejiang, Peoples R China.
   [Hu, Xiaoge; Huang, Dongsheng; Xu, Qiuran] Hangzhou Med Coll, Zhejiang Prov Peoples Hosp, Affiliated Peoples Hosp, Key Lab Tumor Mol Diag & Individualized Med Zhejia, Hangzhou 310014, Zhejiang, Peoples R China.
   [Lu, Qiliang; Fu, Wen] Qingdao Univ, Qingdao Med Coll, Qingdao 266000, Shandong, Peoples R China.
   [Sun, Wen] Zhejiang Chinese Med Univ, Clin Med Inst 2, Hangzhou 310053, Zhejiang, Peoples R China.
   [Ma, Qiancheng] Zhejiang Univ Technol, Inst Bioengn, Hangzhou 310014, Zhejiang, Peoples R China.
   [Huang, Dongsheng; Xu, Qiuran] Hangzhou Med Coll, Zhejiang Prov Peoples Hosp, Affiliated Peoples Hosp, Key Lab Tumor Mol Diag & Individualized Med Zhejia, 158 Shangtang Rd, Hangzhou 310014, Zhejiang, Peoples R China.
C3 Hangzhou Medical College; Hangzhou Medical College; Zhejiang Provincial
   People's Hospital; Qingdao University; Zhejiang Chinese Medical
   University; Zhejiang University of Technology; Hangzhou Medical College;
   Zhejiang Provincial People's Hospital
RP Huang, DS; Xu, QR (corresponding author), Hangzhou Med Coll, Zhejiang Prov Peoples Hosp, Affiliated Peoples Hosp, Key Lab Tumor Mol Diag & Individualized Med Zhejia, 158 Shangtang Rd, Hangzhou 310014, Zhejiang, Peoples R China.
EM dshuang@hmc.edu.cn; windway626@sina.com
RI lu, qiliang/HGC-2565-2022
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NR 114
TC 3
Z9 4
U1 6
U2 22
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 MAR
PY 2023
VL 49
IS 3
AR 63
DI 10.3892/or.2023.8500
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 9F6KL
UT WOS:000937575800001
PM 36799184
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Xu, JB
   Koval, A
   Katanaev, VL
AF Xu, Jiabin
   Koval, Alexey
   Katanaev, Vladimir L.
TI Beyond TNBC: Repositioning of Clofazimine Against a Broad Range of
   Wnt-Dependent Cancers
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE Wnt; repositioning; clofazimine; colorectal cancer; ovarian cancer;
   hepatocellular carcinoma; glioblastoma; breast cancer
ID IN-VITRO; SIGNALING PATHWAY; BETA-CATENIN; PHASE-II; INHIBITORS; TARGET
AB Wnt signaling plays key roles in oncogenic transformation and progression in a number of cancer types, including tumors in the breast, colon, ovaries, liver, and other tissues. Despite this importance, no therapy targeting the Wnt pathway currently exists. We have previously shown that the anti-mycobacterium drug clofazimine is a specific inhibitor of Wnt signaling and cell proliferation in triple-negative breast cancer (TNBC). Here, we expand the applicability of clofazimine to a set of other Wnt-dependent cancers. Using a panel of cell lines from hepatocellular carcinoma, glioblastoma, as well as colorectal and ovarian cancer, we show that the efficacy of clofazimine against a given cancer type correlates with the basal levels of Wnt pathway activation and the ability of the drug to inhibit Wnt signaling in it, being further influenced by the cancer mutational spectrum. Our study establishes the basis for patient stratification in the future clinical trials of clofazimine and may ultimately contribute to the establishment of the Wnt pathway-targeted therapy against a diverse set of cancer types relying on the oncogenic Wnt signaling.
C1 [Xu, Jiabin; Koval, Alexey; Katanaev, Vladimir L.] Univ Geneva, Fac Med, Dept Cell Physiol & Metab, Translat Res Ctr Oncohaematol, Geneva, Switzerland.
   [Xu, Jiabin] Univ Lausanne, Fac Biol & Med, Dept Biomed Sci, Lausanne, Switzerland.
   [Katanaev, Vladimir L.] Far Eastern Fed Univ, Sch Biomed, Vladivostok, Russia.
   [Katanaev, Vladimir L.] Minjiang Univ, Inst Oceanog, Fuzhou, Peoples R China.
C3 University of Geneva; University of Lausanne; Far Eastern Federal
   University; Minjiang University
RP Katanaev, VL (corresponding author), Univ Geneva, Fac Med, Dept Cell Physiol & Metab, Translat Res Ctr Oncohaematol, Geneva, Switzerland.; Katanaev, VL (corresponding author), Far Eastern Fed Univ, Sch Biomed, Vladivostok, Russia.; Katanaev, VL (corresponding author), Minjiang Univ, Inst Oceanog, Fuzhou, Peoples R China.
EM vladimir.katanaev@unige.ch
RI Koval, Alexey/IAP-2281-2023; Katanaev, Vladimir/F-9480-2014
OI Koval, Alexey/0000-0002-8920-4426; Xu, Jiabin/0000-0001-6024-3555;
   Katanaev, Vladimir/0000-0002-7909-5617
FU Novartis Foundation for Medical Biological Research grant [17C153];
   Theodor et Gabriela Kummer fellowship
FX The work was funded by the Novartis Foundation for MedicalBiological
   Research grant #17C153 to VK. JX is a recipient of the Theodor et
   Gabriela Kummer fellowship.
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NR 49
TC 18
Z9 18
U1 0
U2 10
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 10
PY 2020
VL 10
AR 602817
DI 10.3389/fonc.2020.602817
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PI7HY
UT WOS:000601258800001
PM 33363033
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Morales, EV
   Guerrero, GS
   Palacio, LMH
   Maday, Y
AF Morales, Esteban Vallejo
   Guerrero, Gustavo Suarez
   Hoyos Palacio, Lina M. M.
   Maday, Yvon
TI Computational Analysis of Nanocarriers in the Tumor Microenvironment for
   the Treatment of Colorectal Cancer
SO APPLIED SCIENCES-BASEL
LA English
DT Article
DE colorectal cancer; nanocarriers; computational simulation; vectorized
   deposition efficiency; histological samples; selective coupling
ID SIMULATION; MODEL; LIGAND
AB Colorectal cancer is currently treated by surgical procedures, chemotherapy and radiotherapy; however, these latest treatments are highly aggressive, with side effects that affect the patient's quality of life. The scientific union has been investigating other more favorable alternatives, such as targeted therapy, which seeks greater selectivity in the type of target cells. This type of treatment can significantly reduce side effects in the patient. The goal of this research is to computationally visualize the behavior of nanocarriers in the colon tumor microenvironment, as well as their capacity for deepening, selective coupling and differentiating between healthy and cancerous tissue. A group of histological samples of cancerous tissue was selected, based on morphological criteria and the stage of the disease. This was used to elaborate 2D and 3D models to study different cases using artificial vision and computer simulation techniques. The results indicated velocities of the nanocarriers that reached values between 1.40 and 8.69x10-7ms for a time of 3.88 h, with a vectorized deposition efficiency of 1.0 to 4.46%. In addition, selective mating events were achieved at a maximum depth of 4.68 x 10(-4) m. This scientific knowledge can contribute to the estimation of the efficacy of the treatment, as well as the assessment for different dosage levels and frequency of drug administration from the studies carried out on the lesion.
C1 [Morales, Esteban Vallejo] Univ Pontificia Bolivariana, Grp Invest Nuevos Mat, Cir 1 70-01, Medellin 050031, Colombia.
   [Guerrero, Gustavo Suarez] Inst Universitaria Pascual Bravo, Grp Invest Innovac Energia, Cl 73 73a-226, Medellin 050036, Colombia.
   [Hoyos Palacio, Lina M. M.] Univ Pontificia Bolivariana, Grp Invest Biol Sistemas, Cir 1 70-01, Medellin 050031, Colombia.
   [Maday, Yvon] Sorbonne Univ, Univ Paris Diderot SPC, Lab Jacques Louis LJLL L, CNRS, F-75005 Paris, France.
C3 Universidad Pontificia Bolivariana; Universidad Pontificia Bolivariana;
   Universite Paris Cite; Sorbonne Universite; Centre National de la
   Recherche Scientifique (CNRS)
RP Morales, EV (corresponding author), Univ Pontificia Bolivariana, Grp Invest Nuevos Mat, Cir 1 70-01, Medellin 050031, Colombia.; Guerrero, GS (corresponding author), Inst Universitaria Pascual Bravo, Grp Invest Innovac Energia, Cl 73 73a-226, Medellin 050036, Colombia.
EM esteban.vallejomo@upb.edu.co; gustavo.suarez@pascualbravo.edu.co;
   lina.hoyos@upb.edu.co; yvon.maday@sorbonne-universite.fr
OI Vallejo Morales, Esteban/0000-0002-9916-5766; Suarez Guerrero,
   Gustavo/0000-0001-7595-7366
FU MINCIENCIAS; MINEDUCACION; MINCIT; ICETEX, through Program Ecosistema
   Cientifico [FP44842-211-2018, 58962]
FX This research and APC was funded by MINCIENCIAS, MINEDUCACION, MINCIT
   and ICETEX, through the Program Ecosistema Cientifico, grant number
   FP44842-211-2018 Project number 58962.
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NR 55
TC 0
Z9 0
U1 2
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-3417
J9 APPL SCI-BASEL
JI Appl. Sci.-Basel
PD MAY 19
PY 2023
VL 13
IS 10
AR 6248
DI 10.3390/app13106248
PG 17
WC Chemistry, Multidisciplinary; Engineering, Multidisciplinary; Materials
   Science, Multidisciplinary; Physics, Applied
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Engineering; Materials Science; Physics
GA H4JB3
UT WOS:000995632600001
OA gold
DA 2025-01-04
ER

PT J
AU Jia, SY
   Zhang, R
   Lin, GG
   Peng, RX
   Gao, P
   Han, YX
   Fu, Y
   Ding, JS
   Wu, QS
   Zhang, K
   Xie, JH
   Li, JM
AF Jia, Shiyu
   Zhang, Rui
   Lin, Guigao
   Peng, Rongxue
   Gao, Peng
   Han, Yanxi
   Fu, Yu
   Ding, Jiansheng
   Wu, Qisheng
   Zhang, Kuo
   Xie, Jiehong
   Li, Jinming
TI A novel cell line generated using the CRISPR/Cas9 technology as
   universal quality control material for <i>KRAS</i> G12V mutation testing
SO JOURNAL OF CLINICAL LABORATORY ANALYSIS
LA English
DT Article
DE colorectal cancer; CRISPR/Cas9; KRAS; next-generation sequencing;
   quality control material
ID COLORECTAL-CANCER; ACQUIRED-RESISTANCE; DIGITAL PCR; FREE DNA; BRAF
AB BackgroundKRAS mutations are the key indicator for EGFR monoclonal antibody-targeted therapy and acquired drug resistance, and their accurate detection is critical to the clinical decision-making of colorectal cancer. However, no proper quality control material is available for the current detection methods, particularly next-generation sequencing (NGS). The ideal quality control material for NGS needs to provide both the tumor mutation gene and the matched background genomic DNA, which is uncataloged in public databases, to accurately distinguish germline polymorphisms and somatic mutations.
   MethodsWe developed a novel KRAS G12V mutant cell line using the clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR-associated protein 9 (Cas9) technique to make up for the deficiencies in existing quality control material and further validated the feasibility of the cell line as quality control material by amplification refractory mutation system (ARMS), Sanger sequencing, digital PCR (dPCR), and NGS.
   ResultsWe verified that the edited cell line specifically had the G12V mutation, and the validation results presented a high consistency among the four methods of detection. The three cell lines screened contained the G12V mutation and the mutation allele fractions of G12V-1, G12V-2, and G12V-3 were 52.01%, 82.06%, and 17.29%, respectively.
   ConclusionThe novel KRAS G12V cell line generated using the CRISPR/Cas9 gene editing system is suitable as a quality control material for all current detection methods and provides a new direction in the development of quality control material.
C1 [Jia, Shiyu; Li, Jinming] Peking Univ, Sch Clin Med 5, Natl Ctr Clin Labs, Natl Ctr Gerontol, Beijing, Peoples R China.
   [Jia, Shiyu; Zhang, Rui; Lin, Guigao; Peng, Rongxue; Gao, Peng; Han, Yanxi; Fu, Yu; Ding, Jiansheng; Wu, Qisheng; Zhang, Kuo; Xie, Jiehong; Li, Jinming] Beijing Hosp, Natl Ctr Clin Labs, Natl Ctr Gerontol, Beijing, Peoples R China.
   [Jia, Shiyu; Zhang, Rui; Lin, Guigao; Peng, Rongxue; Gao, Peng; Han, Yanxi; Fu, Yu; Ding, Jiansheng; Wu, Qisheng; Zhang, Kuo; Xie, Jiehong; Li, Jinming] Beijing Hosp, Beijing Engn Res Ctr Lab Med, Beijing, Peoples R China.
   [Peng, Rongxue; Gao, Peng; Fu, Yu; Ding, Jiansheng; Wu, Qisheng] Chinese Acad Med Sci, Peking Union Med Coll, Grad Sch, Beijing, Peoples R China.
C3 Peking University; Beijing Hospital; Beijing Hospital; Chinese Academy
   of Medical Sciences - Peking Union Medical College; Peking Union Medical
   College
RP Li, JM (corresponding author), Beijing Hosp, Natl Ctr Clin Labs, Beijing, Peoples R China.
EM jmli@nccl.org.cn
RI wang, rui/JAC-6240-2023; LIN, GUIGAO/KCJ-9774-2024; jia,
   shi/HHS-4172-2022; gao, peng/JHS-8320-2023
FU National Natural Science Foundation of China [81601848]; Beijing Natural
   Science Foundation [7174345]
FX National Natural Science Foundation of China, Grant/Award Number:
   81601848; Beijing Natural Science Foundation, Grant/Award Number:
   7174345
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PY 2018
VL 32
IS 5
AR e22391
DI 10.1002/jcla.22391
PG 7
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA GJ3XQ
UT WOS:000435263900027
PM 29380513
OA Bronze, Green Published
DA 2025-01-04
ER

PT J
AU Ala, M
AF Ala, Moein
TI Sestrin2 in cancer: a foe or a friend?
SO BIOMARKER RESEARCH
LA English
DT Review
DE Sestrin2; Cancer; Oxidative stress; Autophagy; Apoptosis; mTORC1
ID STRESS-MEDIATED APOPTOSIS; AGE-RELATED INTOLERANCE; OXIDATIVE STRESS;
   LUNG-CANCER; ER STRESS; GENETIC POLYMORPHISMS; NRF2 ACTIVATION; FEEDBACK
   LOOP; CELL-GROWTH; AUTOPHAGY
AB Sestrin2 is a conserved antioxidant, metabolism regulator, and downstream of P53. Sestrin2 can suppress oxidative stress and inflammation, thereby preventing the development and progression of cancer. However, Sestrin2 attenuates severe oxidative stress by activating nuclear factor erythroid 2-related factor 2 (Nrf2), thereby enhancing cancer cells survival and chemoresistance. Sestrin2 inhibits endoplasmic reticulum stress and activates autophagy and apoptosis in cancer cells. Attenuation of endoplasmic reticulum stress and augmentation of autophagy hinders cancer development but can either expedite or impede cancer progression under specific conditions. Furthermore, Sestrin2 can vigorously inhibit oncogenic signaling pathways through downregulation of mammalian target of rapamycin complex 1 (mTORC1) and hypoxia-inducible factor 1-alpha (HIF-1 alpha). Conversely, Sestrin2 decreases the cytotoxic activity of T cells and natural killer cells which helps tumor cells immune evasion. Sestrin2 can enhance tumor cells viability in stress conditions such as glucose or glutamine deficiency. Cancer cells can also upregulate Sestrin2 during chemotherapy or radiotherapy to attenuate severe oxidative stress and ER stress, augment autophagy and resist the treatment. Recent studies unveiled that Sestrin2 is involved in the development and progression of several types of human cancer. The effect of Sestrin2 may differ depending on the type of tumor, for instance, several studies revealed that Sestrin2 protects against colorectal cancer, whereas results are controversial regarding lung cancer. Furthermore, Sestrin2 expression correlates with metastasis and survival in several types of human cancer such as colorectal cancer, lung cancer, and hepatocellular carcinoma. Targeted therapy for Sestrin2 or regulation of its expression by new techniques such as non-coding RNAs delivery and vector systems may improve cancer chemotherapy and overcome chemoresistance, metastasis and immune evasion that should be investigated by future trials.
C1 [Ala, Moein] Univ Tehran Med Sci, Sch Med, Tehran, Iran.
C3 Tehran University of Medical Sciences
RP Ala, M (corresponding author), Univ Tehran Med Sci, Sch Med, Tehran, Iran.
EM moinala75@yahoo.com
RI Ala, Moein/AAD-5514-2021
OI Ala, Moein/0000-0001-5951-4864
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NR 143
TC 6
Z9 7
U1 0
U2 18
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 2050-7771
J9 BIOMARK RES
JI Biomark. Res.
PD MAY 8
PY 2022
VL 10
IS 1
AR 29
DI 10.1186/s40364-022-00380-6
PG 13
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA 1A9MV
UT WOS:000792072200001
PM 35527284
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kuderer, NM
   Poniewierski, MS
   Culakova, E
   Lyman, GH
   Khorana, AA
   Pabinger, I
   Agnelli, G
   Liebman, HA
   Vicaut, E
   Meyer, G
   Shepherd, FA
AF Kuderer, Nicole M.
   Poniewierski, Marek S.
   Culakova, Eva
   Lyman, Gary H.
   Khorana, Alok A.
   Pabinger, Ingrid
   Agnelli, Giancarlo
   Liebman, Howard A.
   Vicaut, Eric
   Meyer, Guy
   Shepherd, Frances A.
TI Predictors of Venous Thromboembolism and Early Mortality in Lung Cancer:
   Results from a Global Prospective Study (CANTARISK)
SO ONCOLOGIST
LA English
DT Article
DE Venous thromboembolism; Lung neoplasms; Risk factors; Risk prediction
   model; Mortality; Prognosis
ID PATIENTS RECEIVING CHEMOTHERAPY; METASTATIC COLORECTAL-CANCER; PRACTICE
   GUIDELINE UPDATE; KHORANA SCORE; OUTCOMES VALIDATION; AMERICAN SOCIETY;
   RISK-ASSESSMENT; POOLED ANALYSIS; PHASE-I; THROMBOSIS
AB Background. Patients with lung cancer are known to be at increased risk for venous thromboembolism (VTE). Venous thromboembolism is associated with increased risk for early mortality. However, there have been no studies performing a comprehensive assessment of risk factors for VTE or early mortality in lung cancer patients undergoing systemic chemotherapy in a global real-world setting.
   Materials and Methods. CANTARISK is a prospective, global, noninterventional cohort study including patients with lung cancer initiating a new cancer therapy. Clinical data were collected until 6-month follow-up. The impact of patient-, disease-, and treatment-related factors on the occurrence of VTE and early mortality was evaluated in univariable and multivariable Cox regression analyses. A previously validated VTE risk score (VTE-RS) was also calculated (also known as Khorana score).
   Results. Of 1,980 patients with lung cancer who were enrolled from 2011 to 2012, 84% had non-small cell lung cancer. During the first 6 months, 121 patients developed a VTE (6.1%), of which 47% had pulmonary embolism, 46% deep vein thrombosis, 3% catheter-associated thrombosis, and 4% visceral thrombosis. Independent predictors for VTE included female sex, North America location, leg immobilization, and presence of a central venous catheter. The VTE-RS was not significantly associated with VTE in either univariable or multivariable analysis in this population. During the study period, 472 patients died, representing 20%, 24%, 36%, and 25% with VTE-RS 1, 2, >= 3, or unknown, respectively (p < .0001). Significant independent predictors of early mortality include older age, current/former smoking, chronic obstructive pulmonary disease, Eastern Cooperative Oncology Group performance status >= 2, no prior surgery, and metastatic disease, as well as the VTE-RS.
   Conclusion. In this global, prospective, real-world analysis, several demographic, geographic, and clinical factors are independent risk factors for VTE and early mortality in patients with lung cancer. The VTE-RS represents a significant independent predictor of early mortality but not for VTE in lung cancer in the era of targeted therapy.
C1 [Poniewierski, Marek S.; Lyman, Gary H.] Fred Hutchinson Canc Res Ctr, Hutchinson Inst Canc Outcomes Res, 1124 Columbia St, Seattle, WA 98104 USA.
   [Kuderer, Nicole M.; Lyman, Gary H.] Univ Washington, Dept Med, Seattle, WA USA.
   [Culakova, Eva] Univ Rochester, Dept Med, Rochester, NY USA.
   [Khorana, Alok A.] Cleveland Clin, Dept Oncol, Taussig Canc Inst, Cleveland, OH 44106 USA.
   [Pabinger, Ingrid] Med Univ Vienna, Dept Med, Vienna, Austria.
   [Agnelli, Giancarlo] Univ Perugia, Dept Internal Med, Perugia, Italy.
   [Liebman, Howard A.] Univ Southern Calif, Dept Med, Los Angeles, CA USA.
   [Vicaut, Eric; Meyer, Guy] Univ Paris 05, Dept Med, Paris, France.
   [Shepherd, Frances A.] Princess Margaret Canc Ctr, Canc Clin Res Unit, Toronto, ON, Canada.
C3 Fred Hutchinson Cancer Center; University of Washington; University of
   Washington Seattle; University of Rochester; Cleveland Clinic
   Foundation; Medical University of Vienna; University of Perugia;
   University of Southern California; Sanofi-Aventis; Sanofi France;
   Universite Paris Cite; University of Toronto; University Health Network
   Toronto; Princess Margaret Cancer Centre
RP Lyman, GH (corresponding author), Fred Hutchinson Canc Res Ctr, Publ Hlth Sci Div, Seattle, WA 98109 USA.
EM glyman@fredhutch.org
RI Khorana, Alok/JAO-0943-2023; Lyman, Gary/K-5227-2019; Shepherd,
   Frances/ABR-3795-2022
OI Khorana, Alok/0000-0002-9509-0998
FU Sanofi-Aventis
FX Funding for this study was provided by Sanofi-Aventis. The funding
   agency was involved in study design. The funding agency had no
   involvement in data analysis, data interpretation, manuscript
   preparation, ormanuscript finalization.
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NR 47
TC 66
Z9 71
U1 3
U2 13
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PD FEB
PY 2018
VL 23
IS 2
BP 247
EP 255
DI 10.1634/theoncologist.2017-0205
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FW2LY
UT WOS:000425135900018
PM 28951500
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Deng, YY
   Fu, H
   Han, X
   Li, YX
   Zhao, W
   Zhao, XN
   Yu, CX
   Guo, WQ
   Lei, KJ
   Wang, TX
AF Deng, Yuying
   Fu, Han
   Han, Xue
   Li, Yuxi
   Zhao, Wei
   Zhao, Xuening
   Yu, Chunxue
   Guo, Wenqing
   Lei, Kaijian
   Wang, Tianxiao
TI Activation of DDX58/RIG-I suppresses the growth of tumor cells by
   inhibiting STAT3/CSE signaling in colon cancer
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE DExD/H-box helicase 58; retinoic acid-inducible gene-I; signal
   transducer and activator of transcription 3; cystathionine-gamma-lyase;
   colon cancer
ID RIG-I; HYDROGEN-SULFIDE
AB Some patients with colon cancer eventually develop metastasis during treatment, and the 5-year survival rate of patients with metastatic colon cancer remains relatively low, which is most likely due to the ineffectiveness of the current standard treatment. Systemic treatment for patients with colon cancer has expanded from chemotherapy to targeted therapy and immunotherapy. Immunotherapy holds promise in the treatment of colon cancer. The present study revealed the role of innate immune receptor helicase DExD/H-box helicase 58 (DDX58), which encodes retinoic acid-inducible gene-I (RIG-I), in colon cancer. It was demonstrated that colon cancer patients with a low protein expression of DDX58/RIG-I had a worse 5-year survival rate of patients compared with patients with a high expression of DDX58/RIG-I. The activation of DDX58/RIG-I inhibited the proliferation, migration and invasion of colon cancer cells, as well as tumor growth in a nude mouse xenograft model of colon cancer. To investigate the mechanisms of action of DDX58/RIG-I in colon cancer, the role of signal transducer and activator of transcription 3 (STAT3)/cystathionine-gamma-lyase (CSE) signaling in the up- or downregulation of DDX58 was examined. The data demonstrated that DDX58 regulated the STAT3/CSE signaling pathway by interacting with STAT3 and consequently affecting the proliferation of tumor cells in colon cancer. In addition, the RIG-I agonist, SB9200, induced proliferation, migration and invasion of human colon cancer. On the whole, the present study demonstrates that DDX58/RIG-I affects the proliferation of tumor cells by regulating STAT3/CSE signaling in colon cancer. The findings presented herein suggest that DDX58/RIG-I activation may be an effective treatment strategy, and DDX58/RIG-I agonists may be potential therapeutic candidates for colon cancer.
C1 [Deng, Yuying; Fu, Han; Han, Xue; Li, Yuxi; Zhao, Wei; Zhao, Xuening; Yu, Chunxue; Guo, Wenqing; Lei, Kaijian; Wang, Tianxiao] Henan Univ, Sch Pharm, Biopharmaceut Dept, Kaifeng 475004, Henan, Peoples R China.
   [Lei, Kaijian; Wang, Tianxiao] Henan Univ, Sch Pharm, Biopharmaceut Dept, North Part Jinming Rd, Kaifeng 475004, Henan, Peoples R China.
C3 Henan University; Henan University
RP Lei, KJ; Wang, TX (corresponding author), Henan Univ, Sch Pharm, Biopharmaceut Dept, North Part Jinming Rd, Kaifeng 475004, Henan, Peoples R China.
EM leikaijian@126.com; wtx1975@126.com
RI Wang, Xuemei/GXF-3702-2022; zhao, wei/IQS-1144-2023
FU National Natural Science Foundation of China; Natural Science Foundation
   of Henan Province in China [82072726];  [202300410079]
FX The present study supported by the grants from the National Natural
   Science Foundation of China (no. 82072726), as well as the Natural
   Science Foundation of Henan Province in China (no. 202300410079).
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NR 32
TC 7
Z9 7
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 OCT
PY 2022
VL 61
IS 4
AR 120
DI 10.3892/ijo.2022.5410
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 4N9RC
UT WOS:000854348100001
PM 36004488
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Landi, N
   Ciaramella, V
   Ragucci, S
   Chambery, A
   Ciardiello, F
   Pedone, PV
   Troiani, T
   Di Maro, A
AF Landi, Nicola
   Ciaramella, Vincenza
   Ragucci, Sara
   Chambery, Angela
   Ciardiello, Fortunato
   Pedone, Paolo V.
   Troiani, Teresa
   Di Maro, Antimo
TI A Novel EGFR Targeted Immunotoxin Based on Cetuximab and Type 1 RIP
   Quinoin Overcomes the Cetuximab Resistance in Colorectal Cancer Cells
SO TOXINS
LA English
DT Article
DE Chenopodium quinoa; chemical conjugation; cytotoxicity; GEO-CR cells;
   monoclonal antibody
ID RIBOSOME-INACTIVATING PROTEINS; ACQUIRED-RESISTANCE; ACTIVATION; TOXINS;
   CYTOTOXICITY; PURIFICATION; KRAS
AB Cetuximab is a monoclonal antibody blocking the epidermal growth factor receptor (EGFR) in metastatic colorectal cancer (mCRC). However, cetuximab treatment has no clinical benefits in patients affected by mCRC with KRAS mutation or in the presence of constitutive activation of signalling pathways acting downstream of the EGFR. The aim of this study was to improve cetuximab's therapeutic action by conjugating cetuximab with the type 1 ribosome inactivating protein (RIP) quinoin isolated from quinoa seeds. A chemical conjugation strategy based on the use of heterobifunctional reagent succinimidyl 3-(2-pyridyldithio)propionate (SPDP) was applied to obtain the antibody-type 1 RIP chimeric immunoconjugate. The immunotoxin was then purified by chromatographic technique, and its enzymatic action was evaluated compared to quinoin alone. Functional assays were performed to test the cytotoxic action of the quinoin cetuximab immunoconjugate against the cetuximab-resistant GEO-CR cells. The novel quinoin cetuximab immunoconjugate showed a significant dose-dependent cytotoxicity towards GEO-CR cells, achieving IC50 values of 27.7 nM (similar to 5.0 mu g/mL) at 72 h compared to cetuximab (IC50 = 176.7 nM) or quinoin (IC50 = 149.3 nM) alone assayed in equimolar amounts. These results support the therapeutic potential of quinoin cetuximab immunoconjugate for the EGFR targeted therapy, providing a promising candidate for further development towards clinical use in the treatment of cetuximab-resistant metastatic colorectal cancer.
C1 [Landi, Nicola; Ragucci, Sara; Chambery, Angela; Pedone, Paolo V.; Di Maro, Antimo] Univ Campania Luigi Vanvitelli, Dept Environm Biol & Pharmaceut Sci & Technol DiST, Via Vivaldi 43, I-81100 Caserta, Italy.
   [Ciaramella, Vincenza; Ciardiello, Fortunato; Troiani, Teresa] Univ Campania Luigi Vanvitelli, Dept Precis Med, Med Oncol, Via S Pansini 5, I-80131 Naples, Italy.
C3 Universita della Campania Vanvitelli; Universita della Campania
   Vanvitelli
RP Di Maro, A (corresponding author), Univ Campania Luigi Vanvitelli, Dept Environm Biol & Pharmaceut Sci & Technol DiST, Via Vivaldi 43, I-81100 Caserta, Italy.
EM antimo.dimaro@unicampania.it
RI Di Maro, Antimo/AEM-8941-2022
OI Chambery, Angela/0000-0002-5136-0941; Landi, Nicola/0000-0001-8281-7898;
   Ragucci, Sara/0000-0002-2219-2424; Di Maro, Antimo/0000-0002-9595-9665
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NR 47
TC 1
Z9 1
U1 1
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6651
J9 TOXINS
JI Toxins
PD JAN
PY 2023
VL 15
IS 1
AR 57
DI 10.3390/toxins15010057
PG 13
WC Food Science & Technology; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Food Science & Technology; Toxicology
GA 8A7PP
UT WOS:000916427500001
PM 36668877
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Garcia-Alfonso, P
   Lièvre, A
   Loupakis, F
   Tadmouri, A
   Khan, S
   Barcena, L
   Stintzing, S
AF Garcia-Alfonso, Pilar
   Lievre, Astrid
   Loupakis, Fotios
   Tadmouri, Abir
   Khan, Sadya
   Barcena, Leticia
   Stintzing, Sebastian
TI Systematic review of randomised clinical trials and observational
   studies for patients with RAS wild-type or
   <i>BRAF</i><SUP>V600E</SUP>-mutant metastatic and/or unresectable
   colorectal cancer
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE BRAFV600E; BRAF kinase inhibitor; Efficacy; Metastatic colorectal cancer
ID BRAF MUTATION; ACQUIRED-RESISTANCE; 2ND-LINE TREATMENT; TARGETED
   THERAPY; PHASE-III; PANITUMUMAB; CETUXIMAB; KRAS; INHIBITION; SURVIVAL
AB Approximately 8-10% of metastatic colorectal cancer (mCRC) tumours harbour BRAF(V600E) mutations. Eleven randomised controlled trials (RCTs) and 24 non-RCTs were identified. Seven studies evaluated BRAF inhibitors. Single-agent BRAF inhibitors had minimal efficacy, whereas BRAF inhibitor plus anti-EGFR therapy improved outcomes. In BEACON CRC, overall survival (OS) was significantly longer for patients receiving encorafenib plus cetuximab +/- binimetinib when compared with irinotecan/FOLFIRI plus cetuximab as second- and third-line therapy. Seven prospective non-RCTs reported worse OS and progression-free survival (PFS) for patients with BRAF(V600E)-mutant vs BRAF wild-type mCRC. Eight RCTs reported that PFS and OS were generally shorter for patients with BRAF(V600E)-mutant mCRC vs those with KRAS or RAS wild-type mCRC. Patients with BRAF(V600)-Emutant mCRC have worse outcomes with conventional therapy vs patients with BRAF wild-type tumours. BRAF inhibitors in conjunction with anti-EGFR therapy improves outcomes for patients with BRAF(V600E)-mutant mCRC vs conventional therapy or a BRAF inhibitor alone.
C1 [Garcia-Alfonso, Pilar] Hosp Univ Gregorio Maranon, Med Oncol, Madrid, Spain.
   [Lievre, Astrid] Rennes 1 Univ, Pontchaillou Univ Hosp, Dept Gastroenterol, Rennes, France.
   [Lievre, Astrid] INSERM U1242, Chem Oncogenesis Stress Signaling COSS, Rennes, France.
   [Loupakis, Fotios] Ist Oncol Veneto IOV IRCCS, Dept Oncol, Padua, Italy.
   [Tadmouri, Abir; Khan, Sadya] Pierre Fabre, Boulogne, France.
   [Barcena, Leticia] DRG Abacus Clarivate, Bicester, England.
   [Stintzing, Sebastian] Charite Univ Med Berlin, Div Hematol Oncol & Canc Immunol CCM, Dept Med, Berlin, Germany.
C3 General University Gregorio Maranon Hospital; Universite de Rennes; CHU
   Rennes; Institut National de la Sante et de la Recherche Medicale
   (Inserm); IRCCS Istituto Oncologico Veneto (IOV); Berlin Institute of
   Health; Free University of Berlin; Humboldt University of Berlin;
   Charite Universitatsmedizin Berlin
RP Stintzing, S (corresponding author), Charit Univ Med Berlin, Dept Med, Div Hematol Oncol & Canc Immunol CCM, Charitepl 1, D-10117 Berlin, Germany.
EM pgarcaalfonso@gmail.com; astrid.lievre@chu-rennes.fr;
   fotios.loupakis@iov.veneto.it; abir.tadmouri@pierre-fabre.com;
   sadya.khan@pierre-fabre.com; leticia.Barcena@Clarivate.com;
   sebastian.stintzing@charite.de
RI Stintzing, Sebastian/I-4538-2016
OI Stintzing, Sebastian/0000-0002-3297-5801
FU Pierre Fabre directly to DRG Abacus (Clarivate); Meditech Media
FX The authors received no specific funding for this work. All the work was
   funded by Pierre Fabre directly to DRG Abacus (Clarivate) and Meditech
   Media.
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NR 72
TC 5
Z9 6
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1040-8428
EI 1879-0461
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD MAY
PY 2022
VL 173
AR 103646
DI 10.1016/j.critrevonc.2022.103646
PG 17
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA O5FS6
UT WOS:001044073500001
PM 35344913
DA 2025-01-04
ER

PT J
AU Zhao, CL
   Qiao, CC
   Zong, LG
   Chen, YQ
AF Zhao, Chengling
   Qiao, Chenchen
   Zong, Liguo
   Chen, Yuqing
TI Long non-coding RNA-CCAT2 promotes the occurrence of non-small cell lung
   cancer by regulating the Wnt/-catenin signaling pathway
SO ONCOLOGY LETTERS
LA English
DT Article
DE non-small cell lung carcinoma; colon cancer-associated transcript 2;
   Wnt; -catenin signaling pathway
ID RNA CCAT2; GASTRIC-CANCER; COLON-CANCER; OVEREXPRESSION; PROLIFERATION;
   PROGRESSION; EXPRESSION; RESISTANCE; CARCINOMA; BLOCKADE
AB The present study aimed to investigate the biological function of colon cancer-associated transcript 2 (CCAT2) in the occurrence and progression of non-small cell lung carcinoma (NSCLC) and its potential use in the early diagnosis and molecular-targeted therapy of NSCLC. The tumor tissues, para-carcinoma tissues and associated clinical data of 36 patients with NSCLC were collected in order to detect the expression of CCAT2 and assess the impact of factors including histopathological type, Tumor-Node-Metastasis stage and lymph node metastasis on CCAT2 expression. The lung cancer NCI-H1975 cell line was transfected with a small interfering RNA (siRNA) plasmid to determine the effect of si-CCAT2 on NSCLC proliferation, invasion and metastasis. The effect of si-CCAT2 on the expression of nuclear and cytoplasmic -catenin protein in the lung cancer NCI-H1975 cell line was detected using western blot analysis. The expression levels of CCAT2 in the tumor tissues of patients with NSCLC were significantly higher than those in the normal para-carcinoma tissues (t=8.580, P<0.01). Subsequent to CCAT2 silencing, the proliferation and invasive abilities of NCI-H1975 cells were significantly decreased compared with control cells (P<0.05). In the si-CCAT2 group, the level of nuclear and cytoplasmic -catenin proteins was decreased, and the activity of the Wnt signaling pathway was significantly inhibited compared with the control cells (P<0.01), and a synergistic effect was exerted with the Wnt signaling inhibitor FH535. CCAT2 may therefore promote the occurrence of NSCLC by regulating the Wnt/-catenin signaling pathway.
C1 [Zhao, Chengling] Shandong Univ, Sch Med, Sch Med, Jinan 250100, Shandong, Peoples R China.
   [Zhao, Chengling; Chen, Yuqing] Bengbu Med Coll, Affiliated Hosp 1, Dept Respirat, Anhui Clin & Preclin Key Lab Resp Dis, 803 Changhuai Rd, Bengbu 233004, Anhui, Peoples R China.
   [Qiao, Chenchen] First Municipal Hosp Bengbu, Dept Cardiol, Bengbu 233004, Anhui, Peoples R China.
   [Zong, Liguo] Zaozhuang Municipal Hosp, Dept Intens Care Unit, Zaozhuang 277001, Shandong, Peoples R China.
C3 Shandong University; Bengbu Medical University
RP Zhao, CL (corresponding author), Bengbu Med Coll, Affiliated Hosp 1, Dept Respirat, Anhui Clin & Preclin Key Lab Resp Dis, 803 Changhuai Rd, Bengbu 233004, Anhui, Peoples R China.
EM zhaochengling0708@126.com
RI qi, jinchun/HDM-7017-2022; Chen, Yuqing/GWU-7343-2022
FU Natural Science Foundation of Anhui Province [1608085QH189]; National
   Natural Science Foundation of China [81172213]
FX The present study was supported by the Natural Science Foundation of
   Anhui Province (grant no. 1608085QH189) and the National Natural Science
   Foundation of China (grant no. 81172213).
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NR 28
TC 15
Z9 18
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 OCT
PY 2018
VL 16
IS 4
BP 4600
EP 4606
DI 10.3892/ol.2018.9194
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GU1BU
UT WOS:000444990700066
PM 30214594
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Spelt, L
   Sasor, A
   Ansari, D
   Hilmersson, KS
   Andersson, R
AF Spelt, Lidewij
   Sasor, Agata
   Ansari, Daniel
   Hilmersson, Katarzyna Said
   Andersson, Roland
TI The Prognostic Role of Cancer Stem Cell Markers for Long-term Outcome
   After Resection of Colonic Liver Metastases
SO ANTICANCER RESEARCH
LA English
DT Article
DE Colonic neoplasms; disease-free survival; liver resection; metastasis;
   neoplastic stem cells; survival analysis
ID COLORECTAL-CANCER; EXPRESSION; DIFFERENTIATION; HEPATECTOMY; RECURRENCE;
   SURVIVAL; GROWTH; CD133; CD44
AB Background/Aim: To assess the expression of cancer stem cell (CSC) markers CD44, CD133 and CD24 in colon cancer liver metastases and analyse their predictive value for overall survival (OS) and disease-free survival (DFS) after liver resection. Materials and Methods: Patients operated on for colon cancer liver metastases were included. CSC marker expression was determined through immunohistochemistry analysis. OS and DFS were compared between marker-positive and marker-negative patients. Multivariate analysis was performed to select predictive variables for OS and DFS. Results: CD133-positive patients had a worse DFS than CD133-negative patients, with a median DFS of 12 and 25 months (p=0.051). Multivariate analysis selected CD133 expression as a significant predictor for DFS. CD44 and CD24 were not found to predict OS or DFS. Conclusion: CD133 expression in colonic liver metastases is a negative prognostic factor for DFS after liver resection. In the future, CD133 could be used as a biomarker for risk stratification, and possibly for developing novel targeted therapy.
C1 [Spelt, Lidewij; Ansari, Daniel; Andersson, Roland] Lund Univ, Clin Sci Lund, Dept Surg, Lund, Sweden.
   [Spelt, Lidewij; Ansari, Daniel; Andersson, Roland] Skane Univ Hosp, Lund, Sweden.
   [Sasor, Agata; Hilmersson, Katarzyna Said] Skane Univ Hosp, Dept Pathol, Lund, Sweden.
C3 Lund University; Lund University; Skane University Hospital; Lund
   University; Skane University Hospital
RP Spelt, L (corresponding author), Lund Univ, Skane Univ Hosp, Clin Sci Lund, Dept Surg, SE-22185 Lund, Sweden.
EM lidewij.spelt@med.lu.se
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NR 29
TC 13
Z9 13
U1 0
U2 2
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 JAN
PY 2018
VL 38
IS 1
BP 313
EP 320
DI 10.21873/anticanres.12224
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FR5TW
UT WOS:000419130100041
PM 29277789
OA Bronze
DA 2025-01-04
ER

PT J
AU Cai, W
   Kong, W
   Dong, BJ
   Zhang, J
   Chen, YH
   Xue, W
   Huang, YR
   Zhou, LX
   Huang, JW
AF Cai, Wen
   Kong, Wen
   Dong, Baijun
   Zhang, Jin
   Chen, Yonghui
   Xue, Wei
   Huang, Yiran
   Zhou, Lixin
   Huang, Jiwei
TI Pretreatment Serum Prealbumin as an Independent Prognostic Indicator in
   Patients With Metastatic Renal Cell Carcinoma Using Tyrosine Kinase
   Inhibitors as First-Line Target Therapy
SO CLINICAL GENITOURINARY CANCER
LA English
DT Article
DE Pretreatment prealbumin; Prognosis; Renal cell carcinoma; Sorafenib;
   Sunitinib
ID CANCER-PATIENTS; COLORECTAL-CANCER; PANCREATIC-CANCER; LYMPHOCYTE RATIO;
   BODY-MASS; SURVIVAL; ALBUMIN; MARKERS; ASSOCIATION; SUNITINIB
AB This is a retrospective study on medical records of patients with metastatic renal cell carcinoma to study the prognostic importance of pretreatment prealbumin by evaluating the overall survival (OS) and progression-free survival (PFS), given the scarcity of such data till date. Results found that the pretreatment prealbumin group is an independent prognosticator of risk and survival outcomes, which attenuated the PFS and OS compared with the normal pretreatment prealbumin group.
   Background: Although serum prealbumin is a sensitive marker to assess malnutrition, its prognostic impact in patients with metastatic renal cell carcinoma (mRCC) remains elusive. Methods: Patients' data were retrospectively retrieved from the medical records of Renji Hospital affiliated to Shanghai Jiao Tong University School of Medicine from March 2006 to July 2015 to access overall survival (OS) and progression-free survival (PFS). The survival outcomes of patients with low pretreatment prealbumin (< 200 mg/L) and high pretreatment prealbumin (>= 200 mg/L) were compared using a log-rank test and Cox proportional hazard regression model. Prognostic accuracy was determined using the Harrell concordance index (c-index). Results: The median PFS and OS for 143 patients were 11 months (95% confidence interval [CI], 9-14 months) and 27 months (95% CI, 22-39 months), respectively. The low pretreatment prealbumin group had significantly shorter median PFS (6 vs. 14 months, P<.001) and OS (10 vs. 34 months, P <.001) than the normal pretreatment prealbumin group. Multivariate analysis showed that pretreatment prealbumin was an independent predictor of OS (hazard ratio [HR] 1.963; 95% CI, 1.140-3.381; P=.015) and also an independent predictor of PFS (HR 2.021; 95% CI, 1.227-3.329; P=.006). Further, addition of pretreatment prealbumin to the Heng model enhanced the predictive accuracy of PFS and OS (c-index: 0.70 and 0.74) compared with the Heng model alone (c-index: 0.69 and 0.72). Conclusion: Low pretreatment serum prealbumin is an independent prognosticator of risk and survival outcomes in patients with mRCC receiving tyrosine kinase inhibitors as first-line treatment and also increases the accuracy of established prognostic models. (C) 2017 Elsevier Inc. All rights reserved.
C1 [Cai, Wen; Kong, Wen; Dong, Baijun; Zhang, Jin; Chen, Yonghui; Xue, Wei; Huang, Yiran; Zhou, Lixin; Huang, Jiwei] Shanghai Jiao Tong Univ, Sch Med, Renji Hosp, Dept Urol, 160 Pujian Rd, Shanghai 200127, Peoples R China.
C3 Shanghai Jiao Tong University
RP Zhou, LX; Huang, JW (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Renji Hosp, Dept Urol, 160 Pujian Rd, Shanghai 200127, Peoples R China.
EM zhou_li_xin@hotmail.com; jiweihuang@outlook.com
RI Kong, Wen/GQH-3057-2022; cai, wen/JWP-4797-2024
FU National Natural Science Foundation of China [81402084, 81672513,
   81472378]; Shanghai Municipal Commission of Health and Family Planning
   [2013SY027]; Incubating Program for Clinical Research and Innovation of
   Renji Hospital [PYXJS16-008]
FX The authors acknowledge Ms. Navya Reddy and Dr Amit Bhat (Indegene Pvt
   Ltd, Bangalore, India) for providing medical writing support in the
   preparation of this manuscript. All the authors planned this study and
   contributed to the interpretation of the data, and revisions and inputs
   at all stages of the study. All authors have approved the final version
   of the manuscript. This study was supported by grant numbers 81402084,
   81672513 and 81472378 from the National Natural Science Foundation of
   China and grant number 2013SY027 from the Shanghai Municipal Commission
   of Health and Family Planning and PYXJS16-008 from the Incubating
   Program for Clinical Research and Innovation of Renji Hospital.
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NR 46
TC 30
Z9 31
U1 0
U2 6
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1558-7673
EI 1938-0682
J9 CLIN GENITOURIN CANC
JI Clin. Genitourin. Cancer
PD JUN
PY 2017
VL 15
IS 3
BP E437
EP E446
DI 10.1016/j.clgc.2017.01.008
PG 10
WC Oncology; Urology & Nephrology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Urology & Nephrology
GA FR6XY
UT WOS:000419212000016
PM 28188047
DA 2025-01-04
ER

PT S
AU Donaldson, J
   Park, BH
AF Donaldson, Joshua
   Park, Ben Ho
BE Caskey, CT
TI Circulating Tumor DNA: Measurement and Clinical Utility
SO ANNUAL REVIEW OF MEDICINE, VOL 69
SE Annual Review of Medicine
LA English
DT Review; Book Chapter
DE liquid biopsy; plasma tumor DNA; digital droplet polymerase chain
   reaction; theranostics
ID CELL-FREE-DNA; METASTATIC COLORECTAL-CANCER; ESR1 MUTATIONS; PLASMA DNA;
   BREAST-CANCER; ACQUIRED-RESISTANCE; LIQUID BIOPSIES; RARE MUTATIONS;
   SERUM SAMPLES; BLOOD
AB Circulating tumor DNA (ctDNA) is a component of the "naked" DNA found in blood. It can be isolated from plasma and represents combined genetic material from the primary tumor and metastases. Quantitative and qualitative information about a cancer, including mutations, can be derived using digital polymerase chain reaction and other technologies. This "liquid biopsy" is quicker and more easily repeated than tissue biopsy, yields real-time information about the cancer, and may suggest therapeutic options. All stages of cancer therapy have the ability to benefit from ctDNA, starting with screening for cancer before it is clinically apparent. During treatment of metastatic disease, it is useful to predict response and monitor disease progression. Currently, ctDNA is used in the clinic to select patients who may benefit from epidermal growth factor receptor-targeted therapy in non-small cell lung cancer. In the future, ctDNA technology promises useful applications in every part of clinical oncology care.
C1 [Donaldson, Joshua; Park, Ben Ho] Johns Hopkins Univ, Sch Med, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21287 USA.
   [Park, Ben Ho] Johns Hopkins Univ, Whiting Sch Engn, Dept Chem & Biomol Engn, Baltimore, MD 21218 USA.
C3 Johns Hopkins University; Johns Hopkins Medicine; Johns Hopkins
   University
RP Park, BH (corresponding author), Johns Hopkins Univ, Sch Med, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21287 USA.; Park, BH (corresponding author), Johns Hopkins Univ, Whiting Sch Engn, Dept Chem & Biomol Engn, Baltimore, MD 21218 USA.
EM bpark2@jhmi.edu
OI Donaldson, Joshua/0000-0003-3879-833X
FU NCI NIH HHS [P30 CA006973] Funding Source: Medline
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NR 72
TC 62
Z9 64
U1 0
U2 24
PU ANNUAL REVIEWS
PI PALO ALTO
PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0897 USA
SN 0066-4219
BN 978-0-8243-0569-7
J9 ANNU REV MED
JI Annu. Rev. Med.
PY 2018
VL 69
BP 223
EP 234
DI 10.1146/annurev-med-041316-085721
PG 12
WC Medicine, Research & Experimental
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA BJ3ZL
UT WOS:000424632300016
PM 28846488
DA 2025-01-04
ER

PT J
AU Kothalawala, WJ
   Gyorffy, B
AF Kothalawala, William Jayasekara
   Gyorffy, Balazs
TI Transcriptomic and Cellular Content Analysis of Colorectal Cancer by
   Combining Multiple Independent Cohorts
SO CLINICAL AND TRANSLATIONAL GASTROENTEROLOGY
LA English
DT Article
ID MESSENGER-RNA EXPRESSION; GENE-EXPRESSION; COLON-CANCER; ADENOMA;
   IDENTIFICATION; PROGNOSIS; TARGET; FOXQ1
AB INTRODUCTION: By linking cellular content and molecular subtypes of colorectal cancer (CRC), we aim to uncover novel features useful for targeted therapy. Our first goal was to evaluate gene expression alterations linked to CRC pathogenesis, and then, we aimed to evaluate the cellular composition differences between normal colon mucosa and tumor and between different colon cancer molecular subtypes.
   METHODS: We collected microarray and RNA sequencing data of patients with CRC from the Genome Expression Omnibus and The Cancer Genome Atlas. We combined all cases and performed quantile normalization. Genes with a fold change of >2 were further investigated. We used xCell for cellular decomposition and CMScaller for molecular subtyping. For statistical analyses, the Kruskal-Wallis H test and MannWhitney U tests were performed with Bonferroni correction.
   RESULTS: We established an integrated database of normal colon and CRC using transcriptomic data of 1,082 samples. By using this data set, we identified genes showing the highest differential expression in colon tumors. The top genes were linked to calcium signaling, matrix metalloproteinases, and transcription factors. When compared with normal samples, CD4+ memory T cells, CD8+ naive T cells, CD8+ T cells, Th1 cells, Th2 cells, and regulatory T cells were enriched in tumor tissues. The ImmuneScore was decreased in tumor samples compared with normal samples. The CMS1 and CMS4 molecular subtypes were the most immunogenic, with the highest ImmuneScore but also high infiltration by CD8+ T cells, Th1 cells, and Th2 cells in CMS1 and B-cell subtypes and CD8+ T cells in CMS4.
   DISCUSSION: Our analysis uncovers features enabling advanced treatment selection and the development of novel therapies in CRC.
C1 [Kothalawala, William Jayasekara] Semmelweis Univ, Dept Internal Med, Budapest, Hungary.
   [Gyorffy, Balazs] Semmelweis Univ, Dept Bioinformat, Budapest, Hungary.
   [Gyorffy, Balazs] Semmelweis Univ, Dept Pediat 2, Budapest, Hungary.
   [Gyorffy, Balazs] TTK Canc Biomarker Res Grp, Budapest, Hungary.
C3 Semmelweis University; Semmelweis University; Semmelweis University;
   Hungarian Research Network; HUN-REN Research Centre for Natural Sciences
RP Gyorffy, B (corresponding author), Semmelweis Univ, Dept Bioinformat, Budapest, Hungary.; Gyorffy, B (corresponding author), Semmelweis Univ, Dept Pediat 2, Budapest, Hungary.; Gyorffy, B (corresponding author), TTK Canc Biomarker Res Grp, Budapest, Hungary.
EM gyorffy.balazs@ttk.hu
RI Gyorffy, Balazs/AAA-9135-2021
FU Higher Education Institutional Excellence Programme of the Ministry for
   Innovation and Technology in Hungary [2018-2.1.17-TET-KR-00001,
   2020-1.1.6-JOVO-2021-00013, 2018-1.3.1-VKE-2018-00032,
   2020-4.1.1.-TKP2020]; Ministry for Innovation and Technology; National
   Research, Development and Innovation Fund
FX The research was financed by the 2018-2.1.17-TET-KR-00001,
   2020-1.1.6-JOV}O-2021-00013, and 2018-1.3.1-VKE-2018-00032 grants and by
   the Higher Education Institutional Excellence Programme
   (2020-4.1.1.-TKP2020) of the Ministry for Innovation and Technology in
   Hungary, within the framework of the Bionic thematic programme of the
   Semmelweis University. This study was prepared with the professional
   support of the doctoral student scholarship program of the Cooperative
   Doctoral Program of the Ministry for Innovation and Technology financed
   from the National Research, Development and Innovation Fund.
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NR 47
TC 4
Z9 4
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
EI 2155-384X
J9 CLIN TRANSL GASTROEN
JI Clin. Transl. Gastroenterol.
PD FEB
PY 2023
VL 14
IS 2
AR e00517
DI 10.14309/ctg.0000000000000517
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA H9YM5
UT WOS:000999434700007
PM 35858620
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Jensen, MM
   Kjaer, A
AF Jensen, Mette Munk
   Kjaer, Andreas
TI Monitoring of anti-cancer treatment with <SUP>18</SUP>F-FDG and
   <SUP>18</SUP>F-FLT PET: a comprehensive review of pre-clinical studies
SO AMERICAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
LA English
DT Review
DE F-18-FDG; F-18-FLT; PET; drug development; cancer; response monitoring;
   tyrosine kinase inhibitors; mTOR inhibitors; anti-angiogenic therapy;
   chemotherapy; targeted therapy
ID POSITRON-EMISSION-TOMOGRAPHY; ANTI-ANGIOGENIC THERAPY; THYMIDINE KINASE
   1; C-MET INHIBITOR; TUMOR RESPONSE; COLORECTAL-CANCER; IN-VIVO; KI-67
   IMMUNOHISTOCHEMISTRY; IMAGING PROLIFERATION; NUCLEOSIDE TRANSPORTERS
AB Functional imaging of solid tumors with positron emission tomography (PET) imaging is an evolving field with continuous development of new PET tracers and discovery of new applications for already implemented PET tracers. During treatment of cancer patients, a general challenge is to measure treatment effect early in a treatment course and by that to stratify patients into responders and non-responders. With 2-deoxy-2-[F-18] fluoro-D-glucose (F-18-FDG) and 3'-deoxy-3'-[F-18] fluorothymidine(F-18-FLT) two of the cancer hallmarks, altered energy metabolism and increased cell proliferation, can be visualized and quantified non-invasively by PET. With F-18-FDG and F-18-FLT PET changes in energy metabolism and cell proliferation can thereby be determined after initiation of cancer treatment in both clinical and pre-clinical studies in order to predict, at an early time-point, treatment response. It is hypothesized that decreases in glycolysis and cell proliferation may occur in tumors that are sensitive to the applied cancer therapeutics and that tumors that are resistant to treatment will show unchanged glucose metabolism and cell proliferation. Whether F-18-FDG and/or F-18-FLT PET can be used for prediction of treatment response has been analyzed in many studies both following treatment with conventional chemotherapeutic agents but also following treatment with different targeted therapies, e.g. monoclonal antibodies and small molecules inhibitors. The results from these studies have been most variable; in some studies early changes in F-18-FDG and F-18-FLT uptake predicted later tumor regression whereas in other studies no change in tracer uptake was observed despite the treatment being effective. The present review gives an overview of pre-clinical studies that have used F-18-FDG and/or F-18-FLT PET for response monitoring of cancer therapeutics.
C1 [Jensen, Mette Munk; Kjaer, Andreas] Rigshospitalet & Univ Copenhagen, Dept Clin Physiol Nucl Med & PET & Cluster Mol, Copenhagen, Denmark.
C3 Rigshospitalet
RP Kjaer, A (corresponding author), Natl Univ Hosp, Rigshosp, Dept Clin Physiol Nucl Med & PET KF 4012, Blegdamsvej 9, DK-2100 Copenhagen, Denmark.
EM akjaer@sund.ku.dk
RI Kjaer, Andreas/E-8932-2015
OI Kjaer, Andreas/0000-0002-2706-5547
FU Innovation Fund Denmark; John and Birthe Meyer Foundation; Danish
   Medical Research Council; Rigshospitalets Research Foundation; Svend
   Andersen Foundation; AP Moller Foundation; Novo Nordisk Foundation;
   Lundbeck Foundation; Danish Cancer Society
FX The generous support of the research into the PET imaging in cancer in
   form of unrestriced grants from the Innovation Fund Denmark, the John
   and Birthe Meyer Foundation, the Danish Medical Research Council, the
   Rigshospitalets Research Foundation, the Svend Andersen Foundation, the
   AP Moller Foundation, the Novo Nordisk Foundation, the Lundbeck
   Foundation and the Danish Cancer Society is gratefully acknowledged. The
   authors declare no conflicts of interest.
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NR 120
TC 30
Z9 30
U1 0
U2 4
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 2160-8407
J9 AM J NUCL MED MOLEC
JI Am. J. Nucl. Med. Molec. Imaging
PY 2015
VL 5
IS 5
BP 431
EP 456
PG 26
WC Radiology, Nuclear Medicine & Medical Imaging
WE Emerging Sources Citation Index (ESCI)
SC Radiology, Nuclear Medicine & Medical Imaging
GA V4G9C
UT WOS:000218921100002
PM 26550536
DA 2025-01-04
ER

PT J
AU Liu, XF
   Xu, YX
   Han, LP
   Yi, Y
AF Liu, Xiaofeng
   Xu, Yunxiao
   Han, Liping
   Yi, Yan
TI Reassessing the Potential of Myb-targeted Anti-cancer Therapy
SO JOURNAL OF CANCER
LA English
DT Review
DE MYB; MYB inhibitor; therapeutic strategy; targeted therapy; anti-cancer
   therapy
ID ACUTE MYELOID-LEUKEMIA; ACUTE LYMPHOBLASTIC-LEUKEMIA; DEPENDENT
   GENE-EXPRESSION; HUMAN COLORECTAL-CANCER; C-MYB; BREAST-CANCER;
   TRANSCRIPTION FACTOR; HEMATOPOIETIC-CELLS; ANTISENSE
   OLIGODEOXYNUCLEOTIDES; ABERRANT EXPRESSION
AB Transcription factor MYB is essential for the tumorigenesis of multiple cancers, especially leukemia, breast cancer, colon cancer, adenoid cystic carcinoma and brain cancer. Thus, MYB has been regarded as an attractive target for tumor therapy. However, pioneer studies of antisense oligodeoxynucleotides against MYB, which were launched three decades ago in leukemia therapy, were discontinued because of their unsatisfactory clinical outcomes. In recent years, the roles of MYB in tumor transformation have become increasingly clear. Moreover, the regulatory mechanisms of MYB, such as the vital effects of MYB co-regulators on MYB activity and of transcriptional elongation on MYB expression, have been unveiled. These observations have underpinned novel approaches in inhibiting MYB. This review discusses the structure, function and regulation of MYB, focusing on recent insights into MYB-associated oncogenesis and how MYB-targeted therapeutics can be explored. Additionally, the main MYB-targeted therapies, including novel genetic therapy, RNA interference, microRNAs and low-molecular-weight compounds, which are especially promising inhibitors that target MYB co-regulators and transcriptional elongation, are described, and their prospects are assessed.
C1 [Liu, Xiaofeng; Xu, Yunxiao; Yi, Yan] Cent S Univ, Xiangya Hosp 2, Dept Hematol, 139 Middle Renmin Rd, Changsha 410011, Hunan, Peoples R China.
   [Han, Liping] Changchun Normal Univ, Sch Life Sci, Changchun, Jilin, Peoples R China.
C3 Central South University; Changchun Normal University
RP Yi, Y (corresponding author), Cent S Univ, Xiangya Hosp 2, Dept Hematol, 139 Middle Renmin Rd, Changsha 410011, Hunan, Peoples R China.
EM yiyancsu@csu.edu.cn
RI Yi, Yan/R-8778-2019; Han, Liping/HTQ-5725-2023
FU National Natural Science Foundation of China [81100360]
FX This study was supported in part by the National Natural Science
   Foundation of China (grant no. 81100360).
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NR 73
TC 32
Z9 38
U1 2
U2 26
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 2018
VL 9
IS 7
BP 1259
EP 1266
DI 10.7150/jca.23992
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FZ5KB
UT WOS:000427630100015
PM 29675107
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Zhou, YY
   Li, XY
   Morita, Y
   Hachimura, S
   Miyakawa, T
   Takahashi, S
   Tanokura, M
AF Zhou, Yingyu
   Li, Xuyang
   Morita, Yuki
   Hachimura, Satoshi
   Miyakawa, Takuya
   Takahashi, Sachiko
   Tanokura, Masaru
TI Identification of the Effects of Chondroitin Sulfate on Inhibiting CDKs
   in Colorectal Cancer Based on Bioinformatic Analysis and Experimental
   Validation
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE CDKs; colorectal cancer; bioinformatics; hub genes; chondroitin sulfate;
   MAP kinase pathways
ID WEB SERVER; KINASES; CARCINOGENESIS; EXPRESSION; BIOMARKERS; APOPTOSIS;
   TARGETS; CELLS; PCNA
AB With a high occurrence rate and high mortality, the treatment of colorectal cancer (CRC) is increasingly attracting the attention of scholars. Hub genes that determine the phenotypes of CRC become essential for targeted therapy. In the present study, the importance of cyclin-dependent kinases (CDKs) on the occurrence of CRC was identified by data mining of The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). The results showed that the gene expression levels of CDK1, CDK4, and CDK6 were obviously changed in different stages of CRC. Among the CDKs, CDK4 was suggested as an independent risk factor for CRC based on Cox analysis. Furthermore, chondroitin sulfate (CS), a kind of dietary supplement to treat osteoarthritis, was predicted to treat CRC based on its chemical structure and GEO datasets. Cell assay experiments with the human CRC cell line HCT-116 also verified this prediction. CS inhibited the gene and protein expression levels of CDKs and increased the ratios of apoptotic or dead HCT-116 cells by regulating mitogen-activated protein (MAP) kinase pathways. Our data highlight the essential roles of CDKs in CRC carcinogenesis and the effects of CS on treating CRC, both of which will contribute to the future CRC treatment.</p>
C1 [Zhou, Yingyu; Li, Xuyang; Morita, Yuki; Miyakawa, Takuya; Tanokura, Masaru] Univ Tokyo, Grad Sch Agr & Life Sci, Dept Appl Biol Chem, Tokyo, Japan.
   [Zhou, Yingyu; Hachimura, Satoshi; Tanokura, Masaru] Univ Tokyo, Res Ctr Food Safety, Grad Sch Agr & Life Sci, Tokyo, Japan.
   [Morita, Yuki; Takahashi, Sachiko] Med Viara, Dept Res, Tokyo, Japan.
   [Morita, Yuki; Takahashi, Sachiko] MAF Clin, Dept Res, Tokyo, Japan.
C3 University of Tokyo; University of Tokyo
RP Tanokura, M (corresponding author), Univ Tokyo, Grad Sch Agr & Life Sci, Dept Appl Biol Chem, Tokyo, Japan.; Tanokura, M (corresponding author), Univ Tokyo, Res Ctr Food Safety, Grad Sch Agr & Life Sci, Tokyo, Japan.; Takahashi, S (corresponding author), Med Viara, Dept Res, Tokyo, Japan.; Takahashi, S (corresponding author), MAF Clin, Dept Res, Tokyo, Japan.
EM info@mafclinic.com; amtanok@mail.ecc.u-tokyo.ac.jp
RI Miyakawa, Takuya/IUN-7847-2023
OI Tanokura, Masaru/0000-0001-5072-2480; Miyakawa,
   Takuya/0000-0001-5957-3549; Zhou, Yingyu/0000-0001-9715-7909
FU  [180600000690]
FX This research was supported by the collaboration fund (number
   180600000690) from Medical Viara.
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NR 37
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Z9 5
U1 0
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 SEP 14
PY 2021
VL 11
AR 705939
DI 10.3389/fonc.2021.705939
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UZ6QQ
UT WOS:000702328600001
PM 34595111
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Weng, JY
   Li, SB
   Zhu, ZL
   Liu, Q
   Zhang, RX
   Yang, YF
   Li, XX
AF Weng, Junyong
   Li, Shanbao
   Zhu, Zhonglin
   Liu, Qi
   Zhang, Ruoxin
   Yang, Yufei
   Li, Xinxiang
TI Exploring immunotherapy in colorectal cancer
SO JOURNAL OF HEMATOLOGY & ONCOLOGY
LA English
DT Review
DE Metastatic colorectal cancer; Immune checkpoint blockade; Immunotherapy;
   Biomarkers; Immune desert; Microsatellite instability; Precision
   medicine
ID TUMOR MUTATIONAL BURDEN; MISMATCH REPAIR DEFICIENCY; TO-LYMPHOCYTE
   RATIO; CONSENSUS MOLECULAR SUBTYPES; MHC CLASS-I; MICROSATELLITE
   INSTABILITY; PD-1 BLOCKADE; COLON-CANCER; OPEN-LABEL; MELANOMA-CELLS
AB Chemotherapy combined with or without targeted therapy is the fundamental treatment for metastatic colorectal cancer (mCRC). Due to the adverse effects of chemotherapeutic drugs and the biological characteristics of the tumor cells, it is difficult to make breakthroughs in traditional strategies. The immune checkpoint blockades (ICB) therapy has made significant progress in the treatment of advanced malignant tumors, and patients who benefit from this therapy may obtain a long-lasting response. Unfortunately, immunotherapy is only effective in a limited number of patients with microsatellite instability-high (MSI-H), and segment initial responders can subsequently develop acquired resistance. From September 4, 2014, the first anti-PD-1/PD-L1 drug Pembrolizumab was approved by the FDA for the second-line treatment of advanced malignant melanoma. Subsequently, it was approved for mCRC second-line treatment in 2017. Immunotherapy has rapidly developed in the past 7 years. The in-depth research of the ICB treatment indicated that the mechanism of colorectal cancer immune-resistance has become gradually clear, and new predictive biomarkers are constantly emerging. Clinical trials examining the effect of immune checkpoints are actively carried out, in order to produce long-lasting effects for mCRC patients. This review summarizes the treatment strategies for mCRC patients, discusses the mechanism and application of ICB in mCRC treatment, outlines the potential markers of the ICB efficacy, lists the key results of the clinical trials, and collects the recent basic research results, in order to provide a theoretical basis and practical direction for immunotherapy strategies.
C1 [Weng, Junyong; Zhu, Zhonglin; Liu, Qi; Zhang, Ruoxin; Yang, Yufei; Li, Xinxiang] Fudan Univ, Dept Colorectal Surg, Shanghai Canc Ctr, 270 Dongan Rd, Shanghai 200032, Peoples R China.
   [Li, Shanbao] Shanghai Jiao Tong Univ, Shanghai Gen Hosp, Sch Med, Dept Gen Surg, Shanghai 200080, Peoples R China.
C3 Fudan University; Shanghai Jiao Tong University
RP Li, XX (corresponding author), Fudan Univ, Dept Colorectal Surg, Shanghai Canc Ctr, 270 Dongan Rd, Shanghai 200032, Peoples R China.
EM xinxiangli@fudan.edu.cn
RI Yang, yufei/KHW-2735-2024
FU National Natural Science Foundation of China [82003060, 81772599,
   81972260]
FX This study was supported by the National Natural Science Foundation of
   China (82003060, 81772599, and 81972260).
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NR 220
TC 162
Z9 169
U1 27
U2 116
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1756-8722
J9 J HEMATOL ONCOL
JI J. Hematol. Oncol.
PD JUL 16
PY 2022
VL 15
IS 1
AR 95
DI 10.1186/s13045-022-01294-4
PG 28
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA 2Y8QU
UT WOS:000826155000001
PM 35842707
OA Green Published, gold
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Hechtman, JF
   Zehir, A
   Yaeger, R
   Wang, L
   Middha, S
   Zheng, T
   Hyman, DM
   Solit, D
   Arcila, ME
   Borsu, L
   Shia, J
   Vakiani, E
   Saltz, L
   Ladanyi, M
AF Hechtman, Jaclyn F.
   Zehir, Ahmet
   Yaeger, Rona
   Wang, Lu
   Middha, Sumit
   Zheng, Tao
   Hyman, David M.
   Solit, David
   Arcila, Maria E.
   Borsu, Laetitia
   Shia, Jinru
   Vakiani, Efsevia
   Saltz, Leonard
   Ladanyi, Marc
TI Identification of Targetable Kinase Alterations in Patients with
   Colorectal Carcinoma That are Preferentially Associated with Wild-Type
   RAS/RAF
SO MOLECULAR CANCER RESEARCH
LA English
DT Article
ID CANCER PATIENTS; MUTATIONS; EGFR; HER2; AMPLIFICATION; HYBRIDIZATION;
   FUSIONS; SHOWS; KRAS
AB Targeted therapy for metastatic colorectal carcinoma consists of anti-EGFR therapy for patients with RAS/RAF wild-type tumors. However, the response rate remains low, suggesting the presence of alternative drivers possibly also representing potential therapeutic targets. We investigated receptor tyrosine kinase (RTK) alterations and MAP2K1 (MEK1) mutations in a large cohort of colorectal carcinoma patients studied by Memorial Sloan Kettering-Integrated Mutation Profiling of Actionable Cancer Targets and The Cancer Genome Atlas, focusing on amplifications, fusions, and hotspot mutations in RTK genes and MAP2K1. RTK gene amplifications were confirmed with FISH and immunohistochemical (IHC) staining. Among 751 colorectal carcinoma cases with next-generation sequencing data, 7% and 1% of colorectal carcinoma harbored RTK alterations and MAP2K1 hotspot mutations (n = 7), respectively. RTK-altered cases had fewer concurrent RAS/RAF mutations (P = 0.003) than RTK/MAP2K1 wild-type colorectal carcinoma. MAP2K1-mutated colorectal carcinoma showed no RAS/RAF mutations. ERBB2 (n = 32) and EGFR (n = 13) were the most frequently altered RTKs, both activated by amplification and/or hotspot mutations. Three RTK fusions were identified: NCOA4-RET, ERBB2-GRB7, and ETV6-NTRK3. Only 1 of 6 patients with an RTK or MAP2K1 alteration who received anti-EGFR and/or anti-ERBB2 therapy demonstrated stable disease; the rest progressed immediately. Overall, RTK alterations and MAP2K1 mutations occur in approximately 8% of colorectal carcinoma. In spite of the usual absence of RAS/RAF mutations, response to anti-EGFR and/or anti-ERBB2 therapy was poor in this limited group. Larger studies are warranted to further define these kinase alterations as novel therapeutic targets in colorectal carcinoma and as negative predictors of response to anti-EGFR therapy.
C1 [Hechtman, Jaclyn F.; Zehir, Ahmet; Wang, Lu; Middha, Sumit; Zheng, Tao; Arcila, Maria E.; Borsu, Laetitia; Shia, Jinru; Vakiani, Efsevia; Saltz, Leonard; Ladanyi, Marc] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10065 USA.
   [Yaeger, Rona; Hyman, David M.; Solit, David] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10065 USA.
   [Solit, David; Ladanyi, Marc] Mem Sloan Kettering Canc Ctr, Human Oncol & Pathogenesis Program, New York, NY 10065 USA.
C3 Memorial Sloan Kettering Cancer Center; Memorial Sloan Kettering Cancer
   Center; Memorial Sloan Kettering Cancer Center
RP Hechtman, JF (corresponding author), Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10065 USA.
EM hechtmaj@mskcc.org
RI Zehir, Ahmet/ABE-7155-2020; Ladanyi, Marc/AAG-8585-2019; Hechtman,
   Jaclyn/A-3277-2013; Arcila, Maria/ABE-2235-2021; Solit,
   David/AAC-5309-2019; , Lu/N-8128-2018
OI Hechtman, Jaclyn/0000-0003-2645-0985; , Lu/0000-0002-0073-0666; Shia,
   Jinru/0000-0002-4351-2511; Solit, David/0000-0002-6614-802X; Middha,
   Sumit/0000-0003-4135-6268
FU Marie-Josee and Henry R. Kravis Center for Molecular Oncology; Anbinder
   Fund
FX The MSK-IMPACT program is supported in part by the Marie-Josee and Henry
   R. Kravis Center for Molecular Oncology. The MSKCC Sequenom facility was
   supported by the Anbinder Fund.
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IS 3
BP 296
EP 301
DI 10.1158/1541-7786.MCR-15-0392-T
PG 6
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DG3XM
UT WOS:000372004400006
PM 26660078
OA Green Accepted, Green Submitted, Bronze
DA 2025-01-04
ER

PT J
AU Gondal, MN
   Butt, RN
   Shah, OS
   Sultan, MU
   Mustafa, G
   Nasir, Z
   Hussain, R
   Khawar, H
   Qazi, R
   Tariq, M
   Faisal, A
   Chaudhary, SU
AF Gondal, Mahnoor Naseer
   Butt, Rida Nasir
   Shah, Osama Shiraz
   Sultan, Muhammad Umer
   Mustafa, Ghulam
   Nasir, Zainab
   Hussain, Risham
   Khawar, Huma
   Qazi, Romena
   Tariq, Muhammad
   Faisal, Amir
   Chaudhary, Safee Ullah
TI A Personalized Therapeutics Approach Using an <i>In Silico Drosophila
   Patient Model</i> Reveals Optimal Chemo- and Targeted Therapy
   Combinations for Colorectal Cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE personalized in silico cancer models; Boolean network models; cancer
   systems biology; preclinical in silico drug screening; combinatorial
   therapeutics
ID INTESTINAL STEM-CELL; BORTEZOMIB PLUS DOCETAXEL; HUMAN-DISEASE;
   MULTIDRUG-RESISTANCE; TUMOR HETEROGENEITY; SOLID TUMORS; LUNG-CANCER;
   PHASE-I/II; PATHWAY; DRUG
AB In silico models of biomolecular regulation in cancer, annotated with patient-specific gene expression data, can aid in the development of novel personalized cancer therapeutic strategies. Drosophila melanogaster is a well-established animal model that is increasingly being employed to evaluate such preclinical personalized cancer therapies. Here, we report five Boolean network models of biomolecular regulation in cells lining the Drosophila midgut epithelium and annotate them with colorectal cancer patient-specific mutation data to develop an in silico Drosophila Patient Model (DPM). We employed cell-type-specific RNA-seq gene expression data from the FlyGut-seq database to annotate and then validate these networks. Next, we developed three literature-based colorectal cancer case studies to evaluate cell fate outcomes from the model. Results obtained from analyses of the proposed DPM help: (i) elucidate cell fate evolution in colorectal tumorigenesis, (ii) validate cytotoxicity of nine FDA-approved CRC drugs, and (iii) devise optimal personalized treatment combinations. The personalized network models helped identify synergistic combinations of paclitaxel-regorafenib, paclitaxel-bortezomib, docetaxel-bortezomib, and paclitaxel-imatinib for treating different colorectal cancer patients. Follow-on therapeutic screening of six colorectal cancer patients from cBioPortal using this drug combination demonstrated a 100% increase in apoptosis and a 100% decrease in proliferation. In conclusion, this work outlines a novel roadmap for decoding colorectal tumorigenesis along with the development of personalized combinatorial therapeutics for preclinical translational studies.
C1 [Gondal, Mahnoor Naseer; Butt, Rida Nasir; Shah, Osama Shiraz; Sultan, Muhammad Umer; Mustafa, Ghulam; Nasir, Zainab; Hussain, Risham; Khawar, Huma; Chaudhary, Safee Ullah] Lahore Univ Management Sci, Dept Biol, Biomed Informat Res Lab, Lahore, Pakistan.
   [Qazi, Romena] Shaukat Khanum Mem Canc Hosp & Res Ctr, Dept Pathol, Lahore, Pakistan.
   [Tariq, Muhammad] Lahore Univ Management Sci, Dept Biol, Epigenet Lab, Lahore, Pakistan.
   [Faisal, Amir] Lahore Univ Management Sci, Dept Biol, Canc Therapeut Lab, Lahore, Pakistan.
C3 Lahore University of Management Sciences; Shaukat Khanum Memorial Cancer
   Hospital & Research Centre; Lahore University of Management Sciences;
   Lahore University of Management Sciences
RP Chaudhary, SU (corresponding author), Lahore Univ Management Sci, Dept Biol, Biomed Informat Res Lab, Lahore, Pakistan.
EM safee.ullah.chaudhary@gmail.com
RI Gondal, Mahnoor/LBH-2674-2024; Tariq, Muhammad/KHZ-0791-2024; Chaudhary,
   Safee/JAC-9269-2023
OI Gondal, Mahnoor/0000-0002-9419-6758; Chaudhary, Safee
   Ullah/0000-0002-3758-6581
FU National ICT-RD Fund [SRG-209]; HEC [21-30SRGP/RD/HEC/2014,
   20-2269/NRPU/RD/HEC/12/4792, 20-3629/NRPU/RD/HEC/14/585]; TWAS [RG
   14-319 RG/ITC/AS_C]; LUMS [STG-BIO-1008, FIF-BIO-2052, FIF-BIO-0255,
   SRP-185-BIO, SRP-058-BIO, FIF-477-1819-BIO];  [RF-NCBC-015]; 
   [NGIRI-2020-4771]
FX This work was supported by the National ICT-R&D Fund (SRG-209),
   RF-NCBC-015, NGIRI-2020-4771, HEC (21-30SRGP/R&D/HEC/2014,
   20-2269/NRPU/R&D/HEC/12/4792 and 20-3629/NRPU/R&D/HEC/14/585), TWAS (RG
   14-319 RG/ITC/AS_C) and LUMS (STG-BIO-1008, FIF-BIO-2052, FIF-BIO-0255,
   SRP-185-BIO, SRP-058-BIO and FIF-477-1819-BIO) grants.
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NR 120
TC 6
Z9 6
U1 0
U2 3
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 JUL 16
PY 2021
VL 11
AR 692592
DI 10.3389/fonc.2021.692592
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TT0HA
UT WOS:000680031600001
PM 34336681
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Shi, Y
   Jiang, B
   Zhao, JW
AF Shi, Yan
   Jiang, Bing
   Zhao, Jingwen
TI Induction mechanisms of autophagy and endoplasmic reticulum stress in
   intestinal ischemia-reperfusion injury, inflammatory bowel disease, and
   colorectal cancer
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE Autophagy; Endoplasmic reticulum stress; Intestinal ischemia-reperfusion
   injury; Inflammatory bowel disease; Colorectal cancer
ID ER STRESS; INDUCED APOPTOSIS; TH17 CELLS; EXPRESSION; PATHOGENESIS;
   PROTECTS; PATHWAY; MTOR; ISCHEMIA/REPERFUSION; PROGRESSION
AB In recent years, the incidence of intestinal ischemia-reperfusion injury (II/RI), inflammatory bowel disease (IBD), and colorectal cancer (CRC) has been gradually increasing, posing significant threats to human health. Autophagy and endoplasmic reticulum stress (ERS) play important roles in II/RI. Damage caused by ischemia and cellular stress can activate ERS, which in turn initiates autophagy to clear damaged organelles and abnormal proteins, thereby alleviating ERS and maintaining the intestinal environment. In IBD, chronic inflammation damages intestinal tissues and activates autophagy and ERS. Autophagy is initiated by upregulating ATG genes and downregulating factors that inhibit autophagy, thereby clearing abnormal proteins, damaged organelles, and bacteria. Simultaneously, persistent inflammatory stimulation can also trigger ERS, leading to protein imbalance and abnormal folding in the ER lumen. The activation of ERS can maintain cellular homeostasis by initiating the autophagy process, thereby reducing inflammatory responses and cell apoptosis in the intestine. In CRC, excessive cell proliferation and protein synthesis lead to increased ERS. The activation of ERS, regulated by signaling pathways such as IRE1 alpha and PERK, can initiate autophagy to clear abnormal proteins and damaged organelles, thereby reducing the negative effects of ERS. It can be seen that autophagy and ERS play a crucial regulatory role in the development of intestinal diseases. Therefore, the progress in targeted therapy for intestinal diseases based on autophagy and ERS provides novel strategies for managing intestinal diseases. In this paper, we review the advances in regulation of autophagy and ERS in intestinal diseases, emphasizing the potential molecular mechanisms for therapeutic applications.
C1 [Shi, Yan] Gansu Univ Tradit Chinese Med, Dept Basic Med, Lanzhou 730000, Gansu, Peoples R China.
   [Jiang, Bing] Gansu Univ Tradit Chinese Med, Dept Integrated Chinese & Western Med, Lanzhou 730000, Gansu, Peoples R China.
   [Zhao, Jingwen] Baoji Tradit Chinese Med Hosp, Dept Proctol, 43 Baofu Rd, Baoji 721001, Shanxi, Peoples R China.
C3 Gansu University of Chinese Medicine; Gansu University of Chinese
   Medicine
RP Zhao, JW (corresponding author), Baoji Tradit Chinese Med Hosp, Dept Proctol, 43 Baofu Rd, Baoji 721001, Shanxi, Peoples R China.
EM ZJW1344956830@163.com
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NR 140
TC 11
Z9 12
U1 7
U2 20
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 2024
VL 170
AR 115984
DI 10.1016/j.biopha.2023.115984
EA DEC 2023
PG 17
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA DV7Y9
UT WOS:001134934800001
PM 38070244
OA gold
DA 2025-01-04
ER

PT J
AU Hasbullah, HH
   Musa, M
AF Hasbullah, Hidayati Husainy
   Musa, Marahaini
TI Gene Therapy Targeting p53 and KRAS for Colorectal Cancer Treatment: A
   Myth or the Way Forward?
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE colon cancer; mutation; p53; KRAS; targeted therapy
ID QUADRUPLEX DNA STRUCTURES; KIRSTEN RAS MUTATIONS; COLON-CANCER; K-RAS;
   SIGNALING PATHWAYS; PROGNOSTIC VALUE; PD-1 BLOCKADE; REXIN-G;
   NANOPARTICLE; OXALIPLATIN
AB Colorectal cancer (CRC) is the third most commonly diagnosed malignancy worldwide and is responsible as one of the main causes of mortality in both men and women. Despite massive efforts to raise public awareness on early screening and significant advancements in the treatment for CRC, the majority of cases are still being diagnosed at the advanced stage. This contributes to low survivability due to this cancer. CRC patients present various genetic changes and epigenetic modifications. The most common genetic alterations associated with CRC are p53 and KRAS mutations. Gene therapy targeting defect genes such as TP53 (tumor suppressor gene encodes for p53) and KRAS (oncogene) in CRC potentially serves as an alternative treatment avenue for the disease in addition to the standard therapy. For the last decade, significant developments have been seen in gene therapy for translational purposes in treating various cancers. This includes the development of vectors as delivery vehicles. Despite the optimism revolving around targeted gene therapy for cancer treatment, it also has various limitations, such as a lack of availability of related technology, high cost of the involved procedures, and ethical issues. This article will provide a review on the potentials and challenges of gene therapy targeting p53 and KRAS for the treatment of CRC.
C1 [Hasbullah, Hidayati Husainy; Musa, Marahaini] Univ Sains Malaysia, Sch Med Sci, Human Genome Ctr, Kubang Kerian 16150, Kelantan, Malaysia.
C3 Universiti Sains Malaysia
RP Musa, M (corresponding author), Univ Sains Malaysia, Sch Med Sci, Human Genome Ctr, Kubang Kerian 16150, Kelantan, Malaysia.
EM marahaini.musa@usm.my
RI Musa, Marahaini/E-9987-2019
OI Musa, Marahaini/0000-0002-0165-5741
FU PPSP Incentive Postgraduate Studies Development Fund, School of Medical
   Sciences, USM [1001/PPSP/8070011]
FX FundingThis work was supported by the PPSP Incentive Postgraduate
   Studies Development Fund, School of Medical Sciences, USM (grant account
   number: 1001/PPSP/8070011).
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NR 148
TC 34
Z9 34
U1 2
U2 19
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 NOV
PY 2021
VL 22
IS 21
AR 11941
DI 10.3390/ijms222111941
PG 18
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA WY0KI
UT WOS:000718974900001
PM 34769370
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Baiao, A
   Sousa, F
   Oliveira, AV
   Oliveira, C
   Sarmento, B
AF Baiao, Ana
   Sousa, Flavia
   Oliveira, Ana Vanessa
   Oliveira, Carla
   Sarmento, Bruno
TI Effective intracellular delivery of bevacizumab <i>via</i> PEGylated
   polymeric nanoparticles targeting the CD44v6 receptor in colon cancer
   cells
SO BIOMATERIALS SCIENCE
LA English
DT Article
ID COLORECTAL-CANCER; THERAPEUTIC TARGET; VEGF; ANTIBODY; PLGA;
   PHARMACOKINETICS; EXPRESSION; IMPACT; DRUGS
AB Colorectal cancer (CRC) is one of the most common and deadly cancers in the world, mainly due to its metastatic and metabolic ability. The CD44 receptor isoform containing exon 6 (CD44v6) is a transmembrane protein that plays an important role in the establishment of tumors and metastasis, which make this molecule a potential target for therapy and diagnosis of tumors. Aiming at a targeted therapy, the anti-VEGF monoclonal antibody (mAb) bevacizumab was loaded into poly(lactic-co-glycolic acid)-polyethylene glycol (PLGA-PEG) nanoparticles (NPs) functionalized with an antibody fragment (Fab) specific for CD44v6-expressing human cancer cells. The sizes of NPs were in the range of 150-250 nm and they had a negative charge between -5 and -10 mV, with an association efficiency (AE) of bevacizumab of 86%. v6 Fab-PLGA-PEG NPs containing bevacizumab specifically bonded to the CD44v6 cell surface receptor and exhibited higher internalization into CD44v6+ epithelial cells than bare and (-) Fab-PLGA-PEG NPs. To understand the biological effect of NP targeting, the intracellular levels of bevacizumab and VEGF were evaluated after the incubation of targeted and untargeted NPs. The intracellular levels of bevacizumab were significantly higher in cells incubated with v6 Fab-PLGA-PEG NPs and these NPs resulted in a significant decrease in the intracellular VEGF compared to untargeted NPs and free bevacizumab. PLGA-PEG NPs, surface-functionalized with a v6-specific Fab, have the potential to intracellularly deliver bevacizumab into CD44v6 expressing cancer cells.
C1 [Baiao, Ana; Sousa, Flavia; Oliveira, Ana Vanessa; Oliveira, Carla; Sarmento, Bruno] Univ Porto, i3S Inst Invest & Inovacao Saude, Rua Alfredo Allen 208, P-4200393 Porto, Portugal.
   [Baiao, Ana; Sousa, Flavia; Oliveira, Ana Vanessa; Sarmento, Bruno] Univ Porto, INEB Inst Natl Engn Biomed, Rua Alfredo Allen 208, P-4200393 Porto, Portugal.
   [Baiao, Ana] Univ Aveiro, Dept Ciencias Med, P-3810193 Aveiro, Portugal.
   [Sousa, Flavia; Sarmento, Bruno] CESPU Inst Invest & Formacao Avancada Ciencias, Rua Cent Gandra 1317, P-4585116 Gandra, Portugal.
   [Oliveira, Carla] Univ Porto, IPATIMUP Inst Patol & Imunol Mol, Rua Alfredo Allen 208, P-4200393 Porto, Portugal.
C3 Universidade do Porto; i3S - Instituto de Investigacao e Inovacao em
   Saude, Universidade do Porto; Universidade do Porto; Universidade de
   Aveiro; Universidade do Porto
RP Sarmento, B (corresponding author), Univ Porto, i3S Inst Invest & Inovacao Saude, Rua Alfredo Allen 208, P-4200393 Porto, Portugal.; Sarmento, B (corresponding author), Univ Porto, INEB Inst Natl Engn Biomed, Rua Alfredo Allen 208, P-4200393 Porto, Portugal.; Sarmento, B (corresponding author), CESPU Inst Invest & Formacao Avancada Ciencias, Rua Cent Gandra 1317, P-4585116 Gandra, Portugal.
EM bruno.sarmento@ineb.up.pt
RI Sousa, Flavia/AAY-1208-2020; Baião, Ana/C-7203-2017; Sarmento,
   Bruno/J-6265-2013; Oliveira, Carla/F-8188-2011
OI Sarmento, Bruno/0000-0001-5763-7553; Baiao, Ana/0000-0003-3314-6973;
   Sousa, Flavia/0000-0001-6587-6175; Oliveira, Ana/0000-0003-3162-250X;
   Oliveira, Carla/0000-0001-8340-2264
FU Norte Portugal Regional Operational Programme (NORTE 2020)
   [NORTE-01-0145-FEDER-000012]; COMPETE 2020 - Operacional Programme for
   Competitiveness and Internationalisation (POCI), under the PORTUGAL 2020
   Partnership Agreement, through the FEDER - Fundo Europeu de
   Desenvolvimento Regional [NORTE-01-0145-FEDER-000012]; Portuguese funds
   through FCT - Fundacao para a Ciencia e a Tecnologia/Ministerio da
   Ciencia, Tecnologia e Ensino Superior [UID/BIM/04293/2019]
FX This work was financed by the project NORTE-01-0145-FEDER-000012 by
   Norte Portugal Regional Operational Programme (NORTE 2020), and COMPETE
   2020 - Operacional Programme for Competitiveness and
   Internationalisation (POCI), under the PORTUGAL 2020 Partnership
   Agreement, through the FEDER - Fundo Europeu de Desenvolvimento
   Regional, and by Portuguese funds through FCT - Fundacao para a Ciencia
   e a Tecnologia/Ministerio da Ciencia, Tecnologia e Ensino Superior in
   the framework of the project "Institute for Research and Innovation in
   Health Sciences" UID/BIM/04293/2019.
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NR 44
TC 29
Z9 29
U1 1
U2 18
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 2047-4830
EI 2047-4849
J9 BIOMATER SCI-UK
JI Biomater. Sci.
PD JUL 7
PY 2020
VL 8
IS 13
BP 3720
EP 3729
DI 10.1039/d0bm00556h
PG 10
WC Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Materials Science
GA ME2UU
UT WOS:000544517200010
PM 32500879
DA 2025-01-04
ER

PT J
AU Shida, D
   Tanabe, T
   Boku, N
   Takashima, A
   Yoshida, T
   Tsukamoto, S
   Kanemitsu, Y
AF Shida, Dai
   Tanabe, Taro
   Boku, Narikazu
   Takashima, Atsuo
   Yoshida, Takefumi
   Tsukamoto, Shunsuke
   Kanemitsu, Yukihide
TI Prognostic Value of Primary Tumor Sidedness for Unresectable Stage IV
   Colorectal Cancer: A Retrospective Study
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Article
ID III COLON-CANCER; RESECTION; SUBTYPES; OUTCOMES; SOCIETY
AB Background. When treated with molecular targeted agents, patients with unresectable colorectal cancer with right-sided tumors have poorer prognoses than those with left-sided tumors. While primary tumor sidedness may have prognostic value, the prognostic value of tumor sidedness in chemotherapy regimens without targeted therapy is unclear.
   Methods. Our study population comprised 678 consecutive patients with unresectable stage IV colorectal cancer who received systemic chemotherapy at the National Cancer Center Hospital in Japan from 1999 to 2015. Patients were stratified by treatment subgroup (with or without molecular targeted agents and with or without palliative primary tumor resection), and relationships between overall survival (OS) and primary tumor sidedness were evaluated. Multivariate analyses were also performed.
   Results. Overall, 193 (28%) tumors were right-sided (cecum to transverse colon) and 485 (72%) were left-sided (splenic flexure to rectum). In the overall population, median survival time was 16.4 months for those with right-sided tumors and 23.4 months for those with left-sided tumors (p<0.01). Regardless of the use or non-use of targeted agents and performance or non-performance of palliative resection of the primary tumor, those with right-sided tumors showed significantly poorer prognosis than those with left-sided tumors, in all categories. Multivariate analyses showed right-sided tumors to be associated with shorter OS compared with left-sided tumors (hazard ratio 1.26, 95% confidence interval 1.03-1.53; p=0.024).
   Conclusion. Unresectable stage IV right-sided colorectal tumors were associated with shorter OS compared with left-sided tumors, regardless of treatment strategy. Primary tumor sidedness may be an independent prognostic factor.
C1 [Shida, Dai; Tanabe, Taro; Yoshida, Takefumi; Tsukamoto, Shunsuke; Kanemitsu, Yukihide] Natl Canc Ctr, Dept Colorectal Surg, Tokyo, Japan.
   [Boku, Narikazu; Takashima, Atsuo] Natl Canc Ctr, Gastrointestinal Med Oncol Div, Tokyo, Japan.
C3 National Cancer Center - Japan; National Cancer Center - Japan
RP Shida, D (corresponding author), Natl Canc Ctr, Dept Colorectal Surg, Tokyo, Japan.
EM dshida-tky@umin.ac.jp
OI Shida, Dai/0000-0003-3294-1924
CR AJCC/UICC, 2017, TNM classification of malignant tumours, V8th
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NR 21
TC 28
Z9 29
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9265
EI 1534-4681
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD MAY
PY 2019
VL 26
IS 5
BP 1358
EP 1365
DI 10.1245/s10434-019-07209-x
PG 8
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA HT7DY
UT WOS:000464726300033
PM 30719633
DA 2025-01-04
ER

PT J
AU Zhang, SX
   Duan, JL
   Yang, YP
   Gong, HJ
   Tang, Y
   Xiao, M
   Li, M
   Li, QS
   Wang, YL
AF Zhang, Shuxian
   Duan, Jiale
   Yang, Yanping
   Gong, Hanjuan
   Tang, Yi
   Xiao, Ming
   Li, Ming
   Li, Qingshu
   Wang, Yalan
TI Identification of the role of mono-ADP-ribosylation in colorectal cancer
   by integrated transcriptome analysis
SO MEDICAL ONCOLOGY
LA English
DT Article
DE Colorectal cancer; Mono-ADP-ribosylation; Transcriptome sequencing;
   Endoplasmic reticulum; Alternative splicing
ID ENDOPLASMIC-RETICULUM STRESS; RIBOSYLTRANSFERASE 1; POLY(ADP-RIBOSE)
   POLYMERASE-1; SIGNALING PATHWAYS; CT26 CELLS; APOPTOSIS; PROTEIN; ART1;
   EXPRESSION; MIGRATION
AB Our previous study clarified the carcinogenic properties of arginine-specific mono-ADP-ribosyltransferase 1 (ART1), which results in a critical post-translational modification that changes the structure and function of proteins and is widely involved in important processes. This study provides, for the first time, a comprehensive transcriptomic analysis of colorectal cancer cells with ART1 silencing by Illumina RNA-Seq and related verification experiments. Lentiviral infection was used to construct a CT-26 cell line with stable knockdown of the ART1 gene, and a whole transcriptome sequencing technique was performed to identify differentially expressed genes (DEGs). GO and KEGG classification/enrichment analyses and verification experiments were performed to determine the role of ART1 in the progression of colorectal cancer. A total of 5552 DEGs, GO functions and KEGG pathways with the highest enrichment, various SNPs, and diverse splicing patterns were identified. Importantly, knockdown of ART1 affected the splicing of certain key genes related to tumor cell growth and downregulated the expression of the key gene PTBP1 for alternative splicing. The overall attenuation of the endoplasmic reticulum unfolded protein response (UPR) signaling pathway caused by the inhibition of mono-ADP-ribosylation of GRP78 could disrupt UPR signaling, leading to the occurrence of apoptosis to impede tumorigenesis. ART1, which is clustered in organelles, may promote the development of colorectal cancer by participating in a variety of new mechanisms, including endoplasmic reticulum stress regulation and alternative splicing, and may be a good clinical drug target for targeted therapy of CRC.
C1 [Zhang, Shuxian; Duan, Jiale; Yang, Yanping; Gong, Hanjuan; Tang, Yi; Xiao, Ming; Li, Ming; Li, Qingshu; Wang, Yalan] Chongqing Med Univ, Basic Med Coll, Dept Pathol, Mol Med & Canc Res Ctr, 1 Yixueyuan Rd, Chongqing 400016, Peoples R China.
C3 Chongqing Medical University
RP Wang, YL (corresponding author), Chongqing Med Univ, Basic Med Coll, Dept Pathol, Mol Med & Canc Res Ctr, 1 Yixueyuan Rd, Chongqing 400016, Peoples R China.
EM wangyalan@cqmu.edu.cn
FU Innovation Project of Graduate Student in Chongqing [CYB19160]; National
   Nature Science Foundation of China [30870946]; Science and Technology
   Research Foundation of Chongqing Municipal Education Commission
   [KJQN201800435]
FX The research was supported by Innovation Project of Graduate Student in
   Chongqing (CYB19160); National Nature Science Foundation of China
   (30870946); Science and Technology Research Foundation of Chongqing
   Municipal Education Commission (KJQN201800435).
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NR 30
TC 0
Z9 0
U1 0
U2 5
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 SEP
PY 2021
VL 38
IS 9
AR 111
DI 10.1007/s12032-021-01559-x
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UL0UN
UT WOS:000692376500004
PM 34357465
DA 2025-01-04
ER

PT J
AU Tougeron, D
   Sueur, B
   Zaanan, A
   de la Fouchardiére, C
   Sefrioui, D
   Lecomte, T
   Aparicio, T
   Des Guetz, G
   Artru, P
   Hautefeuille, V
   Coriat, R
   Moulin, V
   Locher, C
   Touchefeu, Y
   Lecaille, C
   Goujon, G
   Ferru, A
   Evrard, C
   Chautard, R
   Gentilhomme, L
   Vernerey, D
   Taieb, J
   André, T
   Henriques, J
   Cohen, R
AF Tougeron, David
   Sueur, Benjamin
   Zaanan, Aziz
   de la Fouchardiere, Christelle
   Sefrioui, David
   Lecomte, Thierry
   Aparicio, Thomas
   Des Guetz, Gaetan
   Artru, Pascal
   Hautefeuille, Vincent
   Coriat, Romain
   Moulin, Valerie
   Locher, Christophe
   Touchefeu, Yann
   Lecaille, Cedric
   Goujon, Gael
   Ferru, Aurelie
   Evrard, Camille
   Chautard, Romain
   Gentilhomme, Lucie
   Vernerey, Dewi
   Taieb, Julien
   Andre, Thierry
   Henriques, Julie
   Cohen, Romain
CA Assoc Gastro-enterologues Oncologu
TI Prognosis and chemosensitivity of deficient MMR phenotype in patients
   with metastatic colorectal cancer: An AGEO retrospective multicenter
   study
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE colorectal cancer; microsatellite instability; deficient mismatch
   repair; metastatic; chemosensitivity
ID MICROSATELLITE-INSTABILITY STATUS; MISMATCH REPAIR STATUS; BRAF
   MUTATION; CONTAINING CHEMOTHERAPY; PRIMARY TUMOR; MONONUCLEOTIDE
   REPEATS; 1ST-LINE CHEMOTHERAPY; POOLED ANALYSIS; BEVACIZUMAB;
   FLUOROURACIL
AB Mismatch repair-deficient (dMMR) and/or microsatellite instability-high (MSI) colorectal cancers (CRC) represent about 5% of metastatic CRC (mCRC). Prognosis and chemosensitivity of dMMR/MSI mCRC remain unclear. This multicenter study included consecutive patients with dMMR/MSI mCRC from 2007 to 2017. The primary endpoint was the progression-free survival (PFS) in a population receiving first-line chemotherapy. Associations between chemotherapy regimen and survival were evaluated using a Cox regression model and inverse of probability of treatment weighting (IPTW) methodology in order to limit potential biases. Overall, 342 patients with dMMR/MSI mCRC were included. Median PFS and overall survival (OS) on first-line chemotherapy were 6.0 and 26.3 months, respectively. For second-line chemotherapy, median PFS and OS were 4.4 and 21.6 months. Longer PFS (8.1 vs. 5.4 months, p = 0.0405) and OS (35.1 vs. 24.4 months, p = 0.0747) were observed for irinotecan-based chemotherapy compared to oxaliplatin-based chemotherapy. The association was no longer statistically significant using IPTW methodology. In multivariable analysis, anti-VEGF as compared to anti-EGFR was associated with a trend to longer OS (HR = 1.78, 95% CI 1.00-3.19, p = 0.0518), whatever the backbone chemotherapy used. Our study shows that dMMR/MSI mCRC patients experienced short PFS with first-line chemotherapy with or without targeted therapy. OS was not different according to the chemotherapy regimen used, but a trend to better OS was observed with anti-VEGF. Our study provides some historical results concerning chemotherapy in dMMR/MSI mCRC in light of the recent nonrandomized trials with immune checkpoint inhibitors.
C1 [Tougeron, David; Sueur, Benjamin] Univ Poitiers Hosp, Gastroenterol Dept, Poitiers, France.
   [Tougeron, David; Sueur, Benjamin] Univ Poitiers, Poitiers, France.
   [Zaanan, Aziz; Taieb, Julien] Paris Descartes Univ, Europeen Georges Pompidou Hosp, Dept Gastroenterol & Digest Oncol, Paris, France.
   [Zaanan, Aziz; Taieb, Julien] Paris Descartes Univ, Sorbonne Paris Cite, Paris, France.
   [de la Fouchardiere, Christelle] Leon Berard Ctr, Med Oncol Dept, Lyon, France.
   [Sefrioui, David; Gentilhomme, Lucie] Univ Normandy, Rouen Univ Hosp, Dept Hepatogastroenterol, Digest Oncol Unit,IRON Grp, Rouen, France.
   [Sefrioui, David; Gentilhomme, Lucie] Univ Normandy, INSERM U1245, Rouen, France.
   [Lecomte, Thierry; Chautard, Romain] Univ Tours, Tours Univ Hosp, Dept Hepatogastroenterol & Digest Oncol, Tours, France.
   [Lecomte, Thierry; Chautard, Romain] Univ Tours, EA 7501 GICC, Tours, France.
   [Aparicio, Thomas] Univ Paris, St Louis Hosp, AP HP, Gastroenterol Dept, Paris, France.
   [Aparicio, Thomas] Avicenne Hosp, Gastroenterol Dept, Bobigny, France.
   [Des Guetz, Gaetan] Avicenne Hosp, Oncol Dept, Bobigny, France.
   [Artru, Pascal] Jean Mermoz Hosp, Lyon, France.
   [Hautefeuille, Vincent] Amiens Univ Hosp, Gastroenterol Dept, Amiens, France.
   [Coriat, Romain] Cochin Univ Hosp, Gastroenterol Dept, Paris, France.
   [Moulin, Valerie] La Rochelle Hosp, Oncol Dept, La Rochelle, France.
   [Locher, Christophe] Meaux Hosp, Gastroenterol & Digest Oncol Dept, Meaux, France.
   [Touchefeu, Yann] Nantes Univ Hosp, Gastroenterol & Digest Oncol Dept, Nantes, France.
   [Lecaille, Cedric] Polyclin Nord Aquitaine, Gastroenterol Dept, Bordeaux, France.
   [Goujon, Gael] Hop Xavier Bichat, Gastroenterol Dept, Paris, France.
   [Ferru, Aurelie; Evrard, Camille] Univ Poitiers Hosp, Med Oncol Dept, Poitiers, France.
   [Vernerey, Dewi; Henriques, Julie] Univ Hosp, Methodol & Qual Life Oncol Unit, INSERM UMR1098, Besancon, France.
   [Andre, Thierry; Cohen, Romain] Sorbonne Univ, Paris, France.
   [Andre, Thierry; Cohen, Romain] St Antoine Hosp, Med Oncol Dept, Paris, France.
C3 CHU Poitiers; Universite de Poitiers; Universite de Poitiers; Assistance
   Publique Hopitaux Paris (APHP); Universite Paris Cite; Hopital
   Universitaire Europeen Georges-Pompidou - APHP; Universite Paris Cite;
   UNICANCER; Centre Leon Berard; Universite de Rouen Normandie; CHU de
   Rouen; Institut National de la Sante et de la Recherche Medicale
   (Inserm); Universite de Rouen Normandie; CHU Tours; Universite de Tours;
   Universite de Tours; Assistance Publique Hopitaux Paris (APHP);
   Universite Paris Cite; Hopital Universitaire Saint-Louis - APHP;
   Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
   Avicenne - APHP; Assistance Publique Hopitaux Paris (APHP); Hopital
   Universitaire Avicenne - APHP; Universite de Picardie Jules Verne
   (UPJV); CHU Amiens; Assistance Publique Hopitaux Paris (APHP);
   Universite Paris Cite; Hopital Universitaire Cochin - APHP; Nantes
   Universite; CHU de Nantes; Assistance Publique Hopitaux Paris (APHP);
   Universite Paris Cite; Hopital Universitaire Bichat-Claude Bernard -
   APHP; CHU Poitiers; Universite de Poitiers; Universite de Franche-Comte;
   CHU Besancon; Institut National de la Sante et de la Recherche Medicale
   (Inserm); Sorbonne Universite; Assistance Publique Hopitaux Paris
   (APHP); Sorbonne Universite; Hopital Universitaire Saint-Antoine - APHP
RP Tougeron, D (corresponding author), Univ Poitiers Hosp, Gastroenterol Dept, Poitiers, France.; Tougeron, D (corresponding author), Univ Poitiers, Poitiers, France.
EM davidtougeron@hotmail.fr
RI Hautefeuille, Vincent/HZJ-6501-2023; André, Thierry/N-8830-2017; de la
   Fouchardiere, Christelle/AAW-7887-2021; Cohen, Romain/AAC-9089-2019;
   tougeron, david/ABF-3217-2020; Touchefeu, Yann/M-2969-2015; APARICIO,
   Thomas/D-6519-2017
OI tougeron, david/0000-0002-8065-9635; Cohen, Romain/0000-0001-9602-5162;
   taieb, julien/0000-0002-9955-4753; DE LA FOUCHARDIERE,
   CHRISTELLE/0000-0003-2291-5693; LECOMTE, Thierry/0000-0001-5093-0212;
   APARICIO, Thomas/0000-0001-8834-6927; Hautefeuille,
   Vincent/0000-0003-2735-6448
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NR 37
TC 60
Z9 62
U1 0
U2 11
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 JUL 1
PY 2020
VL 147
IS 1
BP 285
EP 296
DI 10.1002/ijc.32879
EA FEB 2020
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LI8TI
UT WOS:000513016000001
PM 31970760
OA Bronze
DA 2025-01-04
ER

PT J
AU Ros, J
   Baraibar, I
   Martini, G
   Salvà, F
   Saoudi, N
   Cuadra-Urteaga, JL
   Dienstmann, R
   Tabernero, J
   Élez, E
AF Ros, Javier
   Baraibar, Iosune
   Martini, Giulia
   Salva, Francesc
   Saoudi, Nadia
   Luis Cuadra-Urteaga, Jose
   Dienstmann, Rodrigo
   Tabernero, Josep
   Elez, Elena
TI The Evolving Role of Consensus Molecular Subtypes: a Step Beyond
   Inpatient Selection for Treatment of Colorectal Cancer
SO CURRENT TREATMENT OPTIONS IN ONCOLOGY
LA English
DT Review
DE Consensus molecular subtypes; Immunotherapy; Target therapy; BRAF
   mutation; KRAS mutation; HER2 mutation
ID PLUS CETUXIMAB TREATMENT; MICROSATELLITE INSTABILITY; RAS MUTATIONS;
   COLON-CANCER; INTRATUMORAL HETEROGENEITY; SIGNAL-TRANSDUCTION; PD-1
   BLOCKADE; BRAF MUTATION; EGFR BLOCKADE; SOLID TUMORS
AB Opinion statement The heterogenous nature of colorectal cancer (CRC) renders it a major clinical challenge. Increasing genomic understanding of CRC has improved our knowledge of this heterogeneity and the main cancer drivers, with significant improvements in clinical outcomes. Comprehensive molecular characterization has allowed clinicians a more precise range of treatment options based on biomarker selection. Furthermore, this deep molecular understanding likely extends therapeutic options to a larger number of patients. The biological associations of consensus molecular subtypes (CMS) with clinical outcomes in localized CRC have been validated in retrospective clinical trials. The prognostic role of CMS has also been confirmed in the metastatic setting, with CMS2 having the best prognosis, whereas CMS1 tumors are associated with a higher risk of progression and death after chemotherapy. Similarly, according to mesenchymal features and immunosuppressive molecules, CMS1 responds to immunotherapy, whereas CMS4 has a poorer prognosis, suggesting that a CMS1 signature could identify patients who may benefit from immune checkpoint inhibitors regardless of microsatellite instability (MSI) status. The main goal of these comprehensive analyses is to switch from "one marker-one drug" to "multi-marker drug combinations" allowing oncologists to give "the right drug to the right patient." Despite the revealing data from transcriptomic analyses, the high rate of intra-tumoral heterogeneity across the different CMS subgroups limits its incorporation as a predictive biomarker. In clinical practice, when feasible, comprehensive genomic tests should be performed to identify potentially targetable alterations, particularly in RAS/BRAF wild-type, MSI, and right-sided tumors. Furthermore, CMS has not only been associated with clinical outcomes and specific tumor and patient phenotypes but also with specific microbiome patterns. Future steps will include the integration of clinical features, genomics, transcriptomics, and microbiota to select the most accurate biomarkers to identify optimal treatments, improving individual clinical outcomes. In summary, CMS is context specific, identifies a level of heterogeneity beyond standard genomic biomarkers, and offers a means of maximizing personalized therapy.
C1 [Ros, Javier; Baraibar, Iosune; Salva, Francesc; Saoudi, Nadia; Tabernero, Josep; Elez, Elena] Vall dHebron Univ Hosp, Med Oncol, Barcelona, Spain.
   [Ros, Javier; Baraibar, Iosune; Salva, Francesc; Saoudi, Nadia; Tabernero, Josep; Elez, Elena] Vall DHebron Inst Oncol VHIO, Barcelona, Spain.
   [Ros, Javier; Martini, Giulia] Univ Campania Luigi Vanvitelli, Dept Precis Med, Med Oncol, Naples, Campania, Italy.
   [Luis Cuadra-Urteaga, Jose; Tabernero, Josep] IOB, Barcelona, Spain.
   [Dienstmann, Rodrigo] Hosp Univ Vall DHebron, Vall DHebron Inst Oncol VHIO, Oncol Data Sci ODysSey Grp, Vall DHebron Barcelona Hosp Campus, Barcelona, Spain.
   [Tabernero, Josep] UVic UCC, Vic, Spain.
C3 Hospital Universitari Vall d'Hebron; Vall d'Hebron Institut d'Oncologia
   (VHIO); Universita della Campania Vanvitelli; Vall d'Hebron Institut
   d'Oncologia (VHIO); Hospital Universitari Vall d'Hebron; Universitat de
   Vic - Universitat Central de Catalunya (UVic-UCC)
RP Ros, J (corresponding author), Vall dHebron Univ Hosp, Med Oncol, Barcelona, Spain.; Ros, J (corresponding author), Vall DHebron Inst Oncol VHIO, Barcelona, Spain.; Ros, J (corresponding author), Univ Campania Luigi Vanvitelli, Dept Precis Med, Med Oncol, Naples, Campania, Italy.
EM fjros@vhio.net
RI Ros, Javier/HKF-1171-2023; Baraibar, Iosune/GXF-7067-2022; Martini,
   Giulia/AIB-8246-2022; Gonzalez, Nadia/AAM-9354-2021; Cuadra-Urteaga,
   Jose Luis/C-1783-2016
OI Salva, Francesc/0000-0001-9240-4907; Ros, Javier/0000-0002-8137-5415;
   Cuadra-Urteaga, Jose Luis/0000-0002-9495-7318; Saoudi Gonzalez,
   Nadia/0000-0001-6044-1703; MARTINI, Giulia/0000-0003-4093-2681;
   Baraibar, Iosune/0000-0002-3500-9641
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NR 92
TC 13
Z9 13
U1 0
U2 9
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 DEC
PY 2021
VL 22
IS 12
AR 113
DI 10.1007/s11864-021-00913-5
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA WS2OV
UT WOS:000715027500001
PM 34741675
DA 2025-01-04
ER

PT J
AU Pang, XL
   Li, QX
   Ma, ZP
   Shi, Y
   Ma, YQ
   Li, XX
   Cui, WL
   Zhang, W
AF Pang, Xue-Lian
   Li, Qiao-Xin
   Ma, Zhi-Ping
   Shi, Yi
   Ma, Yu-Qing
   Li, Xin-Xia
   Cui, Wen-Li
   Zhang, Wei
TI Association between clinicopathological features and survival in
   patients with primary and paired metastatic colorectal cancer and
   <i>KRAS</i> mutation
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE CRC; KRAS; primary; metastatic; cetuximab; survival
ID CODON 12 MUTATION; BRAF MUTATIONS; TUMOR; EXPRESSION; IMPACT
AB The KRAS gene mutation is involved in several types of tumors. However, the potential role of the KRAS mutation in human primary and paired metastatic colorectal cancer (CRC) among different nationalities is poorly understood. In the present study, we assessed the relationship between KRAS mutation status and overall survival (OS) and disease-free survival (DFS) in 230 patients with primary and paired metastatic CRC. The KRAS mutation rate in primary CRC tissue was 43.0% (99/230), which was higher than in paired metastatic CRC, which was 31.9% (23/72; P<0.001). Clinicopathologically, the KRAS gene mutation rate was higher in tumors that had infiltrated more deeply (T3, T4) and in lymph node (LN) metastases (N1/N2) (P= 0.029 and P= 0.010, respectively). The KRAS gene status did not differ between the Han and Uyghur nationalities in both primary and metastatic CRC. In 72 paired cases, the KRAS mutation rate in primary CRC was significantly higher than in metastatic CRC (P<0.001) and in metastatic CRC that had infiltrated more deeply (T3, T4) (P= 0.034). In the metastatic cases, the KRAS gene mutation rate was higher in patients aged over 65 years (P= 0.035). Specifically, KRAS mutation was correlated with a poorer OS and DFS (P= 0.004 and P= 0.029, respectively). In our study, 35 patients with wild-type KRAS who received cetuximab targeted therapy had a better DFS than patients with mutant KRAS (P= 0.029). The results of the current study demonstrate that the KRAS status is significantly associated with infiltrating LN metastases and the TNM stage in primary CRC. In addition, the results show that the KRAS mutation is significantly more common in primary tumors than in paired metastatic CRC, and the KRAS mutation is correlated with a shorter OS and DFS, as patients with wild-type KRAS who received cetuximab experienced a longer DFS.
C1 [Pang, Xue-Lian; Li, Qiao-Xin; Ma, Zhi-Ping; Shi, Yi; Ma, Yu-Qing; Li, Xin-Xia; Cui, Wen-Li; Zhang, Wei] Xinjiang Med Univ, Affiliated Hosp 1, Dept Pathol, 137 Liyushan South Rd, Urumqi 830054, Xinjiang, Peoples R China.
C3 Xinjiang Medical University
RP Cui, WL; Zhang, W (corresponding author), Xinjiang Med Univ, Affiliated Hosp 1, Dept Pathol, 137 Liyushan South Rd, Urumqi 830054, Xinjiang, Peoples R China.
EM cwl860@163.com; zwyhr100@163.com
FU National Natural Science Foundation of China [81560035]; Xinjiang Uygur
   Autonomous Region Nature Science Foundation [2014211C032]; Science and
   Technology Talents Training Project of Xinjiang Uyghur Autonomous Region
   [qn2015bs011]; Post-doctor Project of Xinjiang Medical University
FX This work was supported by the National Natural Science Foundation of
   China (No 81560035), The Xinjiang Uygur Autonomous Region Nature Science
   Foundation (No 2014211C032), Science and Technology Talents Training
   Project of Xinjiang Uyghur Autonomous Region (qn2015bs011) and the
   Post-doctor Project of Xinjiang Medical University.
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TC 8
Z9 9
U1 1
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 2017
VL 10
BP 2645
EP 2654
DI 10.2147/OTT.S133203
PG 10
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA EV5WT
UT WOS:000401839800001
PM 28579802
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Yamada, T
   Masuda, M
AF Yamada, Tesshi
   Masuda, Mari
TI Emergence of TNIK inhibitors in cancer therapeutics
SO CANCER SCIENCE
LA English
DT Review
DE Cancer stem cell; colorectal cancer; molecular targeted therapy; TNIK;
   Wnt signaling
ID NCK-INTERACTING KINASE; FACTOR-4-MEDIATED GENE TRANSACTIVATION;
   BETA-CATENIN; POLY(ADP-RIBOSE) POLYMERASE-1; STEM-CELLS; C-JUN; PATHWAY;
   MEBENDAZOLE; TRANSCRIPTION; TARGET
AB The outcome of patients with metastatic colorectal cancer remains unsatisfactory. To improve patient prognosis, it will be necessary to identify new drug targets based on molecules that are essential for colorectal carcinogenesis, and to develop therapeutics that target such molecules. The great majority of colorectal cancers (>90%) have mutations in at least one Wnt signaling pathway gene. Aberrant activation of Wnt signaling is a major force driving colorectal carcinogenesis. Several therapeutics targeting Wnt pathway molecules, including porcupine, frizzled receptors and tankyrases, have been developed, but none of them have yet been incorporated into clinical practice. Wnt signaling is most frequently activated by loss of function of the adenomatous polyposis coli (APC) tumor suppressor gene. Restoration of APC gene function does not seem to be a realistic therapeutic approach, and, therefore, only Wnt signaling molecules downstream of the APC gene product can be considered as targets for pharmacological intervention. Traf2 and Nck-interacting protein kinase (TNIK) was identified as a regulatory component of the beta-catenin and T-cell factor-4 (TCF-4) transcriptional complex. Several small-molecule compounds targeting this protein kinase have been shown to have anti-tumor effects against various cancers. An anthelmintic agent, mebendazole, was recently identified as a selective inhibitor of TNIK and is under clinical evaluation. TNIK regulates Wnt signaling in the most downstream part of the pathway, and its pharmacological inhibition seems to be a promising therapeutic approach. We demonstrated the feasibility of this approach by developing a small-molecule TNIK inhibitor, NCB-0846.
C1 [Yamada, Tesshi; Masuda, Mari] Natl Canc Ctr, Res Inst, Div Chemotherapy & Clin Res, Tokyo, Japan.
C3 National Cancer Center - Japan
RP Yamada, T (corresponding author), Natl Canc Ctr, Res Inst, Div Chemotherapy & Clin Res, Chuo Ku, 5-1-1 Tsukiji, Tokyo 1040045, Japan.
EM tyamada@ncc.go.jp
FU Japan Agency for Medical Research and Development [16im0210804h0001];
   National Cancer Center Research and Development Fund [26-A-13, 26-A-5]
FX Japan Agency for Medical Research and Development, (Grant / Award
   Number: '16im0210804h0001') National Cancer Center Research and
   Development Fund, (Grant / Award Number: '26-A-13 and 26-A-5')
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NR 74
TC 31
Z9 49
U1 1
U2 32
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 MAY
PY 2017
VL 108
IS 5
BP 818
EP 823
DI 10.1111/cas.13203
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EW2AH
UT WOS:000402298000002
PM 28208209
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Jaeger, N
   Czepielewski, RS
   Bagatini, M
   Porto, BN
   Bonorino, C
AF Jaeger, Natalia
   Czepielewski, Rafael Sanguinetti
   Bagatini, Maira
   Porto, Barbara N.
   Bonorino, Cristina
TI Neuropeptide gastrin-releasing peptide induces PI3K/reactive oxygen
   species-dependent migration in lung adenocarcinoma cells
SO TUMOR BIOLOGY
LA English
DT Article
DE Gastrin-releasing peptide; gastrin-releasing peptide receptor; non-small
   cell lung carcinoma; chemotaxis; gastrin-releasing peptide; metastasis;
   neuropeptide; cancer
ID BOMBESIN-LIKE PEPTIDES; ASYMPTOMATIC CIGARETTE SMOKERS; RECEPTOR
   ANTAGONIST RC-3095; GROWTH-FACTOR RECEPTOR; CANCER CELLS; IN-VITRO;
   NERVOUS-SYSTEM; BREAST-CANCER; TUMOR-GROWTH; COLON-CANCER
AB Nerve fibers and neurotransmitters have increasingly been shown to have a role in tumor progression. Gastrin-releasing peptide is a neuropeptide linked to tumor aggressiveness, acting as an autocrine tumor growth factor by binding to its receptor, gastrin-releasing peptide receptor, expressed by many tumors. Although neuropeptides have been previously linked to tumor cell proliferation, more recent studies have uncovered roles for neuropeptides in chemotaxis and metastasis. Understanding the precise roles of such peptides in cancer is crucial to optimizing targeted therapy design. We have previously described that gastrin-releasing peptide acts directly as a chemotactic factor for neutrophils, dependent on PI3K, ERK, and p38. In this study, we investigated roles for gastrin-releasing peptide in lung adenocarcinoma. We asked if gastrin-releasing peptide would act as a proliferative and/or chemotactic stimulus for gastrin-releasing peptide receptor-expressing tumor cells. In A549 cells, a non-small cell lung carcinoma line, the treatment with gastrin-releasing peptide leads to activation of AKT and ERK1/2, and production of reactive oxygen species. Gastrin-releasing peptide induced migration of A549 cells, dependent on gastrin-releasing peptide receptor and PI3K, but not ERK. However, no proliferation was observed in these cells in response to gastrin-releasing peptide, and gastrin-releasing peptide did not promote resistance to treatment with a chemotherapy drug. Our results suggest that, similar to what happens in neutrophils, gastrin-releasing peptide is a migratory, rather than a proliferative, stimulus, for non-small cell lung carcinoma cells, indicating a putative role for gastrin-releasing peptide and gastrin-releasing peptide receptor in metastasis.
C1 [Jaeger, Natalia; Czepielewski, Rafael Sanguinetti; Bagatini, Maira; Bonorino, Cristina] Pontificia Univ Catolica Rio Grande Sul PUCRS, IPB, Hosp Sao Lucas, Lab Imunol Celular & Mol, Av Ipiranga,6690,2nd Floor,Room 6, BR-90610900 Porto Alegre, RS, Brazil.
   [Jaeger, Natalia; Czepielewski, Rafael Sanguinetti; Bonorino, Cristina] Pontificia Univ Catolica Rio Grande Sul PUCRS, Fac Biociencias, Programa Posgrad Biol Celular & Mol, Porto Alegre, RS, Brazil.
   [Porto, Barbara N.] Pontificia Univ Catolica Rio Grande Sul PUCRS, IPB, Hosp Sao Lucas, Lab Imunol Clin & Expt, Porto Alegre, RS, Brazil.
C3 Pontificia Universidade Catolica Do Rio Grande Do Sul; Pontificia
   Universidade Catolica Do Rio Grande Do Sul; Pontificia Universidade
   Catolica Do Rio Grande Do Sul
RP Bonorino, C (corresponding author), Pontificia Univ Catolica Rio Grande Sul PUCRS, IPB, Hosp Sao Lucas, Lab Imunol Celular & Mol, Av Ipiranga,6690,2nd Floor,Room 6, BR-90610900 Porto Alegre, RS, Brazil.
EM cbonorino@pucrs.br
RI Czepielewski, Rafael/ABB-7858-2021; Bonorino, Cristina/U-2780-2019;
   Jaeger, Natalia/ABB-8377-2021
OI Jaeger, Natalia/0000-0003-2875-8297
FU Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
   [485344/2012-2]; Coordenacao de Aperfeicoamento de Pessoal de Nivel
   Superior (CAPES); Fundacao de Amparo a Pesquisa do Estado do Rio Grande
   do Sul (FAPERGS) [13//0829-0]; Cristalia Ltda; CAPES; Cristalia Ltda.
   (Itapira, Brazil)
FX The authors acknowledge grant support from the Conselho Nacional de
   Desenvolvimento Cientifico e Tecnologico (CNPq) Grant No 485344/2012-2.
   N.J. was supported by Coordenacao de Aperfeicoamento de Pessoal de Nivel
   Superior (CAPES) and Fundacao de Amparo a Pesquisa do Estado do Rio
   Grande do Sul (FAPERGS) fellowship (No. 13//0829-0), R.S.C. was
   supported by Cristalia Ltda. and CAPES fellowships, and M.B. received a
   CNPq fellowship. Cristalia Ltda. (Itapira, Brazil) granted a fellowship
   to R.S.C.
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NR 62
TC 9
Z9 9
U1 0
U2 8
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1010-4283
EI 1423-0380
J9 TUMOR BIOL
JI Tumor Biol.
PD MAR
PY 2017
VL 39
IS 3
AR 694321
DI 10.1177/1010428317694321
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ET4OS
UT WOS:000400263700039
PM 28351312
OA gold
DA 2025-01-04
ER

PT J
AU Strickler, JH
   Hsu, L
   Wright, P
   Stecher, M
   Siadak, MF
   Palanca-Wessels, MC
   Yu, JH
   Zhang, NCL
   Espenschied, CR
   Lang, KTY
   Bekaii-Saab, TS
AF Strickler, John H.
   Hsu, Ling-, I
   Wright, Phoebe
   Stecher, Michael
   Siadak, Muriel F.
   Palanca-Wessels, Maria Corinna
   Yu, Junhua
   Zhang, Nicole
   Espenschied, Carin R.
   Lang, Kathryn
   Bekaii-Saab, Tanios S.
TI Real-World Treatment Patterns in Patients With HER2-Amplified Metastatic
   Colorectal Cancer: A Clinical-Genomic Database Study
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
ID TRASTUZUMAB; MUTATIONS; PHASE-2
AB Background: HER2 amplification (HER2+) occurs in approximately 3% of patients with metastatic colorectal cancer (mCRC). Despite the recent addition of HER2-directed therapies to treatment recommendations in the NCCN Guidelines, until more recently there were no FDA-approved treatments. This study examined real-world treatment patterns in patients with HER2+ mCRC in the United States before and after the emerging awareness of HER2-directed therapies in 2018. Methods: This was a retrospective observational study of patients with HER2+ mCRC from the GuardantINFORM database, which contains claims data for patients with Guardant360 genomic testing results. Patients were aged ?18 years, were diagnosed with mCRC between January 2014 and September 2020, and had confirmed ERBB2 amplification via the blood-based Guardant360 test. Treatment patterns and real-world time to next treatment (rwTTNT) were evaluated. Results: This study included 142 patients with a median age of 59 years; 31 (21.8%) patients with ERBB2 amplifications also had ERBB2 mutations. Treatment patterns were heterogeneous and evolved over time; before 2018, the most common regimen prescribed after detection of ERBB2 amplification was anti-VEGF therapy with or without chemotherapy (31.6%; n=25), and after 2018, HER2-directed therapies were the most commonly prescribed (36.5%; n=23). Median rwTTNT among the overall cohort was 8.4 months (95% CI, 6.5-10.0); rwTTNT was numerically longer in patients who received HER2-directed therapy compared with those who received non-HER2-directed therapies (11.0 months [95% CI, 6.3-12.3] vs 7.2 months [95% CI, 5.8-9.6]). Conclusions: This real-world study of the largest clinically annotated dataset of patients with HER2+ mCRC showed that many patients do not receive HER2-directed therapy despite its inclusion in NCCN Guidelines, with heterogeneous treatment patterns suggesting that standard of care remains undefined and targeted therapy remains underutilized. Greater awareness of the unmet need in this patient population, together with new effective therapies, will facilitate strategies for improved, targeted treatment approaches.
C1 [Strickler, John H.] Duke Univ, Med Ctr, Div Med Oncol, Durham, NC USA.
   [Hsu, Ling-, I; Wright, Phoebe; Stecher, Michael; Siadak, Muriel F.; Palanca-Wessels, Maria Corinna] Seagen Inc, Bothell, WA USA.
   [Yu, Junhua; Zhang, Nicole; Espenschied, Carin R.; Lang, Kathryn] Guardant Hlth Inc, Redwood City, CA USA.
   [Bekaii-Saab, Tanios S.] Mayo Clin, Div Hematol Oncol, 5881 E Mayo Blvd, Phoenix, AZ 85054 USA.
C3 Duke University; Guardant Health, Inc.; Mayo Clinic; Mayo Clinic Phoenix
RP Bekaii-Saab, TS (corresponding author), Mayo Clin, Div Hematol Oncol, 5881 E Mayo Blvd, Phoenix, AZ 85054 USA.
EM bekaii-saab.tanios@mayo.edu
RI Bekaii-Saab, Tanios/AGD-6851-2022
FU Seagen Inc
FX This study was sponsored by Seagen Inc., in collaboration with Merck
   Sharp & amp; Dohme Corp., a subsidiary of Merck & amp; Co., Inc.
CR Benson AB III, 2019, NCCN Clinical Practice Guidelines in Oncology: Colon Cancer
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NR 31
TC 0
Z9 0
U1 0
U2 1
PU HARBORSIDE PRESS
PI HUNTINGTON
PA 94 NORTH WOODHULL RD, HUNTINGTON, NY 11743 USA
SN 1540-1405
EI 1540-1413
J9 J NATL COMPR CANC NE
JI J. Natl. Compr. Cancer Netw.
PD AUG
PY 2023
VL 21
IS 8
BP 805
EP +
DI 10.6004/jnccn.2023.7022
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA R4AR9
UT WOS:001063796600006
PM 37549907
OA Bronze
DA 2025-01-04
ER

PT J
AU Jiang, Q
   Zhang, Y
   Qiu, YL
   Quan, MF
   Yang, SY
   Chu, FY
   Wang, R
   Ye, ZC
   Tao, XJ
   Liu, RS
AF Jiang, Qing
   Zhang, Yi
   Qiu, Yilan
   Quan, Meifang
   Yang, Shanyi
   Chu, Feiyi
   Wang, Rong
   Ye, Zhichao
   Tao, Xiaojun
   Liu, Rushi
TI Study on the effect of carrier-free dual-drug nanocrystals against colon
   cancer cells
SO INTERNATIONAL JOURNAL OF NANOTECHNOLOGY
LA English
DT Article
DE nanocrystals; doxorubicin 10-Hydroxycamptothecin synergistic inhibition;
   colon cancer cells
ID ENHANCED PERMEABILITY; 10-HYDROXYCAMPTOTHECIN; DOXORUBICIN; DELIVERY;
   NANOPARTICLES; RELEASE
AB Nano-delivery systems are often used for targeted therapy of tumours, but a single anti-tumour drug often causes drug resistance in tumour cells, thereby reducing the effectiveness of the drug in chemotherapy. Therefore, in order to overcome the drug resistance of tumour cells, nano-formulations of combined drugs have emerged. This work aims to design a carrier-free dual drug-loaded nanocrystalline HCPT-DOX NCs, and verify its possibility of treating colon cancer through experiments. And through the comparison with a single drug, it highlights its advantages in the treatment of colon cancer. The synthesised HD NCs are characterised by dynamic light scattering (DLS), and the best synthesis ratio is selected. Through the drug release experiment, the release efficiency of a single drug in HD NCs is explored. Through MTT experiment, cell scratch experiment, cell cloning experiment, etc., the possibility of HD NCs in the treatment of colon cancer at the cellular level is discussed. The HCPT/DOX (HD) molar ratio of 1:1 is the best choice for the preparation of analytically valuable nanocrystals. Drug release experiments showed that the cumulative release rates of HCPT and DOX in HD NCs at 48 hours were 94.03% and 74.15%, respectively. MTT experiments of the colon cancer cell HCT116 and RKO showed a stronger synergistic inhibitory in low-concentration HD NCs than in drugs that underwent a simple physical mixing, and the RKO cells exhibited a more obvious effect. HD NCs could significantly inhibit colony formation of colon cancer cells in cell cloning experiments. Cell migration experiments showed that drug combination therapy of HD NCs could effectively inhibit the migration of cancer cells. By cell uptake experiments, it was determined that at the same concentration, the drug absorption of HD NCs was much higher than that of the free drug. HD NCs with appropriate particle size can be synthesized at a certain feeding ratio. The dual-drug-loaded HD NCs showed better anti-tumour effects than a single drug and a simple mixture of two drugs.
C1 [Jiang, Qing; Zhang, Yi; Quan, Meifang; Yang, Shanyi; Chu, Feiyi; Wang, Rong; Ye, Zhichao; Tao, Xiaojun; Liu, Rushi] Hunan Normal Univ, Sch Med, Dept Med Lab, Changsha 410013, Peoples R China.
   [Qiu, Yilan] Hunan Normal Univ, Sch Life Sci, Changsha 410018, Peoples R China.
C3 Hunan Normal University; Hunan Normal University
RP Tao, XJ; Liu, RS (corresponding author), Hunan Normal Univ, Sch Med, Dept Med Lab, Changsha 410013, Peoples R China.
EM 1319481873@qq.com; 1003476370@qq.com; qiu730822@qq.com;
   258375240@qq.com; 1923443065@qq.com; 1105906221@qq.com;
   2513638094@qq.com; 1436939860@qq.com; xiaojtao@126.com;
   liurushi@hunnu.edu.cn
RI Zhu, Yifan/GXH-6179-2022
FU Scientific Research Fund of Hunan Provincial Education Department
   [2019A293]; Hunan Provincial Key Research and Development Program
   [2019SK2042]; Hunan Provincial Natural Science Foundation of China
   [2019JJ10002]; National Natural Science Foundation of China [31072141];
   Science and Technology Plan Project of Changsha [kq1907130]
FX We thank the support of grants from Scientific Research Fund of Hunan
   Provincial Education Department (No. 2019A293), Hunan Provincial Key
   Research and Development Program (No. 2019SK2042), Hunan Provincial
   Natural Science Foundation of China (No. 2019JJ10002) and National
   Natural Science Foundation of China (No. 31072141), and Science and
   Technology Plan Project of Changsha (kq1907130).
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NR 33
TC 0
Z9 0
U1 1
U2 10
PU INDERSCIENCE ENTERPRISES LTD
PI GENEVA
PA WORLD TRADE CENTER BLDG, 29 ROUTE DE PRE-BOIS, CASE POSTALE 856, CH-1215
   GENEVA, SWITZERLAND
SN 1475-7435
EI 1741-8151
J9 INT J NANOTECHNOL
JI Int. J. Nanotechnol.
PY 2022
VL 19
IS 12
BP 1158
EP 1176
DI 10.1504/IJNT.2022.129765
PG 20
WC Nanoscience & Nanotechnology; Materials Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Materials Science
GA C0WB0
UT WOS:000959214700006
DA 2025-01-04
ER

PT J
AU Maleki, F
   Noorkhoda, S
   Halabian, R
   Behzadi, E
   Fooladi, AAI
AF Maleki, Farajolah
   Noorkhoda, Sadeghifard
   Halabian, Raheleh
   Behzadi, Elham
   Fooladi, Abbas Ali Imani
TI The Role of Epidermal Growth Factor Receptor in Cancer and their
   Application for New Targeted Cancer Therapy
SO JOURNAL OF CLINICAL AND DIAGNOSTIC RESEARCH
LA English
DT Review
DE Immune system responses; Ligand targeted therapy; Tyrosine kinase
   inhibitor
ID COLORECTAL-CANCER; FACTOR-ALPHA; FACTOR-BETA; TGF-BETA;
   ANTITUMOR-ACTIVITY; IMMUNE-RESPONSES; MUCIN PRODUCTION; EGFR INHIBITORS;
   FUSION PROTEINS; ANTI-EGFR
AB Epidermal Growth Factor Receptor (EGFR) has central role in cancer therapy because it causes tumour progression in many cases. The EGFR has seven ligands. Each factor that can block this binding, inhibits the intracellular signal transduction and prevents progression of the tumours. Immune system response is the most important factor for suppressing the initial stage of tumour growth and destroying some initial malignant cells, daily. On the other hand, tumours have different mechanisms to hide their antigens and escape from immune system responses. In contrary, tumours use some mechanisms to escape from immune system such as: 1) use of TGF-beta to initiate angiogenesis and immune suppression; 2) Induces Treg cell activation to modulate other immune cells; 3) secretion of the prostaglandin E2 to convert T cell into Treg. So, if a superantigen fused to one of the EGFR-ligands, causes the induction of immune system responses against the tumour cells. One of the new methods is based on the use of the fused super antigen with a ligand of the EGFR to inhibit ligand attaching to the EGFR and inducing immune system responses. To achieve this goal, we can block binding of EGFR to their ligands in the extracellular domain by fusing ligands with bacterial superantigens, toxins or cytokines of the viruses and plants that can induce immune system responses and kill malignant cells. So, the fused ligand can both block signal transduction and induce immune system response against malignant cells. In addition, with combining traditional drugs, high efficacy of the tumour treatment can be achieved. The aim of this review is to assess the mentioned strategy for targeting tumours.
C1 [Maleki, Farajolah; Noorkhoda, Sadeghifard] Ilam Univ Med Sci, Clin Microbiol Res Ctr, Ilam, Iran.
   [Halabian, Raheleh; Fooladi, Abbas Ali Imani] Baqiyatallah Univ Med Sci, Appl Microbiol Res Ctr, Syst Biol & Poisonings Inst, Tehran, Iran.
   [Behzadi, Elham] Islamic Azad Univ, Shahr E Qods Branch, Coll Basic Sci, Dept Microbiol, Tehran, Iran.
C3 Baqiyatallah University of Medical Sciences (BMSU); Islamic Azad
   University
RP Fooladi, AAI (corresponding author), Baqiyatallah Univ Med Sci, Appl Microbiol Res Ctr, Syst Biol & Poisonings Inst, Tehran, Iran.
EM imanifouladi.a@gmail.com
RI maleki, farajolah/K-9487-2018; halabian, raheleh/V-4983-2019
OI Imani Fooladi, Abbas Ali/0000-0001-7339-8257
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NR 89
TC 1
Z9 1
U1 0
U2 3
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 2018
VL 12
IS 6
BP XE01
EP XE06
DI 10.7860/JCDR/2018/35499.11680
PG 6
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA GN6MG
UT WOS:000439200700112
OA gold
DA 2025-01-04
ER

PT J
AU Golovko, D
   Kedrin, D
   Yilmaz, ÖH
   Roper, J
AF Golovko, Daniel
   Kedrin, Dmitriy
   Yilmaz, Oemer H.
   Roper, Jatin
TI Colorectal cancer models for novel drug discovery
SO EXPERT OPINION ON DRUG DISCOVERY
LA English
DT Review
DE colorectal cancer mouse models; intestinal organoid; patient-derived
   xenograft; transgenic colorectal cancer mouse model
ID FAMILIAL ADENOMATOUS POLYPOSIS; MULTIPLE INTESTINAL NEOPLASIA;
   PATIENT-DERIVED XENOGRAFTS; ENGINEERED MOUSE MODELS; IN-VITRO EXPANSION;
   COLON-CANCER; STEM-CELLS; TUMOR XENOGRAFTS; RODENT MODELS; MUTANT MICE
AB Introduction: Despite increased screening rates and advances in targeted therapy, colorectal cancer (CRC) remains the third leading cause of cancer-related mortality. CRC models that recapitulate key features of human disease are essential to the development of novel and effective therapeutics. Classic methods of modeling CRC such as human cell lines and xenograft mice, while useful for many applications, carry significant limitations. Recently developed in vitro and in vivo models overcome some of these deficiencies and thus can be utilized to better model CRC for mechanistic and translational research.
   Areas covered: The authors review established models of in vitro cell culture and describe advances in organoid culture for studying normal and malignant intestine. They also discuss key features of classic xenograft models and describe other approaches for in vivo CRC research, including patient-derived xenograft, carcinogen-induced, orthotopic transplantation and transgenic mouse models. We also describe mouse models of metastatic CRC.
   Expert opinion: No single model is optimal for drug discovery in CRC. Genetically engineered models overcome many limitations of xenograft models. Three-dimensional organoids can be efficiently derived from both normal and malignant tissue for large-scale in vitro and in vivo (transplantation) studies and are thus a significant advance in CRC drug discovery.
C1 [Golovko, Daniel; Roper, Jatin] Tufts Med Ctr, Div Gastroenterol & Mol Oncol, Res Inst, Boston, MA 02111 USA.
   [Kedrin, Dmitriy; Yilmaz, Oemer H.; Roper, Jatin] MIT, Dept Biol, David H Koch Inst Integrat Canc Res, Cambridge, MA 02139 USA.
   [Kedrin, Dmitriy; Yilmaz, Oemer H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
   [Kedrin, Dmitriy] Harvard Univ, Sch Med, Div Gastroenterol, Boston, MA 02114 USA.
   [Yilmaz, Oemer H.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02114 USA.
C3 Tufts Medical Center; Massachusetts Institute of Technology (MIT);
   Harvard University; Massachusetts General Hospital; Harvard University;
   Harvard Medical School; Harvard University; Harvard Medical School
RP Roper, J (corresponding author), Tufts Med Ctr, Div Gastroenterol & Mol Oncol, Res Inst, Boston, MA 02111 USA.
EM jroper@tuftsmedicalcenter.org
OI Roper, Jatin/0000-0002-8851-1352
FU Department of Defense through the Peer Reviewed Cancer Research Program
   Career Development Award [CA120198]; Tufts University School of Medicine
   through the Earl P. Charlton Fund Research Award; Tufts University
   School of Medicine through the Rozan Research Fund Pilot Award; V
   Scholar Award through the V Foundation for Cancer Research; National
   Institutes of Health (NIH) through the Center for the Study of
   Inflammatory Bowl Diseases from the Massachusetts General Hospital
   [DK043351]; National Institute of Aging [NIA R00 AG045144]; NIH Cancer
   Center Support (core) grant [P30-CA14051]; National Institute of
   Diabetes and Digestive and Kidney Diseases (NIDDK) T32 grant [DK007191]
FX J Roper was supported by the Department of Defense through the Peer
   Reviewed Cancer Research Program Career Development Award CA120198 and
   by the Tufts University School of Medicine through the Earl P. Charlton
   Fund Research Award and Rozan Research Fund Pilot Award. J Roper and OH
   Yilmaz are supported with a V Scholar Award through the V Foundation for
   Cancer Research. OH Yilmaz is supported by a National Institutes of
   Health (NIH) grant DK043351 through the Center for the Study of
   Inflammatory Bowl Diseases from the Massachusetts General Hospital as
   well as National Institute of Aging grant NIA R00 AG045144 and NIH
   Cancer Center Support (core) grant P30-CA14051. D Kedrin is also
   supported by a National Institute of Diabetes and Digestive and Kidney
   Diseases (NIDDK) T32 grant DK007191. 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 101
TC 34
Z9 42
U1 3
U2 64
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1746-0441
EI 1746-045X
J9 EXPERT OPIN DRUG DIS
JI Expert. Opin. Drug Discov.
PD NOV 2
PY 2015
VL 10
IS 11
BP 1217
EP 1229
DI 10.1517/17460441.2015.1079618
PG 13
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DD5LX
UT WOS:000369966400003
PM 26295972
OA Green Accepted, Green Submitted
DA 2025-01-04
ER

PT J
AU Dommann, N
   Sánchez-Taltavull, D
   Eggs, L
   Birrer, F
   Brodie, T
   Salm, L
   Baier, FA
   Medová, M
   Humbert, M
   Tschan, MP
   Beldi, G
   Candinas, D
   Stroka, D
AF Dommann, Noelle
   Sanchez-Taltavull, Daniel
   Eggs, Linda
   Birrer, Fabienne
   Brodie, Tess
   Salm, Lilian
   Baier, Felix Alexander
   Medova, Michaela
   Humbert, Magali
   Tschan, Mario P.
   Beldi, Guido
   Candinas, Daniel
   Stroka, Deborah
TI The LIM Protein Ajuba Augments Tumor Metastasis in Colon Cancer
SO CANCERS
LA English
DT Article
DE Ajuba; metastasis; proliferation; cell differentiation
ID COLORECTAL-CANCER; CELL-PROLIFERATION; SIGNALING PATHWAY; TYROSINE
   KINASE; DOMAIN PROTEIN; PROMOTES; EPHA2; COMPLEX; OVEREXPRESSION;
   SUPPRESSES
AB Colorectal cancer, along with its high potential for recurrence and metastasis, is a major health burden. Uncovering proteins and pathways required for tumor cell growth is necessary for the development of novel targeted therapies. Ajuba is a member of the LIM domain family of proteins whose expression is positively associated with numerous cancers. Our data shows that Ajuba is highly expressed in human colon cancer tissue and cell lines. Publicly available data from The Cancer Genome Atlas shows a negative correlation between survival and Ajuba expression in patients with colon cancer. To investigate its function, we transduced SW480 human colon cancer cells, with lentiviral constructs to knockdown or overexpress Ajuba protein. The transcriptome of the modified cell lines was analyzed by RNA sequencing. Among the pathways enriched in the differentially expressed genes, were cell proliferation, migration and differentiation. We confirmed our sequencing data with biological assays; cells depleted of Ajuba were less proliferative, more sensitive to irradiation, migrated less and were less efficient in colony formation. In addition, loss of Ajuba expression decreased the tumor burden in a murine model of colorectal metastasis to the liver. Taken together, our data supports that Ajuba promotes colon cancer growth, migration and metastasis and therefore is a potential candidate for targeted therapy.
C1 [Dommann, Noelle; Sanchez-Taltavull, Daniel; Eggs, Linda; Birrer, Fabienne; Brodie, Tess; Salm, Lilian; Baier, Felix Alexander; Beldi, Guido; Candinas, Daniel; Stroka, Deborah] Univ Bern, Bern Univ Hosp, Dept Biomed Res Visceral & Transplantat Surg, Clin Visceral Surg & Med, CH-3008 Bern, Switzerland.
   [Medova, Michaela] Univ Bern, Bern Univ Hosp, Dept Biomed Res, Radiat Oncol, CH-3008 Bern, Switzerland.
   [Humbert, Magali; Tschan, Mario P.] Univ Bern, Inst Pathol, CH-3008 Bern, Switzerland.
C3 University of Bern; University Hospital of Bern; University of Bern;
   University Hospital of Bern; University of Bern
RP Stroka, D (corresponding author), Univ Bern, Bern Univ Hosp, Dept Biomed Res Visceral & Transplantat Surg, Clin Visceral Surg & Med, CH-3008 Bern, Switzerland.
EM noelle.dommann@dbmr.unibe.ch; daniel.sanchez@dbmr.unibe.ch;
   eggsl@hotmail.ch; fabienne.birrer@dbmr.unibe.ch;
   tess.brodie@dbmr.unibe.ch; lilian.salm@insel.ch;
   felix.baier@dbmr.unibe.ch; michaela.medova@dbmr.unibe.ch;
   magali.humbert@pathology.unibe.ch; mario.tschan@pathology.unibe.ch;
   guido.beldi@insel.ch; daniel.candinas@insel.ch;
   deborah.stroka@dbmr.unibe.ch
RI Stroka, Deborah/KSM-8508-2024; Salm, Lilian/KJM-4576-2024; Humbert,
   Magali/KFB-4325-2024; Humbert, Magali/AAC-8951-2020
OI Dommann, Noelle Annick/0000-0003-0475-0899; Salm,
   Lilian/0000-0002-6812-3678; Tschan, Mario P./0000-0001-5897-3647;
   Medova, Michaela/0000-0003-0649-469X; Beldi, Guido/0000-0002-9914-3807;
   Humbert, Magali/0000-0003-3820-0297; Birrer, Fabienne
   Esther/0000-0003-4366-9946; Sanchez-Taltavull,
   Daniel/0000-0002-4944-0360
FU Aclon Foundatio [1/2018]
FX This research was funded by Aclon Foundatio, grant number 1/2018.
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NR 60
TC 11
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 JUL
PY 2020
VL 12
IS 7
AR 1913
DI 10.3390/cancers12071913
PG 21
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA MX9XU
UT WOS:000558071900001
PM 32679899
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Nutthasirikul, N
   Hahnvajanawong, C
   Techasen, A
   Limpaiboon, T
   Leelayuwat, C
   Chau-In, S
   Jearanaikoon, P
AF Nutthasirikul, Nichapavee
   Hahnvajanawong, Chariya
   Techasen, Anchalee
   Limpaiboon, Temduang
   Leelayuwat, Chanvit
   Chau-In, Siri
   Jearanaikoon, Patcharee
TI Targeting the Δ133p53 isoform can restore chemosensitivity in
   5-fluorouracil-resistant cholangiocarcinoma cells
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE p53 isoform; drug resistance; cholangiocarcinoma; reversed
   chemosensitivity; apoptosis; Delta 133p53
ID SYRIAN GOLDEN-HAMSTERS; ACUTE MYELOID-LEUKEMIA; COLON-CANCER CELLS; P53
   ISOFORMS; INTRAHEPATIC CHOLANGIOCARCINOMA; GENE-EXPRESSION; COLORECTAL
   CANCERS; P73 GENE; CHEMOTHERAPY; INDUCTION
AB Lack of the normal p53 transactivation domain, Delta 133p53 isoform exhibits anti-p53 function. Many studies report the correlation between Delta 133p53 expression and poor survival in various cancers, including cholangiocarcinoma (CCA), which is a cancer of the bile ducts. CCA almost always results in short survival times. The relevance of Delta 133p53 to drug resistance in CCA is not yet well understood. This study aimed to demonstrate the association between Delta 133p53 and 5-fluorouracil (5-FU) resistance in CCA. Delta 133p53 protein was highly expressed in CCA patients with poor outcome compared to favorable outcome but was not statistically significant. However, a significant correlation was found between normalized Delta 133p53 levels and 5-FU resistance which was defined by an ex vivo histoculture drug response assay (P=0.019). Two stable 5-FU-resistant CCA cell lines, KKU-M139R (IC50 38.8 mu M) and KKU-M214R (IC50 39.5 mu M), were used as a model to evaluate the role of Delta 133p53. Increased Delta 133p53 was correlated with 5-FU in a dose-dependent manner. The transient knockdown of Delta 133p53 expression can restore drug sensitivity in both resistant CCA cells with 11- to 45-fold reduction of IC50 compared to control. Upon Delta 133p53 silencing, apoptotic signaling was enhanced by the upregulation of Bax and downregulation of Bcl-2. Additionally, p21 and p27 were upregulated, resulting in cell cycle arrest at G2. Inhibition of colony formation and prolong doubling time were also observed. Our findings demonstrated that chemosensitivity can be modulated via targeting of Delta 133p53 suggesting the potential use of Delta 133p53 as a candidate for targeting therapy in CCA.
C1 [Nutthasirikul, Nichapavee; Techasen, Anchalee; Limpaiboon, Temduang; Leelayuwat, Chanvit; Jearanaikoon, Patcharee] Khon Kaen Univ, Fac Associated Med Sci, Res Ctr, Khon Kaen 40002, Thailand.
   [Nutthasirikul, Nichapavee; Techasen, Anchalee; Limpaiboon, Temduang; Leelayuwat, Chanvit; Jearanaikoon, Patcharee] Khon Kaen Univ, Fac Associated Med Sci, Dev Med Diagnost Labs, Khon Kaen 40002, Thailand.
   [Nutthasirikul, Nichapavee; Hahnvajanawong, Chariya; Techasen, Anchalee; Limpaiboon, Temduang; Leelayuwat, Chanvit; Chau-In, Siri; Jearanaikoon, Patcharee] Khon Kaen Univ, Fac Med, Liver Fluke & Cholangiocarcinoma Res Ctr, Khon Kaen 40002, Thailand.
   [Hahnvajanawong, Chariya] Khon Kaen Univ, Fac Med, Dept Microbiol, Khon Kaen 40002, Thailand.
   [Chau-In, Siri] Khon Kaen Univ, Fac Med, Dept Surg, Khon Kaen 40002, Thailand.
C3 Khon Kaen University; Khon Kaen University; Khon Kaen University; Khon
   Kaen University; Khon Kaen University
RP Jearanaikoon, P (corresponding author), Khon Kaen Univ, Fac Associated Med Sci, Res Ctr, Khon Kaen 40002, Thailand.
EM patjea@kku.ac.th
RI , Alsevier/V-1974-2019
FU Higher Education Research Promotion and National Research University
   Project of Thailand, Office of the Higher Education Commission, through
   the Health Cluster (SHeP-GMS), Khon Kaen University [H-2553-Ph.D-06];
   Centre for Research and Development of Medical Diagnostic Laboratories,
   Faculty of Associated Medical Sciences, Khon Kaen University
FX This study was supported by the Higher Education Research Promotion and
   National Research University Project of Thailand, Office of the Higher
   Education Commission, through the Health Cluster (SHeP-GMS), Khon Kaen
   University (Grant no. H-2553-Ph.D-06); the Centre for Research and
   Development of Medical Diagnostic Laboratories, Faculty of Associated
   Medical Sciences, Khon Kaen University.
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NR 55
TC 17
Z9 18
U1 0
U2 6
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 DEC
PY 2015
VL 47
IS 6
BP 2153
EP 2164
DI 10.3892/ijo.2015.3188
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CX1OM
UT WOS:000365465500018
PM 26459801
OA Bronze
DA 2025-01-04
ER

PT J
AU Marcion, G
   Hermetet, F
   Neiers, F
   Uyanik, B
   Dondaine, L
   Dias, AMM
   Da Costa, L
   Moreau, M
   Bellaye, PS
   Collin, B
   Gobbo, J
   Briand, L
   Seigneuric, R
   Kitten, O
   Cinier, M
   Garrido, C
AF Marcion, Guillaume
   Hermetet, Francois
   Neiers, Fabrice
   Uyanik, Burhan
   Dondaine, Lucile
   Dias, Alexandre M. M.
   Da Costa, Laurene
   Moreau, Mathieu
   Bellaye, Pierre-Simon
   Collin, Bertrand
   Gobbo, Jessica
   Briand, Loic
   Seigneuric, Renaud
   Kitten, Olivier
   Cinier, Mathieu
   Garrido, Carmen
TI Nanofitins targeting heat shock protein 110: An innovative
   immunotherapeutic modality in cancer
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE anticancer-targeted therapy; HSP110; Nanofitins; small peptide molecules
AB The presence of an inactivating heat shock protein 110 (HSP110) mutation in colorectal cancers has been correlated with an excellent prognosis and with the ability of HSP110 to favor the formation of tolerogenic (M2-like) macrophages. These clinical and experimental results suggest a potentially powerful new strategy against colorectal cancer: the inhibition of HSP110. In this work, as an alternative to neutralizing antibodies, Nanofitins (scaffold similar to 7 kDa proteins) targeting HSP110 were isolated from the screening of a synthetic Nanofitin library, and their capacity to bind (immunoprecipitation, biolayer interferometry) and to inhibit HSP110 was analyzed in vitro and in vivo. Three Nanofitins were found to inhibit HSP110 chaperone activity. Interestingly, they share a high degree of homology in their variable domain and target the peptide-binding domain of HSP110. In vitro, they inhibited the ability of HSP110 to favor M2-like macrophages. The Nanofitin with the highest affinity, A-C2, was studied in the CT26 colorectal cancer mice model. Our PET/scan experiments demonstrate that A-C2 may be localized within the tumor area, in accordance with the reported HSP110 abundance in the tumor microenvironment. A-C2 treatment reduced tumor growth and was associated with an increase in immune cells infiltrating the tumor and particularly cytotoxic macrophages. These results were confirmed in a chicken chorioallantoic membrane tumor model. Finally, we showed the complementarity between A-C2 and an anti-PD-L1 strategy in the in vivo and in ovo tumor models. Overall, Nanofitins appear to be promising new immunotherapeutic lead compounds.
C1 [Marcion, Guillaume; Hermetet, Francois; Uyanik, Burhan; Dondaine, Lucile; Dias, Alexandre M. M.; Gobbo, Jessica; Seigneuric, Renaud; Garrido, Carmen] INSERM, UMR 1231, Label Ligue Natl Canc & LipST, F-21000 Dijon, France.
   [Marcion, Guillaume; Hermetet, Francois; Neiers, Fabrice; Uyanik, Burhan; Dondaine, Lucile; Dias, Alexandre M. M.; Da Costa, Laurene; Moreau, Mathieu; Gobbo, Jessica; Briand, Loic; Seigneuric, Renaud; Garrido, Carmen] Univ Bourgogne Franche Comte, F-21000 Dijon, France.
   [Neiers, Fabrice; Briand, Loic] INRA, Ctr Sci Gout & Alimentat, F-21000 Dijon, France.
   [Da Costa, Laurene; Moreau, Mathieu; Collin, Bertrand] ICMUB UMR 6302, F-21000 Dijon, France.
   [Da Costa, Laurene; Moreau, Mathieu; Bellaye, Pierre-Simon; Collin, Bertrand; Gobbo, Jessica; Garrido, Carmen] AntiCanc Ctr Georges Francois Leclerc, F-21000 Dijon, France.
   [Kitten, Olivier; Cinier, Mathieu] Affil SAS, F-44200 Nantes, France.
C3 Institut Agro; AgroSup Dijon; Institut National de la Sante et de la
   Recherche Medicale (Inserm); Universite de Bourgogne; INRAE; Institut
   Agro; AgroSup Dijon; Centre National de la Recherche Scientifique
   (CNRS); Universite de Bourgogne; Centre National de la Recherche
   Scientifique (CNRS); CNRS - Institute of Chemistry (INC); Universite de
   Bourgogne; UNICANCER; Centre Georges-Francois Leclerc
RP Garrido, C (corresponding author), INSERM, UMR 1231, Label Ligue Natl Canc & LipST, F-21000 Dijon, France.; Garrido, C (corresponding author), Univ Bourgogne Franche Comte, F-21000 Dijon, France.; Garrido, C (corresponding author), AntiCanc Ctr Georges Francois Leclerc, F-21000 Dijon, France.
EM cgarrido@u-bourgogne.fr
RI Hermetet, François/GPF-8614-2022; Moreau, Mathieu/GRR-7439-2022; Neiers,
   Fabrice/AAM-1637-2021; Bellaye, Pierre-Simon/GLS-4891-2022; Garrido,
   Carmen/G-1633-2018
OI Marcion, Guillaume/0000-0002-3634-6316; Bellaye,
   Pierre-Simon/0000-0002-8498-5163; Neiers, Fabrice/0000-0002-8965-4929;
   Hermetet, Francois/0000-0001-5549-1992; Garrido,
   Carmen/0000-0003-1368-1493
FU French Government grant [ANR-11-LABX-0021, ANR-15-IDEX-0003];
   Association pour la Recherche sur le Cancer; Conseil Regional de
   Bourgogne; Institut National du Cancer; Ligue Nationale contre le Cancer
FX French Government grant managed by the French National Research Agency
   under the program "Investissements d'Avenir", Grant/Award Numbers:
   ANR-11-LABX-0021, ANR-15-IDEX-0003; Ligue Nationale contre le Cancer;
   Association pour la Recherche sur le Cancer; Conseil Regional de
   Bourgogne; Institut National du Cancer
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NR 37
TC 19
Z9 20
U1 1
U2 15
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 JUN 15
PY 2021
VL 148
IS 12
BP 3019
EP 3031
DI 10.1002/ijc.33485
EA MAR 2021
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RP2EO
UT WOS:000625545900001
PM 33506516
OA Bronze
DA 2025-01-04
ER

PT J
AU Gouverneur, A
   Rouyer, M
   Grelaud, A
   Robinson, P
   Colombani, F
   Terrebonne, E
   Smith, D
   Fourrier-Réglat, A
   Noize, P
AF Gouverneur, Amandine
   Rouyer, Magali
   Grelaud, Angela
   Robinson, Philip
   Colombani, Francoise
   Terrebonne, Eric
   Smith, Denis
   Fourrier-Reglat, Annie
   Noize, Pernelle
TI How are elderly patients treated after a diagnosis of metastatic
   colorectal cancer in real-life practice? A study in a French teaching
   hospital
SO FUNDAMENTAL & CLINICAL PHARMACOLOGY
LA English
DT Article
DE aged; antibodies; colorectal neoplasm; interdisciplinary communication;
   monoclonal; neoplasm metastasis
ID OPEN-LABEL; BEVACIZUMAB; TRIAL; CHEMOTHERAPY; CAPECITABINE; OUTCOMES;
   COHORT
AB Metastatic colorectal cancer (mCRC) is frequent among elderly patients. However, in the era of new targeted therapies, little is known about real-life mCRC treatment in this population. This study aimed to describe elderly mCRC patients and the current real-life treatment practices. mCRC patients aged 65 years were identified using the registry of multidisciplinary team meetings, mandatory for all cancer patients, held between January 1, 2013 and June 30, 2014 at the Bordeaux University Hospital. Data were collected from medical records using a standardized questionnaire. Treatment type was defined as follows: at least one anticancer medication administered vs. best supportive care (BSC). A total of 78 patients were included; median age was 74 years and the M/F sex ratio 1.6. Eleven patients (14.1%) were referred to a geriatric oncology consultation. One patient died before treatment initiation, 28 (35.9%) had BSC, and 49 (62.8%) were treated with anticancer medications: 20 (25.6%) had chemotherapy combined with a targeted therapy, and 28 (35.9%) chemotherapy alone (one missing data for treatment). Compared to patients treated with anticancer medications, BSC patients were older (P < 0.0001) and had more often metachronous metastases (P = 0.01), more comorbidities (P = 0.05), and a greater number of concomitant medications (P = 0.004). This study is one of the rare investigations providing insight to treatment practices in all elderly mCRC patients, not just those who receive anticancer medications. Our results suggest that efforts must be pursued to better integrate geriatric oncology in daily clinical practice.
C1 [Gouverneur, Amandine; Colombani, Francoise; Terrebonne, Eric; Smith, Denis; Fourrier-Reglat, Annie; Noize, Pernelle] CHU Bordeaux, F-33000 Bordeaux, France.
   [Gouverneur, Amandine; Fourrier-Reglat, Annie] Univ Bordeaux, F-33076 Bordeaux, France.
   [Gouverneur, Amandine; Fourrier-Reglat, Annie; Noize, Pernelle] INSERM, U1219, F-33076 Bordeaux, France.
   [Gouverneur, Amandine; Rouyer, Magali; Grelaud, Angela; Robinson, Philip; Fourrier-Reglat, Annie; Noize, Pernelle] INSERM, CIC1401, F-33076 Bordeaux, France.
   [Rouyer, Magali; Grelaud, Angela; Robinson, Philip] ADERA, F-33608 Pessac, France.
C3 CHU Bordeaux; Universite de Bordeaux; Universite de Bordeaux; Institut
   National de la Sante et de la Recherche Medicale (Inserm); Universite de
   Bordeaux; Universite de Bordeaux; Institut National de la Sante et de la
   Recherche Medicale (Inserm)
RP Noize, P (corresponding author), CHU Bordeaux, F-33000 Bordeaux, France.; Noize, P (corresponding author), INSERM, U1219, F-33076 Bordeaux, France.; Noize, P (corresponding author), INSERM, CIC1401, F-33076 Bordeaux, France.
EM pernelle.noize@u-bordeaux.fr
RI Noize, Pernelle/T-1955-2019; Gouverneur, Amandine/O-5332-2018
OI Angela, Grelaud/0000-0002-3480-3405; Noize,
   Pernelle/0000-0001-5617-7954; Gouverneur, Amandine/0000-0001-6253-1833
CR Aparicio T, 2016, ANN ONCOL, V27, P121, DOI 10.1093/annonc/mdv491
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   Phelip JM, 2014, CANC COLORECTAL META
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NR 17
TC 6
Z9 6
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0767-3981
EI 1472-8206
J9 FUND CLIN PHARMACOL
JI Fundam. Clin. Pharmacol.
PD FEB
PY 2017
VL 31
IS 1
BP 104
EP 109
DI 10.1111/fcp.12243
PG 6
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA EK2OJ
UT WOS:000393766300008
PM 27600062
DA 2025-01-04
ER

PT J
AU Khan, T
   Lyons, NJ
   Gough, M
   Kwah, KKX
   Cuda, TJ
   Snell, CE
   Tse, BW
   Sokolowski, KA
   Pearce, LA
   Adams, TE
   Rose, SE
   Puttick, S
   Pajic, M
   Adams, MN
   He, YW
   Hooper, JD
   Kryza, T
AF Khan, Tashbib
   Lyons, Nicholas J.
   Gough, Madeline
   Kwah, Kayden K. X.
   Cuda, Tahleesa J.
   Snell, Cameron E.
   Tse, Brian W.
   Sokolowski, Kamil A.
   Pearce, Lesley A.
   Adams, Timothy E.
   Rose, Stephen E.
   Puttick, Simon
   Pajic, Marina
   Adams, Mark N.
   He, Yaowu
   Hooper, John D.
   Kryza, Thomas
TI CUB Domain-Containing Protein 1 (CDCP1) is a rational target for the
   development of imaging tracers and antibody-drug conjugates for cancer
   detection and therapy
SO THERANOSTICS
LA English
DT Article
DE CDCP1; cancer; theranostics; antibody-drug conjugate; receptor
ID COLORECTAL-CANCER; MEMBRANE ANTIGEN; CELL-MIGRATION; ELEVATED CDCP1;
   IDENTIFICATION; CARCINOMA; SURVIVAL; SURFACE
AB Rationale: An antibody-drug conjugate (ADC) is a targeted therapy consisting of a cytotoxic payload that is linked to an antibody which targets a protein enriched on malignant cells. Multiple ADCs are currently used clinically as anti-cancer agents significantly improving patient survival. Herein, we evaluated the rationale of targeting the cell surface oncoreceptor CUB domain-containing protein 1 (CDCP1) using ADCs and assessed the efficacy of CDCP1-directed ADCs against a range of malignant tumors.
   Methods: CDCP1 mRNA expression was evaluated using large transcriptomic datasets of normal/tumor samples for 23 types of cancer and 15 other normal organs, and CDCP1 protein expression was examined in 34 normal tissues, >300 samples from six types of cancer, and in 49 cancer cell lines. A recombinant human/mouse chimeric anti-CDCP1 antibody ( ch10D7) was labelled with 89Zirconium or monomethyl auristatin E (MMAE) and tested in multiple pre-clinical cancer models including 36 cancer cell lines and three mouse xenograft models.
   Results: Analysis of CDCP1 expression indicates elevated CDCP1 expression in the majority of the cancers and restricted expression in normal human tissues. Antibody ch10D7 demonstrates a high affinity and specificity for CDCP1 inducing cell signalling via Src accompanied by rapid internalization of ch10D7/CDCP1 complexes in cancer cells. (89)Zirconium-labelled ch10D7 accumulates in CDCP1 expressing cells enabling detection of pancreatic cancer xenografts in mice by PET imaging. Cytotoxicity of MMAE-labelled ch10D7 against kidney, colorectal, lung, ovarian, pancreatic and prostate cancer cells in vitro, correlates with the level of CDCP1 on the plasma membrane. ch10D7-MMAE displays robust anti-tumor effects against mouse xenograft models of pancreatic, colorectal and ovarian cancer.
   Conclusion: CDCP1 directed imaging agents will be useful for selecting cancer patients for personalized treatment with cytotoxin-loaded CDCP1 targeting agents including antibody-drug conjugates.
C1 [Khan, Tashbib; Lyons, Nicholas J.; Gough, Madeline; Kwah, Kayden K. X.; Cuda, Tahleesa J.; Snell, Cameron E.; He, Yaowu; Hooper, John D.; Kryza, Thomas] Univ Queensland, Translat Res Inst, Mater Res Inst, 37 Kent St, Woolloongabba, Qld, Australia.
   [Snell, Cameron E.] Mater Hlth Serv, South Brisbane, Qld, Australia.
   [Tse, Brian W.; Sokolowski, Kamil A.] Translat Res Inst, Preclin Imaging Facil, Woolloongabba, Qld, Australia.
   [Pearce, Lesley A.; Adams, Timothy E.] Commonwealth Sci & Ind Res Org Mfg, Parkville, Vic, Australia.
   [Rose, Stephen E.; Puttick, Simon] CSIRO, Herston, Qld, Australia.
   [Pajic, Marina] Univ New South Wales, Fac Med, Kinghorn Canc Ctr, Garvan Inst Med Res,St Vincents Clin Sch, Sydney, NSW, Australia.
   [Adams, Mark N.] Queensland Univ Technol, Ctr Genom Cs & Personalised Hlth, Sch Biomed Sci, Brisbane, Qld, Australia.
C3 Mater Research; University of Queensland; Mater Health Services;
   University of Queensland; Commonwealth Scientific & Industrial Research
   Organisation (CSIRO); Commonwealth Scientific & Industrial Research
   Organisation (CSIRO); Garvan Institute of Medical Research; The Kinghorn
   Cancer Centre; University of New South Wales Sydney; Queensland
   University of Technology (QUT)
RP Hooper, JD; Kryza, T (corresponding author), Univ Queensland, Translat Res Inst, Mater Res Inst, 37 Kent St, Woolloongabba, Qld, Australia.
EM john.hooper@mater.uq.edu.au; thomas.kryza@mater.uq.edu.au
RI Tse, Brian/X-8909-2019; Kryza, Thomas/AAX-7681-2020; Puttick,
   Simon/M-1903-2013; Adams, Mark/AAE-1209-2021; Adams,
   Timothy/I-6231-2012; Hooper, John/C-1481-2016; Rose, Stephen/C-8044-2009
OI Kwah, Kayden/0000-0002-0809-9995; Gough, Madeline/0000-0003-3677-9661;
   Rose, Stephen/0000-0003-1558-6297; Adams, Mark/0000-0003-1906-5018
FU National Health and Medical Research Council of Australia [APP1121970];
   Medical Research Future Fund [MRF1199422]; Avner Pancreatic Cancer
   Foundation [R3 JH 2.1]; Therapeutics Innovation Australia; Cancer
   Council Queensland [APP1082040]; NBCF [IIRS-085]; Mater Foundation
FX This work was supported by grants from the National Health and Medical
   Research Council of Australia (APP1121970), Medical Research Future Fund
   (MRF1199422) the Avner Pancreatic Cancer Foundation (R3 JH 2.1),
   Therapeutics Innovation Australia (Pipeline Accelerator 2020-21 Round 1)
   and Cancer Council Queensland (APP1082040) to JDH, and the NBCF
   (IIRS-085) to TK. CES is a Betty McGrath Fellow and CES and JDH are
   supported by the Mater Foundation.
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NR 39
TC 3
Z9 3
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 2022
VL 12
IS 16
BP 6915
EP 6930
DI 10.7150/thno.78171
PG 16
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 8Z4XU
UT WOS:000933383900006
PM 36276654
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Cheng, ZW
   Shao, XY
   Xu, ML
   Wang, JF
   Kuai, XY
   Zhang, LP
   Wu, J
   Zhou, CL
   Mao, JD
AF Cheng, Zhengwu
   Shao, Xinyu
   Xu, Menglin
   Wang, Junfeng
   Kuai, Xiaoyi
   Zhang, Liping
   Wu, Jian
   Zhou, Chunli
   Mao, Jiading
TI Rab1A promotes proliferation and migration abilities via regulation of
   the HER2/AKT-independent mTOR/S6K1 pathway in colorectal cancer
SO ONCOLOGY REPORTS
LA English
DT Article
DE colorectal cancer; Rab1A; mTORC1; prognosis
ID ABERRANT EXPRESSION; MTORC1; GROWTH; CELLS; METASTASIS; INHIBITION
AB Colorectal carcinoma (CRC) is one of the most common malignancies worldwide and the second leading cause of cancer-related deaths in the US. Recently, Rab1A has been reported to be an activator of mTORC1 and p-S6K1, which is downstream of mTORC1. However, the association between Rab1A and p-S6K1 in CRC remains elusive. In the present study, we first demonstrated that Rab1A was overexpressed in CRC tissues and Rab1A overexpression was positively related to lymph node invasion, degree of differentiation, venous invasion and tumor-node-metastasis (TNM) stage. In both TNM stage I-II and III-IV patients, Rab1A-positive patients had a shorter survival time than Rab1A-negative patients. Furthermore, in univariate and multivariate analyses, only Rab1A expression was verified as an independent prognostic factor for survival in CRC patients. The level of p-S6K1 was markedly high in CRC tissues and Rab1A expression level had a positive association with p-S6K1 level. In addition, high levels of both Rab1A and p-S6K1 were associated with a poorer prognosis compared with low expression of either Rab1A or p-S6K1 level. Moreover, high levels of both Rab1A and p-S6K1 were associated with a poorer prognosis than patients with high levels of either Rab1A or p-S6K1 alone. Finally, knockdown of Rab1A expression inhibited migration and proliferation of SW480 and HCT116 cell lines by targeting regulation of p-S6K1. Thus, our findings indicate that Rab1A plays an important role in CRC and may provide a therapeutic target for CRC, particularly for mTORC1-targeted therapy-resistant cancers.
C1 [Cheng, Zhengwu; Wang, Junfeng; Wu, Jian; Mao, Jiading] Wannan Med Coll, Affiliated Hosp 1, Dept Gastrointestinal Surg, 2 Zheshan West Rd, Wuhu 241000, Anhui, Peoples R China.
   [Shao, Xinyu; Kuai, Xiaoyi; Zhang, Liping; Zhou, Chunli] Nanjing Med Univ, Affiliated Suzhou Hosp, Dept Gastroenterol, 242 Guangji Rd, Suzhou 215006, Jiangsu, Peoples R China.
   [Shao, Xinyu] Nanjing Med Univ, Affiliated Suzhou Hosp, Dept Gen Surg, Suzhou 215006, Jiangsu, Peoples R China.
   [Xu, Menglin] Wannan Med Coll, Affiliated Hosp 1, Dept Oncol, Wuhu 241000, Anhui, Peoples R China.
C3 Wannan Medical College; Nanjing Medical University; Nanjing Medical
   University; Wannan Medical College
RP Mao, JD (corresponding author), Wannan Med Coll, Affiliated Hosp 1, Dept Gastrointestinal Surg, 2 Zheshan West Rd, Wuhu 241000, Anhui, Peoples R China.; Zhou, CL (corresponding author), Nanjing Med Univ, Affiliated Suzhou Hosp, Dept Gastroenterol, 242 Guangji Rd, Suzhou 215006, Jiangsu, Peoples R China.
EM zhouchunli079@163.com; maojiadingyjs02@126.com
OI Zhou, Chunli/0000-0001-7369-4320; Shao, Xinyu/0000-0001-9608-455X
FU Beijing Medical and Health Foundation [B17523]
FX This study was supported by the Beijing Medical and Health Foundation
   (B17523).
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NR 36
TC 27
Z9 29
U1 0
U2 5
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 MAY
PY 2019
VL 41
IS 5
BP 2717
EP 2728
DI 10.3892/or.2019.7071
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HS6XZ
UT WOS:000464015900011
PM 30896866
OA Green Published, hybrid, Green Submitted
DA 2025-01-04
ER

PT J
AU Galbraith, NJ
   Wood, C
   Steele, CW
AF Galbraith, Norman J.
   Wood, Colin
   Steele, Colin W.
TI Targeting Metastatic Colorectal Cancer with Immune Oncological Therapies
SO CANCERS
LA English
DT Review
DE colorectal cancer; immunotherapy; metastases; immune checkpoint
   inhibitors; anti-PD1; tumour microenvironment; targeted therapy;
   microsatellite instability; mismatch repair; tumour-associated
   macrophages
ID MISMATCH REPAIR-DEFICIENT; TUMOR MUTATIONAL BURDEN; OPEN-LABEL;
   MONOCLONAL-ANTIBODY; PHASE-II; CHECKPOINT; CLASSIFICATION; MULTICENTER;
   BEVACIZUMAB; NIVOLUMAB
AB Simple Summary Colorectal cancer that has become metastatic continues to have a poor outlook. Many patients will undergo intensive chemotherapy, often with limited effects but many side effects. In other types of cancer, immunotherapy has shown to be effective by targeting the immune cells of the patient and restoring their function to fight off cancer. This review explores the up-to-date evidence for immunotherapy in metastatic colorectal cancer. We have discussed in which patients this treatment is effective, but also why this has not been effective in a large number of patients. By summarizing the key components of the immune cells within the proximity to the tumour and its areas of spread, we discuss how these components can be targeted. Areas of future research are also highlighted, which includes combining immunotherapy with current treatments, such as surgery, radiotherapy and chemotherapy as well as some recent advances from basic and translational studies that promises to improve outcomes in these patients. Metastatic colorectal cancer carries poor prognosis, and current therapeutic regimes convey limited improvements in survival and high rates of detrimental side effects in patients that may not stand to benefit. Immunotherapy has revolutionised cancer treatment by restoring antitumoural mechanisms. However, the efficacy in metastatic colorectal cancer, is limited. A literature search was performed using Pubmed (Medline), Web of Knowledge, and Embase. Search terms included combinations of immunotherapy and metastatic colorectal cancer, primarily focusing on clinical trials in humans. Analysis of these studies included status of MMR/MSS, presence of combination strategies, and disease control rate and median overall survival. Evidence shows that immune checkpoint inhibitors, such as anti-PD1 and anti-PD-L1, show efficacy in less than 10% of patients with microsatellite stable, MMR proficient colorectal cancer. In the small subset of patients with microsatellite unstable, MMR deficient cancers, response rates were 40-50%. Combination strategies with immunotherapy are under investigation but have not yet restored antitumoural mechanisms to permit durable disease regression. Immunotherapy provides the potential to offer additional strategies to established chemotherapeutic regimes in metastatic colorectal cancer. Further research needs to establish which adjuncts to immune checkpoint inhibition can unpick resistance, and better predict which patients are likely to respond to individualised therapies to not just improve response rates but to temper unwarranted side effects.
C1 [Galbraith, Norman J.; Wood, Colin; Steele, Colin W.] Univ Glasgow, Glasgow Royal Infirm, Acad Dept Surg, Level 2 New Lister Bldg,10-16 Alexandra Parade, Glasgow G31 2ER, Lanark, Scotland.
   [Steele, Colin W.] Beatson Inst, Inst Canc Sci, Garscube Campus,Switchback Rd, Bearsden G61 1BD, Scotland.
C3 University of Glasgow; Beatson Institute
RP Galbraith, NJ (corresponding author), Univ Glasgow, Glasgow Royal Infirm, Acad Dept Surg, Level 2 New Lister Bldg,10-16 Alexandra Parade, Glasgow G31 2ER, Lanark, Scotland.
EM norman.galbraith@glasgow.ac.uk; colin.wood@glasgow.ac.uk;
   colin.steele@glasgow.ac.uk
RI Galbraith, Norman/AGS-5023-2022
OI Galbraith, Norman/0000-0002-6354-6946
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NR 83
TC 6
Z9 6
U1 0
U2 11
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUL
PY 2021
VL 13
IS 14
AR 3566
DI 10.3390/cancers13143566
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TO2QH
UT WOS:000676762600001
PM 34298779
OA Green Published, Green Accepted, gold
DA 2025-01-04
ER

PT J
AU Xie, WL
   Xie, L
   Song, XR
AF Xie, Wenli
   Xie, Li
   Song, Xianrang
TI The diagnostic accuracy of circulating free DNA for the detection of
   KRAS mutation status in colorectal cancer: A meta-analysis
SO CANCER MEDICINE
LA English
DT Article
DE cfDNA; colorectal cancer; diagnostic; KRAS mutation; meta-analysis
ID CELL-FREE DNA; K-RAS MUTATIONS; PRIMARY TUMORS; SYSTEMATIC REVIEWS;
   PROGNOSTIC VALUE; BRAF MUTATIONS; DIGITAL-PCR; MUTANT-DNA; PLASMA DNA;
   TISSUE
AB KRAS mutations have been reported as a reliable biomarker for epidermal growth factor receptor (EGFR) targeted therapy and are also associated with poor prognosis in colorectal cancer (CRC) patients. However, limitations of detecting KRAS mutations in tissues are obvious. KRAS mutations in the peripheral blood can be detected as an alternative to tissue analysis. The objective of this meta-analysis was to evaluate the diagnostic value of cfDNA (circulating free DNA) compared with tissues and to investigate the prognostic potential of cfDNA KRAS mutations in CRC patients. Searches were performed in PubMed, Embase, and Cochrane Library for published studies. We extracted true-positive (TP), false-positive (FP), false-negative (FN), true-negative (TN) values, survival rate of CRC patients with mutant and wild-type KRAS and calculated pooled sensitivity and specificity, positive/negative likelihood ratios [PLRs/NLRs], diagnostic odds ratios [DORs], and corresponding 95% confidence intervals [95% CIs]. We also generated a summary receiver operating characteristic (SROC) curve to evaluate the overall diagnostic potential. Totally, 31 relevant studies were recruited and used for the meta-analysis on the efficacy of cfDNA testing in detecting KRAS mutations. The pooled sensitivity, specificity, PLR, NLR, and DOR were 0.637 (95% CI: 0.607-0.666), 0.943 (95% CI: 0.930-0.954), 10.024 (95% CI: 6.912-14.535), 0.347 (95% CI: 0.269-0.447), and 37.882 (95% CI: 22.473-63.857), respectively. The area under the SROC curve was 0.9392. Together, the results suggest that detecting KRAS mutations in cfDNA has adequate diagnostic efficacy in terms of specificity. There is a promising role for cfDNA in the detection of KRAS mutations in CRC patients. However, prospective studies with larger patient cohorts are still required before definitive conclusions of the prognostic potential of cfDNA KRAS mutations in CRC patients were drawn.
C1 [Xie, Wenli; Song, Xianrang] Shandong Univ, Shandong Canc Hosp, Jinan, Shandong, Peoples R China.
   [Xie, Li; Song, Xianrang] Shandong Univ, Shandong Acad Med Sci, Shandong Canc Hosp, Jinan, Shandong, Peoples R China.
C3 Shandong University; Shandong First Medical University & Shandong
   Academy of Medical Sciences; Shandong University; Shandong First Medical
   University & Shandong Academy of Medical Sciences; University of Jinan
RP Song, XR (corresponding author), Shandong Univ, Shandong Acad Med Sci, Shandong Canc Hosp, Jinan, Shandong, Peoples R China.
EM sxr@vip.163.com
OI song, xianrang/0000-0003-1722-8207
FU National Natural Science Foundation of China [81371886]
FX National Natural Science Foundation of China, Grant/Award Number:
   81371886
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NR 64
TC 11
Z9 13
U1 0
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD MAR
PY 2019
VL 8
IS 3
BP 1218
EP 1231
DI 10.1002/cam4.1989
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HQ3YX
UT WOS:000462347500036
PM 30791218
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Cocco, E
   Benhamida, J
   Middha, S
   Zehir, A
   Mullaney, K
   Shia, J
   Yaeger, R
   Zhang, LY
   Wong, D
   Villafania, L
   Nafa, K
   Scaltriti, M
   Drilon, A
   Saltz, L
   Schram, AM
   Stadler, ZK
   Hyman, DM
   Benayed, R
   Ladanyi, M
   Hechtman, JF
AF Cocco, Emiliano
   Benhamida, Jamal
   Middha, Sumit
   Zehir, Ahmet
   Mullaney, Kerry
   Shia, Jinru
   Yaeger, Rona
   Zhang, Liying
   Wong, Donna
   Villafania, Liliana
   Nafa, Khedoudja
   Scaltriti, Maurizio
   Drilon, Alexander
   Saltz, Leonard
   Schram, Alison M.
   Stadler, Zsofia K.
   Hyman, David M.
   Benayed, Ryma
   Ladanyi, Marc
   Hechtman, Jaclyn F.
TI Colorectal Carcinomas Containing Hypermethylated MLH1 Promoter and
   Wild-Type BRAF/KRAS Are Enriched for Targetable Kinase Fusions
SO CANCER RESEARCH
LA English
DT Article
ID CANCER; BRAF
AB Kinase fusions are rare and poorly characterized in colorectal carcinoma, yet they present unique opportunities for targeted therapy. In this study, we characterized kinase fusions from patients with advanced colorectal carcinoma who had MSK-IMPACT testing of their tumors between January 2014 and June 2018. Patients were analyzed for the presence of fusions, microsatellite instability (MSI), and RAS/BRAF mutations. Mismatch repair (MMR), IHC, and promoter hypermethylation status of MLH1 (MLH1ph) in microsatellite instability-high (MSI-H) colorectal carcinoma with fusions were investigated. Fusion transcripts were confirmed using a targeted RNA-seq panel assay. Of 2,314 colorectal carcinomas with MSK-IMPACT testing, 21 harbored kinase fusions. Over-all 57% (12/21) of colorectal carcinoma fusions were MSI-H/MMR-D. Loss of MLH1 and MLH1ph was confirmed in all 12 and all 10 cases with available material, respectively. Fusions were present in 5% of MSI-H/MMR-D colorectal carcinoma compared with 0.4% of MSS/MMR-P colorectal carcinoma (P < 0.001) and 15% of MSI-H/MMR-D colorectal carcinoma with wild-type RAS/BRAF. Of 24 total MLH1-deficient colorectal carcinomas with MLH1ph and wild-type RAS/BRAF, 10 (42%) harbored kinase fusions. Kinase fusions in MSI-H colorectal carcinoma were associated with sporadic MLH1ph rather than with Lynch syndrome, and these patients may be eligible for kinase inhibitors, particularly following resistance or toxicity in response to immunotherapy. These findings identify a molecular subset of colorectal carcinoma with kinase fusions that may be responsive to kinase inhibitors.
C1 [Cocco, Emiliano; Scaltriti, Maurizio; Ladanyi, Marc] Mem Sloan Kettering Canc Ctr, Human Oncol & Pathol Program, 1275 York Ave, New York, NY 10021 USA.
   [Benhamida, Jamal; Middha, Sumit; Zehir, Ahmet; Mullaney, Kerry; Shia, Jinru; Zhang, Liying; Wong, Donna; Villafania, Liliana; Nafa, Khedoudja; Scaltriti, Maurizio; Benayed, Ryma; Ladanyi, Marc; Hechtman, Jaclyn F.] Mem Sloan Kettering Canc Ctr, Dept Pathol, 1275 York Ave, New York, NY 10021 USA.
   [Yaeger, Rona; Drilon, Alexander; Saltz, Leonard; Schram, Alison M.; Stadler, Zsofia K.; Hyman, David M.] Mem Sloan Kettering Canc Ctr, Dept Med, 1275 York Ave, New York, NY 10021 USA.
   [Drilon, Alexander; Schram, Alison M.; Hyman, David M.] Weill Cornell Med Coll, New York, NY USA.
C3 Memorial Sloan Kettering Cancer Center; Memorial Sloan Kettering Cancer
   Center; Memorial Sloan Kettering Cancer Center; Cornell University;
   Weill Cornell Medicine
RP Hechtman, JF (corresponding author), Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10065 USA.
EM hechtmaj@mskcc.org
RI Hechtman, Jaclyn/A-3277-2013; Ladanyi, Marc/AAG-8585-2019; Zehir,
   Ahmet/ABE-7155-2020
OI Schram, Alison/0000-0002-6070-2413; Zehir, Ahmet/0000-0001-5406-4104;
   Hechtman, Jaclyn/0000-0003-2645-0985
FU Cycle for Survival award; NCI under the MSK Cancer Center Support
   Grant/Core Grant [P30 CA008748, R01CA226864]; LOXO Oncology; NIH
   [T32-CA009207]; ASCO Young Investigator Award
FX A. Drilon acknowledges Cycle for Survival award. E. Cocco acknowledges
   MSK society for a scholar prize. This study was funded by the NCI under
   the MSK Cancer Center Support Grant/Core Grant (P30 CA008748) and the
   R01CA226864 (to M. Scaltriti and A. Drilon). Archer testing was
   supported in part by a grant from LOXO Oncology (to M. Ladanyi.). A.
   Schram acknowledges NIH T32-CA009207 and ASCO Young Investigator Award.
CR [Anonymous], 2010, WHO Classification of tumors of the digestive system
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NR 16
TC 105
Z9 109
U1 0
U2 11
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 MAR 15
PY 2019
VL 79
IS 6
BP 1047
EP 1053
DI 10.1158/0008-5472.CAN-18-3126
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HP2CF
UT WOS:000461474900008
PM 30643016
OA Bronze, Green Accepted
DA 2025-01-04
ER

PT J
AU Lehmann, TP
   Golik, M
   Olejnik, J
   Lukaszewska, M
   Markowska, D
   Drozdzynska, M
   Kotecki, A
   Glowacki, M
   Jagodzinski, PP
AF Lehmann, Tomasz P.
   Golik, Marta
   Olejnik, Jolanta
   Lukaszewska, Marianna
   Markowska, Dominika
   Drozdzynska, Martyna
   Kotecki, Aleksander
   Glowacki, Maciej
   Jagodzinski, Pawel P.
TI Potential applications of using tissue-specific EVs in targeted therapy
   and vaccinology
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE MiRNA; Extracellular vesicles; Exosome-based vaccines; Colorectal
   cancer; Parkinson's disease; Leukaemia; Liver fibrosis
ID EXTRACELLULAR VESICLES; PARKINSONS-DISEASE; DENDRITIC CELLS; SURFACE
   FUNCTIONALIZATION; ENGINEERING EXOSOMES; CELLULAR UPTAKE; BLOOD
   EXOSOMES; T-CELLS; DELIVERY; ANTIGEN
AB Many cell types secrete spherical membrane bodies classified as extracellular vesicles (EVs). EVs participate in intercellular communication and are present in body fluids, including blood, lymph, and cerebrospinal fluid. The time of EVs survival in the body varies depending on the body's localisation. Once the EVs reach cells, they trigger a cellular response. Three main modes of direct interaction of EVs with a target cell were described: receptor-ligand interaction mode, a direct fusion of EVs with the cellular membrane and EVs internalisation. Studies focused on the medical application of EVs. Medical application of EVs may require modification of their surface and interior. EVs surface was modified by affecting the parental cells or by the direct amendment of isolated EVs. The interior modification involved introducing materials into the cells or direct administrating isolated EVs. EVs carry proteins, lipids, fragments of DNA, mRNA, microRNA (miRNA) and long non-coding RNA. Because of EVs availability in liquid biopsy, they are potential diagnostic markers. Modified EVs could enhance the treatment of diseases such as colorectal cancer, Parkinson's disease, leukaemia or liver fibrosis. EVs have specific tissue tropisms, which makes them convenient organ-directed carriers of nucleic acids, drugs and vaccines. In conclusion, recently published works have shown that EVs could become biomarkers and modern vehicles of advanced drug forms.
C1 [Lehmann, Tomasz P.; Golik, Marta; Olejnik, Jolanta; Lukaszewska, Marianna; Markowska, Dominika; Drozdzynska, Martyna; Kotecki, Aleksander; Jagodzinski, Pawel P.] Poznan Univ Med Sci, Dept Biochem & Mol Biol, PL-60781 Poznan, Poland.
   [Glowacki, Maciej] Poznan Univ Med Sci, Dept Paediat Orthopaed & Traumatol, PL-61545 Poznan, Poland.
   [Lehmann, Tomasz P.] Poznan Univ Med Sci, Dept Biochem & Mol Biol, Ul Swiecickiego 6, PL-60781 Poznan, Poland.
C3 Poznan University of Medical Sciences; Poznan University of Medical
   Sciences; Poznan University of Medical Sciences
RP Lehmann, TP (corresponding author), Poznan Univ Med Sci, Dept Biochem & Mol Biol, Ul Swiecickiego 6, PL-60781 Poznan, Poland.
EM tlehmann@ump.edu.pl
RI Lehmann, Tomasz/JRX-1433-2023
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NR 129
TC 13
Z9 13
U1 2
U2 16
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 OCT
PY 2023
VL 166
AR 115308
DI 10.1016/j.biopha.2023.115308
EA SEP 2023
PG 11
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA S8DA0
UT WOS:001073405500001
PM 37660644
OA gold
DA 2025-01-04
ER

PT J
AU Druzhkova, IM
   Shirmanova, MV
   Kuznetsova, DS
   Lukina, MM
   Zagaynova, EV
AF Druzhkova, I. M.
   Shirmanova, M., V
   Kuznetsova, D. S.
   Lukina, M. M.
   Zagaynova, E., V
TI Modern Approaches to Testing Drug Sensitivity of Patients' Tumors
SO SOVREMENNYE TEHNOLOGII V MEDICINE
LA English
DT Review
DE medical oncology; individualized cancer therapy; cancer treatment
   selection; molecular genetic tumor testing; drug testing in vitro
ID CANCER-CELL-LINES; COLORECTAL-CANCER; HUMAN COLON; XENOGRAFTS;
   CHEMOTHERAPY; CHEMOSENSITIVITY; EXPRESSION; CETUXIMAB; CHIP;
   TECHNOLOGIES
AB Drug therapy is still one of the basic techniques used to treat cancers of different etiology. However, tumor resistance to drugs is a pressing problem limiting drug treatment efficacy. It is obvious for both modern fundamental and clinical oncology that there is the need for an individual approach to treating cancer taking into account the biological properties of a tumor when prescribing chemo- and targeted therapy. One of the promising strategies is to increase the antitumor therapy efficacy by developing predictive tests, which enable to evaluate the sensitivity of a particular tumor to a specific drug or a drug combination before the treatment initiation and, thus, make individual therapy selection possible.
   The present review considers the main approaches to drug sensitivity assessment of patients' tumors: molecular genetic profiling of tumor cells, and direct efficiency testing of the drugs on tumor cells isolated from surgical or biopsy material. There were analyzed the key directions in research and clinical studies such as: the search for predictive molecular markers, the development of methods to maintain tumor cells or tissue sections viable, i.e. in a condition maximum close to their physiological state, the development of high throughput systems to assess therapy efficiency. Special attention was given to a patient-centered approach to drug therapy in colorectal cancer.
C1 [Druzhkova, I. M.; Shirmanova, M., V; Lukina, M. M.] Privolzhsky Res Med Univ, Fluorescent Bioimaging Lab, Res Inst Expt Oncol & Biomed Technol, 10-1 Minin & Pozharsky Sq, Nizhnii Novgorod 603005, Russia.
   [Shirmanova, M., V] Privolzhsky Res Med Univ, Res Inst Expt OnColog & Biomed Technol, 10-1 Minin & Pozharsky Sq, Nizhnii Novgorod 603005, Russia.
   [Kuznetsova, D. S.] Privolzhsky Res Med Univ, Regenerat Med Lab, Res Inst Expt Oncol & Biomed Technol, 10-1 Minin & Pozharsky Sq, Nizhnii Novgorod 603005, Russia.
   [Zagaynova, E., V] Privolzhsky Res Med Univ, Lab Opt Coherence Tomog, Res Inst Expt Oncol & Biomed Technol, 10-1 Minin & Pozharsky Sq, Nizhnii Novgorod 603005, Russia.
   [Zagaynova, E., V] Natl Res Lobachevsky State Univ Nizhni Novgorod, 23 Prospekt Gagarina, Nizhnii Novgorod 603950, Russia.
C3 Privolzhsky Research Medical University; Privolzhsky Research Medical
   University; Privolzhsky Research Medical University; Privolzhsky
   Research Medical University; Lobachevsky State University of Nizhni
   Novgorod
RP Shirmanova, MV (corresponding author), Privolzhsky Res Med Univ, Fluorescent Bioimaging Lab, Res Inst Expt Oncol & Biomed Technol, 10-1 Minin & Pozharsky Sq, Nizhnii Novgorod 603005, Russia.; Shirmanova, MV (corresponding author), Privolzhsky Res Med Univ, Res Inst Expt OnColog & Biomed Technol, 10-1 Minin & Pozharsky Sq, Nizhnii Novgorod 603005, Russia.
EM Shirmanovam@gmail.com
RI Shirmanova, Marina/M-7635-2016; Lukina, Maria/AAA-7249-2020; Kuznetsova,
   Daria/G-3965-2016
OI Shirmanova, Marina/0000-0002-3207-7227; Lukina,
   Maria/0000-0003-1374-8571; Kuznetsova, Daria/0000-0003-0096-6887
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NR 97
TC 2
Z9 2
U1 0
U2 9
PU NIZHNIY NOVGOROD STATE MEDICAL ACAD
PI NIZHNIY NOVGOROD
PA MININ & POZHARSKY SQUARE, 10-1, NIZHNIY NOVGOROD, 603005, RUSSIA
SN 2076-4243
J9 SOVREM TEHNOL MED
JI Sovrem. Tehnol. Med.
PY 2020
VL 12
IS 4
BP 91
EP 102
DI 10.17691/stm2020.12.4.11
PG 12
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA NI1VF
UT WOS:000565144700011
PM 34795997
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Sartore-Bianchi, A
   Amatu, A
   Bonazzina, E
   Stabile, S
   Giannetta, L
   Cerea, G
   Schiavetto, I
   Bencardino, K
   Funaioli, C
   Ricotta, R
   Cipani, T
   Schirru, M
   Gambi, V
   Palmeri, L
   Carlo-Stella, G
   Rusconi, F
   Di Bella, S
   Burrafato, G
   Cassingena, A
   Valtorta, E
   Lauricella, C
   Pazzi, F
   Gambaro, A
   Ghezzi, S
   Marrapese, G
   Tarenzi, E
   Veronese, S
   Truini, M
   Vanzulli, A
   Siena, S
AF Sartore-Bianchi, Andrea
   Amatu, Alessio
   Bonazzina, Erica
   Stabile, Stefano
   Giannetta, Laura
   Cerea, Giulio
   Schiavetto, Ilaria
   Bencardino, Katia
   Funaioli, Chiara
   Ricotta, Riccardo
   Cipani, Tiziana
   Schirru, Michele
   Gambi, Valentina
   Palmeri, Laura
   Carlo-Stella, Giulia
   Rusconi, Francesca
   Di Bella, Sara
   Burrafato, Giovanni
   Cassingena, Andrea
   Valtorta, Emanuele
   Lauricella, Calogero
   Pazzi, Federica
   Gambaro, Alessandra
   Ghezzi, Silvia
   Marrapese, Giovanna
   Tarenzi, Emiliana
   Veronese, Silvio
   Truini, Mauro
   Vanzulli, Angelo
   Siena, Salvatore
TI Pooled Analysis of Clinical Outcome of Patients with Chemorefractory
   Metastatic Colorectal Cancer Treated within Phase I/II Clinical Studies
   Based on Individual Biomarkers of Susceptibility: A Single-Institution
   Experience
SO TARGETED ONCOLOGY
LA English
DT Article
ID TARGETED THERAPY; RAS MUTATIONS; OPEN-LABEL; OXALIPLATIN; PLUS; KRAS;
   CHEMOTHERAPY; MULTICENTER; IRINOTECAN; TUMORS
AB Background Patients with metastatic colorectal cancer (mCRC) refractory to standard therapies have a poor prognosis. In this setting, recruitment into clinical trials is warranted, and studies driven by selection according to individual tumor molecular characteristics are expected to provide added value.
   Objective We retrospectively analyzed data from patients with mCRC refractory to or following failure of standard therapies who were enrolled into phase I/II clinical studies at the Niguarda Cancer Center based on the presence of a specific molecular profile expected to represent the target of susceptibility to the experimental drug(s).
   Patients and Methods From June 2011 to May 2016, 2044 patients with mCRC underwent molecular screening. Eighty patients (3.9%) were enrolled in ad hoc studies; the median age was 60 years (range 36-86) and the median number of previous treatment lines was five (range 2-8). Molecular characteristics exploited within these studies were MGMT promoter hypermethylation (48.7%), HER2 amplification (28.8%), BRAF (V600E) mutation (20%), and novel gene fusions involving ALK or NTRK (2.5%).
   Results One patient (1%) had RECIST (Response Evaluation Criteria In Solid Tumors) complete response (CR), 13 patients (16.5%) experienced a partial response (PR), and 28 (35%) stable disease (SD). Median progression-free survival (PFS) was 2.8 months (range 2.63-3.83), with 24% of patients displaying PFS >5 months. Median growth modulation index (GMI) was 0.85 (range 0-15.61) and 32.5% of patients had GMI >1.33. KRAS exon 2 mutations were found in 38.5% of patients, and among the 78 patients with known KRAS status, those with wild-type tumors had longer PFS than those with mutated tumors (3.80 [95% CI 2.80-5.03] vs. 2.13 months [95% CI 1.77-2.87], respectively, p = 0.001). Median overall survival (OS) was 7.83 months (range 7.17-9.33) for all patients, and patients with KRAS wild-type tumors had longer OS than those with mutated tumors (7.83 [95% CI 7.33-10.80] vs. 7.18 months [95% CI 5.63-9.33], respectively, p = 0.06).
   Conclusions This single-institution retrospective study indicates that in a heavily pretreated population approximately 4% of mCRC tumors display a potential actionable molecular context suitable for therapeutic intervention. Application of molecular selection is challenging but improves clinical outcome even in later lines of treatment.
C1 [Sartore-Bianchi, Andrea; Amatu, Alessio; Bonazzina, Erica; Stabile, Stefano; Giannetta, Laura; Cerea, Giulio; Schiavetto, Ilaria; Bencardino, Katia; Funaioli, Chiara; Ricotta, Riccardo; Cipani, Tiziana; Schirru, Michele; Gambi, Valentina; Palmeri, Laura; Carlo-Stella, Giulia; Rusconi, Francesca; Di Bella, Sara; Burrafato, Giovanni; Cassingena, Andrea; Valtorta, Emanuele; Lauricella, Calogero; Pazzi, Federica; Gambaro, Alessandra; Ghezzi, Silvia; Marrapese, Giovanna; Tarenzi, Emiliana; Veronese, Silvio; Truini, Mauro; Vanzulli, Angelo; Siena, Salvatore] Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, Piazza Osped Maggiore 3, I-20162 Milan, Italy.
   [Vanzulli, Angelo; Siena, Salvatore] Univ Milan, Dipartimento Oncol & Ematooncol, Milan, Italy.
C3 University of Milan
RP Siena, S (corresponding author), Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, Piazza Osped Maggiore 3, I-20162 Milan, Italy.; Siena, S (corresponding author), Univ Milan, Dipartimento Oncol & Ematooncol, Milan, Italy.
EM salvatore.siena@ospedaleniguarda.it
RI Vanzulli, Angelo/X-4175-2019; Cassingena, Andrea/AGD-7137-2022;
   Sartore-Bianchi, Andrea/AAB-9848-2019; SIENA, SALVATORE/AAC-5806-2019
OI VALTORTA, EMANUELE/0000-0002-5087-6233; Vanzulli,
   Angelo/0000-0002-2452-3370; Veronese, Silvio Marco/0000-0002-5280-3740;
   Cassingena, Andrea/0000-0003-4116-3992; Sartore-Bianchi,
   Andrea/0000-0003-0780-0409; SIENA, SALVATORE/0000-0002-2681-2846
FU grant "Terapia Molecolare dei Tumori" by Fondazione Oncologia Niguarda;
   Associazione Italiana per la Ricerca sul Cancro (AIRC) Special program 5
   x 1000; European Union Horizon research and innovation programme
   [635342]; H2020 Societal Challenges Programme [635342] Funding Source:
   H2020 Societal Challenges Programme
FX The study was partly supported by the grant "Terapia Molecolare dei
   Tumori" by Fondazione Oncologia Niguarda, by Associazione Italiana per
   la Ricerca sul Cancro (AIRC) Special program 5 x 1000, and by the
   European Union Horizon 2020 research and innovation programme 2014-2020
   under grant agreement number 635342 (MoTriColor project).
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NR 45
TC 13
Z9 13
U1 0
U2 4
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 AUG
PY 2017
VL 12
IS 4
BP 525
EP 533
DI 10.1007/s11523-017-0505-6
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FB7JP
UT WOS:000406317200011
PM 28669023
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Cremolini, C
   Antoniotti, C
   Pietrantonio, F
   Berenato, R
   Tampellini, M
   Baratelli, C
   Salvatore, L
   Marmorino, F
   Borelli, B
   Nichetti, F
   Bironzo, P
   Sonetto, C
   Di Bartolomeo, M
   de Braud, F
   Loupakis, F
   Falcone, A
   Di Maio, M
AF Cremolini, Chiara
   Antoniotti, Carlotta
   Pietrantonio, Filippo
   Berenato, Rosa
   Tampellini, Marco
   Baratelli, Chiara
   Salvatore, Lisa
   Marmorino, Federica
   Borelli, Beatrice
   Nichetti, Federico
   Bironzo, Paolo
   Sonetto, Cristina
   Di Bartolomeo, Maria
   de Braud, Filippo
   Loupakis, Fotios
   Falcone, Alfredo
   Di Maio, Massimo
TI Surrogate Endpoints in Second-Line Trials of Targeted Agents in
   Metastatic Colorectal Cancer: A Literature-Based Systematic Review and
   Meta-Analysis
SO CANCER RESEARCH AND TREATMENT
LA English
DT Review
DE Colorectal neoplasms; Biomarkers; Molecular targeted therapy
ID PROGRESSION-FREE SURVIVAL; RANDOMIZED PHASE-II; PLACEBO-CONTROLLED
   PHASE-2; 1ST-LINE THERAPY; DOUBLE-BLIND; BEVACIZUMAB; FOLFIRI;
   OXALIPLATIN; COMBINATION; FLUOROURACIL
AB Purpose
   The purpose of this study was to evaluate progression-free survival (PFS) and objective response rate (ORR) as surrogate endpoints of overall survival (OS) in modern clinical trials investigating the efficacy of targeted agents in the second-line treatment of metastatic colorectal cancer (mCRC).
   Materials and Methods
   A systematic search of literature pertaining to randomized phase II and Ill trials evaluating targeted agents as second-line treatments for mCRC was performed. The strength of the correlation between both PFS and ORR and OS was assessed based on the Pearson's correlation coefficient (R) and the coefficient of determination (R-2).
   Results
   Twenty trials, including a total of 7,571 patients, met the search criteria. The median duration of post-progression survival (PPS) was 7.6 months. The median differences between experimental and control arms were 0.65 months (range,-2.4 to 3.4) for the median PFS and 0.7 months (range,-5.8 to 3.9) for the median OS. PFS and ORR showed moderate (R=0.734, R-2=0.539, p < 0.001) and poor correlation (R=0.169, R-2=0.029, p=0.476) with OS, respectively. No differences between anti-angiogenic agents and other drugs were evident.
   Conclusion
   Targeted agents investigated in the second-line treatment of mCRC provided minimal PFS gains translating into modest OS improvements. Considering both the moderate correlation between PFS and OS and the short duration of PPS, the OS should remain the preferred primary endpoint for randomized clinical trials in the second-line treatment of mCRC.
C1 [Cremolini, Chiara; Antoniotti, Carlotta; Marmorino, Federica; Borelli, Beatrice; Loupakis, Fotios; Falcone, Alfredo] Univ Pisa, Azienda Osped Univ Pisana, Dept Translat Res & New Technol Med, Unit Med Oncol, Pisa, Italy.
   [Pietrantonio, Filippo; Berenato, Rosa; Nichetti, Federico; Di Bartolomeo, Maria; de Braud, Filippo] Fdn IRCCS Ist Nazl Tumori, Med Oncol Dept, Milan, Italy.
   [Tampellini, Marco; Baratelli, Chiara; Bironzo, Paolo; Sonetto, Cristina] Univ Turin, Dept Oncol, AOU San Luigi Gonzaga, Turin, Italy.
   [Di Maio, Massimo] Univ Turin, Dept Oncol, AO Ordine Mauriziano, Turin, Italy.
C3 University of Pisa; Azienda Ospedaliero Universitaria Pisana; Fondazione
   IRCCS Istituto Nazionale Tumori Milan; University of Turin; A.O.U. Citta
   della Salute e della Scienza di Torino; AOU San Giovanni
   Battista-Molinette; University of Turin
RP Di Maio, M (corresponding author), Univ Turin, Osped Umberto 1, Dipartimento Oncol, SCDU Oncol,AO Ordine Mauriziano, Via Magellano 1, I-10128 Turin, Italy.
EM massimo.dimaio@unito.it
RI Nichetti, Federico/AAG-3984-2020; DI MAIO, Massimo/AAB-6074-2019;
   Borelli, B/AAJ-8829-2021; Antoniotti, Carlotta/KIC-8096-2024; Cremolini,
   Chiara/AAC-1889-2019; Falcone, Alfredo/G-5217-2013; Loupakis,
   Fotios/I-7243-2012; Di Bartolomeo, Maria/D-1655-2017; de Braud, Filippo
   Guglielmo Maria/B-9997-2017; DI MAIO, Massimo/K-9990-2016; Pietrantonio,
   Filippo/C-2180-2017; Salvatore, Lisa/L-7746-2019
OI Loupakis, Fotios/0000-0001-9651-0395; Bironzo,
   Paolo/0000-0002-2784-5076; Di Bartolomeo, Maria/0000-0002-7954-6609;
   CREMOLINI, CHIARA/0000-0002-0520-4841; Nichetti,
   Federico/0000-0001-8044-4207; de Braud, Filippo Guglielmo
   Maria/0000-0003-0103-730X; Falcone, Alfredo/0000-0001-5840-2529; DI
   MAIO, Massimo/0000-0001-8906-3785; Pietrantonio,
   Filippo/0000-0002-8530-8420; Salvatore, Lisa/0000-0003-3864-0719
CR [Anonymous], ASCO M S
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NR 35
TC 12
Z9 13
U1 0
U2 1
PU KOREAN CANCER ASSOCIATION
PI SEOUL
PA RM 1824, GWANGHWAMUN OFFICIA, 92 SAEMUNAN-RO, JONGNO-GU, SEOUL, 110-999,
   SOUTH KOREA
SN 1598-2998
EI 2005-9256
J9 CANCER RES TREAT
JI Cancer Res. Treat.
PD JUL
PY 2017
VL 49
IS 3
BP 834
EP 845
DI 10.4143/crt.2016.249
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FA6FD
UT WOS:000405537800029
PM 27857020
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Wu, C
   Liu, XT
   Liu, R
   Song, SY
   Zheng, ZF
   Zeng, YL
   Mei, Y
   Zhang, JY
   Duan, QJ
   Lin, R
   Du, JZ
   He, WL
AF Wu, Chong
   Liu, Xiaoting
   Liu, Rong
   Song, Shiyao
   Zheng, Zi-Fan
   Zeng, Yilin
   Mei, Yong
   Zhang, Jing-Yang
   Duan, Qijia
   Lin, Run
   Du, Jin-Zhi
   He, Weiling
TI Sustained Endocytosis Inhibition via Locally-Injected Drug-Eluting
   Hydrogel Improves ADCC-Mediated Antibody Therapy in Colorectal Cancer
SO ADVANCED SCIENCE
LA English
DT Article; Early Access
DE antibody-dependent cell-mediated cytotoxicity; colorectal cancer;
   endocytosis inhibition; epidermal growth factor receptor; hydrogel;
   targeted therapy
ID ACQUIRED-RESISTANCE; EGFR THERAPY; CETUXIMAB; CHEMOTHERAPY; RECEPTORS;
   EFFICACY; IMPACT
AB The epidermal growth factor receptor (EGFR) is a validated therapeutic target for RAS/RAF wild-type colorectal cancer (CRC). However, monoclonal antibody-based anti-EGFR therapies such as cetuximab have limited effectiveness. Herein, it is identified that EGFR internalization is associated with poor treatment response and prognosis in patients with CRC, based on a retrospective analysis of patients treated with cetuximab. It is further demonstrated that the endocytosis inhibitor prochlorperazine (PCZ) can move EGFR, which is hidden inside the cell, to the cell surface to improve therapeutic antibody binding. Thus, a thermosensitive hydrogel co-loaded with cetuximab and PCZ (Gel@Cmab/PCZ) is constructed for sustained inhibition of endocytosis and effective cetuximab delivery. Peritumoral injection of Gel@Cmab/PCZ shows strong antitumor efficacy in subcutaneous and orthotopic CRC tumor models and completely abrogated liver metastasis when combined with chemotherapy. In a humanized patient-derived xenograft model, a single injection of Gel@Cmab/PCZ with one-third of the conventional cetuximab dose achieved 91% tumor growth inhibition, which promoted NK cell infiltration into tumor tissues and their antibody-dependent cell-mediated cytotoxicity effect. This study represents a novel strategy to boost the monoclonal antibody-mediated anti-tumor response in CRC.
C1 [Wu, Chong; Liu, Xiaoting; Zheng, Zi-Fan; Mei, Yong; He, Weiling] Sun Yat sen Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Guangzhou 510080, Guangdong, Peoples R China.
   [Liu, Xiaoting] Sun Yat sen Univ, Zhongshan Sch Med, Dept Immunol, Guangzhou 510080, Guangdong, Peoples R China.
   [Liu, Rong; Duan, Qijia; Du, Jin-Zhi] South China Univ Technol, Sch Med, Guangzhou 510006, Guangdong, Peoples R China.
   [Liu, Rong] Guangdong Inst Drug Control, NMPA Key Lab Qual Control & Evaluat Pharmaceut Exc, Guangzhou 510663, Peoples R China.
   [Song, Shiyao] Sun Yat sen Univ, Affiliated Hosp 1, Dept Pediat, Guangzhou 510080, Guangdong, Peoples R China.
   [Zeng, Yilin; Lin, Run] Sun Yat sen Univ, Affiliated Hosp 1, Dept Radiol, Guangzhou 510080, Guangdong, Peoples R China.
   [Zhang, Jing-Yang] South China Univ Technol, Sch Biomed Sci & Engn, Guangzhou Int Campus, Guangzhou 511442, Guangdong, Peoples R China.
   [Zhang, Jing-Yang; Du, Jin-Zhi] South China Univ Technol, Natl Engn Res Ctr Tissue Restorat & Reconstruct, Guangzhou 510006, Guangdong, Peoples R China.
   [He, Weiling] Xiamen Univ, Xiangan Hosp, Sch Med, Dept Gastrointestinal Surg, Xiamen 361000, Fujian, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; South China University
   of Technology; Sun Yat Sen University; Sun Yat Sen University; South
   China University of Technology; South China University of Technology;
   Xiamen University
RP He, WL (corresponding author), Sun Yat sen Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Guangzhou 510080, Guangdong, Peoples R China.; Du, JZ (corresponding author), South China Univ Technol, Sch Med, Guangzhou 510006, Guangdong, Peoples R China.; Lin, R (corresponding author), Sun Yat sen Univ, Affiliated Hosp 1, Dept Radiol, Guangzhou 510080, Guangdong, Peoples R China.; Du, JZ (corresponding author), South China Univ Technol, Natl Engn Res Ctr Tissue Restorat & Reconstruct, Guangzhou 510006, Guangdong, Peoples R China.; He, WL (corresponding author), Xiamen Univ, Xiangan Hosp, Sch Med, Dept Gastrointestinal Surg, Xiamen 361000, Fujian, Peoples R China.
EM linrun5@mail.sysu.edu.cn; djzhi@scut.edu.cn; wlhe@xah.xmu.edu.cn
RI Zhang, Jingyang/AAU-7348-2021
FU National Natural Science Foundation of China; National Key Research and
   Development Plan [2022YFC3401000, 2022YFC3401400]; Guangdong Basic and
   Applied Basic Research Foundation [2021B1515230009, 2022B1515120028];
   Guangdong Provincial Key Areas R&D Programs of Precision Medicine and
   Stem Cells [2023B1111020005]; Guangzhou Science and Technology Planning
   Project [2024A04J3631];  [92359302];  [52173122]
FX The authors acknowledge the tissue bank of The First Affiliated Hospital
   of Sun Yat-sen University for providing patient samples. The authors
   also thank Figdraw () for the assistance in creating the Scheme. This
   work was supported by the National Key Research and Development Plan
   (2022YFC3401000, 2022YFC3401400), National Natural Science Foundation of
   China (92359302, 52173122), Guangdong Basic and Applied Basic Research
   Foundation (2021B1515230009, 2022B1515120028), Guangdong Provincial Key
   Areas R&D Programs of Precision Medicine and Stem Cells
   (2023B1111020005) and Guangzhou Science and Technology Planning Project
   (2024A04J3631).
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NR 45
TC 0
Z9 0
U1 12
U2 12
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2198-3844
J9 ADV SCI
JI Adv. Sci.
PD 2024 NOV 19
PY 2024
DI 10.1002/advs.202407239
EA NOV 2024
PG 16
WC Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials
   Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA M5I8P
UT WOS:001357881400001
PM 39560161
OA gold
DA 2025-01-04
ER

PT J
AU Hopirtean, C
   Ciuleanu, T
   Cainap, C
   Todor, N
   Nagy, V
AF Hopirtean, C.
   Ciuleanu, T.
   Cainap, C.
   Todor, N.
   Nagy, V.
TI BODY MASS INDEX AS A PROGNOSTIC FACTOR FOR DISEASE PROGRESSION IN
   PATIENTS WITH METASTATIC COLORECTAL CANCER TREATED WITH BEVACIZUMAB
   BASED SYSTEMIC THERAPY
SO ACTA ENDOCRINOLOGICA-BUCHAREST
LA English
DT Article
DE metastatic colorectal cancer; body mass index; bevacizumab; progression
   free survival; overall survival
ID 1ST-LINE TREATMENT; PLUS IRINOTECAN; CLINICAL-TRIALS; OBESITY;
   FLUOROURACIL; LEUCOVORIN; CHEMOTHERAPY; OVERWEIGHT; MORTALITY; CETUXIMAB
AB Context. Epidemiological data have shown that obesity increases the risk of developing colorectal cancer and also an increased body mass index (BMI) is associated with a worse prognosis. Bevacizumab based systemic therapy, an antiVEGF targeted therapy, is an important treatment option for metastatic colorectal cancer (mCRC) patients. Obesity is associated with high level of vascular endothelial growth factor (VEGF), that might provoke resistance to antiVEGF monoclonal antibody.
   Objective. To evaluate the efficacy in terms of progression free survival (PFS) and overall survival (OS) of bevacizumab systemic therapy in patients with mCRC.
   Design. Retrospective cohort, single center study.
   Subjects and Methods. Between January 2007 and December 2012, 112 patients with mCRC, who followed bevacizumab based systemic therapy in the "Ion Chiricuta" Oncology Institute in Cluj-Napoca, were included in our analysis.
   Results. Values of BMI >= or < 27 kg/sqm was found that PFS is statistically significant superior in patients with BMI < 27 kg/sqm (n=77) than in those with BMI >= 27 kg/sqm (n=35), 24 months versus 17.9 months (p = 0.04). Five years OS was not influenced by the BMI, 35% vs 30% (p=0.29). In patients with liver metastases with values of BMI 2 >= 7 kg/ sqm have PFS lower than patients with a BMI < 27 kg/sqm, 17.5 months versus 24.5 months (p = 0.02). Five years OS was not influenced by the BMI, 39% (BMI < 27 kg/sqm) vs. 22% (BMI >= 27 kg/sqm) (p = 0.09).
   Conclusions. This study demonstrated the negative influence of BMI on both PFS on the entire sample of patients and in patients with liver metastases only, BMI cutoff value proved to be 27 kg/square meter and shows that the BMI may be an important prognostic factor with a high clinical relevance in patients with mCRC.
C1 [Hopirtean, C.; Ciuleanu, T.; Cainap, C.; Todor, N.; Nagy, V.] Ion Chiricuta Oncol Inst, Cluj Napoca, Romania.
   [Ciuleanu, T.; Cainap, C.; Nagy, V.] Iuliu Hatieganu Univ Med & Pharm, Cluj Napoca, Romania.
C3 Oncology Institute Prof. Dr. Ion Chiricuta; Iuliu Hatieganu University
   of Medicine & Pharmacy
RP Hopirtean, C (corresponding author), Prof Dr Ion Chiricuta Oncol Inst, Republicii 34-36, Cluj Napoca 400015, Romania.
EM hopirtean.claudiu@gmail.com
RI Ciuleanu, Tudor-Eliade/ABH-8452-2020; Cainap, Calin/AAU-5665-2020
OI Ciuleanu, Tudor Eliade/0000-0003-0958-5597
CR [Anonymous], 2011, GLOBAL STATUS REPORT
   [Anonymous], 2007, Maedica
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   World Health Organization, OB SIT TRENDS
NR 27
TC 6
Z9 6
U1 0
U2 5
PU EDITURA ACAD ROMANE
PI BUCURESTI
PA CALEA 13 SEPTEMBRIE NR 13, SECTOR 5, BUCURESTI 050711, ROMANIA
SN 1841-0987
EI 1843-066X
J9 ACTA ENDOCRINOL-BUCH
JI Acta Endocrinol.
PD OCT-DEC
PY 2017
VL 13
IS 4
BP 425
EP 430
DI 10.4183/aeb.2017.425
PG 6
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA FT4QQ
UT WOS:000423140200005
PM 31149211
OA Green Published
DA 2025-01-04
ER

PT J
AU Smit, DJ
   Cayrefourcq, L
   Haider, MT
   Hinz, N
   Pantel, K
   Alix-Panabières, C
   Jücker, M
AF Smit, Daniel J.
   Cayrefourcq, Laure
   Haider, Marie-Therese
   Hinz, Nico
   Pantel, Klaus
   Alix-Panabieres, Catherine
   Juecker, Manfred
TI High Sensitivity of Circulating Tumor Cells Derived from a Colorectal
   Cancer Patient for Dual Inhibition with AKT and mTOR Inhibitors
SO CELLS
LA English
DT Article
DE circulating tumor cells; CTCs; drug sensitivity assays; PI3K; AKT; mTOR
   pathway; AKT; MK2206; RAD001; dual targeting; colorectal carcinoma;
   targeted therapy; personalized medicine
ID COLON-CANCER; IN-VITRO; EX-VIVO; SURVIVAL; PATHWAY; PROGRESSION;
   RESISTANCE; EXPRESSION; PATTERNS; AKT/PKB
AB Circulating tumor cells (CTCs) are cells shed from the primary tumor into the bloodstream. While many studies on solid tumor cells exist, data on CTCs are scarce. The mortality of cancer is mostly associated with metastasis and recent research identified CTCs as initiators of metastasis. The PI3K/AKT/mTOR signaling pathway is an intracellular pathway that regulates essential functions including protein biosynthesis, cell growth, cell cycle control, survival and migration. Importantly, activating oncogenic mutations and amplifications in this pathway are frequently observed in a wide variety of cancer entities, underlining the significance of this signaling pathway. In this study, we analyzed the functional role of the PI3K/AKT/mTOR signaling pathway in the CTC-MCC-41 line, derived from a patient with metastatic colorectal cancer. One striking finding in our study was the strong sensitivity of this CTC line against AKT inhibition using MK2206 and mTOR inhibition using RAD001 within the nanomolar range. This suggests that therapies targeting AKT and mTOR could have been beneficial for the patient from which the CTC line was isolated. Additionally, a dual targeting approach of AKT/mTOR inside the PI3K/AKT/mTOR signaling pathway in the colorectal CTCs showed synergistic effects in vitro. Depending on the phenotypical behavior of CTC-MCC-41 in cell culture (adherent vs. suspension), we identified altered phosphorylation levels inside the PI3K/AKT/mTOR pathway. We observed a downregulation of the PI3K/AKT/mTOR signaling pathway, but not of the RAS/RAF/MAPK pathway, in CTCs growing in suspension in comparison to adherent CTCs. Our results highlight distinct functions of AKT isoforms in CTC-MCC-41 cells with respect to cell proliferation. Knockdown of AKT1 and AKT2 leads to significantly impaired proliferation of CTC-MCC-41 cells in vitro. Therefore, our data demonstrate that the PI3K/AKT/mTOR signaling pathway plays a key role in the proliferation of CTC-MCC-41.
C1 [Smit, Daniel J.; Hinz, Nico; Juecker, Manfred] Univ Med Ctr Hamburg Eppendorf, Inst Biochem & Signal Transduct, Martinistr 52, D-20246 Hamburg, Germany.
   [Cayrefourcq, Laure; Alix-Panabieres, Catherine] Univ Med Ctr Montpellier, Lab Rare Human Circulating Cells LCCRH, F-34093 Montpellier, France.
   [Haider, Marie-Therese] Univ Med Ctr Hamburg Eppendorf, Dept Trauma Hand & Reconstruct Surg, Mol Skeletal Biol Lab, D-20246 Hamburg, Germany.
   [Pantel, Klaus] Univ Med Ctr Hamburg Eppendorf, Dept Tumor Biol, Martinistr 52, D-20246 Hamburg, Germany.
C3 University of Hamburg; University Medical Center Hamburg-Eppendorf;
   Universite de Montpellier; CHU de Montpellier; University of Hamburg;
   University Medical Center Hamburg-Eppendorf; University of Hamburg;
   University Medical Center Hamburg-Eppendorf
RP Jücker, M (corresponding author), Univ Med Ctr Hamburg Eppendorf, Inst Biochem & Signal Transduct, Martinistr 52, D-20246 Hamburg, Germany.
EM d.smit@uke.de; l-cayrefourcq@chu-montpellier.fr; m.haider@uke.de;
   hinz_nico@gmx.de; pantel@uke.de; c-panabieres@chu-montpellier.fr;
   juecker@uke.de
RI ALIX-PANABIERES, Catherine/AAC-1773-2019; Smit, Dr. Daniel
   J./AFH-3933-2022
OI Cayrefourcq, Laure/0000-0002-6124-7029; Alix-Panabieres, Prof
   Catherine/0000-0002-6401-2903; Hinz, Nico/0000-0002-6069-9787; Smit,
   Daniel J./0000-0002-3190-9511; Jucker, Manfred/0000-0003-2176-6526;
   Pantel, Klaus/0000-0001-5736-2772
FU National Cancer Institute (INCa); SIRIC Montpellier Cancer Grant
   [INCa_Inserm_DGOS_12553]
FX C.A.-P. and L.C.: The establishment of the CTC-MCC-41 line was supported
   by the National Cancer Institute (INCa). The LCCRH is supported by the
   SIRIC Montpellier Cancer Grant INCa_Inserm_DGOS_12553.
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NR 74
TC 28
Z9 28
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 SEP
PY 2020
VL 9
IS 9
AR 2129
DI 10.3390/cells9092129
PG 16
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA OE0RW
UT WOS:000580250000001
PM 32962206
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Shen, XG
   Zuo, XF
   Liang, L
   Wang, L
   Luo, B
AF Shen, Xiaogang
   Zuo, Xiaofei
   Liang, Liang
   Wang, Lin
   Luo, Bin
TI Integrating machine learning and single-cell trajectories to analyze
   T-cell exhaustion to predict prognosis and immunotherapy in colon cancer
   patients
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE colon adenocarcinoma (COAD); t-cell exhaustion; tumor microenvironment;
   prognosis; immunotherapy
ID TP53 MUTATIONAL STATUS; RESISTANCE; MECHANISMS; BLOCKADE; SURVIVAL;
   THERAPY
AB IntroductionThe incidence of colon adenocarcinoma (COAD) has recently increased, and patients with advanced COAD have a poor prognosis due to treatment resistance. Combining conventional treatment with targeted therapy and immunotherapy has shown unexpectedly positive results in improving the prognosis of patients with COAD. More study is needed to determine the prognosis for patients with COAD and establish the appropriate course of treatment. MethodsThis study aimed to explore the trajectory of T-cell exhaustion in COAD to predict the overall survival and treatment outcome of COAD patients. Clinical data were derived from the TCGA-COAD cohort through "UCSC", as well as the whole genome data. Prognostic genes driving T-cell trajectory differentiation were identified on the basis of single-cell trajectories and univariate Cox regression. Subsequently, T-cell exhaustion score (TES) was created by iterative LASSO regression. The potential biological logic associated with TES was explored through functional analysis, immune microenvironment assessment, immunotherapy response prediction, and in vitro experiments. ResultsData showed that patients with significant TES had fewer favorable outcomes. Expression, proliferation, and invasion of COAD cells treated with TXK siRNA were also examined by cellular experiments. Both univariate and multivariate Cox regression indicated that TES was an independent prognostic factor in patients with COAD; in addition, subgroup analysis supported this finding. Functional assay revealed that immune response and cytotoxicity pathways are associated with TES, as the subgroup with low TES has an active immune microenvironment. Furthermore, patients with low TES responded better to chemotherapy and immunotherapy. ConclusionIn this study, we systematically explored the T-cell exhaustion trajectory in COAD and developed a TES model to assess prognosis and provide guidelines for the treatment decision. This discovery gave rise to a fresh concept for novel therapeutic procedures for the clinical treatment of COAD.
C1 [Shen, Xiaogang; Zuo, Xiaofei; Wang, Lin; Luo, Bin] Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Dept Gastrointestinal Surg, Chengdu, Peoples R China.
   [Shen, Xiaogang; Zuo, Xiaofei; Liang, Liang; Wang, Lin; Luo, Bin] Chinese Acad Sci, Sichuan Translat Med Res Hosp, Chengdu, Peoples R China.
   [Liang, Liang] Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Canc Ctr, Chengdu, Peoples R China.
C3 Sichuan Provincial People's Hospital; University of Electronic Science &
   Technology of China; Chinese Academy of Sciences; Sichuan Provincial
   People's Hospital; University of Electronic Science & Technology of
   China
RP Wang, L; Luo, B (corresponding author), Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Dept Gastrointestinal Surg, Chengdu, Peoples R China.; Wang, L; Luo, B (corresponding author), Chinese Acad Sci, Sichuan Translat Med Res Hosp, Chengdu, Peoples R China.
EM wanglinron@126.com; vibrio@163.com
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NR 46
TC 2
Z9 2
U1 1
U2 2
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 MAY 3
PY 2023
VL 14
AR 1162843
DI 10.3389/fimmu.2023.1162843
PG 15
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA G2PI6
UT WOS:000987635500001
PM 37207222
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Xu, MX
   Li, Q
   Zhang, JF
   Xie, H
AF Xu, Minxian
   Li, Qing
   Zhang, Jianfang
   Xie, Hui
TI Identification of Immune-Related lncRNA Pairs and Construction and
   Validation of a New Prognostic Signature of Colon Cancer
SO CANADIAN JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
ID ANTITUMOR; ACTIVATION; EXPRESSION; CELLS; AXIS
AB Background. More and more evidence has shown that immune-related long noncoding ribonucleic acid (irlncRNAs) is a potential prognostic factor for colon cancer. The relevant gene pair pattern can improve the sensitivity of the prognostic model. Therefore, our present study aimed to identify irlncRNA Pairs and construct and validate a new prognostic signature in colon cancer. Methods. We downloaded the expression matrix of mRNA and lncRNA of patients with colon cancer and their clinical information from the public TCGA database. We obtained immune genes from the ImmPort database. Coexpression analysis was performed to identify irlncRNAs. We built an irlncRNA pair matrix by comparing the expression levels of each lncRNA pair in a cycle. Univariate Cox regression analysis, LASSO penalized regression analysis, and multivariate Cox regression analysis were performed to determine the final variables to construct the prognostic risk score model (a new signature). We draw the receiver operating characteristic (ROC) curves of the signature and clinical characteristics and determine the optimal cutoff value by the optimal Akaike Information Criterion (AIC) value. Based on the optimal cutoff value of the ROC curve of the signature, colon cancer patients were divided into the high- and low-risk groups. Then, the signature was evaluated by clinicopathological features, tumor-infiltrating immune cells, checkpoint-related biomarkers, targeted therapy, and chemotherapy. Results. We identified 8 lncRNA pairs including AC103740.1|LEF1-AS1, LINC02391|AC053503.5, WWC2-AS2|AL355916.2, AC104090.1|NEURL1-AS1, AC099524.1|AL161908.1, AC074011.1|AL078601.2, AL355916.2|LINC01723, and AP003392.4|LINC00598 from 71 differently expressed irlncRNAs. We constructed a prognostic risk score model (a new signature) using these optimal eight irlncRNA pairs. ROC curve analysis revealed that the highest AUC value of the signature was 0.776 at 1 year, with the optimal cutoff value of 1.283. Our present study also showed that the constructed signature could accurately identify adverse survival outcomes, prognostic clinicopathological features, and specify tumor invasion status. The expression of immune checkpoint-related genes and chemical drug sensitivity were related to different risk groups. Conclusion. In our present study, we constructed a new irlncRNA signature of colon cancer based on the irlncRNA pairs instead of the special expression level of lncRNA. We found this signature had not only good prognostic value but also certain clinical value, which might provide a new insight into the treatment and prognosis of colon cancer.
C1 [Xu, Minxian] Xiangnan Univ, Affiliated Hosp, Clin Coll, Dept Oncol, Chenzhou 423000, Hunan, Peoples R China.
   [Li, Qing] Xiangnan Univ, Sch Med Imaging Lab Sci & Rehabil, Chenzhou 423000, Hunan, Peoples R China.
   [Li, Qing; Xie, Hui] Key Lab Med Imaging & Artificial Intelligence Hun, Chenzhou 423000, Hunan, Peoples R China.
   [Zhang, Jianfang] Beihu Ctr Dis Control & Prevent, Dept Phys Examinat, Chenzhou 423000, Hunan, Peoples R China.
   [Xie, Hui] Xiangnan Univ, Clin Coll, Affiliated Hosp, Dept Radiat Oncol, Chenzhou 423000, Hunan, Peoples R China.
C3 Xiangnan University; Xiangnan University; Xiangnan University
RP Xie, H (corresponding author), Key Lab Med Imaging & Artificial Intelligence Hun, Chenzhou 423000, Hunan, Peoples R China.; Xie, H (corresponding author), Xiangnan Univ, Clin Coll, Affiliated Hosp, Dept Radiat Oncol, Chenzhou 423000, Hunan, Peoples R China.
EM xu_mx66846@21cn.com; liq894643@163.com; zhangjf854525@163.com;
   h.xie@xnu.edu.cn
RI Xu, Minxian/LOS-9369-2024; Xie, Hui/ACL-9395-2022
OI xie, hui/0000-0002-8490-1695
FU Key Laboratory of Tumor Precision Medicine, Hunan colleges and
   Universities Project [2019-379]; Scientific Research Fund of Hunan
   Provincial [19JJ80073]
FX AcknowledgmentsAcknowledgements are due to the TCGA databases for
   providing researchable patient data. This study was supported by the Key
   Laboratory of Tumor Precision Medicine, Hunan colleges and Universities
   Project (No. 2019-379), and a project supported by the Scientific
   Research Fund of Hunan Provincial (No. 19JJ80073).
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NR 42
TC 5
Z9 5
U1 0
U2 5
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2291-2789
EI 2291-2797
J9 CAN J GASTROENTEROL
JI Can. J. Gastroenterol. Hepatol.
PD MAR 30
PY 2022
VL 2022
AR 5827544
DI 10.1155/2022/5827544
PG 16
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 2C7QZ
UT WOS:000811059400001
PM 35399646
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Hassan, S
   Mirza, T
   Khatoon, A
   Bukhari, U
   Shaikh, F
AF Hassan, Sobia
   Mirza, Talat
   Khatoon, Ambrina
   Bukhari, Uzma
   Shaikh, Fouzia
TI In Silico Analysis of Differentially Expressed Genes in Colorectal
   Carcinoma
SO ADVANCEMENTS IN LIFE SCIENCES
LA English
DT Article
DE STAT3 drug resistance; targeted therapy; bioinformatics
AB Background: Colorectal carcinoma (CRC) is a primary cause of morbidity and mortality worldwide. Resistance to therapy contributes to poor patient prognosis. The aim of our study is to identify the key proteins and interaction networks implicated in CRC which may serve as possible therapeutic targets and help in overcoming therapy resistance. Methods: The microarray dataset of 58 cases and 62 controls was used to identify Differentially Expressed Genes (DEGs).After constructing protein-protein interaction networks , Cytoscape analysis was done to identify the hub proteins. Based on sub graph centrality, between-ness and degree (=10), hub proteins were selected for further literature search and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. Results: A total of 85 up-regulated genes and 95 down-regulated genes of CRC patients were selected based on criteria of P>0.05 and fold change>2.0. The PPI analysis revealed STAT3, HNRNPA2B1, RBM8A, RBM25, ATM, HIST1H2BK, SRSF5 and HNRNPDLas hub proteins. On the basis of criteria set for cytoscape analysis, STAT3 and HNRNPA2B1 were identified as key hub proteins. KEGG pathway analysis revealed vital role of STAT3in carcinogenesis. Conclusion: In addition of HNRNPA2B1 activation by STAT3, cross talk of STAT3 with other oncogenic signaling pathways signifies its role in colorectal carcinogenesis. Our study highlights thatSTAT3may be a possible therapeutic target which may help in overcoming the dilemma of resistance to drug treatment in advanced cases.
C1 [Hassan, Sobia; Shaikh, Fouzia] Ziauddin Med Univ, Dept Pathol, Karachi, Pakistan.
   [Mirza, Talat; Khatoon, Ambrina] Ziauddin Med Univ, Res Dept, Karachi, Pakistan.
   [Bukhari, Uzma] Dow Univ Hlth Sci, Dept Pathol, Karachi, Pakistan.
C3 Ziauddin University; Ziauddin University; Dow University of Health
   Sciences
RP Hassan, S (corresponding author), Ziauddin Med Univ, Dept Pathol, Karachi, Pakistan.
EM sobia10722@zu.edu.pk
RI Mirza, Talat/KCJ-5401-2024; Khatoon, Ambrina/LWK-4369-2024
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NR 29
TC 0
Z9 0
U1 0
U2 3
PU The Running Line
PI Lahore
PA 79-A Block, Punjab University Town 1, Abdul Sattar Edhi road, Niaz Baig,
   Lahore, PAKISTAN
SN 2310-5380
J9 ADV LIFE SCI-PAK
JI Advan. Life Sci.
PD MAR
PY 2023
VL 10
IS 1
BP 37
EP 41
PG 5
WC Biology
WE Emerging Sources Citation Index (ESCI)
SC Life Sciences & Biomedicine - Other Topics
GA E4EG9
UT WOS:000975085100007
DA 2025-01-04
ER

PT J
AU Mandi, CS
   Mahata, T
   Patra, D
   Chakraborty, J
   Bora, A
   Pal, R
   Dutta, S
AF Mandi, Chandra Sova
   Mahata, Tridib
   Patra, Dipendu
   Chakraborty, Jeet
   Bora, Achyut
   Pal, Ritesh
   Dutta, Sanjay
TI Cleavage of Abasic Sites in DNA by an Aminoquinoxaline Compound:
   Augmented Cytotoxicity and DNA Damage in Combination with an Anticancer
   Drug Chlorambucil in Human Colorectal Carcinoma Cells
SO ACS OMEGA
LA English
DT Article
ID BASE EXCISION-REPAIR; CHRONIC LYMPHOCYTIC-LEUKEMIA; APURINIC SITES;
   APYRIMIDINIC SITES; RESISTANCE; ASSAY; DEPURINATION; GLUTATHIONE;
   SELECTIVITY; MUTAGENESIS
AB The elevated level of endogenous oxidative DNA damage and spontaneous deamination of DNA bases in cancer cells substantially increase the abasic sites in DNA via base excision repairs (BERs). Thus, the predominant BER pathway is a favorable target for cancer therapy. Interestingly, elevated levels of glutathione (GSH) in certain cancer cells, such as colon cancer, are associated with acquired resistance to several chemotherapeutic agents, which increase the difficulty for the treatment of cancer. Here, we have reported an ideal nitro group-containing monoquinoxaline DNA intercalator (1d), which is reduced into a fluorescent quinoxaline amine (1e) in the presence of GSH; concurrently, 1e (similar to 100 nM concentration) selectively causes the in vitro cleavage of abasic sites in DNA. le also binds to the tetrahydrofuran analogue of the abasic site in the nanomolar to low micromolar range depending on the nucleotide sequence opposite to the abasic site and also induces a structural change in abasic DNA. Furthermore, the amine compound (1e) augments the response of the specific bifunctional alkylating drug chlorambucil at a much lower concentration in the human colorectal carcinoma cell (HCT-116), and their combination shows a potential strategy for targeted therapy. Alone or in combination, Id and le lead to a cascade of cellular events such as induction of DNA double-stranded breaks and cell arrest at G(0)/G(1) and G(2)/M phases, eventually leading to apoptotic cell death in HCT-116 cells. Hence, the outcome of this study provides a definitive approach that will help optimize the therapeutic applications for targeting the abasic site in cancer cells.
C1 [Mandi, Chandra Sova; Mahata, Tridib; Patra, Dipendu; Chakraborty, Jeet; Bora, Achyut; Pal, Ritesh; Dutta, Sanjay] CSIR Indian Inst Chem Biol, Organ & Med Chem Div, Kolkata 700032, W Bengal, India.
   [Patra, Dipendu; Bora, Achyut; Pal, Ritesh; Dutta, Sanjay] Acad Sci & Innovat Res AcSIR, Ghaziabad 201002, India.
C3 Council of Scientific & Industrial Research (CSIR) - India; CSIR -
   Indian Institute of Chemical Biology (IICB); Academy of Scientific &
   Innovative Research (AcSIR)
RP Dutta, S (corresponding author), CSIR Indian Inst Chem Biol, Organ & Med Chem Div, Kolkata 700032, W Bengal, India.; Dutta, S (corresponding author), Acad Sci & Innovat Res AcSIR, Ghaziabad 201002, India.
EM sanjaydutta@iicb.res.in
RI Mahata, Tridib/ABC-3455-2021
OI MAHATA, TRIDIB/0000-0002-7145-3715; Bora, Achyut/0000-0003-3964-595X
FU CSIR; DST SERB [EMR/2017/000659]; UGC
FX S.D. acknowledges CSIR (MLP-139) and DST SERB (Grant No.
   EMR/2017/000659) for financial support. C.S.M., J.C., and A.B.
   acknowledge CSIR for fellowship, and R. P. acknowledges UGC for
   fellowship.
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NR 59
TC 3
Z9 5
U1 0
U2 9
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 2470-1343
J9 ACS OMEGA
JI ACS Omega
PD MAR 1
PY 2022
VL 7
IS 8
BP 6488
EP 6501
DI 10.1021/acsomega.1c04962
EA FEB 2022
PG 14
WC Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA 2U4CB
UT WOS:000823588400001
PM 35252645
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Allgayer, H
   Leupold, JH
   Patil, N
AF Allgayer, Heike
   Leupold, Joerg H.
   Patil, Nitin
TI Defining the "Metastasome": Perspectives from the genome and molecular
   landscape in colorectal cancer for metastasis evolution and clinical
   consequences
SO SEMINARS IN CANCER BIOLOGY
LA English
DT Review
DE Metastasis; Whole genome; Colorectal cancer; Sequencing; Metastasome
ID PLASMINOGEN-ACTIVATOR RECEPTOR; MINIMAL RESIDUAL DISEASE; DISSEMINATED
   TUMOR-CELLS; SRC FAMILY KINASES; UROKINASE-RECEPTOR; LOCALIZATION
   MICROSCOPY; BONE-MARROW; U-PAR; SUPERRESOLUTION MICROSCOPY;
   GENE-EXPRESSION
AB Metastasis still poses the highest challenge for personalized therapy in cancer, partly due to a still incomplete understanding of its molecular evolution. We recently presented the most comprehensive whole-genome study of colorectal metastasis vs. matched primary tumors and suggested novel components of disease progression and metastasis evolution, some of them potentially relevant for targeted therapy. In this review, we try to put these findings into perspective with latest discoveries of colleagues and recent literature, and propose a systematic international team effort to collectively define the "metastasome", a term we introduce to summarize all genomic, epigenomic, transcriptomic, further -omic, molecular and functional characteristics rendering metastases different from primary tumors. Based on recent discoveries, we propose a revised metastasis model for colorectal cancer which is based on a common ancestor clone, early dissemination but flexible early or late stage clonal separation paralleling stromal interactions. Furthermore, we discuss hypotheses on site-specific metastasis, colorectal cancer progression, metastasis-targeted diagnosis and therapy, and metastasis prevention based on latest metastasome data.
C1 [Allgayer, Heike; Leupold, Joerg H.; Patil, Nitin] Heidelberg Univ, Med Fac Mannheim, Dept Expt Surg Canc Metastasis, Theodor Kutzer Ufer 1, D-68135 Heidelberg, Germany.
   [Allgayer, Heike; Leupold, Joerg H.; Patil, Nitin] Heidelberg Univ, Med Fac Mannheim, Ctr Biomed & Med Technol Mannheim CBTM, Ludolf Krehl Str 6, D-68135 Heidelberg, Germany.
C3 Ruprecht Karls University Heidelberg; Ruprecht Karls University
   Heidelberg
RP Allgayer, H (corresponding author), Heidelberg Univ, Med Fac Mannheim, Dept Expt Surg, Canc Metastasis, Ludolf Krehl Str 13-17, D-68167 Mannheim, Germany.; Allgayer, H (corresponding author), Heidelberg Univ, Ctr Biomed & Med Technol Mannheim CBTM, Med Fac Mannheim, Ludolf Krehl Str 13-17, D-68167 Mannheim, Germany.
EM heike.allgayer@medma.uni-heidelberg.de
RI Patil, Nitin/B-5113-2014
FU Alfried Krupp von Bohlen und Halbach Foundation, Essen; Deutsche
   Krebshilfe, Bonn [70112168]; Deutsche Forschungsgemeinschaft (DFG) [AL
   465/9-1]; HEiKA Initiative (Karlsruhe Institute of Technology/University
   of Heidelberg collaborative effort); HIPO/POP-Initiative for
   Personalized Oncology, Heidelberg [H032, H027]; Molecular Biomarkers for
   Individualized Therapy (MoBIT) project initiative
FX The work of our group was supported by the Alfried Krupp von Bohlen und
   Halbach Foundation, Essen, the Deutsche Krebshilfe, Bonn (70112168), the
   Deutsche Forschungsgemeinschaft (DFG, grant numberAL 465/9-1), the HEiKA
   Initiative (Karlsruhe Institute of Technology/University of Heidelberg
   collaborative effort), the HIPO/POP-Initiative for Personalized
   Oncology, Heidelberg (H032 and H027) and by the Molecular Biomarkers for
   Individualized Therapy (MoBIT) project initiative.
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NR 149
TC 17
Z9 18
U1 0
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1044-579X
EI 1096-3650
J9 SEMIN CANCER BIOL
JI Semin. Cancer Biol.
PD FEB
PY 2020
VL 60
BP 1
EP 13
DI 10.1016/j.semcancer.2019.07.018
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KU9BK
UT WOS:000520016500002
PM 31362074
OA hybrid
DA 2025-01-04
ER

PT J
AU Potocki, PM
   Wójcik, P
   Chmura, L
   Goc, B
   Fedewicz, M
   Bielanska, Z
   Swadzba, J
   Konopka, K
   Kwinta, L
   Wysocki, PJ
AF Potocki, Pawel M.
   Wojcik, Piotr
   Chmura, Lukasz
   Goc, Bartlomiej
   Fedewicz, Marcin
   Bielanska, Zofia
   Swadzba, Jakub
   Konopka, Kamil
   Kwinta, Lukasz
   Wysocki, Piotr J.
TI Clinical Characterization of Targetable Mutations (BRAF V600E and KRAS
   G12C) in Advanced Colorectal Cancer-A Nation-Wide Study
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE metastatic colorectal cancer; KRAS mutation; BRAF mutation; V600E; G12C;
   tumour sidedness; brain metastases; MANEC; sotorasib; encorafenib
ID STAGE-II
AB BRAF V600E and KRAS mutations that occur in colorectal cancer (CRC) define a subpopulation of patients with an inferior prognosis. Recently, the first BRAF V600E-targeting therapy has been approved and novel agents targeting KRAS G12C are being evaluated in CRC. A better understanding of the clinical characteristics of the populations defined by those mutations is needed. We created a retrospective database that collects clinical characteristics of patients with metastatic CRC evaluated for RAS and BRAF mutations in a single laboratory. A total of 7604 patients tested between October 2017 and December 2019 were included in the analysis. The prevalence of BRAF V600E was 6.77%. Female sex, primary in the right colon, high-grade, mucinous, signet cell, partially neuroendocrine histology, perineural and vascular invasion, and surgical tissue sample were factors associated with increased mutation rates. The prevalence of KRAS G12C was 3.11%. Cancer of primary origin in the left colon and in samples from brain metastases were associated with increased mutation rates. The high prevalence of the BRAF V600E mutation in cancers with a neuroendocrine component identifies a potential candidate population for BRAF inhibition. The association of KRAS G12C with the left part of the intestine and brain metastases of CRC are new findings and require further investigation.
C1 [Potocki, Pawel M.; Konopka, Kamil; Kwinta, Lukasz; Wysocki, Piotr J.] Jagiellonian Univ, Fac Med, Oncol Dept, Med Coll, PL-31008 Krakow, Poland.
   [Wojcik, Piotr; Chmura, Lukasz] Oncogene Diagnost Sp Zoo, PL-31546 Krakow, Poland.
   [Goc, Bartlomiej; Fedewicz, Marcin; Bielanska, Zofia] Jagiellonian Univ, Fac Med, Oncol Dept, Student Res Grp,Med Coll, PL-31008 Krakow, Poland.
   [Goc, Bartlomiej] MSC Natl Res Inst Oncol, Radiotherapy Dept, PL-44102 Gliwice, Poland.
   [Fedewicz, Marcin] Jozef Babinski Clin Hosp, PL-30393 Krakow, Poland.
   [Bielanska, Zofia] Regio Klinikum, Klin Psychiat Psychotherap & Psychosomat, D-25337 Elmshorn, Germany.
   [Swadzba, Jakub] Andrzej Frycz Modrzewski Krakow Univ, Fac Med & Hlth Sci, Dept Lab Med, PL-30705 Krakow, Poland.
C3 Jagiellonian University; Collegium Medicum Jagiellonian University;
   Jagiellonian University; Collegium Medicum Jagiellonian University;
   Andrzej Frycz Modrzewski Krakow University
RP Potocki, PM (corresponding author), Jagiellonian Univ, Fac Med, Oncol Dept, Med Coll, PL-31008 Krakow, Poland.
EM pawel.potocki@uj.edu.pl
RI Swadźba, Jakub/CAH-1228-2022; Wysocki, Piotr/HKF-6762-2023; Konopka,
   Kamil/AAD-7068-2021; Chmura, Łukasz/AAL-5247-2021; Potocki,
   Pawel/AAK-7272-2021
OI Swadzba, Jakub/0000-0001-8757-360X; Wysocki, Piotr/0000-0003-4003-5278;
   Potocki, Pawel/0000-0003-3627-5201; Konopka, Kamil/0000-0003-2848-9832;
   Wojcik, Piotr/0000-0001-6128-4041
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NR 42
TC 6
Z9 6
U1 0
U2 1
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 MAY 22
PY 2023
VL 24
IS 10
AR 9073
DI 10.3390/ijms24109073
PG 17
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA H6MV0
UT WOS:000997090400001
PM 37240418
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Osumi, H
   Shinozaki, E
   Osako, M
   Kawazoe, Y
   Oba, M
   Misaka, T
   Goto, T
   Kamo, H
   Suenaga, M
   Kumekawa, Y
   Ogura, M
   Ozaka, M
   Matsusaka, S
   Chin, K
   Hatake, K
   Mizunuma, N
AF Osumi, Hiroki
   Shinozaki, Eiji
   Osako, Masahiko
   Kawazoe, Yoshimasa
   Oba, Masaru
   Misaka, Takaharu
   Goto, Takashi
   Kamo, Hitomi
   Suenaga, Mitsukuni
   Kumekawa, Yosuke
   Ogura, Mariko
   Ozaka, Masato
   Matsusaka, Satoshi
   Chin, Keisho
   Hatake, Kiyohiko
   Mizunuma, Nobuyuki
TI Cetuximab treatment for metastatic colorectal cancer with KRAS p.G13D
   mutations improves progression-free survival
SO MOLECULAR AND CLINICAL ONCOLOGY
LA English
DT Article
DE Kirsten rat sarcoma viral oncogene homolog p.G13D; cetuximab; vertical
   blockade of Ras pathway
AB A number of previous studies have reported that 30-50% of patients with colorectal cancer (CRC) harbor Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations, which is a major predictive biomarker of resistance to epidermal growth factor (EGFR)-targeted therapy. Treatment with an anti-EGFR inhibitor is recommended for patients with KRAS wild-type metastatic colorectal cancer (mCRC). A recent retrospective study of cetuximab reported that patients with KRAS p.G13D mutations had better outcomes compared with those with other mutations. The aim of this retrospective study was to assess the prevalence of KRAS p.G13D mutations and evaluate the effectiveness of cetuximab in mCRC patients with KRAS p.G13D or other KRAS mutations. We reviewed the clinical records of 98 mCRC patients with KRAS mutations who were treated between August, 2004 and January, 2011 in four hospitals located in Tokyo and Kyushu Island. We also investigated KRAS mutation subtypes and patient characteristics. In the patients who received cetuximab, univariate and multivariate analyses were performed to assess the effect of KRAS p.G13D mutations on progression-free survival (PFS) and overall survival (OS). Of the 98 patients, 23 (23.5%) had KRAS p.G13D-mutated tumors, whereas 75 (76.5%) had tumors harboring other mutations. Of the 31 patients who received cetuximab, 9 (29.0%) had KRAS p.G13D mutations and 22 (71.0%) had other mutations. There were no significant differences in age, gender, primary site, pathological type, history of chemotherapy, or the combined use of irinotecan between either of the patient subgroups. The univariate analysis revealed no significant difference in PFS or OS between the patients with KRAS p.G13D mutations and those with other mutations (median PFS, 4.5 vs. 2.8 months, respectively; P=0.65; and median OS, 15.3 vs. 8.9 months, respectively; P=0.51). However, the multivariate analysis revealed a trend toward better PFS among patients harboring p.G13D mutations (PFS: HR=0.29; 95% CI: 0.08-1.10; P=0.07; OS: HR=0.23; 95% CI: 0.04-1.54; P=0.13). In conclusion, treatment with cetuximab may be more clinically beneficial in mCRC patients with a KRAS p.G13D mutation, compared with those harboring other mutations. However, further investigation is required to clearly determine the benefits of cetuximab treatment in patients with KRAS p.G13D mutation-positive mCRC.
C1 [Osumi, Hiroki; Shinozaki, Eiji; Suenaga, Mitsukuni; Kumekawa, Yosuke; Ogura, Mariko; Ozaka, Masato; Matsusaka, Satoshi; Chin, Keisho; Mizunuma, Nobuyuki] Japanese Fdn Canc Res, Canc Inst Hosp, Dept Gastroenterol, Tokyo, Japan.
   [Osako, Masahiko] Kagoshima Med Assoc Hosp, Dept Surg, Kagoshima, Kagoshima, Japan.
   [Kawazoe, Yoshimasa] Univ Tokyo, Grad Sch Med, Dept Med Informat & Econ, Tokyo, Japan.
   [Oba, Masaru] Univ Tokyo, Grad Sch Med, Div Hepatobiliary & Pancreat Surg, Dept Surg, Tokyo, Japan.
   [Misaka, Takaharu] Kirishima Med Ctr, Dept Gastroenterol, Kirishima, Kagoshima, Japan.
   [Goto, Takashi; Kamo, Hitomi] Koga Gen Hosp, Dept Surg, Miyazaki, Japan.
   [Hatake, Kiyohiko] Japanese Fdn Canc Res, Canc Inst Hosp, New Drug Dev Ctr, Dept Med Oncol & Iematol, Tokyo, Japan.
C3 Japanese Foundation for Cancer Research; University of Tokyo; University
   of Tokyo; Japanese Foundation for Cancer Research
RP Shinozaki, E (corresponding author), Canc Inst Hosp, Japanese Fdn Canc Res, Dept Gastroenterol, Koto Ku, 3-8-31 Ariake, Tokyo 1358550, Japan.
EM eiji.shinozaki@jfcr.or.jp
RI Kawazoe, Yoshimasa/GYU-2868-2022; GOTO, TAKASHI/C-1704-2019
OI Kawazoe, Yoshimasa/0000-0002-7277-0827
CR Bando H, 2012, JPN J CLIN ONCOL, V42, P1146, DOI 10.1093/jjco/hys160
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NR 10
TC 15
Z9 16
U1 0
U2 2
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 SEP
PY 2015
VL 3
IS 5
BP 1053
EP 1057
DI 10.3892/mco.2015.602
PG 5
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA VH4GJ
UT WOS:000453157500014
PM 26623049
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Charlton, ME
   Kahl, AR
   Greenbaum, AA
   Karlitz, JJ
   Lin, C
   Lynch, CF
   Chen, VW
AF Charlton, Mary E.
   Kahl, Amanda R.
   Greenbaum, Alissa A.
   Karlitz, Jordan J.
   Lin, Chi
   Lynch, Charles F.
   Chen, Vivien W.
TI <i>KRAS</i> Testing, Tumor Location, and Survival in Patients With Stage
   IV Colorectal Cancer: SEER 2010-2013
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
ID SIDED COLON-CANCER; PROGNOSTIC-FACTOR; BRAF MUTATIONS; CETUXIMAB;
   DISTAL; EXPRESSION; RESISTANCE; BENEFIT; PTEN
AB Purpose: KRAS mutations and tumor location have been associated with response to targeted therapy among patients with stage IV colorectal cancer (CRC) in various trials. This study performed the first population-based examination of associations between KRAS mutations, tumor location, and survival, and assessed factors associated with documented KRAS testing. Methods: Patients with stage IV adenocarcinoma of the colon/rectum diagnosed from 2010 to 2013 were extracted from SEER data. Analyses of patient characteristics, KRAS testing, and tumor location were conducted using logistic regression. Cox proportional hazards models assessed relationships between KRAS mutations, tumor location, and risk of all-cause death. Results: Of 22,542 patients, 30% received KRAS testing, and 44% of these had mutations. Those tested tended to be younger, married, and metropolitan area residents, and have private insurance or Medicare. Rates of KRAS testing also varied by registry (range, 20%-46%). Patients with right-sided colon cancer (vs left-sided) tended to be older, female, and black; have mucinous, KRAS-mutant tumors; and have a greater risk of death (hazard ratio [HR], 1.27; 95% CI, 1.22-1.32). KRAS mutations were not associated with greater risk of death in the overall population; however, they were associated with greater risk of death among patients with left-sided colon cancer (HR, 1.19; 95% CI, 1.05-1.33). Conclusions: This large population-based study showed that among patients initially diagnosed with stage IV CRC, right-sided colon cancer was associated with greater risk of death compared with left-sided cancer, and KRAS mutations were only associated with risk of death in left-sided colon cancer. An unexpected finding was that among patients with stage IV disease, right-sided cancer was more commonly seen in black patients versus whites. Future studies should further explore these associations and determine the role of biology versus treatment differences. In addition, use of KRAS testing is increasing, but there is wide geographic variation wherein disparities related to insurance coverage and rurality may warrant further study.
C1 [Charlton, Mary E.; Kahl, Amanda R.; Lynch, Charles F.] Univ Iowa, Dept Epidemiol, Coll Publ Hlth, 145 North Riverside Dr,Room S453 CPHB, Iowa City, IA 52242 USA.
   [Greenbaum, Alissa A.] Univ New Mexico, Sch Med, Dept Surg, Albuquerque, NM 87131 USA.
   [Karlitz, Jordan J.] Tulane Univ, Sch Med, Div Gastroenterol, 1430 Tulane Ave, New Orleans, LA 70112 USA.
   [Lin, Chi] Univ Nebraska Med Ctr, Dept Radiat Oncol, Omaha, NE USA.
   [Chen, Vivien W.] Louisiana State Univ, Sch Publ Hlth, Louisiana Tumor Registry, Hlth Sci Ctr, New Orleans, LA USA.
   [Chen, Vivien W.] Louisiana State Univ, Sch Publ Hlth, Program Epidemiol, Hlth Sci Ctr, New Orleans, LA USA.
C3 University of Iowa; University of New Mexico; Tulane University;
   University of Nebraska System; University of Nebraska Medical Center;
   Louisiana State University System; Louisiana State University Health
   Sciences Center New Orleans; Louisiana State University System;
   Louisiana State University Health Sciences Center New Orleans
RP Charlton, ME (corresponding author), Univ Iowa, Dept Epidemiol, Coll Publ Hlth, 145 North Riverside Dr,Room S453 CPHB, Iowa City, IA 52242 USA.
EM mary-charlton@uiowa.edu
RI Lin, Chi/AAE-2495-2019
FU NIH/NCI [HHSN261201000030C, HHSN261201300020I]; Louisiana State
   University Health Sciences Center; University of Iowa
FX This work was supported in part under NIH/NCI contract number
   HHSN261201000030C with Louisiana State University Health Sciences Center
   (V.W.C.); NIH/NCI contract number HHSN261201300020I with University of
   Iowa (M.E.C., A.R.K., C.F.L.).
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NR 42
TC 44
Z9 46
U1 0
U2 4
PU HARBORSIDE PRESS
PI COLD SPRING HARBOR
PA 37 MAIN ST, COLD SPRING HARBOR, NY 11724 USA
SN 1540-1405
EI 1540-1413
J9 J NATL COMPR CANC NE
JI J. Natl. Compr. Cancer Netw.
PD DEC 1
PY 2017
VL 15
IS 12
BP 1484
EP 1493
DI 10.6004/jnccn.2017.7011
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FQ7IR
UT WOS:000418536600008
PM 29223986
OA Bronze, Green Accepted
DA 2025-01-04
ER

PT J
AU Hewitt, DB
   Brown, ZJ
   Pawlik, TM
AF Hewitt, Daniel Brock
   Brown, Zachary J.
   Pawlik, Timothy M.
TI The Role of Biomarkers in the Management of Colorectal Liver Metastases
SO CANCERS
LA English
DT Review
DE colorectal cancer; colorectal liver metastasis; biomarker; ctDNA;
   radiomics
ID CIRCULATING TUMOR DNA; MICROSATELLITE INSTABILITY; NEOADJUVANT
   CHEMOTHERAPY; MESENCHYMAL TRANSITION; EXTRACELLULAR-MATRIX;
   ACQUIRED-RESISTANCE; PROGNOSTIC-FACTORS; HEPATIC RESECTION; TARGETED
   THERAPY; LIQUID BIOPSIES
AB Simple Summary Colorectal cancer remains one of the most significant sources of cancer-related morbidity and mortality worldwide. The liver is the most common site of metastatic spread. Multiple modalities exist to manage and potentially cure patients with metastatic colorectal cancer. However, reliable biomarkers to assist with clinical decision-making are limited. Recent advances in genomic sequencing technology have greatly expanded our knowledge of colorectal cancer carcinogenesis and significantly reduced the cost and timing of the investigation. In this article, we discuss the current utility of biomarkers in the management of colorectal cancer liver metastases. Surgical management combined with improved systemic therapies have extended 5-year overall survival beyond 50% among patients with colorectal liver metastases (CRLM). Furthermore, a multitude of liver-directed therapies has improved local disease control for patients with unresectable CRLM. Unfortunately, a significant portion of patients treated with curative-intent hepatectomy develops disease recurrence. Traditional markers fail to risk-stratify and prognosticate patients with CRLM appropriately. Over the last few decades, advances in molecular sequencing technology have greatly expanded our knowledge of the pathophysiology and tumor microenvironment characteristics of CRLM. These investigations have revealed biomarkers with the potential to better inform management decisions in patients with CRLM. Actionable biomarkers such as RAS and BRAF mutations, microsatellite instability/mismatch repair status, and tumor mutational burden have been incorporated into national and societal guidelines. Other biomarkers, including circulating tumor DNA and radiomic features, are under active investigation to evaluate their clinical utility. Given the plethora of therapeutic modalities and lack of evidence on timing and sequence, reliable biomarkers are needed to assist clinicians with the development of patient-tailored management plans. In this review, we discuss the current evidence regarding biomarkers for patients with CRLM.
C1 [Hewitt, Daniel Brock; Brown, Zachary J.; Pawlik, Timothy M.] Ohio State Univ, Dept Surg, Div Surg Oncol, Wexner Med Ctr, Columbus, OH 43210 USA.
C3 University System of Ohio; Ohio State University
RP Pawlik, TM (corresponding author), Ohio State Univ, Dept Surg, Div Surg Oncol, Wexner Med Ctr, Columbus, OH 43210 USA.
EM tim.pawlik@osumc.edu
RI Pawlik, Timothy/AAO-9335-2020
OI Pawlik, Timothy/0000-0002-7994-9870
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NR 117
TC 8
Z9 9
U1 0
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD OCT
PY 2022
VL 14
IS 19
AR 4602
DI 10.3390/cancers14194602
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 5G0WB
UT WOS:000866727200001
PM 36230522
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Yang, WL
   Zhou, W
   Zhao, XH
   Wang, XQ
   Duan, LL
   Li, YD
   Niu, LR
   Chen, JF
   Zhang, YJ
   Han, Y
   Fan, DM
   Hong, L
AF Yang, Wanli
   Zhou, Wei
   Zhao, Xinhui
   Wang, Xiaoqian
   Duan, Lili
   Li, Yiding
   Niu, Liaoran
   Chen, Junfeng
   Zhang, Yujie
   Han, Yu
   Fan, Daiming
   Hong, Liu
TI Prognostic biomarkers and therapeutic targets in oral squamous cell
   carcinoma: a study based on cross-database analysis
SO HEREDITAS
LA English
DT Article
DE Oral squamous cell carcinoma; Bioinformatics analysis; Differentially
   expressed genes; GEO; TCGA
ID GENE-EXPRESSION; COLORECTAL-CANCER; FOXM1; MIGRATION; PATHWAYS;
   PROLIFERATION; PROMOTES; IDENTIFICATION; VALIDATION; SUPPRESSES
AB Background Oral squamous cell carcinoma (OSCC) is a malignant cancer, the survival rate of patients is disappointing. Therefore, it is necessary to identify the driven-genes and prognostic biomarkers in OSCC. Methods Four Gene Expression Omnibus (GEO) datasets were integratedly analyzed using bioinformatics approaches, including identification of differentially expressed genes (DEGs), GO and KEGG analysis, construction of protein-protein interaction (PPI) network, selection of hub genes, analysis of prognostic information and genetic alterations of hub genes. ONCOMINE, The Cancer Genome Atlas (TCGA) and Human Protein Atlas databases were used to evaluate the expression and prognostic value of hub genes. Tumor immunity was assessed to investigate the functions of hub genes. Finally, Cox regression model was performed to construct a multiple-gene prognostic signature. Results Totally 261 genes were found to be dysregulated. 10 genes were considered to be the hub genes. The Kaplan-Meier analysis showed that upregulated SPP1, FN1, CXCL8, BIRC5, PLAUR, and AURKA were related to poor outcomes in OSCC patients. FOXM1 and TPX2 were considered as the potential immunotherapeutic targets with future clinical significance. Moreover, we constructed a nine-gene signature (TEX101, DSG2, SCG5, ADA, BOC, SCARA5, FST, SOCS1, and STC2), which can be utilized to predict prognosis of OSCC patients effectively. Conclusion These findings may provide new clues for exploring the molecular mechanisms and targeted therapy in OSCC. The hub genes and risk gene signature are helpful to the personalized treatment and prognostic judgement.
C1 [Yang, Wanli; Zhou, Wei; Wang, Xiaoqian; Duan, Lili; Li, Yiding; Niu, Liaoran; Chen, Junfeng; Zhang, Yujie; Fan, Daiming; Hong, Liu] Fourth Mil Med Univ, Xijing Hosp Digest Dis, State Key Lab Canc Biol, 127 Changle West Rd, Xian 710032, Shaanxi, Peoples R China.
   [Yang, Wanli; Zhou, Wei; Wang, Xiaoqian; Duan, Lili; Li, Yiding; Niu, Liaoran; Chen, Junfeng; Zhang, Yujie; Fan, Daiming; Hong, Liu] Fourth Mil Med Univ, Xijing Hosp Digest Dis, Natl Clin Res Ctr Digest Dis, 127 Changle West Rd, Xian 710032, Shaanxi, Peoples R China.
   [Zhao, Xinhui] Northwest Univ, Affiliated Hosp, Dept Thyroid & Breast Surg, Xian 710018, Shaanxi, Peoples R China.
   [Zhao, Xinhui] Northwest Univ, Xian Hosp 3, Xian 710018, Shaanxi, Peoples R China.
   [Han, Yu] Fourth Mil Med Univ, Xijing Hosp, Dept Otolaryngol, 127 Changle West Rd, Xian 710032, Shaanxi, Peoples R China.
C3 Air Force Military Medical University; Air Force Military Medical
   University; Northwest University Xi'an; Northwest University Xi'an; Air
   Force Military Medical University
RP Fan, DM; Hong, L (corresponding author), Fourth Mil Med Univ, Xijing Hosp Digest Dis, State Key Lab Canc Biol, 127 Changle West Rd, Xian 710032, Shaanxi, Peoples R China.; Fan, DM; Hong, L (corresponding author), Fourth Mil Med Univ, Xijing Hosp Digest Dis, Natl Clin Res Ctr Digest Dis, 127 Changle West Rd, Xian 710032, Shaanxi, Peoples R China.; Han, Y (corresponding author), Fourth Mil Med Univ, Xijing Hosp, Dept Otolaryngol, 127 Changle West Rd, Xian 710032, Shaanxi, Peoples R China.
EM hanyufmmu@126.com; hlhyhj@126.com; hongliufmmu@163.com
FU Scientific Foundation of Shaanxi Province [S2019ZDLSF01-02-01,
   2018SF-240]; National Clinical Research Center for Digestive Diseases
   [2015BAI13B07]; Boost Program of Xijing Hospital [XJZT18ML06]
FX This study was supported in part by grant from the Scientific Foundation
   of Shaanxi Province (S2019ZDLSF01-02-01; 2018SF-240) and grant from the
   National Clinical Research Center for Digestive Diseases (2015BAI13B07)
   and Boost Program of Xijing Hospital (XJZT18ML06).
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NR 70
TC 20
Z9 21
U1 1
U2 6
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1601-5223
J9 HEREDITAS
JI Hereditas
PD APR 23
PY 2021
VL 158
IS 1
AR 15
DI 10.1186/s41065-021-00181-1
PG 17
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA RR1ZR
UT WOS:000642905600001
PM 33892811
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Verhoeven, Y
   Tilborghs, S
   Jacobs, J
   De Waele, J
   Quatannens, D
   Deben, C
   Prenen, H
   Pauwels, P
   Trinh, XB
   Wouters, A
   Smits, ELJ
   Lardon, F
   van Dam, PA
AF Verhoeven, Yannick
   Tilborghs, Sam
   Jacobs, Julie
   De Waele, Jorrit
   Quatannens, Delphine
   Deben, Christophe
   Prenen, Hans
   Pauwels, Patrick
   Xuan Bich Trinh
   Wouters, An
   Smits, Evelien L. J.
   Lardon, Filip
   van Dam, Peter A.
TI The potential and controversy of targeting STAT family members in cancer
SO SEMINARS IN CANCER BIOLOGY
LA English
DT Review
DE Signal transducer and activator of transcription (STAT); Cancer;
   JAK-STAT mutations; Targeted therapy; Immunotherapy
ID NF-KAPPA-B; TUMOR-ASSOCIATED MACROPHAGES; LYMPH-NODE METASTASIS; HUMAN
   PROSTATE-CANCER; DNA-BINDING ACTIVITY; CELL-CYCLE ARREST; SIGNAL
   TRANSDUCER; CONSTITUTIVE ACTIVATION; TRANSCRIPTION FACTOR;
   COLORECTAL-CANCER
AB The Signal Transducer and Activator of Transcription (STAT) family of proteins consists of transcription factors that play a complex and essential role in the regulation of physiologic cell processes, such as proliferation, differentiation, apoptosis and angiogenesis, and serves to organize the epigenetic landscape of immune cells. To date, seven STAT genes have been identified in the human genome; STAT1, STAT2, STAT3, STAT4, STAT5a, STAT5b and STAT6. They all account for diverse effects in response to extracellular signaling proteins, mainly by altering gene transcription in the effector cells. Members of the STAT family have been implicated in human cancer development, progression, metastasis, survival and resistance to treatment. Particularly STAT3 and STAT5 are of interest in cancer biology. They are currently considered as oncogenes, but their signaling is embedded into a complex and delicate balance between different (counteracting) transcription factors, and thus, in some contexts they can have a tumor suppressive role. Assessing STAT signaling mutations as well as screening for aberrant STAT pathway activation may have a role to predict sensitivity to immunotherapy and targeted STAT inhibition. In the present comprehensive review of the literature, we discuss in-depth the role of each STAT family member in cancer, assemble cuffing-edge information on the use of these molecules as potential biomarkers and targets for treatment, and address why their clinical implementation is controversy.
C1 [Verhoeven, Yannick; Tilborghs, Sam; Prenen, Hans; Xuan Bich Trinh; van Dam, Peter A.] Antwerp Univ Hosp, Multidisciplinary Oncol Ctr Antwerp, Wilrijkstr 10, B-2650 Edegem, Belgium.
   [Verhoeven, Yannick; Jacobs, Julie; De Waele, Jorrit; Quatannens, Delphine; Deben, Christophe; Prenen, Hans; Pauwels, Patrick; Xuan Bich Trinh; Wouters, An; Smits, Evelien L. J.; Lardon, Filip; van Dam, Peter A.] Univ Antwerp, Ctr Oncol Res CORE, Univ Pl 1, B-2610 Antwerp, Belgium.
   [Prenen, Hans] Antwerp Univ Hosp, Oncol Dept, Wilrijkstr 10, B-2650 Edegem, Belgium.
   [Pauwels, Patrick] Antwerp Univ Hosp, Dept Pathol, Wilrijkstr 10, B-2650 Edegem, Belgium.
   [Xuan Bich Trinh; van Dam, Peter A.] Antwerp Univ Hosp, Gynaecol Oncol Unit, Wilrijkstr 10, B-2650 Edegem, Belgium.
   [Smits, Evelien L. J.] Antwerp Univ Hosp, Ctr Cell Therapy & Regenerat Med, Wilrijkstr 10, B-2650 Edegem, Belgium.
C3 University of Antwerp; University of Antwerp; University of Antwerp;
   University of Antwerp; University of Antwerp; University of Antwerp
RP van Dam, PA (corresponding author), Antwerp Univ Hosp, Multidisciplinary Oncol Ctr Antwerp, Wilrijkstr 10, B-2650 Edegem, Belgium.
EM peter.vandam@uza.be
RI Verhoeven, Yannick/O-7194-2019; Jacobs, Julie/L-6479-2018; Lardon,
   Filip/A-3559-2010; Deben, Christophe/AAB-1636-2019; Wouters,
   An/B-5384-2017; Smits, Evelien/A-3520-2014
OI Prenen, Hans/0000-0001-8802-7352; Deben, Christophe/0000-0001-8085-2040;
   Quatannens, Delphine/0000-0001-5493-5539; Verhoeven,
   Yannick/0000-0002-4168-8222; Smits, Evelien/0000-0001-9255-3435
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NR 321
TC 252
Z9 270
U1 7
U2 117
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1044-579X
EI 1096-3650
J9 SEMIN CANCER BIOL
JI Semin. Cancer Biol.
PD FEB
PY 2020
VL 60
BP 41
EP 56
DI 10.1016/j.semcancer.2019.10.002
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KU9BK
UT WOS:000520016500005
PM 31605750
OA hybrid, Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Hesari, A
   Anoshiravani, AA
   Talebi, S
   Noruzi, S
   Mohammadi, R
   Salarinia, R
   Zare, R
   Ghasemi, F
AF Hesari, Amireza
   Anoshiravani, Ali Arash
   Talebi, Samaneh
   Noruzi, Somayye
   Mohammadi, Rezvan
   Salarinia, Reza
   Zare, Reza
   Ghasemi, Faezeh
TI Knockdown of sal-like 4 expression by small interfering RNA induces
   apoptosis in breast cancer cells
SO JOURNAL OF CELLULAR BIOCHEMISTRY
LA English
DT Article
DE biomarker; breast cancer; diagnosis; spalt-like transcription factor 4
ID MESENCHYMAL STEM-CELLS; CIRCULATING MICRORNAS; GASTRIC-CANCER;
   CLINICAL-SIGNIFICANCE; DIAGNOSTIC BIOMARKER; COLORECTAL-CANCER; T-CELLS;
   GENE; TUMOR; MELANOMA
AB Breast cancer is the most prevalent cancers worldwide and causes a significant amount of deaths annually. Spalt-like transcription factor 4 is known as a transcription factor, which has an important role in the proliferation of cancerous cells. Small interfering RNA (siRNA) is a short-chain molecule of 20 to 25 nucleotides that protrude on two sides of the 3, two nucleotides. In this study, using a specific sequence of siRNA against the sequence of this gene, its activity is investigated in the cell line of breast cancer. The breast cancer cells (MCF-7) were cultured and then, using a specific anti-sal-like 4 (SALL4) siRNA, their toxic doses were determined. Then, the gene is transfected into the cell. Proliferation and expression of the SALL4 and BCL-2 gene were measured using the real-time polymerase chain reaction method. The specific concentration of siRNA IC50 of the SALL4 gene was 40.35nmole. Gene expression results indicated that the expression of the Bcl-2 gene in the siRNA group was significantly reduced (P<0.05). SiRNA can increase the apoptosis of breast cancer cells by reducing the gene expression of SALL4 gene and Bcl-2; it can be used as a novel targeted therapy. This strategy, in addition to increasing the specificity of the drug, also reduces the side effects when compared with conventional chemotherapy.
C1 [Hesari, Amireza; Ghasemi, Faezeh] Arak Univ Med Sci, Dept Biotechnol, Fac Med, Arak, Iran.
   [Anoshiravani, Ali Arash] Arak Univ Med Sci, Dept Internal Med, Arak, Iran.
   [Talebi, Samaneh] Mashhad Univ Med Sci, Avicenna Res Inst, Div Human Genet, Immunol Res Ctr, Mashhad, Razavi Khorasan, Iran.
   [Noruzi, Somayye; Mohammadi, Rezvan; Salarinia, Reza] North Khorasan Univ Med Sci, Sch Med, Student Res Comm, Bojnurd, Iran.
   [Salarinia, Reza] North Khorasan Univ Med Sci, Sch Med, Dept Med Biotechnol & Mol Sci, Bojnurd, Iran.
   [Zare, Reza] Arak Univ Med Sci, Student Res Comm, Fac Med, Arak, Iran.
   [Ghasemi, Faezeh] High Inst Res & Educ Transfus Med, Blood Transfus Res Ctr, Next Milad Tower, Tehran, Iran.
C3 Mashhad University of Medical Sciences; North Khorasan University of
   Medical Sciences; North Khorasan University of Medical Sciences
RP Ghasemi, F (corresponding author), High Inst Res & Educ Transfus Med, Blood Transfus Res Ctr, Next Milad Tower, Tehran, Iran.
EM Ghasemi_808@yahoo.com
RI Talebi, Samaneh/JXN-8673-2024; Salari nia, Reza/ADN-5411-2022
OI Salarinia, Reza/0000-0002-5774-5295; Zarei, Reza/0000-0002-5513-6912;
   Talebi, Samaneh/0000-0003-1142-4557
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   Zhao HB, 2018, REPROD SCI, V25, P435, DOI 10.1177/1933719117715130
NR 97
TC 8
Z9 10
U1 0
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0730-2312
EI 1097-4644
J9 J CELL BIOCHEM
JI J. Cell. Biochem.
PD JUN
PY 2019
VL 120
IS 6
BP 9392
EP 9399
DI 10.1002/jcb.28214
PG 8
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA HX1FO
UT WOS:000467135600054
PM 30520112
DA 2025-01-04
ER

PT J
AU Bhattacharya, R
   Ye, XC
   Wang, R
   Ling, X
   McManus, M
   Fan, F
   Boulbes, D
   Ellis, LM
AF Bhattacharya, Rajat
   Ye, Xiang-Cang
   Wang, Rui
   Ling, Xia
   McManus, Madonna
   Fan, Fan
   Boulbes, Delphine
   Ellis, Lee M.
TI Intracrine VEGF Signaling Mediates the Activity of Prosurvival Pathways
   in Human Colorectal Cancer Cells
SO CANCER RESEARCH
LA English
DT Article
ID ENDOTHELIAL GROWTH-FACTOR; OXALIPLATIN-BASED CHEMOTHERAPY; AUTOCRINE
   SURVIVAL FACTOR; ANTIANGIOGENIC THERAPY; TUMOR ANGIOGENESIS; PHASE-III;
   TARGETED THERAPY; CARCINOMA CELLS; COLON-CANCER; EXPRESSION
AB The effects of vascular endothelial growth factor-A (VEGF-A/VEGF) and its receptors on endothelial cells function have been studied extensively, but their effects on tumor cells are less well defined. Studies of human colorectal cancer cells where the VEGF gene has been deleted suggest an intracellular role of VEGF as a cell survival factor. In this study, we investigated the role of intracrine VEGF signaling in colorectal cancer cell survival. In human colorectal cancer cells, RNAi-mediated depletion of VEGF decreased cell survival and enhanced sensitivity to chemotherapy. Unbiased reverse phase protein array studies and subsequent validation experiments indicated that impaired cell survival was a consequence of disrupted AKT and ERK1/2 (MAPK3/1) signaling, as evidenced by reduced phosphorylation. Inhibition of paracrine or autocrine VEGF signaling had no effect on phospho-AKT or phospho-ERK1/2 levels, indicating that VEGF mediates cell survival via an intracellular mechanism. Notably, RNAi-mediated depletion of VEGF receptor VEGFR1/FLT1 replicated the effects of VEGF depletion on phospho-AKT and phospho-ERK1/2 levels. Together, these studies show how VEGF functions as an intracrine survival factor in colorectal cancer cells, demonstrating its distinct role in colorectal cancer cell survival. (C) 2016 AACR.
C1 [Bhattacharya, Rajat; Ye, Xiang-Cang; Wang, Rui; Ling, Xia; Fan, Fan; Boulbes, Delphine; Ellis, Lee M.] Univ Texas MD Anderson Canc Ctr, Dept Surg Oncol, Houston, TX 77230 USA.
   [McManus, Madonna] Univ Texas MD Anderson Canc Ctr, Dept Pediat, Houston, TX 77230 USA.
   [Ellis, Lee M.] Univ Texas MD Anderson Canc Ctr, Dept Mol & Cellular Oncol, Houston, TX 77230 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
RP Ellis, LM (corresponding author), Univ Texas MD Anderson Canc Ctr, 1400 Pressler St,Unit 1484, Houston, TX 77230 USA.
EM lellis@mdanderson.org
RI fan, fan/KDO-5068-2024; Wang, Rui/JFJ-5076-2023
OI Bhattacharya, Rajat/0000-0001-5693-6754; Wang, Rui/0000-0001-5794-7201
FU NCI NIH HHS [T32 CA009599, R01 CA157880, P30 CA016672] Funding Source:
   Medline
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NR 44
TC 54
Z9 63
U1 0
U2 15
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 MAY 15
PY 2016
VL 76
IS 10
BP 3014
EP 3024
DI 10.1158/0008-5472.CAN-15-1605
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DL7SS
UT WOS:000375841000019
PM 26988990
OA Green Submitted, Bronze, Green Accepted
DA 2025-01-04
ER

PT J
AU Zhang, JY
   Yan, SC
   Liu, XY
   Gan, L
   Wu, ZH
   Gong, YW
   Huang, MZ
   Zhang, XW
   Guo, WJ
AF Zhang, Jieyun
   Yan, Shican
   Liu, Xiyu
   Gan, Lu
   Wu, Zhenhua
   Gong, Yiwei
   Huang, Mingzhu
   Zhang, Xiaowei
   Guo, Weijian
TI Gender-related prognostic value and genomic pattern of intra-tumor
   heterogeneity in colorectal cancer
SO CARCINOGENESIS
LA English
DT Article
ID ISLAND METHYLATOR PHENOTYPE; GENETIC-HETEROGENEITY; DNA-DAMAGE; SMAD4;
   HEAD; INSTABILITY; REPAIR; COLON; PATHWAYS; MATH
AB Intra-tumor heterogeneity (ITH) is crucial in tumorigenesis and resistance to target therapy. Here, we used mutant-allele tumor heterogeneity (MATH) to measure ITH based on next-generation sequencing data and high MATH was proven as an independent risk prognostic factor in male CRC patients in both a training set of 284 colorectal cancer (CRC) patients with from The Cancer Genome Atlas (TCGA) and a validating set of 187 CRC patients from International Cancer Genome Consortium (ICGC). Further, the genomic pattern according to MATH demonstrated that mutation rates of TP53, IRF5 and KRAS were independently associated with MATH, and the latter two were only significant in male patients. As MATH increased, the fraction of somatic copy number alteration (SCNA) elevated. Moreover, more SCNA events was independently associated with MATH in male than in female. WNT pathway, TGF-beta pathway and DNA repair deficiency was enriched in high MATH group and the latter two showed up only in male patients. In summary, we reveal the gender-related prognostic value of MATH and relevant genomic pattern in CRC. Potential mechanisms are provided and it remains to be proven whether they are drivers of subclone formation and ITH. Taking MATH into consideration in clinical trial might contribute to better therapeutic strategies in CRC with researches added on in the future.
C1 [Zhang, Jieyun; Gan, Lu; Wu, Zhenhua; Gong, Yiwei; Huang, Mingzhu; Zhang, Xiaowei; Guo, Weijian] Fudan Univ, Dept Med Oncol, Shanghai Canc Ctr, Shanghai 200032, Peoples R China.
   [Zhang, Jieyun; Liu, Xiyu; Gan, Lu; Wu, Zhenhua; Gong, Yiwei; Huang, Mingzhu; Zhang, Xiaowei; Guo, Weijian] Fudan Univ, Canc Metastasis Inst, Huashan Hosp, Dept Oncol, 12 Urumqi Rd M, Shanghai 200040, Peoples R China.
   [Yan, Shican] Fudan Univ, Canc Metastasis Inst, Huashan Hosp, Dept Gen Surg, 12 Urumqi Rd M, Shanghai 200040, Peoples R China.
   [Yan, Shican] Fudan Univ, Inst Biomed Sci, Shanghai 200032, Peoples R China.
   [Liu, Xiyu] Fudan Univ, Dept Breast Surg, Shanghai Canc Ctr, Shanghai 200032, Peoples R China.
C3 Fudan University; Fudan University; Fudan University; Fudan University;
   Fudan University
RP Guo, WJ (corresponding author), Fudan Univ, Dept Med Oncol, Shanghai Canc Ctr, Shanghai 200032, Peoples R China.; Guo, WJ (corresponding author), Fudan Univ, Canc Metastasis Inst, Huashan Hosp, Dept Oncol, 12 Urumqi Rd M, Shanghai 200040, Peoples R China.
EM guoweijian1@sohu.com
RI Liu, xiyu/KEJ-2349-2024; Zhang, Jieyun/V-7380-2019; zhang,
   xiaowei/GQH-5387-2022; WU, ZHEN/GRN-7688-2022
OI WU, ZHEN/0000-0001-8719-057X
FU Hospital Foundation of Fudan University Shanghai Cancer Center
   [YJ201504]
FX This study was supported by the grant from the Hospital Foundation of
   Fudan University Shanghai Cancer Center (YJ201504).
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NR 42
TC 22
Z9 23
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
EI 1460-2180
J9 CARCINOGENESIS
JI Carcinogenesis
PD AUG
PY 2017
VL 38
IS 8
BP 837
EP 846
DI 10.1093/carcin/bgx046
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FC4SV
UT WOS:000406831800010
PM 28531253
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Zhang, ZY
   Fang, C
   Wang, YX
   Zhang, JH
   Yu, J
   Zhang, YX
   Wang, XW
   Zhong, JT
AF Zhang, Zheying
   Fang, Cheng
   Wang, Yongxia
   Zhang, Jinghang
   Yu, Jian
   Zhang, Yongxi
   Wang, Xianwei
   Zhong, Jiateng
TI COL1A1: A potential therapeutic target for colorectal cancer expressing
   wild-type or mutant KRAS
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE colorectal cancer; collagen type I alpha 1; bioinformatics analysis;
   microarray; KRAS proto-oncogene GTPase
ID STAGING SYSTEM; PROLIFERATION; MICROARRAY; INHIBITOR; MIGRATION;
   PATHWAY; GROWTH; TUMORS; CELLS
AB Colorectal cancer (CRC) treatment primarily relies on chemotherapy along with surgery, radiotherapy and, more recently, targeted therapy at the late stages. However, chemotherapeutic drugs have high cytotoxicity, and the similarity between the effects of these drugs on cancerous and healthy cells limits their wider use in clinical settings. Targeted monoclonal antibody treatment may compensate for this deficiency. Epidermal growth factor receptor (EGFR)-targeted drugs have a positive effect on CRC with intact KRAS proto-oncogene GTPase (KRAS or KRAS(WT)), but may be ineffective or harmful in patients with KRAS mutations (KRAS(MUT)). Therefore, it is important to identify drug target genes that are uniformly effective with regards to KRAS(WT) and KRAS(MUT) CRC. The present study performed gene expression analysis, and identified 294 genes upregulated in KRAS(WT) and KRAS(MUT) CRC samples. Collagen type I 1 (COL1A1) was identified as the hub gene through STRING and Cytoscape analyses. Consistent with results obtained from Oncomine, a cancer microarray database and web-based data-mining platform, it was demonstrated that the expression of COL1A1 was significantly upregulated in CRC tissues and cell lines regardless of KRAS status. Inhibition of COL1A1 in KRAS(WT) and KRAS(MUT) CRC cell lines significantly decreased cell proliferation and invasion. In addition, increased COL1A1 expression in CRC was significantly associated with serosal invasion, lymph metastases and hematogenous metastases. Taken together, the findings of the present study indicated that COL1A1 may serve as a candidate diagnostic biomarker and a promising therapeutic target for CRC.
C1 [Zhang, Zheying; Wang, Yongxia; Zhong, Jiateng] Xinxiang Med Univ, Dept Pathol, 601 Jinsui Rd, Xinxiang 453003, Henan, Peoples R China.
   [Fang, Cheng] Xinxiang Med Univ, Affiliated Hosp 3, Dept Anesthesiol, Xinxiang 453100, Henan, Peoples R China.
   [Zhang, Jinghang; Yu, Jian] Xinxiang Med Univ, Affiliated Hosp 1, Dept Pathol, Xinxiang 453003, Henan, Peoples R China.
   [Zhang, Yongxi] Xinxiang Med Univ, Affiliated Hosp 3, Dept Oncol, Xinxiang 453100, Henan, Peoples R China.
   [Wang, Xianwei] Xinxiang Med Univ, Henan Key Lab Med Tissue Regenerat, 601 Jinsui Rd, Xinxiang 453003, Henan, Peoples R China.
   [Zhong, Jiateng] Xinxiang Med Univ, Collaborat Innovat Ctr Mol Diag & Lab Med Henan P, Sch Lab Med, Xinxiang 453003, Henan, Peoples R China.
C3 Xinxiang Medical University; Xinxiang Medical University; Xinxiang
   Medical University; Xinxiang Medical University; Xinxiang Medical
   University; Xinxiang Medical University
RP Zhong, JT (corresponding author), Xinxiang Med Univ, Dept Pathol, 601 Jinsui Rd, Xinxiang 453003, Henan, Peoples R China.; Wang, XW (corresponding author), Xinxiang Med Univ, Henan Key Lab Med Tissue Regenerat, 601 Jinsui Rd, Xinxiang 453003, Henan, Peoples R China.
EM wangxianwei1116@126.com; zhongjiatengxxmu@163.com
RI Wang, Yongxia/GYU-4895-2022; Wang, Xianwei/AAN-8915-2020; Zhong,
   Jiateng/AAB-2064-2022; Feng, Chao/O-8679-2016; Zhang,
   Caiying/GRX-6292-2022
OI Wang, Xianwei/0000-0002-1490-8736
FU Xinxiang Medical College research funding [XYBSKYZZ201632, 505079];
   Higher Education Institutions of Henan Province, China [17A310023];
   National Natural Science Foundation of China [81702891]; Taihang Young
   Scholar Foundation of Xinxiang Medical University; Science and
   Technology Department of Henan Province, China [172102310651,
   122102310194]
FX The present study was supported by the Xinxiang Medical College research
   funding (grant nos. XYBSKYZZ201632 and 505079), Higher Education
   Institutions of Henan Province, China (grant no. 17A310023), The
   National Natural Science Foundation of China (grant no. 81702891), and
   Taihang Young Scholar Foundation of Xinxiang Medical University and
   Science and Technology Department of Henan Province, China (grant nos.
   172102310651 and 122102310194).
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NR 44
TC 38
Z9 45
U1 0
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 NOV
PY 2018
VL 53
IS 5
BP 1869
EP 1880
DI 10.3892/ijo.2018.4536
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GX4LG
UT WOS:000447703300005
PM 30132520
OA Green Submitted, Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Wan, FQ
   Dong, ZZ
   Liu, B
   Yan, S
   Wu, N
   Yang, MZ
   Chang, LQ
AF Wan, Fengqi
   Dong, Zaizai
   Liu, Bing
   Yan, Shi
   Wu, Nan
   Yang, Mingzhu
   Chang, Lingqian
TI Sensitive Interrogation of Enhancer Activity in Living Cells on a
   Nanoelectroporation-Probing Platform
SO ACS SENSORS
LA English
DT Article
DE enhancer; nanoelectroporation; DNA probe; intracellular analysis;
   biochip
ID AMPLIFICATION; DESIGN
AB Enhancers involved in the upregulation of multiple oncogenes play a fundamental role in tumorigenesis and immortalization. Exploring the activity of enhancers in living cells has emerged as a critical path to a deep understanding of cancer properties, further providing important clues to targeted therapy. However, identifying enhancer activity in living cells is challenging due to the double biological barriers of a cell cytoplasmic membrane and a nuclear membrane, limiting the sensitivity and responsiveness of conventional probing methods. In this work, we developed a nanoelectroporation-probing (NP) platform, which enables intranuclear probe delivery for sensitive interrogation of enhancer activity in living cells. The nanoelectroporation biochip achieved highly focused perforation of the cell cytoplasmic membrane and brought about additional driving force to expedite the delivery of probes into the nucleus. The probes targeting enhancer activity (named "PH probe") are programmed with a cyclic amplification strategy and enable an increase in the fluorescence signals over 100-fold within 1 h. The platform was leveraged to detect the activity of CCAT1 enhancers (CCAT1, colon cancer-associated transcript-1, a long noncoding RNA that functions in tumor invasion and metastasis) in cell samples from clinical lung cancer patients, as well as reveal the heterogeneity of enhancers among different patients. The observations may extend the linkages between enhancers and cancer cells while validating the robustness and reliability of the platform for the assay of enhancer activity. This platform will be a promising toolbox with wide applicable potential for the intranuclear study of living cells.
C1 [Wan, Fengqi; Dong, Zaizai; Yang, Mingzhu; Chang, Lingqian] Beihang Univ, Beijing Adv Innovat Ctr Biomed Engn, Sch Biol Sci & Med Engn, Key Lab Biomech & Mechanobiol,Minist Educ, Beijing 100191, Peoples R China.
   [Chang, Lingqian] Anhui Med Univ, Res & Engn Ctr Biomed Mat, Sch Biomed Engn, Hefei 230032, Peoples R China.
   [Wan, Fengqi] Lanzhou Univ, Cuiying Biomed Res Ctr, Hosp 2, Lanzhou 730030, Peoples R China.
   [Liu, Bing; Yan, Shi; Wu, Nan] Peking Univ, Canc Hosp & Inst, Dept Thorac Surg 2, Key Lab Carcinogenesis & Translat Res,Minist Educ, Beijing 100142, Peoples R China.
C3 Beihang University; Anhui Medical University; Lanzhou University; Peking
   University
RP Dong, ZZ; Chang, LQ (corresponding author), Beihang Univ, Beijing Adv Innovat Ctr Biomed Engn, Sch Biol Sci & Med Engn, Key Lab Biomech & Mechanobiol,Minist Educ, Beijing 100191, Peoples R China.; Chang, LQ (corresponding author), Anhui Med Univ, Res & Engn Ctr Biomed Mat, Sch Biomed Engn, Hefei 230032, Peoples R China.
EM dongzaizai@buaa.edu.cn; lingqianchang@buaa.edu.cn
RI Chang, Lingqian/D-3673-2015
OI Dong, Zaizai/0000-0003-1398-1699; Chang, Lingqian/0000-0003-4116-2711
FU National Natural Science Foundation of China; Beijing Natural Science
   Foundation; Fundamental Research Funds for the Central Universities;
   Cuiying Scientific and Technological Innovation Program of Lanzhou
   University Second Hospital; Science Founda-tion of Peking University
   Cancer Hospital;  [62003023];  [32071407];  [7212204]; 
   [JKF-YG-22-B001];  [CY2018-QN10];  [2022-5 (A002476)]
FX ACKNOWLEDGMENTS This work was supported by funding from the National
   Natural Science Foundation of China (Nos. 62003023 and 32071407) , the
   Beijing Natural Science Foundation (No. 7212204) , the Fundamental
   Research Funds for the Central Universities (JKF-YG-22-B001) , the
   Cuiying Scientific and Technological Innovation Program of Lanzhou
   University Second Hospital (CY2018-QN10) , and the Science Founda-tion
   of Peking University Cancer Hospital 2022-5 (A002476) .
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NR 66
TC 4
Z9 4
U1 6
U2 48
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 2379-3694
J9 ACS SENSORS
JI ACS Sens.
PD DEC 23
PY 2022
VL 7
IS 12
BP 3671
EP 3681
DI 10.1021/acssensors.2c01187
EA NOV 2022
PG 11
WC Chemistry, Multidisciplinary; Chemistry, Analytical; Nanoscience &
   Nanotechnology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics
GA 7S0DL
UT WOS:000889698000001
PM 36410738
DA 2025-01-04
ER

PT J
AU Khoury, JD
   Wang, WL
   Prieto, VG
   Medeiros, LJ
   Kalhor, N
   Hameed, M
   Broaddus, R
   Hamilton, SR
AF Khoury, Joseph D.
   Wang, Wei-Lien
   Prieto, Victor G.
   Medeiros, L. Jeffrey
   Kalhor, Neda
   Hameed, Meera
   Broaddus, Russell
   Hamilton, Stanley R.
TI Validation of Immunohistochemical Assays for Integral Biomarkers in the
   NCI-MATCH EAY131 Clinical Trial
SO CLINICAL CANCER RESEARCH
LA English
DT Review
ID OF-AMERICAN-PATHOLOGISTS; DNA MISMATCH REPAIR; BREAST-CANCER;
   ENDOMETRIAL CARCINOMA; COMPANION DIAGNOSTICS; COLON-CANCER; PTEN
   IMMUNOHISTOCHEMISTRY; SEBACEOUS NEOPLASIA; ANALYTIC VALIDATION;
   COWDEN-SYNDROME
AB Biomarkers that guide therapy selection are gaining unprecedented importance as targeted therapy options increase in scope and complexity. In conjunction with high-throughput molecular techniques, therapy-guiding biomarker assays based upon immunohistochemistry (IHC) have a critical role in cancer care in that they inform about the expression status of a protein target. Here, we describe the validation procedures for four clinical IHC biomarker assays-PTEN, RB, MLH1, and MSH2-for use as integral biomarkers in the nationwide NCI-Molecular Analysis for Therapy Choice (NCI-MATCH) EAY131 clinical trial. Validation procedures were developed through an iterative process based on collective experience and adaptation of broad guidelines from the FDA. The steps included primary antibody selection; assay optimization; development of assay interpretation criteria incorporating biological considerations; and expected staining patterns, including indeterminate results, orthogonal validation, and tissue validation. Following assay lockdown, patient samples and cell lines were used for analytic and clinical validation. The assays were then approved as laboratory-developed tests and used for clinical trial decisions for treatment selection. Calculations of sensitivity and specificity were undertaken using various definitions of gold-standard references, and external validation was required for the PTEN IHC assay. In conclusion, validation of IHC biomarker assays critical for guiding therapy in clinical trials is feasible using comprehensive preanalytic, analytic, and post-analytic steps. Implementation of standardized guidelines provides a useful framework for validating IHC biomarker assays that allow for reproducibility across institutions for routine clinical use. (C) 2017 AACR.
C1 [Khoury, Joseph D.; Medeiros, L. Jeffrey] Univ Texas MD Anderson Canc Ctr, Dept Hematopathol, Houston, TX 77030 USA.
   [Wang, Wei-Lien; Prieto, Victor G.; Kalhor, Neda; Broaddus, Russell; Hamilton, Stanley R.] Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA.
   [Hameed, Meera] Mem Sloan Kettering Canc Ctr, Dept Pathol, 1275 York Ave, New York, NY 10021 USA.
   [Hamilton, Stanley R.] Univ Texas MD Anderson Canc Ctr, Div Pathol & Lab Med, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; University of
   Texas System; UTMD Anderson Cancer Center; Memorial Sloan Kettering
   Cancer Center; University of Texas System; UTMD Anderson Cancer Center
RP Khoury, JD (corresponding author), Univ Texas MD Anderson Canc Ctr, 1515 Holcombe Blvd,MS 072, Houston, TX 77030 USA.
EM jkhoury@mdanderson.org
RI Han, Zhang/KGM-8929-2024; Medeiros, L. Jeffrey/AAB-1018-2019
OI Medeiros, L. Jeffrey/0000-0001-6577-8006
FU NIH/National Cancer Institute [U10CA180820]; Cancer Center Support Grant
   award [P30 CA016672]
FX The authors thank the staff of the Clinical Immunohistochemistry
   Laboratory at The University of Texas MD Anderson Cancer Center,
   especially Janet Quinones and Victor Ortega; the NCI-MATCH support team
   at MD Anderson, especially Dr. Geeta Mantha, Dr. Mark Routbort, Dr.
   Ignacio Wistuba, Dr. Jaime Rodriguez-Canales, and Barbara Mino for
   assistance with external validation studies for PTEN. The authors also
   thank the NCI-MATCH Manuscript Committee for editorial review of this
   manuscript. This study was supported by the NIH/National Cancer
   Institute award U10CA180820 and Cancer Center Support Grant award P30
   CA016672.
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NR 52
TC 60
Z9 60
U1 0
U2 10
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 FEB 1
PY 2018
VL 24
IS 3
BP 521
EP 531
DI 10.1158/1078-0432.CCR-17-1597
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FU6QA
UT WOS:000423975900004
PM 28839110
OA Green Accepted, Bronze
DA 2025-01-04
ER

PT J
AU Grassadonia, A
   Di Marino, P
   Ficorella, C
   Cortellini, A
   Cannita, K
   Parisi, A
   Gamucci, T
   Zoratto, F
   Vici, P
   Barba, M
   Porreca, E
   Neri, M
   Veronese, A
   Natoli, C
   De Tursi, M
   Tinari, N
AF Grassadonia, Antonino
   Di Marino, Pietro
   Ficorella, Corrado
   Cortellini, Alessio
   Cannita, Katia
   Parisi, Alessandro
   Gamucci, Teresa
   Zoratto, Federica
   Vici, Patrizia
   Barba, Maddalena
   Porreca, Ettore
   Neri, Matteo
   Veronese, Angelo
   Natoli, Clara
   De Tursi, Michele
   Tinari, Nicola
TI Impact of primary tumor location in patients with RAS wild-type
   metastatic colon cancer treated with first-line chemotherapy plus
   anti-EGFR or anti-VEGF monoclonal antibodies: a retrospective
   multicenter study
SO JOURNAL OF CANCER
LA English
DT Article
DE Metastatic colorectal cancer (mCRC); RAS wt; Tumor location; Cetuximab;
   Panitumumab; Bevacizumab
ID ADVANCED COLORECTAL-CANCER; BEVACIZUMAB PLUS; MUTATION STATUS;
   OPEN-LABEL; CETUXIMAB; KRAS; SURVIVAL; SITE; FLUOROURACIL; METAANALYSIS
AB Emerging evidence supports a prognostic role of primary tumor location in metastatic colon cancer (mCC). We conducted a retrospective analysis to evaluate the effect of tumor location on prognosis and efficacy of biological agents (anti-EGFR, Cetuximab and Panitumumab, or anti-VEGF, Bevacizumab) added to first-line chemotherapy in patients with RAS wild-type (wt) mCC. Patients with newly diagnosed RAS wt mCC candidates to first-line chemotherapy with anti-EGFRs or Bevacizumab were selected. Clinical outcomes were assessed and stratified by tumor location and type of treatment. Overall, 351 patients met the inclusion criteria. Primary colon cancer was right-sided (RCC) in 105 (29.9%) patients and left-sided (LCC) in 246 (70.1%). Patients with LCC had a better OS compared to those with RCC (33.6 vs 23.5 months, HR 0.74; 95% CI, 0.55 to 0.99; p=0.049). In the overall study population, OS was not significantly different for patients treated with Cetuximab or Panitumumab as compared to those receiving Bevacizumab. However, when comparing treatment outcome according to tumor sidedness, patients with LCC treated with Cetuximab or Panitumumab had a significantly longer PFS (12.4 vs 10.7 months; HR: 0.69; 95% CI, 0.51 to 0.93; p=0.015) and OS (40.7 vs 28.6 months; HR: 0.67; 95% CI 0.47 to 0.95; p=0.026). No relevant differences were observed in patients with RCC.
   We found evidence in support of the impact of tumor location in RAS wt mCC treated with first-line chemotherapy in association with targeted therapy. More favorable outcomes were observed in LCC patients, but not in RCC patients, treated with anti-EGFR agents compared with those who received Bevacizumab. Further, prospective and adequately sized studies are warranted to confirm our findings.
C1 [Grassadonia, Antonino; Di Marino, Pietro; Porreca, Ettore; Natoli, Clara; De Tursi, Michele; Tinari, Nicola] Univ G dAnnunzio, Dept Med Oral & Biotechnol Sci, Via Vestini, I-66100 Chieti, Italy.
   [Grassadonia, Antonino; Neri, Matteo; Veronese, Angelo; Natoli, Clara; Tinari, Nicola] Univ G dAnnunzio, CeSI MeT, Via Vestini, I-66100 Chieti, Italy.
   [Ficorella, Corrado; Cortellini, Alessio; Cannita, Katia; Parisi, Alessandro] Univ Aquila, Dept Biotechnol & Appl Clin Sci, St Salvatore Hosp, Med Oncol Unit, Via Vetoio, I-67100 Laquila, Italy.
   [Gamucci, Teresa] Sandro Pertini Hosp, Med Oncol Unit, Rome, Italy.
   [Zoratto, Federica] F Spaziani Hosp, Med Oncol Unit, Frosinone, Italy.
   [Vici, Patrizia; Barba, Maddalena] IRCCS, Regina Elena Natl Canc Inst, Div Med Oncol 2, Rome, Italy.
   [Neri, Matteo; Veronese, Angelo] Univ G dAnnunzio, Dept Med & Ageing Sci, Chieti, Italy.
C3 G d'Annunzio University of Chieti-Pescara; G d'Annunzio University of
   Chieti-Pescara; University of L'Aquila; Ospedale Sandro Pertini; G
   d'Annunzio University of Chieti-Pescara
RP Grassadonia, A (corresponding author), Univ G dAnnunzio, Dept Med Oral & Biotechnol Sci, Via Vestini, I-66100 Chieti, Italy.; Grassadonia, A (corresponding author), Univ G dAnnunzio, CeSI MeT, Via Vestini, I-66100 Chieti, Italy.
EM grassadonia@unich.it
RI Parisi, Alessandro/AAB-9728-2019; Cortellini, Alessio/AAB-8609-2019; Del
   Mastro, Lucia/J-6163-2016; DE TURSI, MICHELE/L-3427-2016
OI DI MARINO, PIETRO/0000-0002-1330-683X; Parisi,
   Alessandro/0000-0003-4629-7762; DE TURSI, MICHELE/0000-0002-1411-1946;
   Vici, Patrizia/0000-0001-7528-9783; Cortellini,
   Alessio/0000-0002-1209-5735
FU Consorzio Interuniversitario Nazionale per la Bio-Oncologia (CINBO)
FX This work was supported by the Consorzio Interuniversitario Nazionale
   per la Bio-Oncologia (CINBO).
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NR 44
TC 26
Z9 26
U1 1
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 2019
VL 10
IS 24
BP 5926
EP 5934
DI 10.7150/jca.34550
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JE7YF
UT WOS:000490906300004
PM 31762802
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Hubbard, JM
   Yin, J
   Schenk, EL
   Qin, R
   Reid, JM
   Strand, C
   Fiskum, J
   Menefee, M
   Lin, GC
   Doyle, LA
   Ivy, P
   Erlichman, C
   Adjei, A
   Haluska, P
   Costello, BA
AF Hubbard, Joleen M.
   Yin, Jun
   Schenk, Erin L.
   Qin, Rui
   Reid, Joel M.
   Strand, Carrie
   Fiskum, Jack
   Menefee, Michael
   Lin, Grace
   Doyle, L. Austin
   Ivy, Percy
   Erlichman, Charles
   Adjei, Alex
   Haluska, Paul
   Costello, Brian A.
TI Phase I study of cediranib, an oral VEGFR inhibitor, in combination with
   selumetinib, an oral MEK inhibitor, in patients with advanced solid
   malignancies
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE AZD2171; Cediranib; AZD6244; Selumetinib; VEGF; MEK
ID PROGRESSION-FREE SURVIVAL; CELL LUNG-CANCER; TARGETED THERAPY; AZD6244
   ARRY-142886; COLORECTAL-CANCER; TYROSINE KINASE; PLUS DOCETAXEL;
   DOUBLE-BLIND; OPEN-LABEL; BEVACIZUMAB
AB Purpose. Targeting the vascular endothelial growth factor (VEGF) pathway improves progression free survival in multiple advanced malignancies but durable responses are uncommon. Inhibition of the VEGF pathway at multiple levels of signal transduction may improve clinical outcomes. Preclinical data with cediranib, an inhibitor of all 3 VEGF receptors, in combination with selumetinib, an inhibitor of MEK 1/2, demonstrated improved tumor control experimentally. This phase I trial was designed to test the two agents in combination to evaluate the tolerability, safety and assess disease response. Methods. Patients with advanced solid malignancies were enrolled into this phase I trial. Cediranib and selumetinib were dosed using a toxicity-adaptive isotonic design for the dose escalation/de-escalation of each agent. Both cediranib and selumetinib were administered daily and continuously. Cycles were 28 days in length. Results. Eighteen patients were enrolled. At all dose levels, dose limiting toxicities (DLT) were observed, which limited dose escalation and further evaluation. The maximum tolerated dose of cediranib and selumetinib in combination could not be determined. The best response of stable disease was observed in eight patients. Conclusions. Cediranib and selumetinib in combination on a continuous schedule was not tolerable, with patients experiencing cardiovascular and other DLTs. Intermittent schedules may be needed to establish a safe and tolerable combination of cediranib and selumetinib.
C1 [Hubbard, Joleen M.; Schenk, Erin L.; Erlichman, Charles; Adjei, Alex; Haluska, Paul; Costello, Brian A.] Mayo Clin, Div Med Oncol, Rochester, MN 55905 USA.
   [Yin, Jun; Qin, Rui; Strand, Carrie; Fiskum, Jack] Mayo Clin, Div Biomed Stat & Informat, Rochester, MN 55905 USA.
   [Schenk, Erin L.] Univ Colorado, Div Med Oncol, Anschutz Med Campus, Aurora, CO 80045 USA.
   [Reid, Joel M.] Mayo Clin, Div Oncol Res, Rochester, MN 55905 USA.
   [Menefee, Michael] VA Med Ctr, Washington, DC 20422 USA.
   [Lin, Grace] Mayo Clin, Div Cardiovasc Dis, Rochester, MN 55905 USA.
   [Doyle, L. Austin; Ivy, Percy] NCI, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA.
   [Haluska, Paul] Bristol Myers Squibb, Lawrenceville, NJ 08648 USA.
C3 Mayo Clinic; Mayo Clinic; University of Colorado System; University of
   Colorado Anschutz Medical Campus; Mayo Clinic; Mayo Clinic; National
   Institutes of Health (NIH) - USA; NIH National Cancer Institute (NCI);
   Bristol-Myers Squibb
RP Costello, BA (corresponding author), Mayo Clin, Div Med Oncol, Rochester, MN 55905 USA.
EM costello.brian@mayo.edu
RI Qin, Rui/H-5638-2012; Schenk, Erin/CAI-9416-2022; Yin, Jun/ABC-2853-2021
OI Schenk, Erin/0000-0001-9418-9948
FU Mayo Clinic U01 grant [CA069912]; Mayo Clinic UM1 grant [CA186686]
FX Supported by the Mayo Clinic U01 (CA069912) and Mayo Clinic UM1
   (CA186686) grants.
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NR 53
TC 2
Z9 3
U1 0
U2 0
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 2022
VL 40
IS 1
BP 115
EP 123
DI 10.1007/s10637-021-01175-6
EA SEP 2021
PG 9
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA YI0QQ
UT WOS:000695387800002
PM 34515877
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Chandramohan, K
   Balan, DJ
   Devi, KP
   Nabavi, SF
   Reshadat, S
   Khayatkashani, M
   Mahmoodifar, S
   Filosa, R
   Amirkhalili, N
   Pishvaei, S
   Sargazi-Aval, O
   Nabavi, SM
AF Chandramohan, Kiruthiga
   Balan, Devasahayam Jaya
   Devi, Kasi Pandima
   Nabavi, Seyed Fazel
   Reshadat, Sara
   Khayatkashani, Maryam
   Mahmoodifar, Sepideh
   Filosa, Rosanna
   Amirkhalili, Niloufar
   Pishvaei, Soroush
   Sargazi-Aval, Omolbanin
   Nabavi, Seyed Mohammad
TI Short interfering RNA in colorectal cancer: is it wise to shoot the
   messenger?
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE Colorectal cancer; siRNA; RNA interference; Targeted therapy; Gene
   silencing
ID HEDGEHOG SIGNALING PATHWAY; INHIBITS TUMOR-GROWTH; NF-KAPPA-B;
   BETA-CATENIN; SERRATED PATHWAY; SIRNA DELIVERY; POOR-PROGNOSIS; CELL
   SURVIVAL; JANUS KINASES; COLON
AB Colorectal cancer (CRC) is the third most common cancer and the leading cause of gastrointestinal cancer death. 90% of people diagnosed with colorectal cancer are over the age of 50; nevertheless, the illness is more aggressive among those detected at a younger age. Chemotherapy-based treatment has several adverse effects on both normal and malignant cells. The primary signaling pathways implicated in the advancement of CRC include hedgehog (Hh), janus kinase and signal transducer and activator of transcription (JAK/STAT), Wingless-related integration site (Wnt)/beta-catenin, transforming growth factor-beta (TNF-beta), epidermal growth factor receptor (EGFR)/Mitogen-activated protein kinases (MAPK), phosphoinositide 3-kinase (PI3K), nuclear factor kappa B (NF-kappa B), and Notch. Loss of heterozygosity in tumor suppressor genes like adenomatous polyposis coli, as well as mutation or deletion of genes like p53 and Kirsten rat sarcoma viral oncogene (KRAS), are all responsible for the occurrence of CRC. Novel therapeutic targets linked to these signal-transduction cascades have been identified as a consequence of advances in small interfering RNA (siRNA) treatments. This study focuses on many innovative siRNA therapies and methodologies for delivering siRNA therapeutics to the malignant site safely and effectively for the treatment of CRC. Treatment of CRC using siRNA-associated nanoparticles (NPs) may inhibit the activity of oncogenes and MDR-related genes by targeting a range of signaling mechanisms. This study summarizes several siRNAs targeting signaling molecules, as well as the therapeutic approaches that might be employed to treat CRC in the future.
C1 [Chandramohan, Kiruthiga; Balan, Devasahayam Jaya; Devi, Kasi Pandima] Alagappa Univ Sci Campus, Dept Biotechnol, Karaikkudi 630003, Tamil Nadu, India.
   [Nabavi, Seyed Fazel; Khayatkashani, Maryam; Filosa, Rosanna; Amirkhalili, Niloufar; Nabavi, Seyed Mohammad] Biopharmaceut Innovat Ctr, Adv Med Pharm AMP Biotec, Via Cortenocera, I-82030 San Salvatore Telesino, BN, Italy.
   [Nabavi, Seyed Fazel; Khayatkashani, Maryam; Nabavi, Seyed Mohammad] Fed Inst Educ Sci & Technol IFCE, Nutringredientes Res Ctr, Baturite, CE, Brazil.
   [Reshadat, Sara; Mahmoodifar, Sepideh; Pishvaei, Soroush] Semnan Univ Med Sci, Dept Internal Med, Semnan, Iran.
   [Filosa, Rosanna] Univ Sannio, Dept Sci & Technol, I-82100 Benevento, Italy.
   [Sargazi-Aval, Omolbanin] Zabol Univ Med Sci, Zabol, Iran.
C3 Alagappa University; Instituto Federal do Ceara (IFCE); Semnan
   University of Medical Sciences; University of Sannio
RP Devi, KP (corresponding author), Alagappa Univ Sci Campus, Dept Biotechnol, Karaikkudi 630003, Tamil Nadu, India.; Nabavi, SM (corresponding author), Biopharmaceut Innovat Ctr, Adv Med Pharm AMP Biotec, Via Cortenocera, I-82030 San Salvatore Telesino, BN, Italy.
EM devikasi@yahoo.com; nabavi208@gmail.com
RI Sargazi-Aval, Omolbanin/D-1368-2018; Nabavi, Seyed Mohammad/G-5335-2010;
   nabavi, seyed fazel/A-2223-2010; filosa, rosanna/GQR-0571-2022
OI filosa, rosanna/0000-0003-1938-5732
FU DST-FIST [SR/FST/LSI-639/2015 (C)]; UGC-SAP; DST-PURSE; 
   [F.5-1/2018/DRSII (SAP-II)];  [SR/PURSE Phase 2/38 (G)]
FX The authors thankfully acknowledge DST -FIST (GrantNo.
   SR/FST/LSI-639/2015 (C) ) , UGC -SAP (Grant No.F.5-1/2018/DRSII (SAP-II)
   ) , and DST -PURSE (Grant No.SR/PURSE Phase 2/38 (G) ) for providing lab
   facilities. The authors also thank RUSA 2.0 [F. 24-51/2014-U, Policy
   (TNMulti-Gen) , Dept of Edn, GoI] .
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NR 161
TC 5
Z9 5
U1 0
U2 4
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 JUN 15
PY 2023
VL 949
AR 175699
DI 10.1016/j.ejphar.2023.175699
EA APR 2023
PG 13
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA F5GC8
UT WOS:000982620300001
PM 37011722
DA 2025-01-04
ER

PT J
AU Molnar, TF
   Drozgyik, A
AF Molnar, Tamas F.
   Drozgyik, Andras
TI Narrative review of theoretical considerations regarding HITHOC between
   past and future
SO ANNALS OF TRANSLATIONAL MEDICINE
LA English
DT Review
DE Intrapleural hyperthermy; pleurodesis; video-assisted thoracoscopic
   surgery (VATS)
ID MALIGNANT PLEURAL EFFUSIONS; INTRATHORACIC CHEMOTHERAPY HITHOC; CELL
   LUNG-CANCER; INTRAPLEURAL CISPLATIN; HYPOTONIC SOLUTION;
   COLORECTAL-CANCER; DISTILLED WATER; PHASE-II; IN-VITRO; SURGERY
AB Hyppocrates constructed the medicines-surgery-energy triangle which includes all therapeutical modalities. Hyperthermic intraoperative chemotherapy (HITHOC) is a synergy-based single stage multimodality treatment encompassing the locoregional manifestation of the systemic malignant process. Pleural space, thermal effect, lavage/irrigation and chemotherapy represent the basic science ports of the network hub: HITHOC. The malignant transformation and process of the pleural surface (and underlying lung) challenges space management and tissue control. Thermotherapy without local chemotherapy is insufficient, similar to the normothermic local irrigation aligned with anticancer agents. The local administration of combined heat-transfer fluid and chemotherapy with or without subsequent surgical removal offers reasonable outcome in extensive primary pleural neoplasms (malignant mesothelioma), advanced (> Stage IIIA) NSCLC, functionally inoperable lung cancer and pleural carcinosis from extrathoracic malignancies. Measured by symptom-free survival and the quality of life, HITHOC in its present form, offers a modest yet fully substantiated solution. HITHOC in combination with the local application of targeted therapy and/or immunotherapy administered in the pleural space are currently under investigation. Additional development including new acting substances, their solvents and the means regarding surgical delivery and anesthesiology techniques are sign posts up ahead. Level 2 evidence are required in order to stepping up the recommendation levels, rewriting protocols and guidelines, in which HITHOC earns its revered position in the decision making process it deserves.
C1 [Molnar, Tamas F.] Univ Pecs, Dept Operat Med, Fac Med, Pecs Szigeti U 12, H-7622 Pecs, Hungary.
   [Molnar, Tamas F.; Drozgyik, Andras] Aladar Petz Univ, Univ Pecs, Teaching Hosp, Chair Surg,Fac Med,Dept Surg, Gyor, Hungary.
C3 University of Pecs; University of Pecs
RP Molnar, TF (corresponding author), Univ Pecs, Dept Operat Med, Fac Med, Pecs Szigeti U 12, H-7622 Pecs, Hungary.
EM tfmolnar@gmail.com
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NR 72
TC 2
Z9 2
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 JUN
PY 2021
VL 9
IS 11
AR 954
DI 10.21037/atm-20-5855
PG 8
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA SV4CC
UT WOS:000663767300018
PM 34350269
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU McDaniel, AS
   Hovelson, DH
   Cani, AK
   Liu, CJ
   Zhai, YL
   Zhang, YJ
   Weizer, AZ
   Mehra, R
   Feng, FY
   Alva, AS
   Morgan, TM
   Montgomery, JS
   Siddiqui, J
   Sadis, S
   Bandla, S
   Williams, PD
   Cho, KR
   Rhodes, DR
   Tomlins, SA
AF McDaniel, Andrew S.
   Hovelson, Daniel H.
   Cani, Andi K.
   Liu, Chia-Jen
   Zhai, Yali
   Zhang, Yajia
   Weizer, Alon Z.
   Mehra, Rohit
   Feng, Felix Y.
   Alva, Ajjai S.
   Morgan, Todd M.
   Montgomery, Jeffrey S.
   Siddiqui, Javed
   Sadis, Seth
   Bandla, Santhoshi
   Williams, Paul D.
   Cho, Kathleen R.
   Rhodes, Daniel R.
   Tomlins, Scott A.
TI Genomic Profiling of Penile Squamous Cell Carcinoma Reveals New
   Opportunities for Targeted Therapy
SO CANCER RESEARCH
LA English
DT Article
ID HUMAN-PAPILLOMAVIRUS; P16(INK4A) EXPRESSION; COLORECTAL-CANCER; EXTENDED
   RAS; PROGNOSIS; SURVIVAL; METASTASIS; MANAGEMENT; MARKER
AB Penile squamous cell carcinoma (PeSCCA) is a rare malignancy for which there are limited treatment options due to a poor understanding of the molecular alterations underlying disease development and progression. Therefore, we performed comprehensive, targeted next-generation sequencing to identify relevant somatic genomic alterations in a retrospective cohort of 60 fixed tumor samples from 43 PeSCCA cases (including 14 matched primary/metastasis pairs). We identified a median of two relevant somatic mutations and one high-level copy-number alteration per sample (range, 0-5 and 0-6, respectively). Expression of HPV and p16 was detectable in 12% and 28% of patients, respectively. Furthermore, advanced clinical stage, lack of p16 expression, and MYC and CCND1 amplifications were significantly associated with shorter time to progression or PeSCCA-specific survival. Notably, four cases harbored EGFR amplifications and one demonstrated CDK4 amplification, genes for which approved and investigational targeted therapies are available. Importantly, although paired primary tumors and lymph node metastases were largely homogeneous for relevant somatic mutations, we identified heterogeneous EGFR amplification in primary tumor/lymph node metastases in 4 of 14 cases, despite uniform EGFR protein overexpression. Likewise, activating HRAS mutations occurred in 8 of 43 cases. Taken together, we provide the first comprehensive molecular PeSCCA analysis, which offers new insight into potential precision medicine approaches for this disease, including strategies targeting EGFR. (C) 2015 AACR.
C1 [McDaniel, Andrew S.; Cani, Andi K.; Liu, Chia-Jen; Zhai, Yali; Zhang, Yajia; Mehra, Rohit; Siddiqui, Javed; Cho, Kathleen R.; Rhodes, Daniel R.; Tomlins, Scott A.] Univ Michigan, Dept Pathol, Michigan Ctr Translat Pathol, Ann Arbor, MI 48109 USA.
   [Hovelson, Daniel H.] Univ Michigan, Computat Med & Bioinformat, Ann Arbor, MI 48109 USA.
   [Weizer, Alon Z.; Morgan, Todd M.; Montgomery, Jeffrey S.; Tomlins, Scott A.] Univ Michigan, Dept Urol, Ann Arbor, MI 48109 USA.
   [Feng, Felix Y.] Univ Michigan, Dept Radiat Oncol, Ann Arbor, MI 48109 USA.
   [Feng, Felix Y.; Cho, Kathleen R.; Tomlins, Scott A.] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
   [Alva, Ajjai S.] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
   [Sadis, Seth; Bandla, Santhoshi; Williams, Paul D.; Rhodes, Daniel R.] Thermo Fisher Sci, Ann Arbor, MI USA.
C3 University of Michigan System; University of Michigan; University of
   Michigan System; University of Michigan; University of Michigan System;
   University of Michigan; University of Michigan System; University of
   Michigan; University of Michigan System; University of Michigan;
   University of Michigan System; University of Michigan; Thermo Fisher
   Scientific
RP Tomlins, SA (corresponding author), Univ Michigan, Sch Med, 1524 BSRB,109 Zina Pitcher Pl, Ann Arbor, MI 48109 USA.
EM tomlinss@umich.edu
RI Yuanlei, Zhang/AGW-9772-2022; Hovelson, Daniel/JZT-9344-2024; Morgan,
   Todd/A-8531-2012; Cani, Andi/JED-6816-2023
OI Cho, Kathleen/0000-0003-0500-9998; Hovelson, Daniel/0000-0003-1881-4451;
   Morgan, Todd/0000-0002-1140-0603
FU A. Alfred Taubman Medical Research Institute
FX F.Y. Feng, T.M. Morgan, and S.A. Tomlins are supported by the A. Alfred
   Taubman Medical Research Institute.
CR [Anonymous], BJU INT
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NR 28
TC 91
Z9 96
U1 1
U2 9
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 DEC 15
PY 2015
VL 75
IS 24
BP 5219
EP 5227
DI 10.1158/0008-5472.CAN-15-1004
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DA1JL
UT WOS:000367552000008
PM 26670561
OA Green Submitted, Bronze
DA 2025-01-04
ER

PT J
AU Zhao, T
   Su, ZP
   Li, YC
   Zhang, XR
   You, Q
AF Zhao, Ting
   Su, Zhongping
   Li, Yingchang
   Zhang, Xiaoren
   You, Qiang
TI Chitinase-3 like-protein-1 function and its role in diseases
SO SIGNAL TRANSDUCTION AND TARGETED THERAPY
LA English
DT Review
ID HUMAN CARTILAGE GLYCOPROTEIN-39; SERUM YKL-40 LEVEL; COLONIC
   EPITHELIAL-CELLS; INDEPENDENT PROGNOSTIC BIOMARKER; CEREBROSPINAL-FLUID
   BIOMARKERS; PERIPHERAL ARTERIAL-DISEASE; SMOOTH-MUSCLE-CELLS;
   NF-KAPPA-B; 3-LIKE 1; RHEUMATOID-ARTHRITIS
AB Non-enzymatic chitinase-3 like-protein-1 (CHI3L1) belongs to glycoside hydrolase family 18. It binds to chitin, heparin, and hyaluronic acid, and is regulated by extracellular matrix changes, cytokines, growth factors, drugs, and stress. CHI3L1 is synthesized and secreted by a multitude of cells including macrophages, neutrophils, synoviocytes, chondrocytes, fibroblast-like cells, smooth muscle cells, and tumor cells. It plays a major role in tissue injury, inflammation, tissue repair, and remodeling responses. CHI3L1 has been strongly associated with diseases including asthma, arthritis, sepsis, diabetes, liver fibrosis, and coronary artery disease. Moreover, following its initial identification in the culture supernatant of the MG63 osteosarcoma cell line, CHI3L1 has been shown to be overexpressed in a wealth of both human cancers and animal tumor models. To date, interleukin-13 receptor subunit alpha-2, transmembrane protein 219, galectin-3, chemo-attractant receptor-homologous 2, and CD44 have been identified as CHI3L1 receptors. CHI3L1 signaling plays a critical role in cancer cell growth, proliferation, invasion, metastasis, angiogenesis, activation of tumor-associated macrophages, and Th2 polarization of CD4(+) T cells. Interestingly, CHI3L1-based targeted therapy has been increasingly applied to the treatment of tumors including glioma and colon cancer as well as rheumatoid arthritis. This review summarizes the potential roles and mechanisms of CHI3L1 in oncogenesis and disease pathogenesis, then posits investigational strategies for targeted therapies.
C1 [Zhao, Ting; Li, Yingchang; Zhang, Xiaoren; You, Qiang] Guangzhou Med Univ, Affiliated Canc Hosp & Inst, Guangzhou, Peoples R China.
   [Su, Zhongping; You, Qiang] Nanjing Med Univ, Dept Biotherapy, Dept Geriatr, Affiliated Hosp 2, Nanjing, Peoples R China.
   [Li, Yingchang; Zhang, Xiaoren; You, Qiang] Guangzhou Med Univ, Key Lab Cell Homeostasis & Canc Res, Guangdong Higher Educ Inst, Guangzhou, Peoples R China.
C3 Guangzhou Medical University; Nanjing Medical University; Guangzhou
   Medical University
RP You, Q (corresponding author), Guangzhou Med Univ, Affiliated Canc Hosp & Inst, Guangzhou, Peoples R China.; You, Q (corresponding author), Nanjing Med Univ, Dept Biotherapy, Dept Geriatr, Affiliated Hosp 2, Nanjing, Peoples R China.; You, Q (corresponding author), Guangzhou Med Univ, Key Lab Cell Homeostasis & Canc Res, Guangdong Higher Educ Inst, Guangzhou, Peoples R China.
EM qiang.you@live.com
RI zhao, ting/GYJ-2179-2022
OI You, Qiang/0000-0003-3308-4127
FU Guangzhou key medical discipline construction project; National Natural
   Science Foundation of China [81671543, 81870409]
FX This study was supported by Guangzhou key medical discipline
   construction project and the National Natural Science Foundation of
   China (grant numbers 81671543, 81870409 to Q.Y.).
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NR 300
TC 267
Z9 278
U1 9
U2 65
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 SEP 14
PY 2020
VL 5
IS 1
AR 201
DI 10.1038/s41392-020-00303-7
PG 20
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA NS6OQ
UT WOS:000572378800004
PM 32929074
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Yalcin, GS
   Gonultas, MA
   Hucumenoglu, S
   Simsek, G
   Pekcici, MR
AF Yalcin, Gulsum S.
   Gonultas, Mehmet A.
   Hucumenoglu, Sema
   Simsek, Gulcin
   Pekcici, Mevlut R.
TI SATB1 Expression of Colorectal Adenomatous Polyps is Higher than that of
   Colorectal Carcinomas
SO APPLIED IMMUNOHISTOCHEMISTRY & MOLECULAR MORPHOLOGY
LA English
DT Article
DE SATB1; colorectal carcinoma; colorectal adenomatous polyp
ID BINDING-PROTEIN; CANCER; METASTASIS; REGULATOR; GROWTH; GENES
AB "Special AT-rich sequence-binding protein-1" (SATB1) is a global genome organizer and is found to have effects on carcinogenesis and progression of various malignancies including colorectal carcinoma (CRC). We aimed to investigate the expression of SATB1 in CRC and colorectal adenomatous polyps (CAP), the correlation between clinicopathologic parameters, and overall survival. We examined 227 CRCs and 129 CAPs. SATB1 protein expression was evaluated by immunohistochemistry. We found higher SATB1 expression in adenomatous epithelium than in CRC tissues (55.0% vs. 42.7%, respectively) (P<0.05). None of the adjacent normal colorectal mucosa stained positive in CRC cases, and only one of the adjacent normal mucosa of the CAP cases was positive. SATB1 expression of left-sided CRC was higher than that of right-sided CRC (46.3% vs. 28.6%, respectively) (P<0.05), and SATB1 expression of conventional adenocarcinomas was higher than that of mucinous carcinomas (45.5% vs. 6.3%, respectively) (P<0.05). SATB1 expression was higher in CAPs consisting of high-grade dysplasia than in polyps with low-grade dysplasia (77.8% vs. 51.4%) (P<0.05). SATB1 expression did not correlate with patients' overall survival. In conclusion, due to the higher expression of SATB1 in CAP than in CRC, we think SATB1 may have a role in the early stages of carcinogenesis of CRCs. This is the first study investigating SATB1 expression in CAPs. Besides this is the first report that shows different SATB1 expressions in conventional colorectal adenocarcinoma and mucinous carcinoma, and also in right-sided and left-sided CRC. Our results, with supporting new studies, can provide SATB1 as a possible candidate for targeted therapy for CRC patients.
C1 [Yalcin, Gulsum S.; Simsek, Gulcin] Univ Hlth Sci, Kecioren Training & Res Hosp, Dept Pathol, Ankara, Turkey.
   [Gonultas, Mehmet A.; Hucumenoglu, Sema] Univ Hlth Sci, Ankara Training & Res Hosp, Dept Pathol, Ankara, Turkey.
   [Pekcici, Mevlut R.] Univ Hlth Sci, Ankara Training & Res Hosp, Dept Gen Surg, Ankara, Turkey.
C3 Ankara Kecioren Training & Research Hospital; University of Health
   Sciences Turkey; University of Health Sciences Turkey; Ankara Training &
   Research Hospital; Ankara Training & Research Hospital; University of
   Health Sciences Turkey
RP Yalcin, GS (corresponding author), Univ Hlth Sci, Kecioren Educ & Res Hosp, Dept Pathol, Sanatoryum Ave,25 Ardahan St, TR-06280 Ankara, Turkey.
EM drgsu@hotmail.com
RI simsek, gulcin/HJZ-1520-2023; gönültaş, mehmet/HKW-2330-2023; Yalçın,
   Gülsüm/AAE-5837-2020
OI Yalcin, Gulsum Seyma/0000-0002-1944-2955
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NR 27
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 1541-2016
EI 1533-4058
J9 APPL IMMUNOHISTO M M
JI Appl. Immunohistochem.
PD AUG
PY 2020
VL 28
IS 7
BP 532
EP 537
DI 10.1097/PAI.0000000000000791
PG 6
WC Anatomy & Morphology; Medical Laboratory Technology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Anatomy & Morphology; Medical Laboratory Technology; Pathology
GA NP5SF
UT WOS:000570235200012
PM 31290787
DA 2025-01-04
ER

PT J
AU Hess, LM
   Brnabic, A
   Mason, O
   Lee, P
   Barker, S
AF Hess, Lisa M.
   Brnabic, Alan
   Mason, Oksana
   Lee, Pablo
   Barker, Scott
TI Relationship between Progression-free Survival and Overall Survival in
   Randomized Clinical Trials of Targeted and Biologic Agents in Oncology
SO JOURNAL OF CANCER
LA English
DT Review
DE biologic therapy; overall survival; post-progression survival; disease
   progression; oncology
ID CELL LUNG-CANCER; PHASE-III TRIAL; METASTATIC COLORECTAL-CANCER;
   SOFT-TISSUE SARCOMA; VANDETANIB PLUS GEMCITABINE; BILIARY-TRACT CANCER;
   OPEN-LABEL; DOUBLE-BLIND; 1ST-LINE TREATMENT; GASTROESOPHAGEAL JUNCTION
AB Introduction: With a gap in a full understanding of the mechanisms by which survival is extended for patients with cancer who are treated with novel biologic and targeted agents, there is the risk that discordant progression-free and overall survival outcomes are observed due to poor clinical trial design or biases in the interpretation of data. This study was designed to examine the role of study quality and design on the outcomes observed with biologic and targeted agents.
   Methods: A review of studies in clinicaltrials.gov supplemented with a literature review in OVID Medline was conducted to identify all randomized trials of a biologic/targeted agent versus a non-biologic/targeted comparator in oncology that report both median overall and progression-free survival outcomes. Details of the study, design, population, drugs, and outcomes were extracted. Study quality was evaluated using the PEDro scale. Data were summarized using SPSS 22.0.0.0.
   Results: A total of 192 unique studies of 206 pairwise comparisons between a biologic/targeted and comparator were identified. The average absolute magnitude of post-progression survival (difference between OS and PFS) was 9.7 months for biologic/targeted therapy and 9.8 for the comparator. A total of 64 comparisons (31.1%) showed an increase in OS and decrease in PFS, or vice versa, and 25 (12.1%) showed a magnitude of more than 4 months difference between the delta of OS and delta of PFS between the biologic/targeted and comparator arms. Average study quality was high overall (7.7/10), and was comparable for studies with directional differences (7.2/10) as well as for those with the greatest magnitude in post-progression survival (7.4/10).
   Conclusion: This review and analysis specifically examined small PFS benefit with large OS benefit as well as small OS benefit with large PFS benefit, including differences in direction of PFS and OS outcomes. No evidence was identified that these are the result of poor study design, but may rather be due to the mechanism of action, specific disease, and population under study. Further work is needed to understand the mechanism of action of novel biologic/targeted agents to better understand their interaction with the tumor microenvironment.
C1 [Hess, Lisa M.; Mason, Oksana; Lee, Pablo; Barker, Scott] Eli Lilly & Co, Indianapolis, IN 46285 USA.
   [Brnabic, Alan] Eli Lilly & Co, Sydney, NSW, Australia.
C3 Eli Lilly; Eli Lilly
RP Hess, LM (corresponding author), Eli Lilly & Co, Indianapolis, IN 46285 USA.
EM Hess_lisa_m@lilly.com
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NR 84
TC 59
Z9 65
U1 0
U2 2
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 2019
VL 10
IS 16
BP 3717
EP 3727
DI 10.7150/jca.32205
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IC9AH
UT WOS:000471273000015
PM 31333789
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Lin, JZ
   Sun, H
   Zhang, WL
   Hong, ZG
   Lu, ZH
   Pan, ZZ
   Hou, ZL
   Peng, JH
AF Lin, Junzhong
   Sun, Hui
   Zhang, Weili
   Hong, Zhigang
   Lu, Zhenhai
   Pan, Zhizhong
   Hou, Zhenlin
   Peng, Jianhong
TI Conversion therapy with the intent to perform radical local treatment
   may not be suitable for patients with 10 or more liver metastases from
   colorectal cancer
SO CANCER MEDICINE
LA English
DT Article
ID LONG-TERM OUTCOMES; PREOPERATIVE CHEMOTHERAPY; COLON-CANCER;
   FLUOROURACIL; LEUCOVORIN; IRINOTECAN; CONSENSUS; RESECTION; SURGERY
AB Background The number of colorectal cancer liver metastases (CRLMs) is usually considered a contradictory indicator to surgical resection. However, some patients with initially unresectable CRLMs can receive radical local treatment after conversion therapy. This study aimed to evaluate the effect of radical local treatment after conversion therapy and the prognosis of patients with more than 10 initially unresectable CRLMs. Methods Data for a total of 229 patients with initially unresectable CRLMs were retrospectively reviewed between December 2012 and January 2020. Among these patients, 107 had >= 10 CRLMs, and 122 had <10 CRLMs. Overall survival (OS) and progression-free survival (PFS) were used to reflect the prognosis of different groups of patients. Conversion therapy was defined as an initially unresectable liver metastasis converted into an R0 resectable lesion after systemic chemotherapy. Radical local treatment included hepatectomy and radiofrequency ablation (RFA). Results Patients with >= 10 CRLMs had a lower conversion rate (42.7% vs. 56.6%, p = 0.001). Baseline clinical N stage 1-2, >= 8 first-line chemotherapy courses, and stable disease (SD) according to the Response Evaluation Criteria in Solid Tumours (RECIST) were independent factors predictive of conversion failure. Primary tumour location in the right colon, RECIST response of SD, and the absence of targeted therapy were independent factors predictive of unfavourable OS. The survival curves revealed that the OS of patients with or without conversion could be distinguished only among patients with <10 CRLMs (89.9% [95% CI, 82.5%-98.0%] vs. 58.9% [95% CI, 45.2%-76.7%], p < 0.001); this cut-off point could also distinguish patients with a successful conversion outcome according to OS (89.9% [95% CI, 82.5-98.0%] vs. 58.2% [95% CI, 42.2-80.4%], p = 0.008). Conclusion For CRLMs >= 10, patients with a successful conversion outcome cannot be distinguished from those without successful conversion outcome according to OS. Thus, conversion therapy with the intent to perform radical local treatment may not be suitable for patients with 10 or more liver metastases from colorectal cancer.
C1 [Lin, Junzhong; Zhang, Weili; Hong, Zhigang; Lu, Zhenhai; Pan, Zhizhong; Hou, Zhenlin; Peng, Jianhong] Sun Yat Sen Univ Canc Ctr, Dept Colorectal Surg, 651 Dongfeng Rd East, Guangzhou 510060, Guangdong, Peoples R China.
   [Lin, Junzhong; Zhang, Weili; Hong, Zhigang; Lu, Zhenhai; Pan, Zhizhong; Hou, Zhenlin; Peng, Jianhong] Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Guangzhou, Peoples R China.
   [Sun, Hui] Sun Yat Sen Univ, Zhongshan Sch Med, Guangzhou, Peoples R China.
C3 Sun Yat Sen University; State Key Lab Oncology South China; Sun Yat Sen
   University
RP Hou, ZL; Peng, JH (corresponding author), Sun Yat Sen Univ Canc Ctr, Dept Colorectal Surg, 651 Dongfeng Rd East, Guangzhou 510060, Guangdong, Peoples R China.
EM houzl@sysucc.org.cn; pengjh@sysucc.org.cn
OI Zhang, Weili/0000-0003-4703-3486; Peng, Jianhong/0000-0002-0769-8195
FU National Natural Science Foundation of China [82003051, 82072606]
FX This study was funded by grants from the National Natural Science
   Foundation of China (no. 82003051 and no. 82072606).
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NR 26
TC 1
Z9 1
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD NOV
PY 2022
VL 11
IS 22
BP 4225
EP 4235
DI 10.1002/cam4.4775
EA APR 2022
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 6L5ME
UT WOS:000786538200001
PM 35466587
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Brunello, A
   Galiano, A
   Finotto, S
   Monfardini, S
   Colloca, G
   Balducci, L
   Zagonel, V
AF Brunello, Antonella
   Galiano, Antonella
   Finotto, Silvia
   Monfardini, Silvio
   Colloca, Giuseppe
   Balducci, Lodovico
   Zagonel, Vittorina
TI Older cancer patients and COVID-19 outbreak: Practical considerations
   and recommendations
SO CANCER MEDICINE
LA English
DT Review
DE cancer; chemotherapy; COVID-19; elderly; guidelines; management;
   treatment
ID CELL LUNG-CANCER; COMPREHENSIVE GERIATRIC ASSESSMENT; MULTIDIMENSIONAL
   PROGNOSTIC INDEX; INTEGRATED PALLIATIVE CARE; ADVANCED
   COLORECTAL-CANCER; BREAST-CONSERVING SURGERY; TARGETED THERAPY; ADJUVANT
   CHEMOTHERAPY; CLINICAL ONCOLOGY; AMERICAN SOCIETY
AB Since the COVID-19 outbreak started, it has been affecting mainly older individuals. Among the most vulnerable older individuals are those with cancer. Many published guidelines and consensus papers deal with prioritizing cancer care. Given the lack of high-quality evidence for management of cancer in older patients also in normal times, it is even more stringent to provide some resources on how to avoid both undertreatment and overtreatment in this population, who as of now is twice challenged to death, due to both a greater risk of getting infected with COVID-19 as well as from cancer not adequately addressed and treated. We hereby discuss some general recommendations (implement triage procedures; perform geriatric assessment; carefully assess comorbidity; promote early integration of palliative care in oncology; acknowledge the role of caregivers; maintain active take in charge to avoid feeling of abandonment; mandate seasonal flu vaccination) and discuss practical suggestions for specific disease settings (early-stage and advanced-stage disease for solid tumors, and hematological malignancies). The manuscript provides resources on how to avoid both undertreatment and overtreatment in older patients with cancer, who as of now is twice challenged to death, due to both a greater risk of getting infected with COVID-19 as well as from cancer not adequately addressed and treated.
C1 [Brunello, Antonella; Galiano, Antonella; Finotto, Silvia; Zagonel, Vittorina] Ist Oncol Veneto IOV IRCCS, Dept Oncol, Oncol 1 Unit, Via Gattamelata 64, I-35128 Padua, Italy.
   [Monfardini, Silvio] Ist Palazzolo Fdn Don Gnocchi, Milan, Italy.
   [Colloca, Giuseppe] Univ Cattolica Sacro Cuore, Fdn Policlin A Gemelli IRCCS, Ist Radiol, Dipartimento Diagnost Immagini Radioterapia Oncol, Rome, Italy.
   [Balducci, Lodovico] Univ S Florida, Coll Med, Moffitt Canc Ctr, Tampa, FL 33620 USA.
C3 IRCCS Istituto Oncologico Veneto (IOV); Catholic University of the
   Sacred Heart; IRCCS Policlinico Gemelli; H Lee Moffitt Cancer Center &
   Research Institute; State University System of Florida; University of
   South Florida
RP Brunello, A (corresponding author), Ist Oncol Veneto IOV IRCCS, Dept Oncol, Oncol 1 Unit, Via Gattamelata 64, I-35128 Padua, Italy.
EM antonella.brunello@iov.veneto.it
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   Giuseppe/0000-0001-6763-0793
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NR 83
TC 15
Z9 16
U1 0
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD DEC
PY 2020
VL 9
IS 24
BP 9193
EP 9204
DI 10.1002/cam4.3517
EA NOV 2020
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PM5KW
UT WOS:000590869600001
PM 33219746
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU He, Q
   Xu, Q
   Wu, W
   Chen, L
   Sun, WJ
   Ying, JE
AF He, Qiong
   Xu, Qi
   Wu, Wei
   Chen, Lei
   Sun, Weijing
   Ying, Jieer
TI Comparison of <i>KRAS</i> and <i>PIK3CA</i> gene status between primary
   tumors and paired metastases in colorectal cancer
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE KRAS; PIK3CA; colorectal cancer; primary tumor; metastatic site
ID MUTATIONS; CETUXIMAB; HETEROGENEITY; CONCORDANCE; EVOLUTION; BENEFIT;
   BRAF
AB Purpose: In metastatic or recurrent colorectal cancer (MRCRC), the concordance of Kirsten rat sarcoma viral oncogene homolog (KRAS) and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) mutation status between the primary tumors and metastases is still controversial. The purpose of this study was to evaluate the association between KRAS and PIK3CA mutational status and various clinicopathologic features, and compare their genotype in primary tumors with that of the paired metastatic tumors.
   Method: We compared the mutation status of KRAS and PIK3CA between the primary tumors and the paired metastases of 59 MRCRC patients with available tissues (resection or biopsy). The presence of KRAS and PIK3CA mutations were determined by direct sequencing analysis.
   Results: Seventeen patients (28.8%) had the KRAS mutation and 46 patients (80.0%) had the PIK3CA mutation when considering both the primary and metastatic sites. KRAS mutation was observed in ten primary tumors and eleven related metastases (16.9% vs 18.6%), while PIK3CA mutation was found in 26 primary tumors and 32 related metastases (44.1% vs 54.2%). KRAS status was concordant between primary and metastatic sites in 45 patients (76.3%, kappa = 0.157), while the concordance of PIK3CA status was only found in 25 patients (42.4%, kappa =-0.141). The PIK3CA status discordance rate was significantly higher in 40 patients undergoing metachronous resection of primary tumor or metastasis, compared with that in 19 patients with synchronous resection of primary tumor or metastasis (67.5% [27/40] vs 36.8% [7/19]; P= 0.026).
   Conclusion: Our results demonstrate that low concordance of KRAS and high discordance of PIK3CA mutational status exist between the primary tumors and paired metastasis, and these findings remind us to have second thoughts about the need to evaluate metastatic tumors separately rather than only based on the primary tumor data when targeted therapy is considered.
C1 [He, Qiong; Xu, Qi; Wu, Wei; Chen, Lei; Ying, Jieer] Zhejiang Canc Hosp, Dept Chemotherapy, 38 Guangji Rd, Hangzhou 310022, Zhejiang, Peoples R China.
   [Sun, Weijing] Univ Pittsburgh, Sch Med, Dept Gastrointestinal Med Oncol, 1218 Scaife Hall,3550 Terrace St, Pittsburgh, PA 15261 USA.
C3 Zhejiang Cancer Hospital; Pennsylvania Commonwealth System of Higher
   Education (PCSHE); University of Pittsburgh
RP Ying, JE (corresponding author), Zhejiang Canc Hosp, Dept Chemotherapy, 38 Guangji Rd, Hangzhou 310022, Zhejiang, Peoples R China.; Sun, WJ (corresponding author), Univ Pittsburgh, Sch Med, Dept Gastrointestinal Med Oncol, 1218 Scaife Hall,3550 Terrace St, Pittsburgh, PA 15261 USA.
EM sunw@upmc.edu; jieerying@aliyun.com
RI XU, Qi/KIC-2811-2024
FU Natural Science Foundation of Zhejiang Province [LY14H160008]
FX This work was supported by Natural Science Foundation of Zhejiang
   Province (No LY14H160008).
CR Baas JM, 2011, ONCOLOGIST, V16, P1239, DOI 10.1634/theoncologist.2011-0024
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NR 24
TC 12
Z9 15
U1 0
U2 3
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 2329
EP 2335
DI 10.2147/OTT.S97668
PG 7
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA DJ8ZW
UT WOS:000374504500001
PM 27143928
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Norris, RP
   Dew, R
   Sharp, L
   Greystoke, A
   Rice, S
   Johnell, K
   Todd, A
AF Norris, Ruth P.
   Dew, Rosie
   Sharp, Linda
   Greystoke, Alastair
   Rice, Stephen
   Johnell, Kristina
   Todd, Adam
TI Are there socio-economic inequalities in utilization of predictive
   biomarker tests and biological and precision therapies for cancer? A
   systematic review and meta-analysis
SO BMC MEDICINE
LA English
DT Review
DE Precision medicine; Molecular targeted therapy; Immunotherapy;
   Biological therapy; Pharmacogenomic testing; Drug utilization;
   Socio-economic factors; Meta-analysis
ID TRASTUZUMAB-BASED CHEMOTHERAPY; METASTATIC BREAST-CANCER; ADJUVANT
   TRASTUZUMAB; OLDER PATIENTS; ELDERLY-PATIENTS; CARBOPLATIN-PACLITAXEL;
   PERSONALIZED MEDICINE; COLORECTAL-CANCER; MEDICARE PATIENTS; LUNG-CANCER
AB BackgroundNovel biological and precision therapies and their associated predictive biomarker tests offer opportunities for increased tumor response, reduced adverse effects, and improved survival. This systematic review determined if there are socio-economic inequalities in utilization of predictive biomarker tests and/or biological and precision cancer therapies.MethodsMEDLINE, Embase, Scopus, CINAHL, Web of Science, PubMed, and PsycINFO were searched for peer-reviewed studies, published in English between January 1998 and December 2019. Observational studies reporting utilization data for predictive biomarker tests and/or cancer biological and precision therapies by a measure of socio-economic status (SES) were eligible. Data was extracted from eligible studies. A modified ISPOR checklist for retrospective database studies was used to assess study quality. Meta-analyses were undertaken using a random-effects model, with sub-group analyses by cancer site and drug class. Unadjusted odds ratios (ORs) and 95% confidence intervals (CIs) were computed for each study. Pooled utilization ORs for low versus high socio-economic groups were calculated for test and therapy receipt.ResultsAmong 10,722 citations screened, 62 papers (58 studies; 8 test utilization studies, 37 therapy utilization studies, 3 studies on testing and therapy, 10 studies without denominator populations or which only reported mean socio-economic status) met the inclusion criteria. Studies reported on 7 cancers, 5 predictive biomarkers tests, and 11 biological and precision therapies. Thirty-eight studies (including 1,036,125 patients) were eligible for inclusion in meta-analyses. Low socio-economic status was associated with modestly lower predictive biomarker test utilization (OR 0.86, 95% CI 0.71-1.05; 10 studies) and significantly lower biological and precision therapy utilization (OR 0.83, 95% CI 0.75-0.91; 30 studies). Associations with therapy utilization were stronger in lung cancer (OR 0.71, 95% CI 0.51-1.00; 6 studies), than breast cancer (OR 0.93, 95% CI 0.78-1.10; 8 studies). The mean study quality score was 6.9/10.ConclusionsThese novel results indicate that there are socio-economic inequalities in predictive biomarker tests and biological and precision therapy utilization. This requires further investigation to prevent differences in outcomes due to inequalities in treatment with biological and precision therapies.
C1 [Norris, Ruth P.; Todd, Adam] Newcastle Univ, Sch Pharm, King George VI Bldg,Kings Rd, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
   [Norris, Ruth P.; Dew, Rosie; Sharp, Linda; Todd, Adam] Newcastle Univ, Ctr Canc, Populat Hlth Sci Inst, Newcastle Upon Tyne, Tyne & Wear, England.
   [Greystoke, Alastair] Newcastle Univ, Ctr Canc, Newcastle Upon Tyne, Tyne & Wear, England.
   [Rice, Stephen] Newcastle Univ, Populat Hlth Sci Inst, Hlth Econ Grp & Evidence Synth Team, Newcastle Upon Tyne, Tyne & Wear, England.
   [Johnell, Kristina] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
C3 Newcastle University - UK; Newcastle University - UK; Newcastle
   University - UK; Newcastle University - UK; Karolinska Institutet
RP Todd, A (corresponding author), Newcastle Univ, Sch Pharm, King George VI Bldg,Kings Rd, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.; Todd, A (corresponding author), Newcastle Univ, Ctr Canc, Populat Hlth Sci Inst, Newcastle Upon Tyne, Tyne & Wear, England.
EM adam.todd@newcastle.ac.uk
RI Rice, Stephen/LPQ-9019-2024
OI Rice, Stephen/0000-0002-6767-0813; Norris, Ruth/0000-0002-7015-8722;
   Todd, Adam/0000-0003-1496-9341
FU Barbour Foundation PhD Studentship
FX This work was funded by a Barbour Foundation PhD Studentship. The
   funding source had no role in the design and conduct of the study; the
   collection, management, analysis, and interpretation of the data; the
   preparation, review, or approval of the manuscript; and the decision to
   submit the manuscript for publication.
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NR 104
TC 39
Z9 40
U1 0
U2 4
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1741-7015
J9 BMC MED
JI BMC Med.
PD OCT 23
PY 2020
VL 18
IS 1
AR 282
DI 10.1186/s12916-020-01753-0
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA OP4CU
UT WOS:000588029200001
PM 33092592
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Sanz-Garcia, E
   Argiles, G
   Elez, E
   Tabernero, J
AF Sanz-Garcia, E.
   Argiles, G.
   Elez, E.
   Tabernero, J.
TI BRAF mutant colorectal cancer: prognosis, treatment, and new
   perspectives
SO ANNALS OF ONCOLOGY
LA English
DT Review
DE colorectal cancer; BRAF; targeted therapy; clinical trials; anti-EGFR
ID FOLFOXIRI PLUS BEVACIZUMAB; III COLON-CANCER; K-RAS MUTATIONS; KRAS
   WILD-TYPE; 1ST-LINE TREATMENT; MICROSATELLITE INSTABILITY;
   ACQUIRED-RESISTANCE; RANDOMIZED-TRIAL; MISMATCH REPAIR; POOLED ANALYSIS
AB The MAPK cascade plays a crucial role in tumor cell proliferation and survival. Accumulating evidence suggests that mutations in the BRAF oncogene are not only associated with poor prognosis but also linked with less benefit when treated with anti-epidermal growth factor receptor antibodies in metastatic colorectal cancer (mCRC). Targeting this molecular aberration has thus become a matter of particular interest in mCRC drug development. In contrast to other malignances such as BRAF mutant melanoma, efficacy observed with BRAF inhibitors in monotherapy in mCRC is poor. Several mechanisms of resistance have been identified leading to the development of different treatment strategies that have shown promising activity in early clinical trials. Hence, rational combination of targeted therapies is expected to further increase the efficacy of selective BRAF inhibitors. Herein, we discuss the main clinical and molecular characteristics of BRAF mutant colorectal cancer and its translation into the clinic, with a focus on developmental therapeutics and combination strategies. In addition, we contextualize the available data with potential future approaches that include the extended access to next-generation sequencing platforms and gene expression strategies for molecular subtyping. These approaches will facilitate the identification of certain patient profiles providing more therapeutic possibilities.
C1 [Sanz-Garcia, E.; Argiles, G.; Elez, E.; Tabernero, J.] Vall dHebron Univ Hosp, Dept Med Oncol, Barcelona, Spain.
   [Sanz-Garcia, E.; Argiles, G.; Elez, E.; Tabernero, J.] Vall dHebron Inst Oncol VHIO, Dept Med Oncol, Barcelona, Spain.
C3 Vall d'Hebron Institut d'Oncologia (VHIO); Hospital Universitari Vall
   d'Hebron; Vall d'Hebron Institut d'Oncologia (VHIO)
RP Tabernero, J (corresponding author), Vall dHebron Univ Hosp, Vall dHebron Inst Oncol VHIO, Dept Med Oncol, P Vall dHebron 119-129, Barcelona 08035, Spain.
EM jtabernero@vhio.net
RI Tabernero, Josep/AAG-5026-2019; Élez, Elena/AAH-2945-2019; Argiles,
   Guillem/KQU-7406-2024
OI Sanz Garcia, Enrique/0000-0002-3119-3832; Tabernero,
   Josep/0000-0002-2495-8139; Elez, Elena/0000-0002-4653-6324; Argiles,
   Guillem/0000-0002-1487-7108
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NR 80
TC 201
Z9 215
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 NOV
PY 2017
VL 28
IS 11
BP 2648
EP 2657
DI 10.1093/annonc/mdx401
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FL8IJ
UT WOS:000414493200005
OA Bronze
DA 2025-01-04
ER

PT J
AU Mitchell, AP
   Sanoff, HK
AF Mitchell, Aaron P.
   Sanoff, Hanna K.
TI Anti-EGFR and Anti-VEGF Agents in First-Line Therapy for Advanced
   Colorectal Cancer
SO CURRENT COLORECTAL CANCER REPORTS
LA English
DT Article
DE Colorectal cancer; Targeted therapy; Anti-VEGF; Anti-EGFR; Panitumumab;
   Cetuximab; Bevacizumab
ID FOLFIRI PLUS CETUXIMAB; GROWTH-FACTOR THERAPY; OPEN-LABEL; PHASE-III;
   BEVACIZUMAB; FLUOROURACIL; CHEMOTHERAPY; PANITUMUMAB; LEUCOVORIN;
   METAANALYSIS
AB Outcomes for metastatic colorectal cancer have improved progressively with the incorporation of new drugs into standard treatment regimens. Most recently, targeted therapies against VEGF and EGFR have improved upon the prior standard for first-line therapy with FOLFOX or FOLFIRI. As attempts to combine anti-VEGF and anti-EGFR drugs have been unsuccessful, it is necessary to choose between them when beginning first-line therapy. This review summarizes the existing literature to best inform this decision. To date, three head-to-head trials have compared anti-EGFR and anti-VEGF therapy in RAS wild-type patients: PEAK, FIRE-3, and CALGB/SWOG 80405. PEAK and FIRE-3 suggested a survival advantage for anti-EGFR therapy over anti-VEGF therapy, though CALGB/SWOG 80405 did not. Results have emerged recently to suggest that tumors arising from the right colon are resistant to anti-EGFR therapy, and that any advantage of anti-EGFR therapy over anti-VEGF therapy may be limited to left-sided tumors.
C1 [Mitchell, Aaron P.; Sanoff, Hanna K.] Univ N Carolina, Dept Med, Div Hematol Oncol, 3rd Floor,Phys Off Bldg,170 Manning Dr, Chapel Hill, NC 27599 USA.
C3 University of North Carolina; University of North Carolina Chapel Hill
RP Sanoff, HK (corresponding author), Univ N Carolina, Dept Med, Div Hematol Oncol, 3rd Floor,Phys Off Bldg,170 Manning Dr, Chapel Hill, NC 27599 USA.
EM hanna_sanoff@med.unc.edu
OI Mitchell, Aaron/0000-0003-3639-3515
FU Bayer; Novartis; Merck; Precision Biologics; Immunomedics
FX Aaron P. Mitchell declares that he has no conflict of interest. Hanna K.
   Sanoff has received research support through grants from Bayer,
   Novartis, Merck, Precision Biologics, and Immunomedics.
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NR 30
TC 1
Z9 1
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1556-3790
EI 1556-3804
J9 CURR COLORECT CANC R
JI Curr. Colorectal Cancer Rep.
PD JUN
PY 2017
VL 13
IS 3
BP 257
EP 263
DI 10.1007/s11888-017-0372-7
PG 7
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA EY9BY
UT WOS:000404295300010
DA 2025-01-04
ER

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   Soliman, Ghada
   Saleh, Amany A.
TI Long Non-Coding RNAs ASB16-AS1 and AFAP1-AS1: Diagnostic, Prognostic
   Impact and Survival Analysis in Colorectal Cancer
SO APPLICATION OF CLINICAL GENETICS
LA English
DT Article
DE CRC; expression; lncRNA; overall survival; progression-free survival
ID HEPATOCELLULAR-CARCINOMA; LNCRNA AFAP1-AS1; TUMORIGENESIS; EPIDEMIOLOGY;
   EXPRESSION; GROWTH
AB Background: We aimed to evaluate the diagnostic roles of AFAP1-AS1 and ASB16-AS1 in colorectal cancer and highlight their roles in predicting colorectal cancer patients' prognosis.Methods: In this case-control study, 146 participants were involved. Group I included 47 patients with CRC. Group II composed of 49 patients with benign lesions in the colon, and Group III included 50 apparently normal subjects of coincided age and gender as controls. All participants were subjected to clinical and endoscopic evaluations, CA19-9, CEA, and quantification of relative expression of lncRNAs ASB16-AS1 and AFAP1-AS1.Results: CRC patients had significantly elevated expression levels of both lncRNAs in tissue and plasma samples versus benign and control groups (p < 0.001). Despite the higher sensitivity of tissue samples results, the relative expression of both lncRNAs in plasma samples was very encouraging in the discrimination between patients with CRC versus control and benign groups. Furthermore, both lncRNAs could discriminate patients with early-stage CRC (stage I&II) from being colonic lesion and control groups with better sensitivity and specificity presented by ASB16-AS1 in tissue and plasma than results detailed by AFAP1-AS1. High expression levels of ASB16-AS1 in tissue and plasma and tissue lncRNA AFAP1-AS1 are significantly correlated with decreased overall survival (p < 0.001) and reduced progression-free (p < 0.001) compared to low expression in CRC patients.Conclusion: We propose the utilization of lncRNA ASB16-AS1 and lncRNA AFAP1-AS1 as biomarkers in diagnosis and prognosis estimation for CRC patients. Moreover, their value in early CRC patients may affect the assortment of target therapy and treatment protocols.
C1 [Elabd, Naglaa S.; Elhamouly, Moamena S.] Menoufia Univ, Fac Med, Trop Med Dept, Menoufia, Egypt.
   [Soliman, Shimaa E.; Saleh, Amany A.] Menoufia Univ, Fac Med, Med Biochem & Mol Biol Dept, Menoufia, Egypt.
   [Gohar, Suzy F.; Soliman, Ghada] Menoufia Univ, Fac Med, Clin Oncol Dept, Menoufia, Egypt.
   [Elgamal, Ayman] Menoufia Univ, Fac Med, Trop Med Dept, Menoufia, Egypt.
   [Alabassy, Mahmoud Magdy; Soliman, Haitham A.] Menoufia Univ, Fac Med, Gen Med Dept, Menoufia, Egypt.
   [Gadallah, Abdelnaser A.] Menoufia Univ, Fac Med, Internal Med Dept, Menoufia, Egypt.
   [Elbahr, Osama D.] Menoufia Univ, Natl Liver Inst, Hepatol & Gastroenterol Dept, Menoufia, Egypt.
   [Elabd, Naglaa S.] Menoufia Univ Egypt, Fac Med, Trop Med, Cairo, Egypt.
C3 Egyptian Knowledge Bank (EKB); Menofia University; Egyptian Knowledge
   Bank (EKB); Menofia University; Egyptian Knowledge Bank (EKB); Menofia
   University; Egyptian Knowledge Bank (EKB); Menofia University; Egyptian
   Knowledge Bank (EKB); Menofia University; Egyptian Knowledge Bank (EKB);
   Menofia University; Egyptian Knowledge Bank (EKB); Menofia University;
   Egyptian Knowledge Bank (EKB); Menofia University
RP Elabd, NS (corresponding author), Menoufia Univ Egypt, Fac Med, Trop Med, Cairo, Egypt.
EM naglaa_elabd@yahoo.com
RI Soliman, Shimaa/AAJ-7216-2021; Elbahr, Osama/AAO-9459-2021; Abassy,
   Mahmoud/ABS-6990-2022; Gohar, Suzy/AAA-8004-2021; Saleh,
   Amany/AAP-9743-2020
OI Elabd, Naglaa/0000-0001-8786-0190; El-Hamouly,
   Moamena/0000-0002-2018-042X; Gohar, Suzy/0000-0003-3250-5954; ,
   shimaa/0000-0003-3919-3818; Elbahr, Osama/0000-0001-6902-8982; Saleh,
   Amany/0000-0003-0182-3343
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NR 42
TC 5
Z9 5
U1 0
U2 3
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
EI 1178-704X
J9 APPL CLIN GENET
JI Appl. Clin. Genet.
PY 2022
VL 15
BP 97
EP 109
DI 10.2147/TACG.S370242
PG 13
WC Genetics & Heredity
WE Emerging Sources Citation Index (ESCI)
SC Genetics & Heredity
GA 3X4XP
UT WOS:000843045900001
PM 35937710
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Pan, TM
   Liao, PY
AF Pan, Tung -Ming
   Liao, Pei-You
TI High sensitivity and rapid detection of KRAS and BRAF gene mutations in
   colorectal cancer using YbTixOy electrolyte-insulator-semiconductor
   biosensors
SO MATERIALS TODAY CHEMISTRY
LA English
DT Article
DE Available online xxx; Colorectal cancer (CRC); KRAS; BRAF; Gene
   mutation; Electrolyte-insulator-semiconductor (EIS); YbTi x O y
ID FIELD-EFFECT-TRANSISTOR; SENSING CHARACTERISTICS; DNA HYBRIDIZATION;
   EGFR THERAPY; HYSTERESIS; SURFACE; FET
AB The KRAS and BRAF genes are attractive for a predictive biomarker to determine whether the colorectal cancer (CRC) patient predicts response to anti-epidermal growth factor receptor treatment. The detection of KRAS and BRAF mutation statuses has to be considered as a diagnostic and prognostic factor for the treatment of metastatic CRC patients because the targeted therapy may be expensive as well as toxic. In this work, we develop an YbTixOy electrolyte-insulator-semiconductor (EIS) biosensor to detect the KRAS and BRAF gene mutations in CRC. X-ray diffraction, atomic force microscopy, X-ray photoelectron spectroscopy, and secondary ion mass spectrometry were used to explore the structural features of YbTixOy films prepared under three Ti plasma power conditions. We found that the YbTixOy-based EIS sensor fabricated at the 80 W condition exhibited a higher sensitivity of 69.54 mV/pH (in pH range 2 e12), a lower hysteresis voltage of 1 mV (in pH loop of 7->4->7->10->7), and a smaller drift rate of 0.15 mV/h (in pH 7) than those of the other Ti plasma power conditions. Furthermore, we successfully demonstrated that the single strain DNA probe-immobilized YbTixOy EIS biosensors functionalized with 3-aminopropyl triethoxysilane followed by glutaraldehyde were screened for the KRAS and BRAF gene mutations in CRC. High sensitivity and rapid detection of the YbTixOy-based EIS biosensor are expected to serve as the diagnostic tool for clinical examination and screening with CRC. (c) 2022 Elsevier Ltd. All rights reserved.
C1 [Pan, Tung -Ming; Liao, Pei-You] Chang Gung Univ, Dept Elect Engn, Taoyuan 33302, Taiwan.
   [Pan, Tung -Ming] Chang Gung Mem Hosp, Linkou Med Ctr, Div Urol, Taoyuan City 33305, Taiwan.
C3 Chang Gung University; Chang Gung Memorial Hospital
RP Pan, TM (corresponding author), Chang Gung Univ, Dept Elect Engn, Taoyuan 33302, Taiwan.; Pan, TM (corresponding author), Chang Gung Mem Hosp, Linkou Med Ctr, Div Urol, Taoyuan City 33305, Taiwan.
EM tmpan@mail.cgu.edu.tw
OI Pan, Tung-Ming/0000-0002-1013-2571
FU Ministry of Science and Technology of Taiwan [MOST-106-2221-E-182-063]
FX Acknowledgments The authors would like to thank the Ministry of Science
   and Technology of Taiwan for financially supporting this research under
   contract of MOST-106-2221-E-182-063.
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NR 47
TC 6
Z9 6
U1 3
U2 21
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 2468-5194
J9 MATER TODAY CHEM
JI Mater. Today Chem.
PD SEP
PY 2022
VL 25
AR 100979
DI 10.1016/j.mtchem.2022.100979
EA MAY 2022
PG 11
WC Chemistry, Multidisciplinary; Materials Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Materials Science
GA 2B5DM
UT WOS:000810208700006
DA 2025-01-04
ER

PT J
AU Yang, F
   Gong, LC
   Jin, H
   Pi, J
   Bai, HH
   Wang, H
   Cai, H
   Yang, PH
   Cai, JY
AF Yang, Fen
   Gong, Longcai
   Jin, Hua
   Pi, Jiang
   Bai, Haihua
   Wang, Hong
   Cai, Huaihong
   Yang, Peihui
   Cai, Jiye
TI Chrysin-organogermanium (IV) complex induced Colo205 cell
   apoptosis-associated mitochondrial function and anti-angiogenesis
SO SCANNING
LA English
DT Article
DE Chrysin; Chry-Ge; Colo205; laser scanning confocal microscope (LSCM);
   atomic force microscopy (AFM)
ID EMBRYO CHORIOALLANTOIC MEMBRANE; FLAVONOID-RICH FRACTION; CYCLE ARREST;
   IN-VITRO; TUMOR; ACTIVATION; GROWTH; PATHWAY; AGENT
AB Colorectal cancer, a kind of malignant cancer, has more than 1 million new patients and results in 0.5 million deaths every year globally based on the estimation of Globocan in 2008. One of the most important issues against colon cancer is tumor metastasis. Anti-angiogenesis, a form of targeted therapy uses drugs or other substances to prevent the new blood vessel formation, which is critical for tumor metastasis. In our previous studies, we have demonstrated a simple method to synthesize Chry-Ge complex through the reaction between chrysin and triphenylgermanium bromide. In this work, we investigated the mechanism of Chry-Ge induced Colo205 cell apoptosis. We found that Chry-Ge could induce apoptosis in Colo205 cells in mitochondrial-dependent pathway, cause the reorganization of cytoskeleton and induce the damage of nucleus in Colo205 cells. Besides, Chry-Ge was also found to induce membrane ultrastructural changes in Colo205 cells by AFM. Further, we found that Chry-Ge can inhibit tube formation of human umbilical vascular endothelial cell in vitro. Chry-Ge was also tested in vivo in the chicken chorioallantoic membrane (CAM) assay and found to inhibit bFGF-treated CAMs development. These results suggested that Chry-Ge could induce Colo205 cell apoptosis by mitochondrial pathway and anti-angiogenesis, highlighting the use of organic germanium agents for the treatment of colorectal cancer. SCANNING 37:246-257, 2015. (c) 2015 Wiley Periodicals, Inc.
C1 [Yang, Fen; Jin, Hua; Pi, Jiang; Bai, Haihua; Cai, Huaihong; Yang, Peihui; Cai, Jiye] Jinan Univ, Dept Chem, Guangzhou, Guangdong, Peoples R China.
   [Yang, Fen; Jin, Hua; Pi, Jiang; Cai, Jiye] Macau Univ Sci & Technol, State Key Lab Qual Res Chinese Med, Taipa, Macau, Peoples R China.
   [Gong, Longcai; Wang, Hong] Jinan Univ, Dept Bioengn, Guangdong Prov Key Lab Mol Immunol & Antibody Eng, Guangzhou, Guangdong, Peoples R China.
C3 Jinan University; Macau University of Science & Technology; Jinan
   University
RP Cai, JY (corresponding author), Jinan Univ, Dept Chem, Guangzhou, Guangdong, Peoples R China.
EM tjycai@jnu.edu.cn
RI Pi, Jiang/AAJ-7366-2021
OI pi, jiang/0000-0003-4418-1248; Cai, Jiye/0000-0002-4791-3320
FU National Natural Science Foundation of China [2010CB833603]; Overseas,
   Hong Kong, and Macao Scholars Collaborated Researching Fund [30828028]
FX Contract grant sponsor: National Natural Science Foundation of China;
   Contract grant number: 2010CB833603; Contract grant sponsor: Overseas,
   Hong Kong, and Macao Scholars Collaborated Researching Fund; Contract
   grant number: 30828028.
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NR 40
TC 10
Z9 10
U1 2
U2 35
PU WILEY-HINDAWI
PI LONDON
PA ADAM HOUSE, 3RD FL, 1 FITZROY SQ, LONDON, WIT 5HE, ENGLAND
SN 0161-0457
EI 1932-8745
J9 SCANNING
JI Scanning
PD JUL-AUG
PY 2015
VL 37
IS 4
BP 246
EP 257
DI 10.1002/sca.21205
PG 12
WC Instruments & Instrumentation; Microscopy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Instruments & Instrumentation; Microscopy
GA CO7VU
UT WOS:000359372000002
PM 25914235
DA 2025-01-04
ER

PT J
AU Carvalho, TGD
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   Soares, LAL
   Guedes, PMD
   Araújo, RFD Jr
AF Carvalho, Thais Gomes de
   Lara, Pablo
   Jorquera-Cordero, Carla
   Araga, Cicero Flavio Soares
   Oliveira, Artur de Santana
   Garcia, Vinicius Barreto
   Souza, Shirley Vitoria de Paiva
   Schomann, Timo
   Soares, Luiz Alberto Lira
   Guedes, Paulo Marcos da Matta
   Araujo Junior, Raimundo Fernandes de
TI Inhibition of murine colorectal cancer metastasis by targeting M2-TAM
   through STAT3/NF-kB/AKT signaling using macrophage 1-derived
   extracellular vesicles loaded with oxaliplatin, retinoic acid, and
   Libidibia ferrea
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE EVs; Macrophages 1; STAT3; AKT; NF; kappa B; Metastasis; Colorectal
   cancer
ID EXOSOMES; CELLS; THERAPY; POLARIZATION; DOXORUBICIN; PACLITAXEL;
   RESISTANCE; MODELS; BREAST; BRAIN
AB Colorectal cancer is still unmanageable despite advances in target therapy. However, extracellular vesicles (EVs) have shown potential in nanomedicine as drug delivery systems, especially for modulating the immune cells in the tumor microenvironment (TME). In this study, M1 Macrophage EVs (M1EVs) were used as nanocarriers of oxaliplatin (M1EV1) associated with retinoic acid (M1EV2) and Libidibia ferrea (M1EV3), alone or in combination (M1EV4) to evaluate their antiproliferative and immunomodulatory potential on CT-26 and MC-38 colorectal cancer cell lines and prevent metastasis in mice of allograft and peritoneal colorectal cancer models. Tumors were evaluated by qRT-PCR and immunohistochemistry. The cell death profile and epithelial-mesenchymal transition process (EMT) were analyzed in vitro in colorectal cancer cell lines. Polarization of murine macrophages (RAW264.7 cells) was also carried out. M1EV2 and M1EV3 used alone or particularly M1EV4 downregulated the tumor progression by TME immunomodulation, leading to a decrease in primary tumor size and metastasis in the peritoneum, liver, and lungs. STAT3, NF-kB, and AKT were the major genes downregulated by of M1EV systems. Tumor-associated macrophages (TAMs) shifted from an M2 phenotype (CD163) to an M1 phenotype (CD68) reducing levels of IL-10, TGF-beta and CCL22. Furthermore, malignant cells showed overexpression of FADD, APAF-1, caspase-3, and E-cadherin, and decreased expression of MDR1, survivin, vimentin, and PD-L1 after treatment with systems of M1EVs. The study shows that EVs from M1 antitumor macrophages can transport drugs and enhance their immunomodulatory and antitumor activity by modulating pathways associated with cell proliferation, migration, survival, and drug resistance.
C1 [Carvalho, Thais Gomes de; Souza, Shirley Vitoria de Paiva; Araujo Junior, Raimundo Fernandes de] Fed Univ Rio Grande Norte UFRN, Postgrad Program Hlth Sci, Natal, RN, Brazil.
   [Jorquera-Cordero, Carla] Univ Med Ctr Utrecht, Dept Orthoped, NL-3584 CX Utrecht, Netherlands.
   [Araga, Cicero Flavio Soares; Oliveira, Artur de Santana] Fed Univ Rio Grande Norte UFRN, Dept Pharmacol, Postgrad Program Pharmaceut Sci, Natal, RN, Brazil.
   [Lara, Pablo; Schomann, Timo] Leiden Univ, Med Ctr, Dept Radiol, Leiden, Netherlands.
   [Garcia, Vinicius Barreto; Souza, Shirley Vitoria de Paiva; Araujo Junior, Raimundo Fernandes de] Fed Univ Rio Grande Norte UFRN, Dept Morphol, Inflammat & Canc Res Lab, Natal, RN, Brazil.
   [Araga, Cicero Flavio Soares; Oliveira, Artur de Santana] Univ Fed Rio Grande do Norte, Dept Pharm, Med Qual Control Lab LCQMed, Natal, RN, Brazil.
   [Guedes, Paulo Marcos da Matta] Univ Fed Rio Grande do Norte, Dept Parasitol & Microbiol, Natal, RN, Brazil.
   [Soares, Luiz Alberto Lira] Fed Univ Pernambuco UFPE, Dept Pharmaceut Sci, Post Grad Program Therapeut Innovat, Recife, PE, Brazil.
   [Araujo Junior, Raimundo Fernandes de] Univ Fed Rio Grande do Norte, Morphol Dept, Univ Campus, Natal, Brazil.
C3 Universidade Federal do Rio Grande do Norte; Utrecht University; Utrecht
   University Medical Center; Universidade Federal do Rio Grande do Norte;
   Leiden University; Leiden University Medical Center (LUMC); Leiden
   University - Excl LUMC; Universidade Federal do Rio Grande do Norte;
   Universidade Federal do Rio Grande do Norte; Universidade Federal do Rio
   Grande do Norte; Universidade Federal de Pernambuco; Universidade
   Federal do Rio Grande do Norte
RP Lara, P (corresponding author), Leiden Univ, Med Ctr, Dept Radiol, Leiden, Netherlands.; Araújo, RFD Jr (corresponding author), Univ Fed Rio Grande do Norte, Morphol Dept, Univ Campus, Natal, Brazil.
EM p.lara_arenas@lumc.nl
RI GUEDES, PAULO/IZP-6459-2023; Soares, Luiz/R-3373-2016; Lara,
   Pablo/ABA-5691-2021; Araujo Junior, Raimundo/JWA-1491-2024; Schomann,
   Timo/P-7294-2018
OI Lara, Pablo/0000-0001-7791-647X
FU KWF Kankerbestrijding (Dutch Cancer Society) [13167]
FX Thais Gomes de Carvalho received financial support No 968572355 of
   ERASMUS (UE-LUMC). We acknowledge the support of a postdoctoral
   fellowship from Raimundo Fernandes de Araujo Junior by
   CNPq/200989/2022-7 and CNPq (Productivity in Research, Grant No
   <EM><STRONG> </STRONG></EM>3018770/2019). KWF Kankerbestrijding (Dutch
   Cancer Society), grant number 13167.r 3018770/2019) . KWF
   Kankerbestrijding (Dutch Cancer Society) , grant number 13167.
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NR 70
TC 13
Z9 13
U1 8
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 DEC
PY 2023
VL 168
AR 115663
DI 10.1016/j.biopha.2023.115663
EA OCT 2023
PG 16
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA X5BR7
UT WOS:001098606700001
PM 37832408
OA gold
DA 2025-01-04
ER

PT J
AU Jacobsen, IC
   Spanggaard, I
   Hojgaard, M
   Belcaid, L
   Qvortrup, C
   Yde, CW
   Schmidt, AY
   Nielsen, FC
   Willemoe, GL
   Dam, MS
   Lassen, U
   Rohrberg, KS
AF Jacobsen, Ida Christine
   Spanggaard, Iben
   Hojgaard, Martin
   Belcaid, Laila
   Qvortrup, Camilla
   Yde, Christina Westmose
   Schmidt, Ane Yde
   Nielsen, Finn Cilius
   Willemoe, Gro Linno
   Dam, Mikkel Seidelin
   Lassen, Ulrik
   Staal Rohrberg, Kristoffer
TI Extensive genomic analysis in patients with <i>KRAS</i>-mutated solid
   tumors shows high frequencies of concurrent alterations and potential
   targets but has limited clinical impact
SO ACTA ONCOLOGICA
LA English
DT Article
DE KRAS mutation; genomic alterations; actionable targets; personalized
   medicine
ID MUTATIONS; CANCER; RESISTANCE; BRAF
AB BackgroundThis study aimed to investigate the distribution and frequency of concurrent alterations in different cancers across KRAS subtypes and in different KRAS subtypes across cancers, and to identify potentially actionable targets and patients who received targeted treatment matched to their genomic profile (GP).Materials and MethodsIn this descriptive and single-center study, we included 188 patients with solid tumors harboring KRAS mutations in codon 12, 13, 61, 117, or 146, referred to the Phase 1 Unit, Rigshospitalet, Copenhagen, Denmark from mid-2016 to 2020. Genomic co-alterations were detected with whole-exome sequencing, RNA sequencing, SNP array, and mRNA expression array on fresh biopsies. The study is part of the Copenhagen Prospective Personalized Oncology study (NCT02290522).ResultsThe majority of patients had colorectal cancer (60.1%), non-small cell lung cancer (11.2%), or pancreatic cancer (10.6%). Most tumors were KRAS-mutated in codon 12 or 13 (93.7%) including G12D (27.1%), G12V (26.6%), G12C (11.7%), and G13D (11.2%). A total of 175 different co-alterations were found, most frequently pathogenic APC and TP53 mutations (55.9% and 46.4%, respectively) and high expression of CEACAM5 (73.4%). Different cancers and KRAS subtypes showed different patterns of co-alterations, and 157 tumors (83.5%) had potentially actionable targets with varying evidence of targetability (assessed using ESMO Scale for Clinical Actionability of molecular Targets). Of the 188 patients included in the study, 15 (7.4%) received treatment matched to their GP (e.g., immunotherapy and synthetic lethality drugs), of whom one had objective partial response according to Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1.ConclusionPerforming extensive genomic analysis in patients with known KRAS-mutated solid tumors may contribute with information to the genomic landscape of cancers and identify targets for immunotherapy or synthetic lethality drugs, but currently appears to have overall limited clinical impact, as few patients received targeted therapy matched to their GP.
C1 [Jacobsen, Ida Christine; Spanggaard, Iben; Hojgaard, Martin; Belcaid, Laila; Qvortrup, Camilla; Lassen, Ulrik; Staal Rohrberg, Kristoffer] Univ Hosp Copenhagen, Dept Oncol, Phase Unit 1, Rigshosp, Copenhagen, Denmark.
   [Yde, Christina Westmose; Schmidt, Ane Yde; Nielsen, Finn Cilius] Univ Hosp Copenhagen, Ctr Genom Med, Rigshosp, Copenhagen, Denmark.
   [Willemoe, Gro Linno] Univ Hosp Copenhagen, Dept Pathol, Rigshosp, Copenhagen, Denmark.
   [Dam, Mikkel Seidelin] Univ Hosp Copenhagen, Dept Diagnost Radiol, Rigshosp, Copenhagen, Denmark.
   [Jacobsen, Ida Christine] Univ Hosp Copenhagen, Dept Oncol, Phase Unit 1, Rigshosp, Blegdamsvej 9, DK-2100 Copenhagen, Denmark.
C3 Rigshospitalet; University of Copenhagen; Rigshospitalet; University of
   Copenhagen; Rigshospitalet; University of Copenhagen; University of
   Copenhagen; Rigshospitalet; Rigshospitalet; University of Copenhagen
RP Jacobsen, IC (corresponding author), Univ Hosp Copenhagen, Dept Oncol, Phase Unit 1, Rigshosp, Blegdamsvej 9, DK-2100 Copenhagen, Denmark.
EM idachristinejacobsen@gmail.com
RI Lassen, Ulrik/AAH-2799-2021; Qvortrup, Camilla/AAD-3366-2019; Nielsen,
   Finn/AAA-4926-2020; Rohrberg, Kristoffer/HHZ-8445-2022
OI Rohrberg, Kristoffer/0000-0002-5448-9003; Jacobsen, Ida
   Christine/0000-0003-0653-4364; Lassen, Ulrik/0000-0002-3865-4574;
   Belcaid, Laila/0000-0001-8062-1533
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NR 39
TC 0
Z9 0
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 DEC 2
PY 2022
VL 61
IS 12
BP 1499
EP 1506
DI 10.1080/0284186X.2022.2156809
EA DEC 2022
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 7T5SP
UT WOS:000898960200001
PM 36529989
DA 2025-01-04
ER

PT J
AU Jo, H
   Lee, MS
   Lee, YP
   Kim, H
   Hong, JY
   Lee, J
   Park, SH
   Park, JO
   Park, YS
   Lim, HY
   Kang, WK
   Kim, ST
AF Jo, H.
   Lee, M-S
   Lee, Y-P
   Kim, H.
   Hong, J. Y.
   Lee, J.
   Park, S. H.
   Park, J. O.
   Park, Y. S.
   Lim, H. Y.
   Kang, W. K.
   Kim, S. T.
TI A Comparison of Folinic Acid, Fluorouracil and Irinotecan (FOLFIRI) plus
   Bevacizumab and FOLFIRI plus Aflibercept as Second-line Treatment for
   Metastatic Colorectal Cancer
SO CLINICAL ONCOLOGY
LA English
DT Article
DE Aflibercept; bevacizumab; colorectal cancer; target therapy
ID RANDOMIZED-TRIAL; VEGF-TRAP; SURVIVAL; EFFICACY; CHEMOTHERAPY;
   LEUCOVORIN; BIOMARKERS; CETUXIMAB
AB Aim: To compare the efficacy and safety of folinic acid, fluorouracil and irinotecan (FOLFIRI) plus bevacizumab or aflibercept in metastatic colorectal cancer (mCRC) patients pretreated with oxaliplatin-based chemotherapy.
   Materials and methods: We analysed the treatment outcomes of patients receiving FOLFIRI in combination with bevacizumab or aflibercept as second-line treatment for mCRC between October 2017 and March 2020. This analysis included 67 patients receiving FOLFIRI plus aflibercept and 83 receiving FOLFIRI plus bevacizumab.
   Results: The overall response rate (ORR) was 13.6% (95% confidence interval 4.85-22.34) in the FOLFIRI-aflibercept group and 14.7% (95% confidence interval 6.68-22.71) in the FOLFIRI-bevacizumab group. This difference in ORR was not statistically significant. The median progression-free survival was 8.6 months in the FOLFIRI-bevacizumab group and 8.5 months in the FOLFIRI-aflibercept group (P = 0.752). Patients in the FOLFIRI-bevacizumab group showed a median overall survival of 12.4 months, whereas patients in the FOLFIRI-aflibercept group had a median overall survival of 13.7 months (P = 0.276). There were no significant differences in survival between the two treatment groups. The adverse events were also largely similar between the two groups. However, hy-pertension of grade 3 or more was more frequent in the FOLFIRI-aflibercept group.
   Conclusion: FOLFIRI plus bevacizumab and FOLFIRI plus aflibercept had similar anti-tumour activities and toxicity profiles when used as second-line therapy in mCRC patients. Based on these data, both aflibercept and bevacizumab are suitable anti-angiogenic agents when used in combination with FOLFIRI for mCRC. (C) 2022 The Author(s). Published by Elsevier Ltd on behalf of The Royal College of Radiologists.
C1 [Jo, H.; Lee, M-S; Lee, Y-P; Kim, H.; Hong, J. 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, Div Hematol Oncol,Dept Med, 81 Irwon Ro, Seoul 06351, South Korea.
C3 Sungkyunkwan University (SKKU); Samsung Medical Center
RP Kim, ST (corresponding author), Sungkyunkwan Univ, Samsung Med Ctr, Sch Med, Div Hematol Oncol,Dept Med, 81 Irwon Ro, Seoul 06351, South Korea.
EM shty1@skku.edu
RI kim, st/O-5928-2014; Kim, Tae/B-9921-2013
OI Kim, Hongsik/0000-0003-1232-9439; LEE, Min-Sang/0000-0001-8517-1789; Jo,
   Hyunji/0000-0002-4830-0833
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NR 23
TC 2
Z9 2
U1 0
U2 1
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0936-6555
EI 1433-2981
J9 CLIN ONCOL-UK
JI Clin. Oncol.
PD AUG
PY 2022
VL 34
IS 8
BP E323
EP E328
DI 10.1016/j.clon.2022.02.011
EA JUL 2022
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3Y9NA
UT WOS:000844048000002
PM 35248464
OA hybrid
DA 2025-01-04
ER

PT J
AU Van Krieken, JHJM
   Rouleau, E
   Ligtenberg, MJL
   Normanno, N
   Patterson, SD
   Jung, A
AF Van Krieken, J. Han J. M.
   Rouleau, Etienne
   Ligtenberg, Marjolijn J. L.
   Normanno, Nicola
   Patterson, Scott D.
   Jung, Andreas
TI <i>RAS</i> testing in metastatic colorectal cancer: advances in Europe
SO VIRCHOWS ARCHIV
LA English
DT Review
DE Colorectal cancer; RAS; Biomarkers; Sequencing; Quality assurance
   programs
ID EXTERNAL-QUALITY-ASSESSMENT; KRAS MUTATION DETECTION; CETUXIMAB PLUS
   IRINOTECAN; PICODROPLET DIGITAL PCR; RANDOMIZED PHASE-III; WILD-TYPE
   KRAS; 1ST-LINE TREATMENT; CODON 12; PRACTICE GUIDELINES; TARGETED
   THERAPY
AB Personalized medicine shows promise for maximizing efficacy and minimizing toxicity of anti-cancer treatment. KRAS exon 2 mutations are predictive of resistance to epidermal growth factor receptor-directed monoclonal antibodies in patients with metastatic colorectal cancer. Recent studies have shown that broader RAS testing (KRAS and NRAS) is needed to select patients for treatment. While Sanger sequencing is still used, approaches based on various methodologies are available. Few CE-approved kits, however, detect the full spectrum of RAS mutations. More recently, "next-generation" sequencing has been developed for research use, including parallel semiconductor sequencing and reversible termination. These techniques have high technical sensitivities for detecting mutations, although the ideal threshold is currently unknown. Finally, liquid biopsy has the potential to become an additional tool to assess tumor-derived DNA. For accurate and timely RAS testing, appropriate sampling and prompt delivery of material is critical. Processes to ensure efficient turnaround from sample request to RAS evaluation must be implemented so that patients receive the most appropriate treatment. Given the variety of methodologies, external quality assurance programs are important to ensure a high standard of RAS testing. Here, we review technical and practical aspects of RAS testing for pathologists working with metastatic colorectal cancer tumor samples. The extension of markers from KRAS to RAS testing is the new paradigm for biomarker testing in colorectal cancer.
C1 [Van Krieken, J. Han J. M.; Ligtenberg, Marjolijn J. L.] Radboud Univ Nijmegen, Med Ctr, Dept Pathol, POB 9101, NL-6500 HB Nijmegen, Netherlands.
   [Rouleau, Etienne] Inst Curie, Paris, France.
   [Normanno, Nicola] INT Fdn Pascale, Cell Biol & Biotherapy Unit, Naples, Italy.
   [Patterson, Scott D.] Amgen Inc, Thousand Oaks, CA 91320 USA.
   [Jung, Andreas] Univ Munich, Inst Pathol, Thalkirchner Str 36, D-80539 Munich, Germany.
   [Jung, Andreas] German Canc Res Ctr, German Canc Consortium DKTK, Heidelberg, Germany.
   [Patterson, Scott D.] Gilead Sci Inc, 353 Lakeside Dr, Foster City, CA 94404 USA.
C3 Radboud University Nijmegen; UNICANCER; Universite PSL; Institut Curie;
   IRCCS Fondazione Pascale; Amgen; University of Munich; Helmholtz
   Association; German Cancer Research Center (DKFZ); Gilead Sciences
RP Van Krieken, JHJM (corresponding author), Radboud Univ Nijmegen, Med Ctr, Dept Pathol, POB 9101, NL-6500 HB Nijmegen, Netherlands.
EM Han.vanKrieken@radboudumc.nl
RI Ligtenberg, Marjolijn/N-9666-2013; Normanno, Nicola/AAT-1107-2021; van
   Krieken, Joannes/D-4138-2009; Patterson, Scott/A-7404-2009
OI Normanno, Nicola/0000-0002-7158-2605; Patterson, Scott
   Donald/0000-0002-9840-4964; van Krieken, Joannes/0000-0002-8105-0450
FU Amgen (Europe) GmbH
FX Medical writing assistance with this manuscript was provided by Daniel
   Booth, PhD (Bioscript Medical, UK) and funded by Amgen (Europe) GmbH.
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NR 112
TC 23
Z9 23
U1 2
U2 8
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0945-6317
EI 1432-2307
J9 VIRCHOWS ARCH
JI Virchows Arch.
PD APR
PY 2016
VL 468
IS 4
BP 383
EP 396
DI 10.1007/s00428-015-1876-7
PG 14
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA DJ6HT
UT WOS:000374312900002
PM 26573425
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Huang, WL
   Hsu, YC
   Luo, CW
   Chang, SJ
   Hung, YH
   Lai, CY
   Yang, YT
   Chen, YZ
   Wu, CC
   Chen, FM
   Hou, MF
   Pan, MR
AF Huang, Wei-Lun
   Hsu, Yin-Chou
   Luo, Chi-Wen
   Chang, Shu-Jyuan
   Hung, Yu-Hsuan
   Lai, Chiao-Ying
   Yang, Yu-Tzu
   Chen, Yi-Zi
   Wu, Chun-Chieh
   Chen, Fang-Ming
   Hou, Ming-Feng
   Pan, Mei-Ren
TI Targeting the CDK7-MDK axis to suppresses irinotecan resistance in
   colorectal cancer
SO LIFE SCIENCES
LA English
DT Article
DE CDK7; Colorectal cancer; Chemoresistance
ID 1ST-LINE TREATMENT; GEMCITABINE RESISTANCE; CONTROLLED-TRIAL;
   GROWTH-FACTOR; MIDKINE; TRANSCRIPTION; FLUOROURACIL; LEUCOVORIN;
   EXPRESSION; FOLFIRI
AB Aims: Colorectal cancer (CRC) remains a major global health issue, with metastatic cases presenting poor prognosis despite advances in chemotherapy and targeted therapy. Irinotecan, a key drug for advanced CRC treatment, faces challenges owing to the development of resistance. This study aimed to understand the mechanisms underlying irinotecan resistance in colorectal cancer. Main methods: We created a cell line resistant to irinotecan using HT29 cells. These resistant cells were utilized to investigate the role of the CDK7-MDK axis. We employed bulk RNA sequencing, conducted in vivo experiments with mice, and analyzed patient tissues to examine the effects of the CDK7-MDK axis on the cellular response to irinotecan. Key findings: Our findings revealed that HT29 cells resistant to irinotecan, a crucial colorectal cancer medication, exhibited significant phenotypic and molecular alterations compared to their parental counterparts, including elevated stem cell characteristics and increased levels of cytokines and drug resistance proteins. Notably, CDK7 expression was substantially higher in these resistant cells, and targeting CDK7 effectively decreased their survival and tumor growth, enhancing irinotecan sensitivity. RNA-seq analysis indicated that suppression of CDK7 in irinotecan-resistant HT29 cells significantly reduced Midkine (MDK) expression. Decreased CDK7 and MDK levels, achieved through siRNA and the CDK7 inhibitor THZ1, enhanced the sensitivity of resistant HT29 cells to irinotecan. Significance: Our study sheds light on how CDK7 and MDK influence irinotecan resistance in colorectal and highlights the potential of MDK-targeted therapies. We hypothesized that irinotecan sensitivity and overall treatment efficacy would improve by inhibiting MDK. This finding encourages a careful yet proactive investigation of MDK as a therapeutic target to enhance outcomes in colorectal cancer patients.
C1 [Huang, Wei-Lun; Hsu, Yin-Chou; Chang, Shu-Jyuan; Lai, Chiao-Ying; Yang, Yu-Tzu; Chen, Yi-Zi; Pan, Mei-Ren] Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, 100 Tzyou1st Rd, Kaohsiung, Taiwan.
   [Huang, Wei-Lun] Kaohsiung Vet Gen Hosp, Dept Radiat Oncol, Kaohsiung 813, Taiwan.
   [Hsu, Yin-Chou] I Shou Univ, E Da Dachang Hosp, Dept Emergency Med, Kaohsiung 824, Taiwan.
   [Luo, Chi-Wen; Chen, Fang-Ming; Hou, Ming-Feng] Kaohsiung Med Univ Hosp, Dept Surg, Div Breast Oncol & Surg, Kaohsiung 807, Taiwan.
   [Luo, Chi-Wen] Chia Nan Univ Pharm & Sci, Inst Cosmet Sci, Dept Cosmet Sci, Tainan 717, Taiwan.
   [Hung, Yu-Hsuan; Pan, Mei-Ren] Kaohsiung Med Univ Hosp, Dept Med Res, Kaohsiung 807, Taiwan.
   [Wu, Chun-Chieh] Kaohsiung Med Univ, Dept Pathol, Kaohsiung Med Univ Hosp, Kaohsiung 807, Taiwan.
   [Hou, Ming-Feng] Kaohsiung Med Univ, Coll Life Sci, Dept Biomed Sci & Environm Biol, Kaohsiung 807, Taiwan.
   [Pan, Mei-Ren] Kaohsiung Med Univ, Drug Dev & Value Creat Res Ctr, Kaohsiung 807, Taiwan.
C3 Kaohsiung Medical University; Kaohsiung Veterans General Hospital; I
   Shou University; E-Da Hospital; Kaohsiung Medical University; Kaohsiung
   Medical University Hospital; Chia Nan University of Pharmacy & Science;
   Kaohsiung Medical University; Kaohsiung Medical University Hospital;
   Kaohsiung Medical University; Kaohsiung Medical University Hospital;
   Kaohsiung Medical University; Kaohsiung Medical University
RP Pan, MR (corresponding author), Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, 100 Tzyou1st Rd, Kaohsiung, Taiwan.; Luo, CW (corresponding author), Kaohsiung Med Univ Hosp, Dept Surg, 100 Tzyou 1st Rd, Kaohsiung 807, Taiwan.
EM 1070598@mail.kmuh.org.tw; mrpan@kmu.edu.tw
RI Chen, Fang-Ming/D-4721-2009
FU Ministry of Science and Technology, Taiwan [113-2320-B-037-005,
   113-2320-B-037-006, 112-2314-B037-045-, 111-2314-B-650-006-MY3,
   113-2811-B-037-001, 112-2320-B-037-002, 112-2628-B-037-002,
   112-2314-B-037-044]; Kaohsiung Medical University, Kaohsiung, Taiwan
   [KMUH-DK(C)111003, KMUH111-1R34, KMUH112-2R41]; E-DA hospital,
   Kaohsiung, Taiwan [EDAHP-108-027]
FX This work was supported by the following grants: 1) 113-2320-B-037-005,
   113-2320-B-037-006-, 112-2314-B037-045-, 111-2314-B-650-006-MY3,
   113-2811-B-037-001-, 112-2320-B-037-002-, 112-2628-B-037-002-and
   112-2314-B-037-044 from the Ministry of Science and Technology, Taiwan.
   2) KMUH-DK(C)111003, KMUH111-1R34, and KMUH112-2R41 from the Kaohsiung
   Medical University, Kaohsiung, Taiwan. 3) EDAHP-108-027 from E-DA
   hospital, Kaohsiung, Taiwan.
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NR 66
TC 0
Z9 0
U1 2
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0024-3205
EI 1879-0631
J9 LIFE SCI
JI Life Sci.
PD SEP 15
PY 2024
VL 353
AR 122914
DI 10.1016/j.lfs.2024.122914
EA JUL 2024
PG 12
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA ZO5N7
UT WOS:001276253600001
PM 39004275
DA 2025-01-04
ER

PT J
AU Hirashita, Y
   Tsukamoto, Y
   Kudo, Y
   Kakisako, D
   Kurogi, S
   Hijiya, N
   Nakada, C
   Uchida, T
   Hirashita, T
   Hiratsuka, T
   Akagi, T
   Ueda, Y
   Shiroshita, H
   Etoh, T
   Mizukami, K
   Honda, K
   Okimoto, T
   Kodama, M
   Inomata, M
   Moriyama, M
   Murakami, K
AF Hirashita, Yuka
   Tsukamoto, Yoshiyuki
   Kudo, Yoko
   Kakisako, Daisuke
   Kurogi, Shusaku
   Hijiya, Naoki
   Nakada, Chisato
   Uchida, Tomohisa
   Hirashita, Teijiro
   Hiratsuka, Takahiro
   Akagi, Tomonori
   Ueda, Yoshitake
   Shiroshita, Hidefumi
   Etoh, Tsuyoshi
   Mizukami, Kazuhiro
   Honda, Koichi
   Okimoto, Tadayoshi
   Kodama, Masaaki
   Inomata, Masafumi
   Moriyama, Masatsugu
   Murakami, Kazunari
TI Early response in phosphorylation of ribosomal protein S6 is associated
   with sensitivity to trametinib in colorectal cancer cells
SO LABORATORY INVESTIGATION
LA English
DT Article
ID PATIENT-DERIVED ORGANOIDS; MUTATION STATUS; CETUXIMAB; BRAF; INHIBITION;
   ACTIVATION; THERAPY
AB Reduced pS6 correlates with sensitivity to MEK inhibition in colorectal cancer organoids as well as cell lines. This study shows the potential applicability of MEK inhibitors for a subset of colorectal cancer patients with RAS/BRAF mutation by using the change in pS6 levels as a predictive diagnostic marker.
   Mutations in RAS or BRAF are associated with poor prognosis and resistance to epidermal growth factor receptor (EGFR)-targeted therapy in colorectal cancer (CRC). Despite their common ability to activate downstream genes such as MEK and ERK, the therapeutic benefit of MEK inhibitors for patients with RAS/BRAF mutant CRC is limited, highlighting the need for biomarkers to predict the efficacy of MEK inhibition. Previously, we reported that a change in phosphorylation of ribosomal protein S6 (pS6) after MEK inhibition was significantly associated with sensitivity to MEK inhibition in gastric cancer cells. Here, we investigated the value of the response in pS6 for predicting the efficacy of trametinib, a MEK inhibitor, in patients with RAS/BRAF mutant CRC using patient-derived CRC organoids. We found that a subset of CRC cell lines and organoids were sensitive to trametinib. The change in phosphorylated ERK, a downstream molecule of the RAS/RAF/MEK pathway, was not significantly associated with trametinib sensitivity. On the other hand, only those with sensitivity showed a reduction of pS6 levels in response to trametinib. The change in pS6 after trametinib treatment was detectable by Western blotting, immunohistochemistry or immunocytochemistry. We also demonstrated an impact of MEK inhibition on pS6 in vivo using a xenograft model. Our data suggest that, in combination with patient-derived organoids, immunostaining-based detection of pS6 could be useful for prediction of trametinib sensitivity.
C1 [Hirashita, Yuka; Kudo, Yoko; Kakisako, Daisuke; Mizukami, Kazuhiro; Honda, Koichi; Okimoto, Tadayoshi; Kodama, Masaaki; Murakami, Kazunari] Oita Univ, Dept Gastroenterol, Fac Med, Oita, Japan.
   [Hirashita, Yuka; Tsukamoto, Yoshiyuki; Kurogi, Shusaku; Hijiya, Naoki; Nakada, Chisato; Uchida, Tomohisa; Moriyama, Masatsugu] Oita Univ, Dept Mol Pathol, Fac Med, Oita, Japan.
   [Hirashita, Teijiro; Hiratsuka, Takahiro; Akagi, Tomonori; Shiroshita, Hidefumi; Etoh, Tsuyoshi; Inomata, Masafumi] Oita Univ, Dept Gastroenterol & Pediat Surg, Fac Med, Oita, Japan.
   [Ueda, Yoshitake] Oita Univ, Dept Comprehens Surg Community Med, Oita, Japan.
C3 Oita University; Oita University; Oita University; Oita University
RP Hirashita, Y (corresponding author), Oita Univ, Dept Gastroenterol, Fac Med, Oita, Japan.; Hirashita, Y; Tsukamoto, Y (corresponding author), Oita Univ, Dept Mol Pathol, Fac Med, Oita, Japan.
EM not-minamino@oita-u.ac.jp; tuka@oita-u.ac.jp
RI Ueda, Yoshitake/LSK-0856-2024
OI Tsukamoto, Yoshiyuki/0000-0002-2827-8974; Hirashita,
   Yuka/0000-0002-8111-8638
FU JSPS KAKENHI [18K15283]; Grants-in-Aid for Scientific Research
   [23K21375, 21H02703, 21K06888, 21K06924, 20K07394, 18K15283] Funding
   Source: KAKEN
FX This work was supported at the Discretion of the President of Oita
   University (2019) and partly by JSPS KAKENHI Grant Number 18K15283.
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NR 36
TC 9
Z9 10
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0023-6837
EI 1530-0307
J9 LAB INVEST
JI Lab. Invest.
PD AUG
PY 2021
VL 101
IS 8
BP 1036
EP 1047
DI 10.1038/s41374-021-00590-w
EA APR 2021
PG 12
WC Medicine, Research & Experimental; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pathology
GA TL5ZO
UT WOS:000645162200001
OA hybrid
DA 2025-01-04
ER

PT J
AU Ghosh, P
   Muhasina, KM
   Pandey, N
   Basavan, D
AF Ghosh, Puja
   Muhasina, K. M.
   Pandey, Neelaxi
   Basavan, Duraiswamy
TI Jackfruit waste: an invented anticancer therapy using Jacalin lectin
   from jackfruit seed
SO ANTI-CANCER DRUGS
LA English
DT Review
DE cell apoptosis; cellular dynamics; jackfruit wastage; jacalin lectin;
   nano formulation; targeted cancer therapy
ID THOMSEN-FRIEDENREICH-ANTIGEN; N-ACETYLGLUCOSAMINYLTRANSFERASE-III;
   PLANT-LECTINS; SILVER NANOPARTICLES; GOLD NANOPARTICLES; BINDING;
   CANCER; CELL; GLYCOSYLATION; RECOGNITION
AB Every food source contains both edible and inedible waste components. Millions of tonnes of trash from the food business are made from fruits, and these wastes are containing higher-value medicinal components, such as alkaloids, flavonoids, phenolic contents, a huge amount of proteins and secondary metabolites. These bioactive phytoconstituents are being used for the treatment of many serious fatal diseases. So, utilizing the recovered bioactive molecules from food wastes as functional ingredients offers a long-term alternative source of therapeutically active components that will lead to the discovery of novel phytoconstituents or novel treatment approaches. The goal of this systematic study is to provide an overview of the jackfruit (Artocarpus heterophyllus Lam, Moraceae) edible byproducts, such as jackfruit seeds that are largely neglected. This seed contains numerous bioactive lead molecules, such as carbohydrate-binding protein jacalin, which exhibits potent anticancer activity against colon cancer, blood cancer and breast cancer as well as can enlighten the new possible treatment approaches in targeted therapy and photodynamic chemotherapy. Moreover, jackfruit waste seed can be taken as a dietary food, which is having property to prevent and treat cancer and other lifestyle diseases. The works that have been carried out to utilize jackfruit waste other than the juicy edible bulbs have been reviewed in this article.
C1 [Ghosh, Puja; Muhasina, K. M.; Basavan, Duraiswamy] JSS Coll Pharm, Dept Pharmacognosy, Ooty, Tamil Nadu, India.
   [Pandey, Neelaxi] Motherhood Univ, Fac Sci, Dept Zool, Roorkee, Uttarakhand, India.
C3 JSS Academy of Higher Education & Research; JSS College of Pharmacy,
   Ooty
RP Ghosh, P (corresponding author), JSS Coll Pharm, Dept Pharmacognosy, Ooty, Tamil Nadu, India.
EM Ghoshpuja392@gmail.com
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NR 72
TC 2
Z9 2
U1 2
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0959-4973
EI 1473-5741
J9 ANTI-CANCER DRUG
JI Anti-Cancer Drugs
PD NOV
PY 2023
VL 34
IS 10
BP 1085
EP 1093
DI 10.1097/CAD.0000000000001447
PG 9
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA U1PA5
UT WOS:001082579800004
PM 37823283
DA 2025-01-04
ER

PT J
AU Chen, YT
   Lu, AN
   Hu, ZL
   Li, JY
   Lu, J
AF Chen, Yutao
   Lu, Anni
   Hu, Zhangli
   Li, Jinyao
   Lu, Jun
TI ERBB3 targeting: A promising approach to overcoming cancer therapeutic
   resistance
SO CANCER LETTERS
LA English
DT Article
DE ERBB3; Cell signalling; Resistance; Mechanism; Cancer; Cancer therapy
ID GROWTH-FACTOR RECEPTOR; SQUAMOUS-CELL CARCINOMA; ANTI-ERBB3
   MONOCLONAL-ANTIBODY; PRIMARY COLORECTAL-CANCER; BREAST-CANCER;
   ESTROGEN-RECEPTOR; UP-REGULATION; HER3 EXPRESSION; POOR-PROGNOSIS;
   HER2-OVEREXPRESSING BREAST
AB Human epidermal growth factor receptor-3 (ERBB3) is a member of the ERBB receptor tyrosine kinases (RTKs) and is expressed in many malignancies. Along with other ERBB receptors, ERBB3 is associated with regulating normal cell proliferation, apoptosis, differentiation, and survival, and has received increased research attention for its involvement in cancer therapies. ERBB3 expression or co-expression levels have been investigated as predictive factors for cancer prognosis and drug sensitivity. Additionally, the association between the elevated expression of ERBB3 and treatment failure in cancer therapy further established ERBB3-targeting therapy as a crucial therapeutic approach. This review delves into the molecular mechanisms of ERBB3-driven resistance to targeted therapeutics against ERBB2 and EGFR and other signal transduction inhibitors, endocrine therapy, chemotherapy, and radiotherapy. Using preclinical and clinical evidence, we synthesise and explicate how various aspects of aberrant ERBB3 activities-such as compensatory activation, signal crosstalk interactions, dysregulation in the endocytic pathway, mutations, ligand-independent activation, intrinsic kinase activity, and homodimerisation-can lead to resistance development and/or treatment failures. Several ERBB3-directed monoclonal antibodies, bispecific antibodies, and the emerging antibody-drug conjugate demonstrate encouraging clinical outcomes for improving therapeutic efficacy and overcoming resistance, especially when combined with other anti-cancer approaches. More research efforts are needed to identify appropriate biomarkers tailored for ERBB3-targeted therapies.
C1 [Chen, Yutao; Lu, Jun] Univ Auckland, Auckland Bioengn Inst, Private Bag 92019, Auckland 1142, New Zealand.
   [Lu, Anni] Pinehurst Sch, Auckland, New Zealand.
   [Hu, Zhangli] Shenzhen Univ, Coll Life Sci & Oceanog, Shenzhen, Peoples R China.
   [Li, Jinyao] Xinjiang Agr Univ, Coll Life Sci, Urumqi, Peoples R China.
   [Lu, Jun] Shaanxi Normal Univ, Coll Food Engn & Nutr Sci, Xian 710119, Shaanxi, Peoples R China.
   [Lu, Jun] Nanchang Univ, Coll Food Sci & Technol, Nanchang 330031, Jiangxi, Peoples R China.
   [Lu, Jun] Yangtze Delta Reg Inst Tsinghua Univ, Dept Food & Agr Technol, Jiaxing 314006, Zhejiang, Peoples R China.
C3 University of Auckland; Shenzhen University; Xinjiang Agricultural
   University; Shaanxi Normal University; Nanchang University; Tsinghua
   University
RP Lu, J (corresponding author), Univ Auckland, Auckland Bioengn Inst, Private Bag 92019, Auckland 1142, New Zealand.
EM jun.lu@auckland.ac.nz
RI Wuyan, Li/GMX-2504-2022; Hu, Zhangli/AAY-3061-2020
OI Chen, Yutao/0000-0002-0702-2662; Lu, Jun/0000-0003-0225-6643
FU Royal Society of New Zealand Catalyst Fund [CSG-UOA2108]
FX Funding support from Royal Society of New Zealand Catalyst Fund
   (CSG-UOA2108) to Professors Jun Lu and Jinyao Li.
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NR 218
TC 1
Z9 1
U1 2
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0304-3835
EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PD SEP 1
PY 2024
VL 599
AR 217146
DI 10.1016/j.canlet.2024.217146
EA AUG 2024
PG 29
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA C7Y5M
UT WOS:001291491100001
PM 39098760
OA hybrid
DA 2025-01-04
ER

PT J
AU Hou, HL
   Liu, D
   Zhang, CT
   Jiang, YX
   Lu, GF
   Zhou, N
   Yang, XN
   Zhang, XP
   Li, ZK
   Zhu, HM
   Qian, ZY
   Zhang, XC
AF Hou, Helei
   Liu, Dong
   Zhang, Chuantao
   Jiang, Yanxia
   Lu, Guifang
   Zhou, Na
   Yang, Xiaonan
   Zhang, Xiaoping
   Li, Zhuokun
   Zhu, Hongmei
   Qian, Zhaoyang
   Zhang, Xiaochun
TI Targeted next generation sequencing in Chinese colorectal cancer
   patients guided anti-EGFR treatment and facilitated precision cancer
   medicine
SO ONCOTARGET
LA English
DT Article
DE next generation sequencing; colorectal cancer; genetic alteration;
   targeted therapy; personalized therapy
ID KRAS; MUTATIONS; PATHWAYS; PTEN; NRAS; VALIDATION; EXPRESSION; MELANOMA;
   EFFICACY; THERAPY
AB Objective: Colorectal cancer (CRC) patients with both RAS and BRAF wild-type tumors determined by non-next generation sequencing (NGS) testing may still not respond due to the presence of additional mutated genes such as PIK3CA or PTEN. In this study, a broad, hybrid capture-based NGS assay was used to identify RAS, BRAF and additional targetable genetic alterations from Chinese CRC tissues.
   Methods: Fifty-seven cases of CRC were enrolled, and all the patients signed the informed consent. In total, 7708 exons of 508 tumor-related genes and 78 introns of 19 frequently rearranged genes were assessed for base substitutions, INDELs, copy number alterations, and gene fusions.
   Results: The study found that 50.9% (29/57) of the tumors harbored KRAS mutations, 3.5% (2/57) harbored NRAS mutations and 3.5% (2/57) harbored BRAF mutations. More specifically, 89.7% (26/29) of RAS mutations were located in codon 12. Except for RAS and RAF, anti-EGFR therapy response genetic mutations in PTEN (n=2) and PIK3CA (n=1) were found in 4.7% (3/64) of the samples. Actionable alterations were found in HER2 (n =7), CCND2 (n =2), NF1 (n =1), and BRCA1 (n =1).
   Conclusions: Our results illustrated that 82.5% (47/57) of the samples harbored at least one actionable genetic alteration identified by NGS. HER2 amplifications or mutations, which were identified in 12.3% of the tissues, defined a unique molecular subtype of CRC. The study suggests that high-throughput NGS testing in CRC tissues is a comprehensive and efficient genomic profiling assay to guide personalized therapy.
C1 [Hou, Helei; Liu, Dong; Zhang, Chuantao; Zhou, Na; Zhang, Xiaochun] Qingdao Univ, Dept Med Oncol, Affiliated Hosp, Qingdao 266005, Peoples R China.
   [Jiang, Yanxia] Qingdao Univ, Affiliated Hosp, Dept Pathol, Qingdao 266005, Peoples R China.
   [Lu, Guifang] Xi An Jiao Tong Univ, Dept Gastroenterol, Affiliated Hosp 1, Xian 710061, Shaanxi, Peoples R China.
   [Yang, Xiaonan; Li, Zhuokun] Qingdao SINO GERMAN Ecopk, BGI Qingdao Inst, Qingdao 266555, Peoples R China.
   [Zhang, Xiaoping] BGI Shenzhen, Dept Clin Lab, Shenzhen 518083, Peoples R China.
   [Zhu, Hongmei; Qian, Zhaoyang] BGI Shenzhen, Binhai Genom Inst, BGI Tianjin, Tianjin 300308, Peoples R China.
C3 Qingdao University; Qingdao University; Xi'an Jiaotong University;
   Beijing Genomics Institute (BGI); Beijing Genomics Institute (BGI)
RP Zhang, XC (corresponding author), Qingdao Univ, Dept Med Oncol, Affiliated Hosp, Qingdao 266005, Peoples R China.
EM zhangxiaochun9670@126.com
RI Zhang, Xiaoping/AFW-5367-2022; Zhu, Hongmei/HKF-2068-2023; Yang,
   Xiaonan/AAL-5154-2020; xiang, li/JDN-4098-2023; Qian,
   Zhaoyang/JVN-3181-2024
FU Taishan Scholar foundation [tshw201502061]; Qingdao Key Discipline
   foundation; Qingdao people's Livelihood Science and technology program
   [16-6-2-3-nsh]; third batch of Qingdao entrepreneurial innovation
   leading talent program
FX This work was supported by the Taishan Scholar foundation (No.
   tshw201502061), the Qingdao Key Discipline foundation, the Qingdao
   people's Livelihood Science and technology program (16-6-2-3-nsh) and
   the third batch of Qingdao entrepreneurial innovation leading talent
   program.
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NR 34
TC 2
Z9 3
U1 0
U2 6
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
SN 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD DEC 1
PY 2017
VL 8
IS 62
BP 105072
EP 105080
DI 10.18632/oncotarget.21349
PG 9
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FS1UI
UT WOS:000419563600029
PM 29285234
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Helgadottir, H
   Matikas, A
   Fernebro, J
   Frödin, JE
   Ekman, S
   Rodriguez-Wallberg, KA
AF Helgadottir, Hildur
   Matikas, Alexios
   Fernebro, Josefin
   Frodin, Jan-Erik
   Ekman, Simon
   Rodriguez-Wallberg, Kenny A.
TI Fertility and reproductive concerns related to the new generation of
   cancer drugs and the clinical implication for young individuals
   undergoing treatments for solid tumors
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE Oncofertility; Melanoma; Lung cancer; Colorectal cancer; Breast cancer;
   Gynecological cancer; Immunotherapy; Targeted therapy; Fertility
   preservation; Breast feeding
ID PREOPERATIVE RADIOTHERAPY; METASTATIC MELANOMA; IMPROVED SURVIVAL;
   OVARIAN RESERVE; BREAST-CANCER; LUNG-CANCER; STAGE-III; PREGNANCY;
   IPILIMUMAB; BRAF
AB The treatment landscape of solid tumors has changed markedly in the last years. Molecularly targeted treatments and immunotherapies have been implemented and have, in many cancers, lowered the risk of relapse and prolonged survival. Patients with tumors harboring specific targetable molecular alterations or mutations are often of a younger age, and hence future fertility and family building can be important concerns in this group. However, there are great uncertainties regarding the effect of the new drugs on reproductive functions, including fertility, pregnancy and lactation and how young patients with cancers, both women and men should be advised. The goal with this review is to gather the current knowledge regarding oncofertility and the different novel therapies, including immune checkpoint inhibitors, antibody -drug conjugates, small molecules and monoclonal antibody targeted therapies. The specific circumstances and reproductive concerns in different patient groups where novel treatments have been broadly introduced are also discussed, including those with melanoma, lung, breast, colorectal and gynecological cancers. It is clear, that more awareness is needed regarding potential drug toxicity on reproductive tissues, and it is of essence that individuals are informed based on current expertise and on available fertility preservation methods.
C1 [Helgadottir, Hildur; Matikas, Alexios; Fernebro, Josefin; Frodin, Jan-Erik; Ekman, Simon; Rodriguez-Wallberg, Kenny A.] Karolinska Inst, Dept Oncol & Pathol, S-17177 Stockholm, Sweden.
   [Helgadottir, Hildur] Karolinska Univ Hosp, Skin Canc Ctr, Theme Canc, S-17176 Stockholm, Sweden.
   [Matikas, Alexios] Karolinska Comprehens Canc Ctr, Breast Ctr, Stockholm, Sweden.
   [Matikas, Alexios] Karolinska Univ Hosp, Stockholm, Sweden.
   [Fernebro, Josefin] Karolinska Univ Hosp, Dept Pelv Canc, Div Gynecol Canc, Theme Canc, Stockholm, Sweden.
   [Frodin, Jan-Erik] Karolinska Univ Hosp, Dept Upper Abdomen, Div Gastrointestinal Oncol, Solna, Sweden.
   [Ekman, Simon] Karolinska Univ Hosp, Thorac Oncol Ctr, Theme Canc, Stockholm, Sweden.
   [Rodriguez-Wallberg, Kenny A.] Karolinska Univ Hosp, Dept Reprod Med, Div Gynecol & Reprod, Stockholm, Sweden.
C3 Karolinska Institutet; Karolinska Institutet; Karolinska University
   Hospital; Karolinska Institutet; Karolinska University Hospital;
   Karolinska Institutet; Karolinska University Hospital; Karolinska
   Institutet; Karolinska University Hospital; Karolinska Institutet;
   Karolinska University Hospital; Karolinska Institutet; Karolinska
   University Hospital
RP Helgadottir, H (corresponding author), Karolinska Inst, Karolinska Univ Hosp, Dept Oncol & Pathol, Theme Canc, S-17176 Stockholm, Sweden.
EM hildur.helgadottir@sll.se
RI Helgadottir, Hildur/AEJ-4358-2022; Matikas, Alexios/O-1407-2016; Ekman,
   Simon/AAB-9387-2021
OI Ekman, Simon/0000-0002-8343-6226; Helgadottir,
   Hildur/0000-0002-0735-4771
FU Swedish Cancer Society [20 0156F, 200170F]
FX This work was supported by a grant to HH from the Swedish Cancer
   Society, grant numbers 20 0156F (HH) and 200170F (KARW) . The funders
   had no role in the preparation or writing of this review or in the
   decision to submit the article for publication.
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NR 117
TC 4
Z9 4
U1 3
U2 10
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 MAY
PY 2024
VL 202
AR 114010
DI 10.1016/j.ejca.2024.114010
EA MAR 2024
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QO4Z4
UT WOS:001221813500001
PM 38520926
OA hybrid
DA 2025-01-04
ER

PT J
AU Abdo, J
   Wichman, CS
   Dietz, NE
   Ciborowski, P
   Fleegel, J
   Mittal, SK
   Agrawal, DK
AF Abdo, Joe
   Wichman, Christopher S.
   Dietz, Nicholas E.
   Ciborowski, Pawel
   Fleegel, John
   Mittal, Sumeet K.
   Agrawal, Devendra K.
TI Discovery of Novel and Clinically Relevant Markers in Formalin-Fixed
   Paraffin-Embedded Esophageal Cancer Specimen
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE mass spectrometry; formalin-fixed paraffin-embedded tissue; SWATH
   analysis; proliferation markers; proteomics; molecular oncology;
   chemoresistance markers
ID EPITHELIAL-MESENCHYMAL-TRANSITION; SQUAMOUS-CELL CARCINOMA;
   GASTRIC-CANCER; CISPLATIN RESISTANCE; COLORECTAL-CANCER;
   DRUG-RESISTANCE; DOWN-REGULATION; LUNG-CANCER; EXPRESSION; PRMT1
AB Due to the ineffectiveness of chemoradiation and targeted therapy in esophageal anticancer care and the subsequent low survival rates, we constructed a high throughput method to discover and investigate new markers with prognostic, diagnostic, and therapeutic clinical utility. This was accomplished by developing a quick, inexpensive, and dependable platform to simultaneously quantify thousands of proteins which subsequently revealed novel markers involved in the pathogenesis of esophageal adenocarcinoma (EAC) via discovery mass spectrometry paired with conservative biostatistics. Our method uncovered a perfect storm of tumor suppressors being downregulated, proliferation markers ramped up, and chemoresistance markers overexpressed-many of which could serve as new therapy targets for EAC. The 12 markers discovered by this method are novel regarding their involvement in the pathogenesis of EAC. The molecular oncology arena now has a dozen new proteomic targets suitable for validation and elucidation of their clinical utility via gene knockdown in cellular and animal models. This new method can be replicated and applied to other cancers or disease states for research and development and discovery-based investigations. Our findings, which serve as a proof of concept, will hopefully motivate research groups to further expound on the molecular processes involved in the aggressiveness of EAC and other solid tumor diseases, ultimately leading to improved patient management strategies.
C1 [Abdo, Joe; Dietz, Nicholas E.; Fleegel, John; Mittal, Sumeet K.; Agrawal, Devendra K.] Creighton Univ, Sch Med, Dept Clin & Translat Sci, Omaha, NE 68178 USA.
   [Wichman, Christopher S.] Univ Nebraska, Med Ctr, Coll Publ Hlth, Dept Biostat, Omaha, NE USA.
   [Dietz, Nicholas E.] CHI Hlth Creighton Univ, Med Ctr, Coll Med, Dept Pathol, Omaha, NE USA.
   [Ciborowski, Pawel] Univ Nebraska, Med Ctr, Dept Pharmacol, Omaha, NE USA.
   [Mittal, Sumeet K.] St Josephs Hosp, Dign Hlth, Norton Thorac Inst, Phoenix, AZ USA.
C3 Creighton University; University of Nebraska System; University of
   Nebraska Medical Center; Creighton University; University of Nebraska
   System; University of Nebraska Medical Center; St. Joseph's Hospital and
   Medical Center
RP Agrawal, DK (corresponding author), Creighton Univ, Sch Med, Dept Clin & Translat Sci, Omaha, NE 68178 USA.
EM dkagr@creighton.edu
RI Agrawal, Devendra/GLR-3925-2022
OI Abdo, Joe/0000-0002-1463-9038
FU Department of Clinical and Translational Science, Creighton University;
   National Heart, Lung, and Blood Institute, National Institutes of
   Health, USA [R01 HL116042, R01 HL120659, R01 HL128063]
FX This work was supported by funds provided by the Department of Clinical
   and Translational Science, Creighton University. Dr. D. K. Agrawal is
   funded by the research grants R01 HL116042, R01 HL120659, and R01
   HL128063 from the National Heart, Lung, and Blood Institute, National
   Institutes of Health, USA. The content of this publication is solely the
   responsibility of the authors and does not necessarily represent the
   official views of the National Institutes of Health. We would also like
   to acknowledge Ms. Jayme Horning for her hard work in analyzing our
   samples via mass spectrometry and for consulting on our proteomic
   inquiries over the last 2 years.
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NR 40
TC 5
Z9 6
U1 0
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 MAY 9
PY 2018
VL 8
AR 157
DI 10.3389/fonc.2018.00157
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GF2JK
UT WOS:000431764200001
PM 29868478
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Cheng, B
   Xu, L
   Zhang, YZ
   Yang, HM
   Liu, S
   Ding, SS
   Zhao, H
   Sui, Y
   Wang, C
   Quan, LJ
   Liu, JH
   Liu, Y
   Wang, HM
   Zheng, ZQ
   Wu, XZ
   Guo, J
   Wen, ZH
   Zhang, RY
   Wang, F
   Liu, HM
   Sun, SZ
AF Cheng, Bo
   Xu, Lin
   Zhang, Yunzhi
   Yang, Huimin
   Liu, Shan
   Ding, Shanshan
   Zhao, Huan
   Sui, Yi
   Wang, Chan
   Quan, Lanju
   Liu, Jinhong
   Liu, Ye
   Wang, Hongming
   Zheng, Zhaoqing
   Wu, Xizhao
   Guo, Jing
   Wen, Zhaohong
   Zhang, Ruya
   Wang, Fei
   Liu, Hongmei
   Sun, Suozhu
TI Correlation between NGS panel-based mutation results and clinical
   information in colorectal cancer patients
SO HELIYON
LA English
DT Article
DE Colorectal cancer; Next-generation sequencing; gene mutation;
   microsatellite instability; Molecular targeted therapy
ID MICROSATELLITE-INSTABILITY STATUS; MSI-H; SURVIVAL; BENEFIT;
   CHEMOTHERAPY; PREDICTION
AB Early mutation identification guides patients with colorectal cancer (CRC) toward targeted therapies. In the present study, 414 patients with CRC were enrolled, and amplicon-based targeted next-generation sequencing (NGS) was then performed to detect genomic alterations within the 73 cancer-related genes in the OncoAim panel. The overall mutation rate was 91.5 % (379/414). Gene mutations were detected in 38/73 genes tested. The most frequently mutated genes were TP53 (60.9 %), KRAS (46.6 %), APC (30.4 %), PIK3CA (15.9 %), FBXW7 (8.2 %), SMAD4 (6.8 %), BRAF (6.5 %), and NRAS (3.9 %). Compared with the wild type, TP53 mutations were associated with low microsatellite instability/microsatellite stability (MSI-L/MSS) (P = 0.007), tumor location (P = 0.043), and histological grade (P = 0.0009); KRAS mutations were associated with female gender (P = 0.026), distant metastasis (P = 0.023), TNM stage (P = 0.013), and histological grade (P = 0.004); APC mutations were associated with patients <64 years of age at diagnosis (P = 0.04); PIK3CA mutations were associated with tumor location (P = 4.97e-06) and female gender (P = 0.018); SMAD4 mutations were associated with tumor location (P = 0.033); BRAF mutations were associated with high MSI (MSI-H; P = 6.968e-07), tumor location (P = 1.58e-06), and histological grade (P = 0.04). Mutations in 164 individuals were found to be pathogenic or likely pathogenic. A total of 26 patients harbored MSI-H tumors and they all had at least one detected gene mutation. Mutated genes were enriched in signaling pathways associated with CRC. The present findings have important implications for improving the personalized treatment of patients with CRC in China.
C1 [Cheng, Bo; Xu, Lin; Liu, Shan; Ding, Shanshan; Zhao, Huan; Quan, Lanju; Liu, Jinhong; Liu, Ye; Wu, Xizhao; Guo, Jing; Zhang, Ruya; Wang, Fei; Sun, Suozhu] Chinese Peoples Liberat Army Rocket Force Characte, Dept Pathol, Beijing 100037, Peoples R China.
   [Zhang, Yunzhi; Yang, Huimin; Sui, Yi; Wang, Chan; Wang, Hongming; Zheng, Zhaoqing; Wen, Zhaohong; Liu, Hongmei] Singlera Genom Shanghai Ltd, Shanghai 201318, Peoples R China.
   [Zhang, Yunzhi] Fudan Univ, Sch Life Sci, Shanghai 200438, Peoples R China.
C3 Fudan University
RP Sun, SZ (corresponding author), Chinese Peoples Liberat Army Rocket Force Characte, Dept Pathol, Beijing 100037, Peoples R China.; Liu, HM (corresponding author), Singlera Genom Shanghai Ltd, Shanghai 201318, Peoples R China.
EM hmliu1989@126.com; mingzhu0368@sina.com
RI Yang, Huiming/AAR-1956-2021; Wang, Lei/AGQ-4540-2022; Guo,
   Jing/IWD-9275-2023; liu, jinhong/GZH-3251-2022
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NR 47
TC 0
Z9 0
U1 1
U2 1
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 e29299
DI 10.1016/j.heliyon.2024.e29299
PG 11
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA RM7Y8
UT WOS:001228157700001
PM 38623252
OA gold
DA 2025-01-04
ER

PT J
AU Maurya, P
   Rawat, RS
   Gupta, S
   Krishna, S
   Siddiqi, MI
   Sashidhara, KV
   Banerjee, D
AF Maurya, Pooja
   Rawat, Rohit Singh
   Gupta, Sampa
   Krishna, Shagun
   Siddiqi, Mohammad Imran
   Sashidhara, Koneni V.
   Banerjee, Dibyendu
TI Synergy between human DNA ligase I and topoisomerase 1 unveils new
   therapeutic strategy for the management of colorectal cancer
SO JOURNAL OF BIOMOLECULAR STRUCTURE & DYNAMICS
LA English
DT Article; Early Access
DE Topo 1; hLig I; Topotecan; compound 27; drug resistance; Synergistic
   effect; colorectal cancer; Bliss synergy score
ID ORAL ETOPOSIDE; REPAIR; RESISTANCE; INHIBITORS; TOPOTECAN; OVARIAN;
   RECOMBINATION; CAMPTOTHECIN; SENSITIVITY; MECHANISMS
AB DNA topoisomerase 1 (Topo 1) is a pivotal player in various DNA processes, including replication, repair, and transcription. It serves as a target for anticancer drugs like camptothecin and its derivatives (Topotecan and SN-38/Irinotecan). However, the emergence of drug resistance and the associated adverse effects, such as alopecia, anemia, dyspnea, fever, chills, and painful or difficult urination, pose significant challenges in Topo 1-targeted therapy, necessitating urgent attention. Human DNA Ligase 1 (hLig I), recognized primarily for its role in DNA replication and repair of DNA breaks, intriguingly exhibits a DNA relaxation activity akin to Topo 1. This raised the hypothesis that hLig I might compensate for Topo 1 inhibition, contributing to resistance against Topo 1 inhibitors. To explore this hypothesis, we assessed the efficacy of hLig I inhibition alone and in combination with Topo 1 in cancer cells. As anticipated, the overexpression of hLig I was observed after Topo 1 inhibition in colorectal cancer cells, affirming our hypothesis. Previously identified as an inhibitor of hLig I's DNA relaxation activity, compound 27 (C 27), when combined with Topotecan, demonstrated a synergistic antiproliferative effect on colorectal cancer cells. Notably, cells with downregulated hLig I (via siRNA, inhibitors, or genetic manipulation) exhibited significantly heightened sensitivity to Topotecan. This observation strongly supports the concept that hLig I contribute to resistance against clinically relevant Topo 1 inhibitors in colorectal cancers. In conclusion, our findings offer evidence for the synergistic impact of combining hLig I inhibitors with Topotecan in the treatment of colorectal cancers, providing a promising strategy to overcome resistance to Topo 1 inhibitors.
C1 [Maurya, Pooja; Rawat, Rohit Singh; Banerjee, Dibyendu] CSIR Cent Drug Res Inst, Canc Biol Div, Lucknow, India.
   [Maurya, Pooja; Rawat, Rohit Singh; Gupta, Sampa; Krishna, Shagun] Jawaharlal Nehru Univ, New Delhi, India.
   [Gupta, Sampa; Sashidhara, Koneni V.] CSIR Cent Drug Res Inst, Med & Proc Chem Div, Lucknow, India.
   [Krishna, Shagun; Siddiqi, Mohammad Imran] CSIR Cent Drug Res Inst, Biochem & Struct Biol Div, Lucknow, India.
   [Siddiqi, Mohammad Imran; Sashidhara, Koneni V.; Banerjee, Dibyendu] Acad Sci & Innovat Res AcSIR, New Delhi, India.
   [Banerjee, Dibyendu] CSIR Cent Drug Res Inst CSIR CDRI, Canc Biol Div, Sitapur Rd, Lucknow 226031, India.
C3 Council of Scientific & Industrial Research (CSIR) - India; CSIR -
   Central Drug Research Institute (CDRI); Jawaharlal Nehru University, New
   Delhi; Council of Scientific & Industrial Research (CSIR) - India; CSIR
   - Central Drug Research Institute (CDRI); Council of Scientific &
   Industrial Research (CSIR) - India; CSIR - Central Drug Research
   Institute (CDRI); Academy of Scientific & Innovative Research (AcSIR);
   Council of Scientific & Industrial Research (CSIR) - India; CSIR -
   Central Drug Research Institute (CDRI)
RP Banerjee, D (corresponding author), CSIR Cent Drug Res Inst CSIR CDRI, Canc Biol Div, Sitapur Rd, Lucknow 226031, India.
RI Koneni, Sashidhara/B-7845-2009
OI RAWAT, ROHIT SINGH/0000-0001-6329-6636
FU Department of Science and Technology (DST-SERB), Government of India;
   DBT, New Delhi; UGC, New Delhi; Jawaharlal Nehru University, New Delhi;
   CSIR; ICMR
FX The authors express gratitude to the Sophisticated Analytical Instrument
   Facility (SAIF) at CDRI for their assistance in cell-based flow
   cytometry experiments. We further acknowledge Dr. Shahid Parwez
   (Biochemistry and Structural Biology Division, CSIR-CDRI) for his
   assistance in molecular docking studies. PM acknowledges financial
   support from DBT, New Delhi. RSR is thankful for research fellowship
   support from UGC, New Delhi. RSR also acknowledges Jawaharlal Nehru
   University, New Delhi. SG expresses gratitude to CSIR, and SK
   acknowledges support from ICMR.
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NR 35
TC 1
Z9 1
U1 2
U2 4
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 0739-1102
EI 1538-0254
J9 J BIOMOL STRUCT DYN
JI J. Biomol. Struct. Dyn.
PD 2023 DEC 22
PY 2023
DI 10.1080/07391102.2023.2297817
EA DEC 2023
PG 16
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA EE0C3
UT WOS:001137113800001
PM 38179981
DA 2025-01-04
ER

PT J
AU Khalili-Tanha, G
   Fiuji, H
   Gharib, M
   Moghbeli, M
   Khalili-Tanha, N
   Rahmani, F
   Shakour, N
   Maftooh, M
   Hassanian, SM
   Asgharzadeh, F
   Shahidsales, S
   Anvari, K
   Mozafari, MR
   Ferns, GA
   Batra, J
   Giovannetti, E
   Khazaei, M
   Avan, A
AF Khalili-Tanha, Ghazaleh
   Fiuji, Hamid
   Gharib, Masoumeh
   Moghbeli, Meysam
   Khalili-Tanha, Nima
   Rahmani, Farzad
   Shakour, Neda
   Maftooh, Mina
   Hassanian, Seyed Mahdi
   Asgharzadeh, Fereshteh
   Shahidsales, Soodabeh
   Anvari, Kazem
   Mozafari, M. R.
   Ferns, Gordon A.
   Batra, Jyotsna
   Giovannetti, Elisa
   Khazaei, Majid
   Avan, Amir
TI Dual targeting of TGF-ß and PD-L1 inhibits tumor growth in
   TGF-ß/PD-L1-driven colorectal carcinoma
SO LIFE SCIENCES
LA English
DT Article
DE Colorectal Cancer; Bifunctional fusion protein; PD-L1/TGF-beta; Targeted
   therapy
ID CELL-MEDIATED CYTOTOXICITY; M7824 MSB0011359C; FACTOR-BETA; EXPRESSION;
   RESISTANCE; ACTIVATION; AVELUMAB; ALPHA
AB Immunosuppressive factors within the tumor microenvironment (TME), such as Transforming growth factor beta (TGF-ss), constitute a crucial hindrance to immunotherapeutic approaches in colorectal cancer (CRC). Furthermore, immune checkpoint factors (e.g., programmed death-ligand 1 [PD-L1]) inhibit T-cell proliferation and activation. To cope with the inhibitory effect of immune checkpoints, the therapeutic value of dual targeting PDL1 and TGF-ss pathways via M7824 plus 5-FU in CRC has been evaluated. Integrative-systems biology approaches and RNAseq were used to assess the differential level of genes associated with 88 metastatic-CRC patients. The level of PD-L1 and TGF-ss was evaluated in a validation cohort. The anti-proliferative, migratory, and apoptotic effects of PD-L1/TGF-ss inhibitor, M7824, were assessed by MTT, wound-healing assay, and flow cytometry. Antitumor activity was assessed in a xenograft model, followed by biochemical studies and histological staining, and gene/protein expression analyses by RT-PCR and ELISA/IHC. The result of differentially expressed genes (DEGs) analysis showed 1268 upregulated and 1074 downregulated genes in CRC patients. Among the highest scoring genes and dysregulated pathways associated with CRC, PD-L1, and TGF- ss were identified and further validated in 92 CRC patients. Targeting of PD-L1-TGF- ss inhibited cell growth and migration, associated with modulation of CyclinD1 and MMP9. Furthermore, M7824 inhibited tumor growth via targeting TGF-ss and PD-L1 pathways, resulting in modulation of inflammatory response and fibrosis via TNF-alpha/IL6/CD4-8 and COL1A1/1A2, respectively. In conclusion, our data illustrated that co-targeting PD-L1 and TGF-ss pathways increased the effect of Fluorouracil (5-FU) and reduced the tumor growth in PD-L1/TGF-ss expressing tumors, providing a new therapeutic option in the treatment of CRC.
C1 [Khalili-Tanha, Ghazaleh; Fiuji, Hamid; Moghbeli, Meysam; Khalili-Tanha, Nima; Rahmani, Farzad; Maftooh, Mina; Hassanian, Seyed Mahdi; Khazaei, Majid; Avan, Amir] Mashhad Univ Med Sci, Metab Syndrome Res Ctr, Mashhad, Iran.
   [Gharib, Masoumeh] Mashhad Univ Med Sci, Fac Med, Dept Pathol, Mashhad, Iran.
   [Rahmani, Farzad; Hassanian, Seyed Mahdi] Mashhad Univ Med Sci, Fac Med, Dept Med Biochem, Mashhad, Iran.
   [Shakour, Neda] Mashhad Univ Med Sci, Sch Pharm, Dept Med Chem, Mashhad, Iran.
   [Asgharzadeh, Fereshteh; Khazaei, Majid] Mashhad Univ Med Sci, Fac Med, Dept Physiol, Mashhad, Iran.
   [Shahidsales, Soodabeh; Anvari, Kazem] Mashhad Univ Med Sci, Canc Res Ctr, Mashhad, Iran.
   [Avan, Amir] Univ Warith Al Anbiyaa, Coll Med, Karbala, Iraq.
   [Mozafari, M. R.] Monash Univ LPO, Australasian Nanosci & Nanotechnol Initiat ANNI, Clayton, Vic, Australia.
   [Ferns, Gordon A.] Brighton & Sussex Med Sch, Div Med Educ, Brighton BN1 9PH, Sussex, England.
   [Batra, Jyotsna; Avan, Amir] Queensland Univ Technol, Fac Hlth, Sch Biomed Sci, Brisbane, Qld 4059, Australia.
   [Avan, Amir] Queensland Univ Technol, Sci & Engn Fac, Sch Mech Med & Proc Engn, 2 George St, Brisbane, Qld 4000, Australia.
   [Batra, Jyotsna] Translat Res Inst, 37 Kent St, Woolloongabba, Qld 4102, Australia.
   [Giovannetti, Elisa] VU Univ Med Ctr VUMC, Canc Ctr Amsterdam, Dept Med Oncol, Amsterdam UMC, Amsterdam, Netherlands.
   [Giovannetti, Elisa] Fdn Pisana Sci, AIRC Start Unit, Canc Pharmacol Lab, Pisa, Italy.
C3 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; University of Warith Alanbiyaa; Monash
   University; University of Brighton; University of Sussex; Queensland
   University of Technology (QUT); Queensland University of Technology
   (QUT); University of Queensland; Vrije Universiteit Amsterdam; VU
   UNIVERSITY MEDICAL CENTER; University of Amsterdam
RP Khazaei, M; Avan, A (corresponding author), Mashhad Univ Med Sci, Metab Syndrome Res Ctr, Mashhad, Iran.
EM Khazaeim@mums.ac.ir; Avana@mums.ac.ir
RI Hassanian, Seyed Mahdi/KAL-9917-2024; MOZAFARI, Marcel/V-9077-2019;
   Khazaei, Majid/A-6143-2018; Gharib, Masoumeh/GLT-0844-2022; shakour,
   neda/ADU-5645-2022; Batra, Jyotsna/B-4130-2011; Avan,
   Amir/AAK-7543-2021; Moghbeli, Meysam/Q-7916-2019; Anvari,
   Kazem/AAZ-3481-2020; giovannetti, elisa/F-4261-2011; Asgharzadeh,
   Fereshteh/AFE-8923-2022
OI Shakour, Neda/0000-0002-9874-1397; batra, Jyotsna/0000-0003-4646-6247;
   Khalili-Tanha, Ghazaleh/0000-0001-5824-1390
FU Mashhad University of Medical Sciences, Iran [991114]
FX Funding This research is part of the Ph.D. thesis of Ms. Ghazaleh
   Khalili- Tanha, which was supported by the Mashhad University of Medical
   Sciences, Iran. Grant No. 991114 (Amir Avan) .
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NR 51
TC 10
Z9 10
U1 0
U2 16
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0024-3205
EI 1879-0631
J9 LIFE SCI
JI Life Sci.
PD SEP 1
PY 2023
VL 328
AR 121865
DI 10.1016/j.lfs.2023.121865
EA JUN 2023
PG 12
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA M8VY3
UT WOS:001032949100001
PM 37336360
DA 2025-01-04
ER

PT J
AU Yang, Y
   Shen, XY
   Li, RT
   Shen, J
   Zhang, H
   Yu, LX
   Liu, BR
   Wang, LF
AF Yang, Yang
   Shen, Xiaoyan
   Li, Rutian
   Shen, Jie
   Zhang, Hang
   Yu, Lixia
   Liu, Baorui
   Wang, Lifeng
TI The detection and significance of <i>EGFR</i> and <i>BRAF</i> in
   cell-free DNA of peripheral blood in NSCLC
SO ONCOTARGET
LA English
DT Article
DE NSCLC; cfDNA; CastPCR; driver mutation; EGFR
ID LUNG-CANCER PATIENTS; METASTATIC COLORECTAL-CANCER; FACTOR RECEPTOR
   MUTATIONS; CIRCULATING FREE DNA; DROPLET DIGITAL PCR; PLASMA DNA;
   BREAST-CANCER; KRAS; CHEMOTHERAPY; GEFITINIB
AB Objective: Although driver mutation status is crucial to targeted therapy decisionmaking in non-small cell lung cancer (NSCLC), due to unavailable or inadequate biopsies, there are still many patients with unknown mutation status. A promising way to solve this problem is liquid biopsy, such as cell-free DNA (cfDNA) in peripheral blood. Additionally, due to the little amount of cfDNA, detecting methods with high sensitivity, specificity and economy are required in clinical practice. Here, we explored the feasibility of Competitive Allele-Specific TaqMan (R) PCR (CastPCR) detecting driver mutations in cfDNA from plasma in lung adenocarcinoma patients.
   Results: Sensitivity, specificity, concordance, PPV and NPV of CastPCR detecting EGFR mutations in cfDNA was 56.4% (31/55), 94.2% (49/52), 74.8% (80/107), 91.2% (31/34) and 67.1% (49/73), respectively. Notably, specificity and PPV for p. T790M both reached 100.0%. For BRAF detection, it was 28.6% (2/7), 93.0% (93/100), 88.8% (95/107), 22.2% (2/9) and 94.9% (93/98), respectively.
   Materials and Methods: Plasma specimens of 107 lung adenocarcinoma patients and their matched tumor formalin fixed paraffin embedded (FFPE) samples were analyzed. CastPCR was used to detect EGFR (c. 2235_ 2249del, c. 2236_2250del, c. 2369C> T p. T790M, c. 2573T>G p. L858R) and BRAF (c. 1406G>C p. G469A, c. 1799T>A p. V600E, c. 1781A>G p. D594G) mutations. Mutation results of tumor tissue was set as gold standard, and the sensitivity, specificity, concordance, positive predictive value (PPV) and negative predictive value (NPV) were calculated for each mutation.
   Conclusions: For patients whose tumor tissue is unavailable or inadequate, EGFR mutation detection in cfDNA with CastPCR could be first choice. Mutation positive results may provide reference for further clinical medication. While negative results indicate that detection in tissue should be considered as the following step. In this way, tumor tissue could be economized to the maximum extent and the risk of repeated percutaneous transthoracic lung biopsy could also be lowered to the maximum extent. For BRAF detection in cfDNA, CastPCR is a specific method while the sensitivity needs further exploration.
C1 [Yang, Yang; Shen, Xiaoyan; Li, Rutian; Shen, Jie; Zhang, Hang; Yu, Lixia; Liu, Baorui; Wang, Lifeng] Nanjing Univ, Comprehens Canc Ctr, Drum Tower Hosp, Med Sch, Nanjing 210008, Jiangsu, Peoples R China.
   [Yang, Yang; Shen, Xiaoyan; Li, Rutian; Shen, Jie; Zhang, Hang; Yu, Lixia; Liu, Baorui; Wang, Lifeng] Nanjing Univ, Clin Canc Inst, Nanjing 210008, Jiangsu, Peoples R China.
   [Yang, Yang] Nanjing Xianlin Drum Tower Hosp, Nanjing 210046, Jiangsu, Peoples R China.
C3 Nanjing University; Nanjing University
RP Wang, LF (corresponding author), Nanjing Univ, Comprehens Canc Ctr, Drum Tower Hosp, Med Sch, Nanjing 210008, Jiangsu, Peoples R China.; Wang, LF (corresponding author), Nanjing Univ, Clin Canc Inst, Nanjing 210008, Jiangsu, Peoples R China.
EM lifengwang@nju.edu.cn
RI Li, Rutian/JZD-9096-2024; shen, jie/JJF-0994-2023
OI Li, Rutian/0000-0003-4800-6156
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NR 58
TC 28
Z9 28
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 JUL 25
PY 2017
VL 8
IS 30
BP 49773
EP 49782
DI 10.18632/oncotarget.17937
PG 10
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FB6DV
UT WOS:000406232400105
PM 28572536
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Prieur, A
   Cappellini, M
   Habif, G
   Lefranc, MP
   Mazard, T
   Morency, E
   Pascussi, JM
   Flacelière, M
   Cahuzac, N
   Vire, B
   Dubuc, B
   Durochat, A
   Liaud, P
   Ollier, J
   Pfeiffer, C
   Poupeau, S
   Saywell, V
   Planque, C
   Assenat, E
   Bibeau, F
   Bourgaux, JF
   Pujol, P
   Sézeur, A
   Ychou, M
   Joubert, D
AF Prieur, Alexandre
   Cappellini, Monica
   Habif, Guillaume
   Lefranc, Marie-Paule
   Mazard, Thibault
   Morency, Eric
   Pascussi, Jean-Marc
   Flaceliere, Maud
   Cahuzac, Nathalie
   Vire, Berengere
   Dubuc, Benjamin
   Durochat, Amandine
   Liaud, Pierre
   Ollier, Jeremy
   Pfeiffer, Caroline
   Poupeau, Sophie
   Saywell, Veronique
   Planque, Chris
   Assenat, Eric
   Bibeau, Frederic
   Bourgaux, Jean-Francois
   Pujol, Pascal
   Sezeur, Alain
   Ychou, Marc
   Joubert, Dominique
TI Targeting the Wnt Pathway and Cancer Stem Cells with Anti-progastrin
   Humanized Antibodies as a Potential Treatment for K-RAS-Mutated
   Colorectal Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID SIGNALING PATHWAY; ONCOGENIC RAS; GASTRIN; THERAPIES; EXPRESSION;
   INHIBITION; ACTIVATION; GROWTH; METASTASIS; RESISTANCE
AB Purpose: Patients with metastatic colorectal cancer suffer from disease relapse mainly due to cancer stem cells (CSC). Interestingly, they have an increased level of blood progastrin, a tumor-promoting peptide essential for the self-renewal of colon CSCs, which is also a direct beta-catenin/TCF4 target gene. In this study, we aimed to develop a novel targeted therapy to neutralize secreted progastrin to inhibit Wnt signaling, CSCs, and reduce relapses.
   Experimental Design: Antibodies (monoclonal and humanized) directed against progastrin were produced and selected for target specificity and affinity. After validation of their effectiveness on survival of colorectal cancer cell lines harboring B-RAF or K-RAS mutations, their efficacy was assessed in vitro and in vivo, alone or concomitantly with chemotherapy, on CSC self-renewal capacity, tumor recurrence, and Wnt signaling.
   Results: We show that anti-progastrin antibodies decrease self-renewal of CSCs both in vitro and in vivo, either alone or in combination with chemotherapy. Furthermore, migration and invasion of colorectal cancer cells are diminished; chemosensitivity is prolonged in SW620 and HT29 cells and posttreatment relapse is significantly delayed in T84 cells, xenografted nude mice. Finally, we show that the Wnt signaling activity in vitro is decreased, and, in transgenic mice developing Wnt-driven intestinal neoplasia, the tumor burden is alleviated, with an amplification of cell differentiation in the remaining tumors.
   Conclusions: Altogether, these data show that humanized anti-progastrin antibodies might represent a potential new treatment for K-RAS-mutated colorectal patients, for which there is a crucial unmet medical need. (C) 2017 AACR.
C1 [Prieur, Alexandre; Joubert, Dominique] Accompagnement Pharma, 11 Cote Eich, L-1450 Luxembourg, Luxembourg.
   [Cappellini, Monica; Habif, Guillaume; Morency, Eric; Flaceliere, Maud; Cahuzac, Nathalie; Vire, Berengere; Dubuc, Benjamin; Durochat, Amandine; Liaud, Pierre; Ollier, Jeremy; Pfeiffer, Caroline; Poupeau, Sophie; Saywell, Veronique] Eurobiodev, Montpellier, France.
   [Lefranc, Marie-Paule] Inst Genet Humaine, IMGT, Montpellier, France.
   [Mazard, Thibault; Assenat, Eric; Bibeau, Frederic; Ychou, Marc] Inst Reg Canc Montpellier, Montpellier, France.
   [Pascussi, Jean-Marc; Planque, Chris] Inst Genom Fonct, Montpellier, France.
   [Bourgaux, Jean-Francois] CHU Caremeau, Serv Hepatogastroenterol, Nimes, France.
   [Pujol, Pascal] CHRU Montpellier, Dept Oncogenet Clin, Montpellier, France.
   [Sezeur, Alain] Grp Hosp Diaconesses Croix St Simon Chirurg Diges, Paris, France.
C3 Universite de Montpellier; UNICANCER; Universite de Montpellier;
   Institut Regional du Cancer Montpellier / Val d'Aurelle (ICM);
   Universite de Montpellier; Universite de Montpellier; CHU de Nimes;
   Universite de Montpellier; CHU de Montpellier
RP Prieur, A (corresponding author), Accompagnement Pharma, 11 Cote Eich, L-1450 Luxembourg, Luxembourg.
EM a.prieur@accompagnementpharma.com
RI MAZARD, Thibault/ABH-6334-2020; Wegglin, Reto/AAV-4341-2021; pascussi,
   jean marc/F-9311-2013
OI pascussi, jean marc/0000-0002-5168-5383; Lefranc,
   Marie-Paule/0000-0003-0116-9353; Ychou, Marc/0000-0001-7378-9469
FU Agence National de la Recherche [ANR-08-Biot-019-01]; "Institut National
   du Cancer" (INCa)
FX Dominique Joubert was supported by "Agence National de la Recherche"
   (ANR-08-Biot-019-01) and the "Institut National du Cancer" (INCa).
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NR 47
TC 31
Z9 34
U1 0
U2 12
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 SEP 1
PY 2017
VL 23
IS 17
BP 5267
EP 5280
DI 10.1158/1078-0432.CCR-17-0533
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FF5NB
UT WOS:000409037300032
PM 28600477
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Plangger, A
   Rath, B
   Hochmair, M
   Funovics, M
   Hamilton, G
AF Plangger, Adelina
   Rath, Barbara
   Hochmair, Maximilian
   Funovics, Martin
   Hamilton, Gerhard
TI Cytotoxicity of combinations of the pan-KRAS inhibitor BAY-293 against
   primary non-small lung cancer cells
SO TRANSLATIONAL ONCOLOGY
LA English
DT Article
DE Non-small cell lung cancer; KRAS inhibitor; BAY-293; Drug combination;
   Osimertinib; Cytotoxicity
ID ONCOGENIC KRAS; COLORECTAL-CANCER; MOLECULAR PATHWAYS; HSP90 INHIBITOR;
   MYC EXPRESSION; MEK INHIBITOR; RAS ONCOGENES; IN-VITRO; RESISTANCE;
   GROWTH
AB KRAS is mutated in approximately 25% of Non-small Cell Lung Cancer (NSCLC) patients and first specific in-hibitors showed promising responses that may be improved by concurrent interference with downstream signaling pathways. Cell lines exhibiting KRAS mutations show specific sensitivities to modulators affecting glucose utilization, signal transduction and cell survival. Novel SOS1-directed inhibitors with a broader anti-cancer coverage such as BAY-293 and BI-3406 inhibit KRAS through the hindrance of SOS1-KRAS interactions. The aim of this study was to check the putative synergy of BAY-293 with modulators having revealed specific vulnerabilities of KRAS-mutated cell lines. The present investigation tested the cytotoxicity of BAY-293 combi -nations against a series of Osimertinib-resistant primary NSCLC cell lines using MTT tests and calculation of combination indices according to the Chou-Talalay method. The results show that BAY-293 synergizes with modulators of glucose metabolism, inhibitors of cellular proliferation, several chemotherapeutics and a range of diverse modulators, thus corroborating the chemosensitivities of cells expressing mutated KRAS. In conclusion, BAY-293 exerts cytotoxicity with a wide range of drugs against Osimertinib-resistant primary NSCLC cell lines. The administration of pan-KRAS inhibitors alone may be limited in vivo by toxicity to normal tissues but made feasible by its use as part of suitable drug combinations. This study shows that BAY-293 combinations are active against NSCLC cells not further amenable to mutated EGFR-directed targeted therapy and results likewise hold relevance for pancreatic and colon cancer.
C1 [Plangger, Adelina; Rath, Barbara; Hamilton, Gerhard] Med Univ Vienna, Inst Pharmacol, Wahringer Str 13A, A-1090 Vienna, Austria.
   [Hochmair, Maximilian] Karl Landsteiner Inst Lung Res & Pulm Oncol, Dept Resp & Crit Care Med, Vienna, Austria.
   [Funovics, Martin] Med Univ Vienna, Dept Bioimaging & Image Guided Therapy, Cardiovasc & Intervent Radiol, Vienna, Austria.
C3 Medical University of Vienna; Medical University of Vienna
RP Hamilton, G (corresponding author), Med Univ Vienna, Inst Pharmacol, Wahringer Str 13A, A-1090 Vienna, Austria.
EM gerhard.hamilton@meduniwien.ac.at
OI Funovics, Martin/0000-0002-7300-1288
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NR 81
TC 11
Z9 12
U1 3
U2 29
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1936-5233
J9 TRANSL ONCOL
JI Transl. Oncol.
PD DEC
PY 2021
VL 14
IS 12
AR 101230
DI 10.1016/j.tranon.2021.101230
EA SEP 2021
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA XG5XO
UT WOS:000724825900001
PM 34598083
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ren, YC
   Mu, Y
   Song, YP
   Xie, JX
   Yu, H
   Gao, SN
   Li, S
   Peng, HS
   Zhou, YL
   Lu, WY
AF Ren, Yachao
   Mu, Yu
   Song, Yanping
   Xie, Jinxin
   Yu, Hui
   Gao, Sainan
   Li, Sen
   Peng, Haisheng
   Zhou, Yulong
   Lu, Weiyue
TI A new peptide ligand for colon cancer targeted delivery of micelles
SO DRUG DELIVERY
LA English
DT Article
DE Colonic drug delivery; DOX; integrin alpha(6)beta(1) receptor; micelles;
   peptide ligand
ID INTEGRIN; TUMOR; NANOPARTICLES; DOXORUBICIN; PENETRATION; RECEPTORS;
   MECHANISM; CULTURE; CELL
AB Ligands are an imperative part of targeted drug delivery systems, and choosing a ligand with high affinity is a subject of considerable interest. In this study, we first synthesized a 12-residue peptide (TK) that interacts with integrin alpha(6)beta(1) overexpressed on colonic cancer cells. The molecular binding affinity assay indicated that TK had a high binding affinity for integrin alpha(6)beta(1). The results of cellular and tumor spheroid uptake suggested that TK peptide not only increases Caco-2 cells uptake, but also effectively increases penetration of the tumor spheroids. TK-conjugated PEG-PLA was synthesized to prepare a novel PEG-PLA micelles loading DOX or coumarin-6 (TK-MS/DOX or TK-MS/C6). The obtained TK-MS/DOX exhibited uniform, spherical shape with a size of 23.80 +/- 0.32 nm and zeta potential of 12.21 +/- 0.31 mV. The release behavior of DOX from micelles were observed no significant changes after TK modification, however, the release profile exhibited pH-sensitive properties. Compared with MS/DOX, TK-MS/DOX exhibited significantly stronger cytotoxicity for Caco-2. Confocal laser microscopy and flow cytometry data further indicated that the targeting micelles not only had higher uptake by Caco-2 cells, but also more effectively penetrated the tumor spheroids. Therefore, TK peptide appears to be suitable as a targeting ligand with potential applications in colonic targeted therapy.
C1 [Ren, Yachao; Song, Yanping; Yu, Hui; Gao, Sainan; Li, Sen; Peng, Haisheng] Harbin Med Univ Daqing, Coll Pharm, Daqing, Peoples R China.
   [Ren, Yachao; Lu, Weiyue] Fudan Univ, Sch Pharm, Dept Pharmaceut, Key Lab Smart Drug Delivery,Minist Educ, Shanghai 201203, Peoples R China.
   [Mu, Yu; Xie, Jinxin] Jilin Univ, Coll Vet Med, Changchun, Peoples R China.
   [Zhou, Yulong] Heilongjiang Bayi Agr Univ, Anim Technol Coll, Daqing 163319, Peoples R China.
C3 Harbin Medical University; Fudan University; Jilin University;
   Heilongjiang Bayi Agricultural University
RP Lu, WY (corresponding author), Fudan Univ, Sch Pharm, Dept Pharmaceut, Key Lab Smart Drug Delivery,Minist Educ, Shanghai 201203, Peoples R China.; Zhou, YL (corresponding author), Heilongjiang Bayi Agr Univ, Anim Technol Coll, Daqing 163319, Peoples R China.
EM zhouyulong1980@163.com; wylu@shmu.edu.cn
RI mu, yu/KJM-2653-2024; Lu, Weiyue/E-7938-2010
OI Xie, Jinxin/0000-0003-4772-7162
FU Wu Liande Fund for the Youth of Harbin Medical University [WLD-QN1111];
   Natural Science Foundation Project for the Youth of Heilongjiang
   province [QC2013C029]; Post-Doctoral Scientific Research Startup Fund
   [LBH-Q13131]
FX The authors report no conflicts of interest. This work was supported by
   the Wu Liande Fund for the Youth of Harbin Medical University
   (WLD-QN1111), Natural Science Foundation Project for the Youth of
   Heilongjiang province (QC2013C029) and Post-Doctoral Scientific Research
   Startup Fund (LBH-Q13131).
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U1 1
U2 31
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1071-7544
EI 1521-0464
J9 DRUG DELIV
JI Drug Deliv.
PY 2016
VL 23
IS 5
SI SI
BP 1763
EP 1772
DI 10.3109/10717544.2015.1077293
PG 10
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DV5EM
UT WOS:000382949300027
PM 26289214
OA Bronze
DA 2025-01-04
ER

PT J
AU Tang, HM
   Li, YX
   Lian, JJ
   Ng, HY
   Wang, SSY
AF Tang, Haoming
   Li, Yi Xin
   Lian, Jun Jie
   Ng, Hsin-Yueh
   Wang, Samuel Sherng Young
TI Personalized treatment using predictive biomarkers in solid organ
   malignancies: A review
SO TUMORI JOURNAL
LA English
DT Review
DE personalized treatment; predictive biomarkers; malignancies; solid organ
ID RENAL-CELL CARCINOMA; PATHOLOGICAL COMPLETE RESPONSE; HER2-POSITIVE
   BREAST-CANCER; PANCREATIC DUCTAL ADENOCARCINOMA; SERUM CARCINOEMBRYONIC
   ANTIGEN; PLATINUM-BASED CHEMOTHERAPY; ENDOTHELIAL GROWTH-FACTOR;
   VEGF-TARGETED THERAPY; CARBONIC-ANHYDRASE-IX; COLORECTAL-CANCER
AB In recent years, the influence of specific biomarkers in the diagnosis and prognosis of solid organ malignancies has been increasingly prominent. The relevance of the use of predictive biomarkers, which predict cancer response to specific forms of treatment provided, is playing a more significant role than ever before, as it affects diagnosis and initiation of treatment, monitoring for efficacy and side effects of treatment, and adjustment in treatment regimen in the long term. In the current review, we explored the use of predictive biomarkers in the treatment of solid organ malignancies, including common cancers such as colorectal cancer, breast cancer, lung cancer, prostate cancer, and cancers associated with high mortalities, such as pancreatic cancer, liver cancer, kidney cancer and cancers of the central nervous system. We additionally analyzed the goals and types of personalized treatment using predictive biomarkers, and the management of various types of solid organ malignancies using predictive biomarkers and their relative efficacies so far in the clinical settings.
C1 [Tang, Haoming; Li, Yi Xin; Lian, Jun Jie; Ng, Hsin-Yueh] Duke NUS Med Sch, Singapore, Singapore.
   [Wang, Samuel Sherng Young] Singhealth, Singapore Gen Hosp, Internal Med Residency, Outram Rd, Singapore 169608, Singapore.
C3 National University of Singapore; Singapore General Hospital
RP Wang, SSY (corresponding author), Singhealth, Singapore Gen Hosp, Internal Med Residency, Outram Rd, Singapore 169608, Singapore.
EM samuel.wang@mohh.com.sg
OI Tang, Haoming/0009-0005-7510-1599
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NR 258
TC 0
Z9 0
U1 7
U2 7
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0300-8916
EI 2038-2529
J9 TUMORI J
JI Tumori J.
PD OCT
PY 2024
VL 110
IS 5
BP 386
EP 404
DI 10.1177/03008916241261484
EA AUG 2024
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA I1Q2K
UT WOS:001282512700001
PM 39091157
DA 2025-01-04
ER

PT J
AU Nakamura, Y
   Fujisawa, T
   Taniguchi, H
   Bando, H
   Okamoto, W
   Tsuchihara, K
   Yoshino, T
   Ohtsu, A
AF Nakamura, Yoshiaki
   Fujisawa, Takao
   Taniguchi, Hiroya
   Bando, Hideaki
   Okamoto, Wataru
   Tsuchihara, Katsuya
   Yoshino, Takayuki
   Ohtsu, Atsushi
TI SCRUM-Japan GI-SCREEN and MONSTAR-SCREEN: Path to the realization of
   biomarker-guided precision oncology in advanced solid tumors
SO CANCER SCIENCE
LA English
DT Review
DE circulating tumor DNA; multiomics; next-generation sequencing; precision
   oncology; real-world data
ID METASTATIC COLORECTAL-CANCER; DNA; MEDICINE; THERAPY; TISSUE
AB Comprehensive genomic profiling enables the detection of genomic biomarkers in advanced solid tumors. However, efficient patient screening for the success of precision oncology remains challenging due to substantial barriers, such as genotyping costs and accessibility to matched therapies. To address these challenges, we launched GI-SCREEN, a nationwide gastrointestinal cancer genomic screening project within the SCRUM-Japan network in 2015 with the specific purpose of matching patients with a diverse portfolio of affiliated interventional targeted therapy trials. Subsequently, we initiated the molecular profiling projects GOZILA, MONSTAR-SCREEN-1, and MONSTAR-SCREEN-2, which incorporate tissue and plasma multiomics approaches to accurately identify patients with advanced solid tumors who would benefit from matched therapies. These projects have led to a significant increase in patient participation in targeted clinical trials and the approval of several therapeutics and companion diagnostics. Additionally, clinicogenomic analyses utilizing the SCRUM-Japan database have provided new insights into the molecular mechanisms of advanced solid tumors. In this review, we describe the path to the realization of cancer precision medicine for patients with advanced solid tumors based on the SCRUM-Japan GI-SCREEN and MONSTAR-SCREEN platforms.
C1 [Nakamura, Yoshiaki; Taniguchi, Hiroya; Bando, Hideaki; Yoshino, Takayuki; Ohtsu, Atsushi] Natl Canc Ctr Hosp East, Dept Gastroenterol & Gastrointestinal Oncol, 6-5-1 Kashiwanoha, Kashiwa, Chiba 2778577, Japan.
   [Nakamura, Yoshiaki; Fujisawa, Takao; Taniguchi, Hiroya; Bando, Hideaki] Natl Canc Ctr Hosp East, Translat Res Support Sect, Kashiwa, Chiba, Japan.
   [Fujisawa, Takao] Natl Canc Ctr Hosp East, Dept Head & Neck Med Oncol, Kashiwa, Chiba, Japan.
   [Taniguchi, Hiroya] Aichi Canc Ctr Hosp, Dept Clin Oncol, Nagoya, Aichi, Japan.
   [Okamoto, Wataru] Hiroshima Univ Hosp, Canc Treatment Ctr, Hiroshima, Japan.
   [Tsuchihara, Katsuya] Natl Canc Ctr, Exploratory Oncol Res & Clin Trial Ctr, Div Translat Informat, Kashiwa, Chiba, Japan.
C3 National Cancer Center - Japan; National Cancer Center - Japan; National
   Cancer Center - Japan; Aichi Cancer Center; Hiroshima University;
   National Cancer Center - Japan
RP Yoshino, T (corresponding author), Natl Canc Ctr Hosp East, Dept Gastroenterol & Gastrointestinal Oncol, 6-5-1 Kashiwanoha, Kashiwa, Chiba 2778577, Japan.
EM tyoshino@east.ncc.go.jp
RI Okamoto, Wataru/AIE-0808-2022
OI Tsuchihara, Katsuya/0000-0001-7507-2349; Bando,
   Hideaki/0000-0001-5041-2765; Yoshino, Takayuki/0000-0002-0489-4756
CR [Anonymous], 2018, ANN ONCOL
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NR 34
TC 32
Z9 32
U1 1
U2 3
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 NOV
PY 2021
VL 112
IS 11
BP 4425
EP 4432
DI 10.1111/cas.15132
EA SEP 2021
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA WV8CN
UT WOS:000696395900001
PM 34510657
OA Green Published
DA 2025-01-04
ER

PT J
AU Tsuchida, N
   Murugan, AK
   Grieco, M
AF Tsuchida, Nobuo
   Murugan, Avaniyapuram Kannan
   Grieco, Michele
TI Kirsten <i>Ras</i>* oncogene: Significance of its discovery in human
   cancer research
SO ONCOTARGET
LA English
DT Review
DE Kirsten ras; K-ras; KRAS; human cancer; oncogene; EGFR-targeted therapy
ID MURINE SARCOMA-VIRUS; BLADDER-CARCINOMA ONCOGENE; EGFR-TARGETED
   THERAPIES; P21 TRANSFORMING PROTEIN; SRC FAMILY KINASES; KRAS CODON 12;
   COLORECTAL-CANCER; LUNG-CARCINOMA; NUCLEOTIDE-SEQUENCE;
   ACQUIRED-RESISTANCE
AB The KRAS/K-RAS oncogene is crucially involved in human cancer. The term "oncogene" -i.e., a gene able to transform a normal cell into a tumor cell - was introduced in 1969, but the word was not used in the human carcinogenesis literature until much later. Transforming Kras and Hras oncogenes from the Kirsten and Harvey sarcoma viruses were not identified until the early 1980s due to the complicated structures of the viral genomes. Orthologs of these viral oncogenes were then found in transforming DNA fragments in human cancers in the form of mutated versions of the HRAS and KRAS proto-oncogenes. Thus, RAS genes were the first human oncogenes to be identified. Subsequent studies showed that mutated KRAS acted as an in vivo oncogenic driver, as indicated by studies of anti-EGFR therapy for metastatic colorectal cancers. This review addresses the historical background and experimental studies that led to the discovery of Kirsten Ras as an oncogene, the role of mutated KRAS in human carcinogenesis, and recent therapeutic studies of cancer cells with KRAS mutations.
C1 [Tsuchida, Nobuo] Tokyo Med Dent Univ, Grad Sch Med & Dent Sci, Bunkyo Ku, Tokyo, Japan.
   [Murugan, Avaniyapuram Kannan] King Faisal Specialist Hosp & Res Ctr, Dept Mol Oncol, Riyadh, Saudi Arabia.
   [Grieco, Michele] Seconda Univ Napoli, Dipartimento Sci & Tecnol Ambientali Biol & Farma, DiSTABiF, Caserta, Italy.
C3 Institute of Science Tokyo; Tokyo Medical & Dental University (TMDU);
   King Faisal Specialist Hospital & Research Center; Universita della
   Campania Vanvitelli
RP Tsuchida, N (corresponding author), Tokyo Med Dent Univ, Grad Sch Med & Dent Sci, Bunkyo Ku, Tokyo, Japan.
EM ntutid.eme@tmd.ac.jp
RI Murugan, Avaniyapuram Kannan/AAI-8222-2020
OI Grieco, Michele/0000-0002-4212-7814; Murugan, Avaniyapuram
   Kannan/0000-0002-3096-6100
FU NIH [CA-22701]
FX Sincere thanks to Masakazu Hatanaka for providing the opportunity to
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   interests in Kras work. Works for the cloning of the Ki-SV genomic DNA
   and the identification of viral Kras oncogene were supported by NIH
   grant CA-22701 to N.T. as the P.I.
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NR 142
TC 48
Z9 54
U1 0
U2 25
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 JUL 19
PY 2016
VL 7
IS 29
BP 46717
EP 46733
DI 10.18632/oncotarget.8773
PG 17
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DY8SX
UT WOS:000385402300145
PM 27102293
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Yu, Z
   Hao, YY
   Huang, YH
   Ling, L
   Hu, XG
   Qiao, SM
AF Yu, Zhen
   Hao, Yuying
   Huang, Yuhua
   Ling, Ling
   Hu, Xigang
   Qiao, Simiao
TI Radiotherapy in the preoperative neoadjuvant treatment of locally
   advanced rectal cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE locally advanced rectal cancer; neoadjuvant treatment; total neoadjuvant
   treatment; radiotherapy; immunotherapy; targeted therapy
ID TOTAL MESORECTAL EXCISION; SHORT-TERM RADIOTHERAPY; PHASE-II TRIAL;
   VENOUS INFUSION 5-FLUOROURACIL; EPIDERMAL-GROWTH-FACTOR;
   RANDOMIZED-TRIAL; RADIATION-THERAPY; OPEN-LABEL; POSTOPERATIVE
   CHEMORADIOTHERAPY; ADJUVANT CHEMOTHERAPY
AB Radiotherapy and chemotherapy are effective treatments for patients with locally advanced rectal cancer (LARC) and can significantly improve the likelihood of R0 resection. Radiotherapy can be used as a local treatment to reduce the size of the tumor, improve the success rate of surgery and reduce the residual cancer cells after surgery. Early chemotherapy can also downgrade the tumor and eliminate micrometastases throughout the body, reducing the risk of recurrence and metastasis. The advent of neoadjuvant concurrent radiotherapy (nCRT) and total neoadjuvant treatment (TNT) has brought substantial clinical benefits to patients with LARC. Even so, given increasing demand for organ preservation and quality of life and the disease becoming increasingly younger in its incidence profile, there is a need to further explore new neoadjuvant treatment options to further improve tumor remission rates and provide other opportunities for patients to choose watch-and-wait (W&W) strategies that avoid surgery. Targeted drugs and immunologic agents (ICIs) have shown good efficacy in patients with advanced rectal cancer but have not been commonly used in neoadjuvant therapy for patients with LARC. In this paper, we review several aspects of neoadjuvant therapy, including radiation therapy and chemotherapy drugs, immune drugs and targeted drugs used in combination with neoadjuvant therapy, with the aim of providing direction and thoughtful perspectives for LARC clinical treatment and research trials.
C1 [Yu, Zhen; Hao, Yuying; Huang, Yuhua; Ling, Ling; Hu, Xigang; Qiao, Simiao] Southern Med Univ, Zhujiang Hosp, Dept Radiat Oncol, Guangzhou, Peoples R China.
C3 Southern Medical University - China
RP Hu, XG; Qiao, SM (corresponding author), Southern Med Univ, Zhujiang Hosp, Dept Radiat Oncol, Guangzhou, Peoples R China.
EM huxxgg@126.com; zjjxqsm2008@sina.cn
RI Huang, Yu-hua/IAP-2895-2023
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NR 161
TC 1
Z9 1
U1 1
U2 1
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 23
PY 2023
VL 13
AR 1300535
DI 10.3389/fonc.2023.1300535
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AI7W7
UT WOS:001117912800001
PM 38074690
OA gold
DA 2025-01-04
ER

PT J
AU Foda, AM
   AbdelAziz, A
   El-Hawary, AK
   Hosni, A
   Zalata, KR
   Gado, AI
AF Foda, Abd AlRahman M.
   AbdelAziz, Azza
   El-Hawary, Amira K.
   Hosni, Ali
   Zalata, Khalid R.
   Gado, Asmaa I.
TI Mucinous Colorectal Adenocarcinoma: Influence of EGFR and E-Cadherin
   Expression on Clinicopathologic Features and Prognosis
SO APPLIED IMMUNOHISTOCHEMISTRY & MOLECULAR MORPHOLOGY
LA English
DT Article
DE EGFR; E-cadherin; mucinous; nonmucinous; colorectal carcinoma;
   microarray
ID IN-SITU HYBRIDIZATION; BETA-CATENIN; TISSUE MICROARRAYS;
   COLON-CARCINOMA; CANCER PATIENTS; SURVIVAL; GROWTH; THERAPY; OUTCOMES;
   PATTERN
AB Previous studies have shown conflicting results on epidermal growth factor receptor (EGFR) and E-cadherin expression in colorectal carcinoma and their prognostic significance. To the best of our knowledge, this study is the first to investigate EGFR and E-cadherin expression, interrelation and relation to clinicopathologic, histologic parameters, and survival in rare colorectal mucinous adenocarcinoma (MA). In this study, we studied tumor tissue specimens from 150 patients with colorectal MA and nonmucinous adenocarcinoma (NMA). High-density manual tissue microarrays were constructed using modified mechanical pencil tips technique, and immunohistochemistry for EGFR and E-cadherin was performed. All relations were analyzed using established statistical methodologies. NMA expressed EGFR and E-cadherin in significantly higher rates with significant heterogenous pattern than MA. EGFR and E-cadherin positivity rates were significantly interrelated in both NMA and MA groups. In the NMA group, high EGFR expression was associated with old age, male sex, multiplicity of tumors, lack of mucinous component, and association with schistosomiasis. However, in the MA group, high EGFR expression was associated only with old age and MA subtype rather than signet ring carcinoma subtype. Conversely, high E-cadherin expression in MA cases was associated with old age, fungating tumor configuration, MA subtype, and negative intratumoral lymphocytic response. However, in the NMA cases, none of these factors was statistically significant. In a univariate analysis, neither EGFR nor E-cadherin expression showed a significant impact on disease-free or overall survival. Targeted therapy against EGFR and E-cadherin may not be useful in patients with MA. Neither EGFR nor E-cadherin is an independent prognostic factor in NMA or MA.
C1 [Foda, Abd AlRahman M.; AbdelAziz, Azza; El-Hawary, Amira K.; Zalata, Khalid R.; Gado, Asmaa I.] Mansoura Univ, Fac Med, Dept Pathol, Mansoura 35516, Egypt.
   [Hosni, Ali] Mansoura Univ, Fac Med, Dept Clin Oncol & Nucl Med, Mansoura 35516, Egypt.
C3 Egyptian Knowledge Bank (EKB); Mansoura University; Egyptian Knowledge
   Bank (EKB); Mansoura University
RP Foda, AM (corresponding author), Mansoura Univ, Fac Med, Dept Pathol, Mansoura 35516, Egypt.
EM abdofoda2009@yahoo.com
RI El-Hawary, Amira/O-3978-2018; foda, Abd/N-3683-2018; AbdelAziz,
   Azza/W-9980-2019
OI foda, abd elrahman/0000-0002-6858-9822; Abdel-Aziz,
   Azza/0000-0003-4403-7123
CR Alshenawy HA, 2013, ANN DIAGN PATHOL, V17, P476, DOI 10.1016/j.anndiagpath.2013.05.007
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NR 39
TC 3
Z9 3
U1 0
U2 4
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 AUG
PY 2015
VL 23
IS 7
BP 506
EP 515
DI 10.1097/PAI.0000000000000112
PG 10
WC Anatomy & Morphology; Medical Laboratory Technology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Anatomy & Morphology; Medical Laboratory Technology; Pathology
GA CQ1CV
UT WOS:000360335800005
PM 26262813
DA 2025-01-04
ER

PT J
AU Dal Buono, A
   Gaiani, F
   Poliani, L
   Correale, C
   Laghi, L
AF Dal Buono, Arianna
   Gaiani, Federica
   Poliani, Laura
   Correale, Carmen
   Laghi, Luigi
TI Defects in MMR Genes as a Seminal Example of Personalized Medicine: From
   Diagnosis to Therapy
SO JOURNAL OF PERSONALIZED MEDICINE
LA English
DT Article
DE microsatellite instability; colorectal cancer; immunotherapy; targeted
   therapy
ID III COLON-CANCER; NONPOLYPOSIS COLORECTAL-CANCER; MISMATCH-REPAIR
   DEFICIENCY; ISLAND METHYLATOR PHENOTYPE; MICROSATELLITE-INSTABILITY;
   LYNCH-SYNDROME; STAGE-II; POOLED ANALYSIS; HMLH1 PROMOTER; BRAF MUTATION
AB Microsatellite instability (MSI) is the landmark feature of DNA mismatch repair deficiency, which can be found in 15-20% of all colorectal cancers (CRC). This specific set of tumors has been initially perceived as a niche for geneticists or gastroenterologists focused on inherited predispositions. However, over the years, MSI has established itself as a key biomarker for the diagnosis, then extending to forecasting the disease behavior and prognostication, including the prediction of responsiveness to immunotherapy and eventually to kinase inhibitors, and possibly even to specific biological drugs. Thanks to the contribution of the characterization of MSI tumors, researchers have first acknowledged that a strong lymphocytic reaction is associated with a good prognosis. This understanding supported the prognostic implications in terms of the low metastatic potential of MSI-CRC and has led to modifications in the indications for adjuvant treatment. Furthermore, with the emergence of immunotherapy, this strong biomarker of responsiveness has exemplified the capability of re-activating an effective immune control by removing the brakes of immune evasion. Lately, a subset of MSI-CRC emerged as the ideal target for kinase inhibitors. This therapeutic scenario implies a paradox in which appropriate treatments for advanced disease are effective in a set of tumors that seldom evolve towards metastases.
C1 [Dal Buono, Arianna; Poliani, Laura; Correale, Carmen] Humanitas Res Hosp IRCCS, Dept Gastroenterol, Div Gastroenterol, I-20089 Rozzano, Italy.
   [Gaiani, Federica; Laghi, Luigi] Univ Parma, Dept Med & Surg, I-43121 Parma, Italy.
   [Poliani, Laura] IRCCS Osped San Raffaele, Gastroenterol & Endoscopy Unit, I-20132 Milan, Italy.
   [Laghi, Luigi] Humanitas Res Hosp IRCCS, Lab Mol Gastroenterol, I-20089 Rozzano, Italy.
C3 IRCCS Humanitas Research Hospital; University of Parma; Vita-Salute San
   Raffaele University; IRCCS Ospedale San Raffaele; IRCCS Humanitas
   Research Hospital
RP Laghi, L (corresponding author), Univ Parma, Dept Med & Surg, I-43121 Parma, Italy.; Laghi, L (corresponding author), Humanitas Res Hosp IRCCS, Lab Mol Gastroenterol, I-20089 Rozzano, Italy.
EM arianna.dalbuono@humanitas.it; federica.gaiani@unipr.it;
   poliani.laura@hsr.it; carmen.correale@humanitasresearch.it;
   luigiandreagiuseppe.laghi@unipr.it
RI correale, carmen/LFU-0222-2024; Dal Buono, Arianna/HLG-1576-2023; Laghi,
   Luigi/GZM-5831-2022
OI Dal Buono, Arianna/0000-0002-8543-4355; Laghi,
   Luigi/0000-0003-4187-1059; correale, carmen/0000-0002-6950-2987; Gaiani,
   Federica/0000-0001-9615-0086
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NR 100
TC 11
Z9 11
U1 0
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4426
J9 J PERS MED
JI J. Pers. Med.
PD DEC
PY 2021
VL 11
IS 12
AR 1333
DI 10.3390/jpm11121333
PG 13
WC Health Care Sciences & Services; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Health Care Sciences & Services; General & Internal Medicine
GA YI4DZ
UT WOS:000743801300001
PM 34945805
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Chou, AG
   Fraser, T
   Ahadi, M
   Fuchs, T
   Sioson, L
   Clarkson, A
   Sheen, A
   Singh, N
   Corless, CL
   Gill, AJ
AF Chou, Angela
   Fraser, Tamara
   Ahadi, Mahsa
   Fuchs, Talia
   Sioson, Loretta
   Clarkson, Adele
   Sheen, Amy
   Singh, Nisha
   Corless, Christopher L.
   Gill, Anthony J.
TI <i>NTRK</i> gene rearrangements are highly enriched in MLH1/PMS2
   deficient, <i>BRAF</i> wild-type colorectal carcinomas-a study of 4569
   cases
SO MODERN PATHOLOGY
LA English
DT Article
ID BRAFV600E IMMUNOHISTOCHEMISTRY; LAROTRECTINIB; CANCERS
AB NTRK gene rearrangements are important to identify as predictors of response to targeted therapy in many malignancies. Only 0.16-0.3% of colorectal carcinomas (CRCs) harbor these fusions making universal screening difficult. We therefore investigated whether pan-Trk immunohistochemistry (IHC), mismatch repair deficiency (MMRd), and BRAFV600E mutation status could be used to triage molecular testing for NTRK gene rearrangements in CRC. CRCs from 4569 unselected patients underwent IHC in TMA format with two different anti-pan-Trk rabbit monoclonal antibodies. All positive cases were confirmed on whole sections and underwent RNA-sequencing. Pan-Trk IHC was positive in 0.2% of CRCs (9/4569). Both antibodies demonstrated similar staining characteristics with diffuse positive staining in all neoplastic cells. Of note 8/9 (89%) IHC positive cases were both MMRd (all showing MLH1/PMS2 loss) and lacked BRAFV600E mutation. That is, IHC was positive in 5.3% (8/152) MLH1/PMS2/BRAFV600E triple negative CRCs, but only 0.02% (1/4417) not showing this phenotype. All nine IHC positive CRCs demonstrated gene rearrangements (LMNA-NTRK1 in 5 CRCs, TPR-NTRK1, STRM-NTRK1, MUC2-NTRK2, and NTRK1 with an unknown partner in one each), suggesting close to 100% specificity for IHC in this sub-population. NTRK fusions were associated with right sided (p = 0.02), larger tumors (p = 0.029) with infiltrative growth (p = 0.021). As a part of universal Lynch syndrome screening many institutions routinely test all CRCs for MMRd, and then proceed to reflex BRAFV600E mutation testing in MLH1/PMS2 negative CRCs. We conclude that performing pan-Trk IHC on this preselected subgroup of MLH1/PMS2/BRAFV600E triple negative CRCs (only 3.3% of all CRC patients) is a resource effective approach to identify the overwhelming majority of CRC patients with NTRK gene fusions.
C1 [Chou, Angela; Fraser, Tamara; Ahadi, Mahsa; Fuchs, Talia; Sioson, Loretta; Clarkson, Adele; Sheen, Amy; Gill, Anthony J.] Royal North Shore Hosp, Kolling Inst Med Res, Canc Diag & Pathol Grp, St Leonards, NSW 2065, Australia.
   [Chou, Angela; Ahadi, Mahsa; Fuchs, Talia; Gill, Anthony J.] Univ Sydney, Sydney, NSW 2006, Australia.
   [Chou, Angela; Fraser, Tamara; Ahadi, Mahsa; Fuchs, Talia; Sioson, Loretta; Clarkson, Adele; Sheen, Amy; Singh, Nisha; Gill, Anthony J.] Royal North Shore Hosp, NSW Hlth Pathol, St Leonards, NSW 2065, Australia.
   [Fraser, Tamara] Univ Technol Sydney, Sch Life Sci, Ultimo, NSW 2007, Australia.
   [Corless, Christopher L.] Oregon Hlth & Sci Univ, Dept Pathol, Portland, OR 97239 USA.
   [Corless, Christopher L.] Oregon Hlth & Sci Univ, Knight Canc Inst, Portland, OR 97239 USA.
C3 Royal North Shore Hospital; University of Sydney; Kolling Institute of
   Medical Research; University of Sydney; Royal North Shore Hospital;
   University of Technology Sydney; Oregon Health & Science University;
   Oregon Health & Science University
RP Gill, AJ (corresponding author), Royal North Shore Hosp, Kolling Inst Med Res, Canc Diag & Pathol Grp, St Leonards, NSW 2065, Australia.; Gill, AJ (corresponding author), Univ Sydney, Sydney, NSW 2006, Australia.; Gill, AJ (corresponding author), Royal North Shore Hosp, NSW Hlth Pathol, St Leonards, NSW 2065, Australia.
EM affgill@med.usyd.edu.au
RI Gill, Anthony/D-4215-2015; Fuchs, Talia/N-7416-2019
OI Gill, Anthony/0000-0002-9447-1967; Seyed Ahadi,
   Mahsa/0000-0002-4687-8666; Chou, Angela/0000-0001-9212-6927; Fuchs,
   Talia/0000-0002-9166-6822; Fraser, Tamara/0000-0001-9947-5361
CR Amatu A, 2016, ESMO OPEN, V1, DOI 10.1136/esmoopen-2015-000023
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NR 30
TC 49
Z9 51
U1 0
U2 3
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 MAY
PY 2020
VL 33
IS 5
BP 924
EP 932
DI 10.1038/s41379-019-0417-3
PG 9
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA LI5XT
UT WOS:000529559200016
PM 31792356
OA Bronze
DA 2025-01-04
ER

PT J
AU Knott, EA
   Ziemlewicz, TJ
   Lubner, SJ
   Swietlik, JF
   Weber, SM
   Zlevor, AM
   Longhurst, C
   Hinshaw, JL
   Lubner, MG
   Mulkerin, DL
   Abbott, DE
   Deming, D
   LoConte, NK
   Uboha, N
   Couillard, AB
   Wells, SA
   Laeseke, PF
   Alexander, ML
   Lee, FT 
AF Knott, Emily A.
   Ziemlewicz, Timothy J.
   Lubner, Sam J.
   Swietlik, John F.
   Weber, Sharon M.
   Zlevor, Annie M.
   Longhurst, Colin
   Hinshaw, J. Louis
   Lubner, Meghan G.
   Mulkerin, Daniel L.
   Abbott, Daniel E.
   Deming, Dustin
   LoConte, Noelle K.
   Uboha, Nataliya
   Couillard, Allison B.
   Wells, Shane A.
   Laeseke, Paul F.
   Alexander, Marci L.
   Lee, Fred T., Jr.
TI Microwave ablation for colorectal cancer metastasis to the liver: a
   single-center retrospective analysis
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Colorectal cancer; ablation; hepatic metastasis; treatment of
   metastasis; liver targeted therapy
ID LOCAL TUMOR PROGRESSION; PERCUTANEOUS RADIOFREQUENCY ABLATION; LONG-TERM
   SURVIVAL; HEPATIC RESECTION; EXPERIENCE; MARGINS; COMPLICATIONS;
   CRYOABLATION; CHEMOTHERAPY; SIZE
AB Background: The purpose of this study is to evaluate the safety and intermediate-term efficacy of percutaneous microwave (MW) ablation for the treatment of colorectal liver metastases (CRLM) at a single institution. Methods: A retrospective review was performed of all CRLM treated with MW ablation from 3/2011 to 7/2020 (102 tumors; 72 procedures; 57 patients). Mean age was 60 years (range, 36-88) and mean tumor size was 1.8 cm (range, 0.5-5.0 cm). The patient population included 19 patients with extra-hepatic disease. Chemotherapy (pre-and/or post-ablation) was given in 98% of patients. Forty-five sessions were preceded by other focal CRLM treatments including resection, ablation, radiation, and radioembolization. Kaplan-Meier curves were used to estimate local tumor progression-free survival (LTPFS), disease-free survival (DFS), and overall survival (OS) and multivariate analysis (Cox Proportional Hazards model) was used to test predictors of OS. Results: Technical success (complete ablation) was 100% and median follow-up was 42 months (range, 1-112). There was a 4% major complication rate and an overall complication rate of 8%. Local tumor progression (LTP) rate during the entire study period was 4/98 (4%), in which 2 were retreated with MW ablation for a secondary LTP-rate of 2%. LTP-free survival at 1, 3, and 5 years was 93%, 58%, and 39% and median LTP-free survival was 48 months. OS at 1, 3, and 5 years was 96%, 66%, 47% and median OS was 52 months. There were no statistically significant predictors of OS. Conclusions: MW ablation of hepatic colorectal liver metastases appears safe with excellent local tumor control and prolonged survival compared to historical controls in selected patients. Further comparative studies with other local treatment strategies appear indicated.
C1 [Knott, Emily A.; Ziemlewicz, Timothy J.; Swietlik, John F.; Weber, Sharon M.; Zlevor, Annie M.; Hinshaw, J. Louis; Lubner, Meghan G.; Couillard, Allison B.; Wells, Shane A.; Laeseke, Paul F.; Alexander, Marci L.; Lee, Fred T., Jr.] Univ Wisconsin, Dept Radiol, Madison, WI 53706 USA.
   [Lubner, Sam J.; Mulkerin, Daniel L.; Deming, Dustin; LoConte, Noelle K.; Uboha, Nataliya] Univ Wisconsin, Dept Med, Madison, WI USA.
   [Lubner, Sam J.; Weber, Sharon M.; Longhurst, Colin; Mulkerin, Daniel L.; Abbott, Daniel E.; Deming, Dustin; LoConte, Noelle K.; Uboha, Nataliya; Laeseke, Paul F.; Lee, Fred T., Jr.] Univ Wisconsin, Carbone Canc Ctr, Madison, WI USA.
   [Weber, Sharon M.; Abbott, Daniel E.] Univ Wisconsin, Dept Surg, Madison, WI USA.
   [Longhurst, Colin] Univ Wisconsin, Dept Biostat & Med Informat, Madison, WI USA.
   [Hinshaw, J. Louis; Lee, Fred T., Jr.] Univ Wisconsin, Dept Urol, Madison, WI USA.
   [Lee, Fred T., Jr.] Univ Wisconsin, Dept Biomed Engn, Madison, WI USA.
C3 University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison;
   University of Wisconsin System; University of Wisconsin Madison
RP Lee, FT  (corresponding author), 600 Highland Ave, Madison, WI 53792 USA.
RI Weber, Michele/H-1001-2012; Ziemlewicz, Timothy/C-3995-2015
OI Zlevor, Annie/0000-0003-4990-9461; Swietlik, John/0000-0002-7180-794X;
   Lubner, Sam/0000-0002-5732-2938
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NR 65
TC 13
Z9 13
U1 0
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 AUG
PY 2021
VL 12
IS 4
BP 1454
EP 1469
DI 10.21037/jgo-21-159
PG 16
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA UK6RI
UT WOS:000692094500023
PM 34532102
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Middleton, G
   Yang, YQ
   Campbell, CD
   André, T
   Atreya, CE
   Schellens, JHM
   Yoshino, T
   Bendell, JC
   Hollebecque, A
   Mcree, AJ
   Siena, S
   Gordon, MS
   Tabernero, J
   Yaeger, R
   O'Dwyer, PJ
   De Vos, F
   Van Cutsem, E
   Millholland, JM
   Brase, JC
   Rangwala, F
   Gasal, E
   Corcoran, RB
AF Middleton, Gary
   Yang, Yiqun
   Campbell, Catarina D.
   Andre, Thierry
   Atreya, Chloe E.
   Schellens, Jan H. M.
   Yoshino, Takayuki
   Bendell, Johanna C.
   Hollebecque, Antoine
   McRee, Autumn J.
   Siena, Salvatore
   Gordon, Michael S.
   Tabernero, Josep
   Yaeger, Rona
   O'Dwyer, Peter J.
   De Vos, Filip
   Van Cutsem, Eric
   Millholland, John M.
   Brase, Jan C.
   Rangwala, Fatima
   Gasal, Eduard
   Corcoran, Ryan B.
TI <i>BRAF</i>-Mutant Transcriptional Subtypes Predict Outcome of Combined
   BRAF, MEK, and EGFR Blockade with Dabrafenib, Trametinib, and
   Panitumumab in Patients with Colorectal Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID CONSENSUS MOLECULAR SUBTYPES; CELL LUNG-CANCER; OPEN-LABEL; INHIBITION;
   MULTICENTER; MELANOMA; EXPRESSION
AB Purpose: The influence of the transcriptional and immunologic context of mutations on therapeutic outcomes with targeted therapy in cancer has not been well defined. BRAF V600E-mutant (BM) colorectal cancer comprises two main transcriptional subtypes, BM1 and BM2. We sought to determine the impact of BM subtype, as well as distinct biological features of those subtypes, on response to BRAF/MEK/EGFR inhibition in patients with colorectal cancer.
   Patients and Methods: Paired fresh tumor biopsies were acquired at baseline and on day 15 of treatment from all consenting patients withBMcolorectal cancer enrolled in a phase II clinical trial of dabrafenib, trametinib, and panitumumab. For each sample, BM subtype, cell cycle, and immune gene signature expression were determined using RNA-sequencing (RNA-seq), and a Cox proportional hazards model was applied to determine association with progression-free survival (PFS).
   Results: Confirmed response rates, median PFS, and median overall survival (OS) were higher in BM1 subtype patients compared with BM2 subtype patients. Evaluation of immune contexture identified greater immune reactivity in BM1, whereas cell-cycle signatures were more highly expressed in BM2. A multivariate model of PFS incorporating BM subtype plus immune and cell-cycle signatures revealed that BM subtype encompasses the majority of the effect.
   Conclusions: BM subtype is significantly associated with the outcome of combination dabrafenib, trametinib, and panitumumab therapy and may serve as a standalone predictive biomarker beyond mutational status. Our findings support a more nuanced approach to targeted therapeutic decisions that incorporates assessment of transcriptional context.
C1 [Middleton, Gary] Univ Birmingham, Inst Immunol & Immunotherapy, Birmingham, W Midlands, England.
   [Yang, Yiqun; Campbell, Catarina D.; Millholland, John M.] Novartis Inst BioMed Res, Cambridge, MA USA.
   [Andre, Thierry] Hop St Antoine, Paris, France.
   [Andre, Thierry] Sorbonne Univ, UPMC Paris 06, Paris, France.
   [Atreya, Chloe E.] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.
   [Schellens, Jan H. M.] Netherlands Canc Inst, Amsterdam, Netherlands.
   [Yoshino, Takayuki] Natl Canc Ctr Hosp East, Chiba, Japan.
   [Bendell, Johanna C.] Sarah Cannon Res Inst Tennessee Oncol, Nashville, TN USA.
   [Hollebecque, Antoine] Inst Gustave Roussy, Villejuif, France.
   [McRee, Autumn J.] Univ N Carolina, Chapel Hill, NC 27515 USA.
   [Siena, Salvatore] Univ Milan, Dept Oncol & Hematooncol, Milan, Italy.
   [Siena, Salvatore] Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, Milan, Italy.
   [Gordon, Michael S.] Pinnacle Oncol Hematol, Scottsdale, AZ USA.
   [Tabernero, Josep] Vall dHebron Univ Hosp, Barcelona, Spain.
   [Yaeger, Rona] Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10021 USA.
   [O'Dwyer, Peter J.] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
   [De Vos, Filip] Univ Utrecht, Univ Med Ctr Utrecht, Dept Med Oncol, Utrecht, Netherlands.
   [Van Cutsem, Eric] Univ Hosp Leuven, Leuven, Belgium.
   [Van Cutsem, Eric] Katholieke Univ Leuven, Leuven, Belgium.
   [Brase, Jan C.] Novartis Pharma AG, Basel, Switzerland.
   [Rangwala, Fatima; Gasal, Eduard] Novartis Pharmaceut, E Hanover, NJ USA.
   [Corcoran, Ryan B.] Massachusetts Gen Hosp, Canc Ctr, Boston, MA 02114 USA.
   [Corcoran, Ryan B.] Harvard Med Sch, Dept Med, Boston, MA 02115 USA.
C3 University of Birmingham; Novartis; Novartis USA; Assistance Publique
   Hopitaux Paris (APHP); Sorbonne Universite; Hopital Universitaire
   Saint-Antoine - APHP; Sorbonne Universite; University of California
   System; University of California San Francisco; UCSF Medical Center;
   UCSF Helen Diller Family Comprehensive Cancer Center; Netherlands Cancer
   Institute; National Cancer Center - Japan; Tennessee Oncology; Sarah
   Cannon Research Institute; UNICANCER; Gustave Roussy; University of
   North Carolina; University of North Carolina Chapel Hill; University of
   Milan; Hospital Universitari Vall d'Hebron; Memorial Sloan Kettering
   Cancer Center; University of Pennsylvania; Utrecht University; Utrecht
   University Medical Center; KU Leuven; University Hospital Leuven; KU
   Leuven; Novartis; Novartis; Novartis USA; Harvard University;
   Massachusetts General Hospital; Harvard University; Harvard Medical
   School
RP Middleton, G (corresponding author), Univ Birmingham, Vincent Dr, Birmingham B15 2TT, W Midlands, England.
EM g.middleton@bham.ac.uk
RI Siena, Salvatore/ACK-2413-2022; Schellens, Jan/O-8444-2016; li,
   yue/IXD-9935-2023; Van+Cutsem, Eric/ABE-1762-2021; André,
   Thierry/N-8830-2017; Hollebecque, Antoine/M-2695-2013
OI Middleton, Gary/0000-0001-5695-3474; Hollebecque,
   Antoine/0000-0003-2869-7551; Andre, Thierry/0000-0002-5103-7095
FU GlaxoSmithKline; Novartis; Novartis Pharmaceuticals Corporation
FX This study was supported by GlaxoSmithKline and Novartis. As of March 2,
   2015, dabrafenib and trametinib are assets of Novartis AG. The authors
   would like to acknowledge the investigators of this trial for providing
   all the biopsies that were so critical to this work. The authors would
   also like to thank Ilona Tala for assistance with biosample management
   and Rebecca Leary for her efforts in directing the lab work associated
   with this study as well as helpful scientific discussion. Medical
   writing assistance was provided by Amy Ghiretti, PhD (ArticulateScience
   LLC), funded by Novartis Pharmaceuticals Corporation.
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NR 36
TC 40
Z9 41
U1 0
U2 1
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 JUN 1
PY 2020
VL 26
IS 11
BP 2466
EP 2476
DI 10.1158/1078-0432.CCR-19-3579
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LU6GQ
UT WOS:000537852100007
PM 32047001
OA Bronze, Green Accepted, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Song, QL
   Jia, JJ
   Niu, XX
   Zheng, CX
   Zhao, HJ
   Sun, LL
   Zhang, HL
   Wang, L
   Zhang, ZZ
   Zhang, Y
AF Song, Qingling
   Jia, Jiajia
   Niu, Xiuxiu
   Zheng, Cuixia
   Zhao, Hongjuan
   Sun, Lingling
   Zhang, Hongling
   Wang, Lei
   Zhang, Zhenzhong
   Zhang, Yun
TI An oral drug delivery system with programmed drug release and imaging
   properties for orthotopic colon cancer therapy
SO NANOSCALE
LA English
DT Article
ID MESOPOROUS SILICA; HYDROXYAPATITE NANORODS; TARGETED DELIVERY;
   NANOPARTICLES; 5-FLUOROURACIL; NANOCOMPOSITE; RESISTANCE; CELLS
AB Oral drug delivery systems (ODDSs) have attracted considerable attention in relation to orthotopic colon cancer therapy due to certain popular advantages. Unfortunately, their clinical applications are generally limited by the side-effects caused by systemic drug exposure and poor real-time monitoring capabilities. Inspired by the characteristics of pH changes of the gastrointestinal tract (GIT) and specific enzymes secreted by the colonic microflora, we anchored polyacrylic acid (PAA) and chitosan (CS) on Gd3+-doped mesoporous hydroxyapatite nanoparticles (Gd-MHAp NPs) to realize programmed drug release and magnetic resonance imaging (MRI) at the tumor sites. In particular, the grafted PAA, as a pH-responsive switch, could effect controlled drug release in the colon. Further, CS is functionalized as the enzyme-sensitive moiety, which could be degraded by beta-glycosidase in the colon. Gadolinium is a paramagnetic lanthanide element used in chelates, working as a contrast medium agent for an MRI system. Interestingly, after oral administration, CS and PAA could protect the drug-loaded nanoparticles (NPs) against variable physiological conditions in the GIT, allowing the drug to reach the colon tumor sites, preventing premature drug release. Enhanced drug concentrations at the colon tumor sites were achieved via this programmed drug release, which subsequently ameliorated the therapeutic effect. In addition, encapsulating both chemotherapeutic (5-fluorouracil, 5-FU) and targeted therapy drug (gefitinib, Gef) within Gd-MHAp NPs produced a synergistic therapeutic effect. In summary, this study demonstrated that such a novel drug system (Gd-MHAp/5-FU/Gef/CS/PAA NPs) could protect, transport, and program drug release locally within the colonic environment; further, this system exhibited a worthwhile therapeutic effect, providing a promising novel treatment strategy for orthotopic colon cancer.
C1 [Song, Qingling; Jia, Jiajia; Niu, Xiuxiu; Zheng, Cuixia; Zhao, Hongjuan; Sun, Lingling; Zhang, Hongling; Wang, Lei; Zhang, Zhenzhong; Zhang, Yun] Zhengzhou Univ, Sch Pharmaceut Sci, 100 Kexue Ave, Zhengzhou 450001, Henan, Peoples R China.
   [Song, Qingling; Jia, Jiajia; Niu, Xiuxiu; Zheng, Cuixia; Zhao, Hongjuan; Sun, Lingling; Zhang, Hongling; Wang, Lei; Zhang, Zhenzhong; Zhang, Yun] Key Lab Targeting Therapy & Diag Crit Dis, 100 Kexue Ave, Zhengzhou 450001, Henan, Peoples R China.
   [Song, Qingling; Jia, Jiajia; Niu, Xiuxiu; Zheng, Cuixia; Zhao, Hongjuan; Sun, Lingling; Zhang, Hongling; Wang, Lei; Zhang, Zhenzhong; Zhang, Yun] Collaborat Innovat Ctr New Drug Res & Safety Eval, Henan Prov 100 Kexue Ave, Zhengzhou 450001, Henan, Peoples R China.
C3 Zhengzhou University
RP Wang, L; Zhang, ZZ; Zhang, Y (corresponding author), Zhengzhou Univ, Sch Pharmaceut Sci, 100 Kexue Ave, Zhengzhou 450001, Henan, Peoples R China.; Wang, L; Zhang, ZZ; Zhang, Y (corresponding author), Key Lab Targeting Therapy & Diag Crit Dis, 100 Kexue Ave, Zhengzhou 450001, Henan, Peoples R China.; Wang, L; Zhang, ZZ; Zhang, Y (corresponding author), Collaborat Innovat Ctr New Drug Res & Safety Eval, Henan Prov 100 Kexue Ave, Zhengzhou 450001, Henan, Peoples R China.
EM hahalei@139.com; zhangzz08@126.com; zhang_yun@ymail.com
RI zhang, zhanzhan/HNS-0642-2023; huang, lei/GQP-8739-2022; Zhang,
   Zhen/GXH-3666-2022
FU National Science Foundation of China [81773276, 81673021, 81572991,
   81874304, U1804183]; Scientific and Technological Project of Henan
   Province [182102310117]
FX All authors gratefully acknowledge financial support from the National
   Science Foundation of China under grant No. 81773276, 81673021,
   81572991, 81874304 and U1804183, and the Scientific and Technological
   Project of Henan Province (182102310117).
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TC 54
Z9 59
U1 7
U2 184
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 14
PY 2019
VL 11
IS 34
BP 15958
EP 15970
DI 10.1039/c9nr03802g
PG 13
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 IU6IZ
UT WOS:000483691300019
PM 31418432
DA 2025-01-04
ER

PT J
AU Islam, F
   Gopalan, V
   Vider, J
   Lu, CT
   Lam, AKY
AF Islam, Farhadul
   Gopalan, Vinod
   Vider, Jelena
   Lu, Cu-tai
   Lam, Alfred K. -Y.
TI <i>MiR</i>-<i>142</i>-<i>5p</i> act as an oncogenic microRNA in
   colorectal cancer: Clinicopathological and functional insights
SO EXPERIMENTAL AND MOLECULAR PATHOLOGY
LA English
DT Article
DE Colorectal cancer; miR-142-5p; KLF6; Targeted therapy; Onco-miRNA
ID SQUAMOUS-CELL CARCINOMA; COLON-CANCER; EXPRESSION; OVEREXPRESSION;
   THERAPY; GROWTH; PREDICTION; MUTATIONS; APOPTOSIS; MIRNAS
AB Objectives: miR-142-5p was noted aberrantly expressed and plays important roles in different pathophysiological conditions in human. The present study aims to examine the expression of miR-142-5p and its association with clinicopathological factors in a large cohort of patients with colorectal cancer. In addition, the cellular effects of miR-142-5p and its interacting targets in colon cancer cells were investigated.
   Methods: Expression of miR-142-5p in colorectal cancer tissues (n = 125) and colon cancer cell lines were analysed using real-time polymerase chain reaction. In vitro assays (cell proliferation, wound healing and colony formation) were used to study the miR-142-5p induced cellular effects. Western blots were used to examine the modulation of FAM134B, KRAS, EPAS1 and KLF6 proteins expression followed by miR-142-5p expression-manipulation.
   Results: Significant high expression of miR-142-5p was noted in cancer tissues and cells when compared to the controls (p < 0.001). Overexpression of miR-142-5p in patients with colorectal cancer was common (72%; 90/125). miR-142-Sp overexpression was associated with cancer in the proximal colorectum and with B-ref positive patients (p = 0.05). Exogenous overexpression of miR-142-5p resulted in significantly increased cell proliferation, colony formation, and wound healing capacities, whereas inhibition of endogenous miR-142-5p led reduced cancer growth properties. The cellular effects of miR-142-5p were mediated by the modulation of tumour suppressor KLF6 expression, as the expression of miR-142-5p and KLF6 protein are inversely correlated in colon cancer cells.
   Conclusion: High miR-142-5p expression was associated with the biological aggressiveness of cancer. Thus, suppression of miR-142-5p could be a therapeutic strategy for patients with colorectal cancers.
C1 [Islam, Farhadul; Gopalan, Vinod; Lam, Alfred K. -Y.] Griffith Univ, Sch Med, Canc Mol Pathol, Gold Coast, Qld 4222, Australia.
   [Islam, Farhadul; Gopalan, Vinod; Lam, Alfred K. -Y.] Griffith Univ, Griffith Hlth Inst, Gold Coast, Qld 4222, Australia.
   [Islam, Farhadul] Univ Rajshahi, Dept Biochem & Mol Biol, Rajshahi 6205, Bangladesh.
   [Gopalan, Vinod; Vider, Jelena] Griffith Univ, Sch Med Sci, Gold Coast, Qld, Australia.
   [Gopalan, Vinod; Vider, Jelena] Griffith Univ, Menzies Hlth Inst Queensland, Gold Coast, Qld, Australia.
   [Lu, Cu-tai] Gold Coast Univ Hosp, Dept Surg, Gold Coast, Qld, Australia.
C3 Griffith University; Griffith University - Gold Coast Campus; Griffith
   University; Griffith University - Gold Coast Campus; Menzies Health
   Institute Queensland; University of Rajshahi; Griffith University;
   Griffith University - Gold Coast Campus; Griffith University; Griffith
   University - Gold Coast Campus; Menzies Health Institute Queensland;
   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 Vider, Jelena/AAW-8577-2020; Islam, Farhadul/R-5643-2017; Lam,
   Alfred/C-1652-2008; Gopalan, Vinod/C-4269-2016
OI Islam, Farhadul/0000-0001-5262-4702; Lam, Alfred/0000-0003-2771-564X;
   Lu, Cu Tai/0000-0001-9565-3749; Gopalan, Vinod/0000-0003-0366-9482
FU Griffith University; Menzies Health Institute Queensland
FX The project was supported by the student scholarship from Griffith
   University and funding from Menzies Health Institute Queensland.
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NR 39
TC 49
Z9 53
U1 0
U2 10
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4800
EI 1096-0945
J9 EXP MOL PATHOL
JI Exp. Mol. Pathol.
PD FEB
PY 2018
VL 104
IS 1
BP 98
EP 107
DI 10.1016/j.yexmp.2018.01.006
PG 10
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA FV8SS
UT WOS:000424857700015
PM 29337244
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Huo, JT
   Tuersun, A
   Yu, SY
   Zhang, YC
   Feng, WQ
   Xu, ZQ
   Zhao, JK
   Zong, YP
   Lu, AG
AF Huo, Jian-Ting
   Tuersun, Abudumaimaitijiang
   Yu, Su-Yue
   Zhang, Yu-Chen
   Feng, Wen-Qing
   Xu, Zhuo-Qing
   Zhao, Jing-Kun
   Zong, Ya-Ping
   Lu, Ai-Guo
TI Leveraging a KRAS-based signature to predict the prognosis and drug
   sensitivity of colon cancer and identifying SPINK4 as a new biomarker
SO SCIENTIFIC REPORTS
LA English
DT Article
ID COLORECTAL-CANCER; MICROSATELLITE INSTABILITY; RAS MUTATIONS;
   LUNG-CANCER; BRAF; CHEMOTHERAPY; INFLAMMATION; PROGRESSION; SURVIVAL;
   IL-6
AB KRAS is one of the leading mutations reported in colon cancer. However, there are few studies on the application of KRAS related signature in predicting prognosis and drug sensitivity of colon cancer patient. We identified KRAS related differentially expressed genes (DEGs) using The Cancer Genome Atlas (TCGA) database. A signature closely related to overall survival was recognized with Kaplan-Meier survival analysis and univariate cox regression analysis. Then we validated this signature with overall expression score (OE score) algorithm using both scRNA-seq and bulk RNA-seq data. Based on this signature, we performed LASSO cox regression to establish a prognostic model, and corresponding scores were calculated. Differences in genomic alteration, immune microenvironment, drug sensitivity between high- and low-KRD score groups were investigated. A KRAS related signature composed of 80 DEGs in colon cancer were recognized, among which 19 genes were selected to construct a prognostic model. This KRAS related signature was significantly correlated with worse prognosis. Furthermore, patients who scored lower in the prognostic model presented a higher likelihood of responding to chemotherapy, targeted therapy and immunotherapy. Furthermore, among the 19 selected genes in the model, SPINK4 was identified as an independent prognostic biomarker. Further validation in vitro indicated the knockdown of SPINK4 promoted the proliferation and migration of SW48 cells. In conclusion, a novel KRAS related signature was identified and validated based on clinical and genomic information from TCGA and GEO databases. The signature was proved to regulate genomic alteration, immune microenvironment and drug sensitivity in colon cancer, and thus might serve as a predictor for individual prognosis and treatment.
C1 [Huo, Jian-Ting; Tuersun, Abudumaimaitijiang; Yu, Su-Yue; Zhang, Yu-Chen; Feng, Wen-Qing; Xu, Zhuo-Qing; Zhao, Jing-Kun; Zong, Ya-Ping; Lu, Ai-Guo] Shanghai Jiao Tong Univ, Ruijin Hosp, Shanghai Minimally Invas Surg Ctr, Dept Gen Surg,Sch Med, Shanghai 200020, Peoples R China.
C3 Shanghai Jiao Tong University
RP Zhao, JK; Zong, YP; Lu, AG (corresponding author), Shanghai Jiao Tong Univ, Ruijin Hosp, Shanghai Minimally Invas Surg Ctr, Dept Gen Surg,Sch Med, Shanghai 200020, Peoples R China.
EM zhaojk8891@126.com; angela_zyp@126.com; luaiguo1965@163.com
RI Tuersun, Abudumaimaitijiang/HZH-3259-2023; Zhang, Wanying/IXD-8104-2023
FU National Natural Science Foundation of China General Program
FX We appreciated to all the patients and the medical staff for their
   outstanding contribution.
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NR 66
TC 0
Z9 0
U1 2
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 DEC 14
PY 2023
VL 13
IS 1
AR 22230
DI 10.1038/s41598-023-48768-0
PG 23
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA CL2L3
UT WOS:001125340600027
PM 38097680
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Ibrahiem, AT
   Eladl, E
   Toraih, EA
   Fawzy, MS
   Abdelwahab, K
   Elnaghi, K
   Emarah, Z
   Shaalan, AAM
   Ehab, Z
   Soliman, NA
AF Ibrahiem, Afaf T.
   Eladl, Entsar
   Toraih, Eman A.
   Fawzy, Manal S.
   Abdelwahab, Khaled
   Elnaghi, Khaled
   Emarah, Ziad
   Shaalan, Aly A. M.
   Ehab, Ziad
   Soliman, Nahed A.
TI Prognostic Value of BRAF, Programmed Cell Death 1 (PD1), and PD Ligand 1
   (PDL1) Protein Expression in Colon Adenocarcinoma
SO DIAGNOSTICS
LA English
DT Article
DE BRAF; colorectal cancer; protein expression; PD1; PDL1; prognosis;
   survival
ID COLORECTAL-CANCER; PD-L1 EXPRESSION; V600E; IMMUNOHISTOCHEMISTRY;
   RESISTANCE; MUTATIONS; CARCINOMA
AB Patients with colorectal cancer in different stages show variable outcomes/therapeutic responses due to their distinct tumoral biomarkers and biological features. In this sense, this study aimed to explore the prognostic utility of BRAF, programmed death-1 (PD1), and its ligand (PDL1) protein signatures in colon adenocarcinoma. The selected protein markers were explored in 64 archived primary colon adenocarcinomas in relation to clinicopathological features. BRAF overexpression was found in 39% of the cases and was significantly associated with grade 3, N1, advanced Dukes stage, presence of relapse, and shorter overall survival (OS). PD1 expression in the infiltrating immune cells (IICs) exhibited significant association with T2/T3, N0/M0, early Dukes stage, and absence of relapse. PDL1 expression in IICs is significantly associated with advanced nodal stage/distant metastasis, advanced Dukes stage, and shorter OS. Meanwhile, PDL1 expression in neoplastic cells (NC) was associated with the advanced lymph node/Dukes stage. A positive combined expression pattern of PDL1 in NC/IICs was associated with poor prognostic indices. Tumor PDL1 expression can be an independent predictor of OS and DFS. The multivariate analyses revealed that short OS was independently associated with the RT side location of the tumor, PD1 expression in stromal IICs, and PDL1 expression in NC. In conclusion, overexpression of BRAF in colon adenocarcinoma is considered a poor prognostic pathological marker. In addition, PDL1 expression in NC is considered an independent prognostic factor for DFS/OS. Combined immunohistochemical assessment for BRAF and PD1/PDL1 protein expressions in colon adenocarcinoma might be beneficial for selecting patients for future targeted therapy.
C1 [Ibrahiem, Afaf T.; Eladl, Entsar] Mansoura Univ, Fac Med, Dept Pathol, Mansoura 35516, Egypt.
   [Eladl, Entsar] Univ Toronto, Dept Lab Med & pathobiol, Toronto, ON M5S 1A8, Canada.
   [Toraih, Eman A.] Tulane Univ, Sch Med, Dept Surg, Div Endocrine & Oncol Surg, New Orleans, LA 70112 USA.
   [Toraih, Eman A.] Suez Canal Univ, Fac Med, Histol & Cell Biol Dept, Med Genet Unit, Ismailia 41522, Egypt.
   [Fawzy, Manal S.] Suez Canal Univ, Fac Med, Dept Med Biochem & Mol Biol, Ismailia 41522, Egypt.
   [Fawzy, Manal S.] Northern Border Univ, Fac Med, Dept Biochem, Ar Ar 73213, Saudi Arabia.
   [Abdelwahab, Khaled] Mansoura Univ, Fac Med, Surg Oncol Dept, Mansoura 35516, Egypt.
   [Elnaghi, Khaled; Emarah, Ziad] Mansoura Univ, Fac Med, Oncol Ctr, Internal Med Dept,Med Onco Unit, Mansoura 35516, Egypt.
   [Elnaghi, Khaled; Emarah, Ziad] King Abdullah Med City, Oncol Ctr, Mecca 24246, Saudi Arabia.
   [Shaalan, Aly A. M.] Jazan Univ, Fac Med, Dept Anat, Jazan 82621, Saudi Arabia.
   Suez Canal Univ, Fac Med, Dept Histol & Cell Biol, Ismailia 41522, Egypt.
   Mansoura Univ, Fac Med, Mansoura 21955, Egypt.
   Helwan Univ, Fac Med, Dept Pathol, Cairo 11795, Egypt.
C3 Egyptian Knowledge Bank (EKB); Mansoura University; University of
   Toronto; Tulane University; Egyptian Knowledge Bank (EKB); Suez Canal
   University; Egyptian Knowledge Bank (EKB); Suez Canal University;
   Northern Border University; Egyptian Knowledge Bank (EKB); Mansoura
   University; Egyptian Knowledge Bank (EKB); Mansoura University; King
   Abdullah Medical City; Jazan University; Egyptian Knowledge Bank (EKB);
   Suez Canal University; Egyptian Knowledge Bank (EKB); Mansoura
   University; Egyptian Knowledge Bank (EKB); Helwan University
RP Fawzy, MS (corresponding author), Suez Canal Univ, Fac Med, Dept Med Biochem & Mol Biol, Ismailia 41522, Egypt.; Fawzy, MS (corresponding author), Northern Border Univ, Fac Med, Dept Biochem, Ar Ar 73213, Saudi Arabia.
EM manal2_khashana@ymail.com
RI naghi, Khaled/AAF-4408-2021; soliman, nahed/HNR-5238-2023; Toraih,
   Eman/I-3024-2019; Ibrahiem, Afaf/AEJ-2582-2022; Emarah,
   Ziad/E-2511-2018; Abdelwahab, khaled/W-3392-2018; Fawzy, Manal
   Said/L-1516-2016
OI Emarah, Ziad/0000-0003-0622-2598; Abdelwahab,
   khaled/0000-0002-3679-8718; soliman, nahed/0000-0001-8376-9744; Fawzy,
   Manal Said/0000-0003-1252-8403; El naghi, Khaled/0000-0002-0403-5134
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NR 46
TC 1
Z9 1
U1 4
U2 10
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4418
J9 DIAGNOSTICS
JI Diagnostics
PD JAN
PY 2023
VL 13
IS 2
AR 237
DI 10.3390/diagnostics13020237
PG 19
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 7Y1AN
UT WOS:000914621300001
PM 36673047
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhu, DH
   Sun, YF
   Zhang, DH
   Dong, M
   Jiang, GY
   Zhang, XP
   Zhou, JP
AF Zhu, Dehua
   Sun, Yefei
   Zhang, Danhua
   Dong, Ming
   Jiang, Guiyang
   Zhang, Xiupeng
   Zhou, Jianping
TI miR-1 inhibits the progression of colon cancer by regulating the
   expression of vascular endothelial growth factor
SO ONCOLOGY REPORTS
LA English
DT Article
DE colorectal cancer; miR-1; VEGF; oncosuppressive
ID METASTATIC COLORECTAL-CANCER; SQUAMOUS-CELL CARCINOMA; DOWN-REGULATION;
   PROGNOSTIC-SIGNIFICANCE; TARGETED THERAPY; VEGF-A; TUMOR; ANGIOGENESIS;
   BIOMARKERS; DYSREGULATION
AB MicroRNA (miR)-1 is associated with various human malignancies through repressing tumor growth, migration and angiogenesis. Recently, high-throughput transcriptional profiling confirmed that miR-1 is markedly downregulated in metastatic colorectal cancer; however, its biological functions and the specific underlying mechanisms in colorectal cancer (CRC) require further investigation. In this study, the expression of miR-1 in 111 CRC and paired normal tissue samples was measured using quantitative polymerase chain reaction analysis, and the association between miR-1 expression and clinical characteristics was evaluated. miR-1 was found to be significantly downregulated in CRC tissues compared with paired normal tissues, and in CRC cell lines compared with non-cancer cells (P<0.001), and was negatively associated with tumor size (P=0.001), differentiation (P=0.011), lymph node metastasis (P=0.001) and TNM stage (P=0.001). Further experiments revealed that miR-1 inhibited the migration and invasion of HCT116 and ClonA1 cells, and inhibited cell proliferation by affecting the cell cycle. Vascular endothelial growth factor (VEGF) was found to be a potential target of miR-1 by biological prediction, and further investigation confirmed that miR-1 significantly inhibited the expression and paracrine function of VEGF. In CRC tissues, the expression of VEGF was negatively correlated with miR-1. The low expression of miR-1 in CRC may be one of the reasons for the abnormally high expression of VEGF; the upregulation of miR-1 expression may inhibit cancer progression by downregulating VEGF. These findings indicate that treatment with miR-1 may be a novel method of tumor suppression, and provide a theoretical and experimental basis for the further targeted treatment of CRC through the regulation of miR-1 and VEGF expression.
C1 [Zhu, Dehua; Sun, Yefei; Zhang, Danhua; Dong, Ming; Zhou, Jianping] China Med Univ, Hosp 1, Gastrointestinal Surg, Dept Gen Surg, 155 Nanjing North St, Shenyang 110001, Liaoning, Peoples R China.
   [Jiang, Guiyang; Zhang, Xiupeng] China Med Univ, Dept Pathol, Affiliated Hosp 1, Shenyang, Liaoning, Peoples R China.
   [Jiang, Guiyang; Zhang, Xiupeng] China Med Univ, Coll Basic Med Sci, Shenyang, Liaoning, Peoples R China.
C3 China Medical University; China Medical University; China Medical
   University
RP Zhou, JP (corresponding author), China Med Univ, Hosp 1, Gastrointestinal Surg, Dept Gen Surg, 155 Nanjing North St, Shenyang 110001, Liaoning, Peoples R China.
EM zjphama@163.com
FU Shenyang Science and Technology Project of China [F14-158-9-35];
   Educational Department of Liaoning Province, China [2012-512]
FX The present study was supported by the Shenyang Science and Technology
   Project of China (grant no. F14-158-9-35) and the Special-Term Professor
   from the Educational Department of Liaoning Province, China (Liao Cai
   Zhi Jiao no. 2012-512).
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NR 42
TC 20
Z9 22
U1 0
U2 6
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 AUG
PY 2018
VL 40
IS 2
BP 589
EP 598
DI 10.3892/or.2018.6463
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GP1OL
UT WOS:000440585500003
PM 29845255
OA hybrid, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Koh, EK
   Lee, HR
   Son, WC
   Park, GY
   Bae, J
   Park, YS
AF Koh, Eun-Kyoung
   Lee, Hong-Rae
   Son, Woo-Chang
   Park, Ga-Young
   Bae, Jaeho
   Park, You-Soo
TI Antitumor effects of NK cells expanded by activation pre-processing of
   autologous feeder cells before irradiation in colorectal cancer
SO ONCOLOGY LETTERS
LA English
DT Article
DE radiotherapy; natural killer cell expansion; antibody-dependent cellular
   cytotoxicity; colorectal cancer; cetuximab
ID NATURAL-KILLER-CELLS; EX-VIVO EXPANSION; I CLINICAL-TRIAL; PHASE-I;
   NKG2D LIGANDS; CYTOTOXICITY; RECEPTORS; THERAPY; IMMUNOTHERAPY;
   EXPRESSION
AB Natural killer (NK) cells play a crucial role in early immune defenses against transformed cells and are used in the therapeutic management of cancer. However, it is difficult to sufficiently obtain high purity activated NK cells for clinical application. The function of NK cells is dependent on the balance of activating and inhibitory signals. Strong and diverse stimuli are required to increase the function of NK cells. Radiotherapy modulates the expression of various immunomodulatory molecules that recruit and activate NK cells. NK cell-mediated antibody-dependent cellular cytotoxicity is one of the most potent cytotoxic effects of NK cells against target cancer cells. To generate activated and irradiated autologous peripheral blood mononuclear cells (PBMCs), cytokine and monoclonal antibody stimulation followed by ionizing radiation was performed in the present study. The expanded NK cells were cultured for 21 days using activated/irradiated autologous PBMCs. Colorectal cancer cells (SW480 and HT-29) were used to analyze the expression of NK group 2D ligands and EGFR by radiation. The cytotoxicity of radiation plus NK cell-based targeted therapy against colorectal cancer cell lines was analyzed using flow cytometry. Activated and irradiated PBMCs exhibited significantly increased expression of various activating ligands that stimulated NK cells. In total, >10,000-fold high-purity activated NK cells were obtained, with negligible T-cell contamination. To confirm the antitumor activity of the NK cells expanded by this method, the expanded NK cells were treated with cetuximab, radiotherapy, or a combination of cetuximab and radiotherapy in the presence of human colorectal cancer cells. Expanded NK cells were effective at targeting human colorectal cancer cells, particularly when combined with cetuximab and radiotherapy. Thus, in the present study, a novel method for high-purity activated NK cell expansion was developed using activated and irradiated PBMCs. In addition, combined radiotherapy and antibody-based immunotherapy with expanded NK cells may be an effective strategy to enhance the efficiency of treatment against colorectal cancer.
C1 [Koh, Eun-Kyoung; Lee, Hong-Rae; Son, Woo-Chang; Park, Ga-Young; Park, You-Soo] Dongnam Inst Radiol & Med Sci, Dept Res Ctr, Busan 46033, South Korea.
   [Koh, Eun-Kyoung; Bae, Jaeho] Pusan Natl Univ, Sch Med, Dept Biochem, Yangsan 50612, Gyeongsangnam D, South Korea.
   [Park, You-Soo] Dongnam Inst Radiol & Med Sci, Dept Res Ctr, 40 Jwadong Gil, Busan 46033, South Korea.
   [Bae, Jaeho] Pusan Natl Univ, Sch Med, Dept Biochem, 49 Busandaehak Ro, Yangsan 50612, Gyeongsangnam D, South Korea.
C3 Korea Institute of Radiological & Medical Sciences; Pusan National
   University; Korea Institute of Radiological & Medical Sciences; Pusan
   National University
RP Park, YS (corresponding author), Dongnam Inst Radiol & Med Sci, Dept Res Ctr, 40 Jwadong Gil, Busan 46033, South Korea.; Bae, J (corresponding author), Pusan Natl Univ, Sch Med, Dept Biochem, 49 Busandaehak Ro, Yangsan 50612, Gyeongsangnam D, South Korea.
EM biotek01@hanmail.net; biosole@pusan.ac.kr
FU Dongnam Institute of Radiological & Medical Sciences; Korean government
   [50593-2022]
FX The present study was supported by the Dongnam Institute of Radiological
   & Medical Sciences grant funded by the Korean government (grant no.
   50593-2022).
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NR 46
TC 1
Z9 1
U1 0
U2 6
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 JUN
PY 2023
VL 25
IS 6
AR 232
DI 10.3892/ol.2023.13818
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA F3RI6
UT WOS:000981546500001
PM 37153058
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Rajakannu, M
   Magdeleinat, P
   Vibert, E
   Ciacio, O
   Pittau, G
   Innominato, P
   SaCunha, A
   Cherqui, D
   Morère, JF
   Castaing, D
   Adam, R
AF Rajakannu, Muthukumarassamy
   Magdeleinat, Pierre
   Vibert, Eric
   Ciacio, Oriana
   Pittau, Gabriella
   Innominato, Pasquale
   SaCunha, Antonio
   Cherqui, Daniel
   Morere, Jean-Francois
   Castaing, Denis
   Adam, Rene
TI Is Cure Possible After Sequential Resection of Hepatic and Pulmonary
   Metastases From Colorectal Cancer?
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE Colorectal adenocarcinoma; Extrahepatic metastases; Hepatectomy; Liver
   and lung metastasis; Metastatic colorectal cancer
ID LONG-TERM SURVIVAL; LIVER METASTASES; EXTRAHEPATIC DISEASE; 2-STAGE
   HEPATECTOMY; CHEMOTHERAPY; STRATEGY; SURGERY; MODEL
AB Retrospective analysis of 150 patients who had undergone sequential surgery for liver and lung metastasis from colorectal cancer identified prognostic factors for survival and cure. Median and 5-year overall survival were 76 months and 60% respectively. Twenty percent of patients were potential cured by this onco-surgical strategy.
   Background: Surgical resection is an established therapeutic strategy for colorectal cancer (CRC) metastasis. However, controversies exist when CRC liver and lung metastases (CLLMs) are found concomitantly or when recurrence develops after either liver or lung resection. No predictive score model is available to risk stratify these patients in preparation for surgery, and cure has not yet been reported. Patients and Methods: All consecutive patients who had undergone surgery for CLLMs at our institution during a 20-year period were reviewed. Our policy was to propose sequential surgery of both sites with perioperative chemotherapy, if the strategy was potentially curative. Overall survival, disease-free survival, and cure were evaluated. Results: Sequential resection was performed in 150 patients with CLLMs. The median number of liver and lung metastases resected was 3 and 1, respectively. The median follow-up period was 59 months (range, 7-274 months). The median, 5-year, and 10-year overall survival was 76 months, 60%, and 35% respectively. CRC that was metastatic at the initial diagnosis (P = .012), a prelung resection carcinoembryonic antigen level > 100 ng/mL (P = .014), a prelung resection cancer antigen 19-9 level > 37 U/ mL (P = .034), and an interval between liver and lung resection of < 24 months (P = .024) were independent poor prognostic factors for survival. The 5-year survival was significantly different for patients with <= 2 and >= 3 risk factors (77.3% vs. 26.5%). Of 75 patients with >= 5 years of follow-up data available from the first metastasis resection, 15 (20%) with disease-free survival >= 5 years were considered cured. The use of targeted therapy was the only independent predictor of cure. Conclusion: Curative-intent surgery provides good long-term survival and offers a chance of cure in select patients. Patients with <= 2 risk factors are good candidates for sequential resection.
C1 [Rajakannu, Muthukumarassamy; Magdeleinat, Pierre; Vibert, Eric; Ciacio, Oriana; Pittau, Gabriella; SaCunha, Antonio; Cherqui, Daniel; Castaing, Denis; Adam, Rene] Hop Paul Brousse, AP HP, Ctr Hepatobiliaire, Villejuif, France.
   [Rajakannu, Muthukumarassamy; Vibert, Eric; SaCunha, Antonio; Cherqui, Daniel; Castaing, Denis; Adam, Rene] Univ Paris Sud, Fac Med, Le Kremlin Bicetre, France.
   [Rajakannu, Muthukumarassamy; Vibert, Eric; Castaing, Denis] INSERM, Unite Mixte Rech S1193, Villejuif, France.
   [Magdeleinat, Pierre] Hop Cochin, AP HP, Serv Chirurg Thorac, Paris, France.
   [Innominato, Pasquale; Morere, Jean-Francois] Hop Paul Brousse, AP HP, Serv Oncol Med, Villejuif, France.
   [Adam, Rene] INSERM, Unite Mixte Rech S776, Villejuif, France.
C3 Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
   Paul-Brousse - APHP; Universite Paris Saclay; Institut National de la
   Sante et de la Recherche Medicale (Inserm); Assistance Publique Hopitaux
   Paris (APHP); Universite Paris Cite; Hopital Universitaire Cochin -
   APHP; Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
   Paul-Brousse - APHP; Institut National de la Sante et de la Recherche
   Medicale (Inserm)
RP Adam, R (corresponding author), Hop Paul Brousse, Ctr Hepatobiliaire, 12-14 Ave Paul Vaillant Couturier, F-94804 Villejuif, France.
EM rene.adam@aphp.fr
RI Cherqui, Daniel/T-6831-2018; Ciaccio, Oriana/V-5934-2018; Pitau,
   Gabriella/V-5917-2018; VIBERT, Eric/T-7746-2018; sa cunha,
   antonio/B-5781-2012
OI Morere, Jean-francois/0000-0002-8745-8414; sa cunha,
   antonio/0000-0003-4015-5368; Rajakannu,
   Muthukumarassamy/0000-0001-6600-7553
CR Adam R, 2004, ANN SURG, V240, P644, DOI 10.1097/01.sla.0000141198.92114.16
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NR 30
TC 15
Z9 15
U1 0
U2 7
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 2018
VL 17
IS 1
BP 41
EP 49
DI 10.1016/j.clcc.2017.06.006
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FY0HC
UT WOS:000426490300006
PM 28709876
DA 2025-01-04
ER

PT J
AU Yang, IP
   Yip, KL
   Chang, YT
   Chen, YC
   Huang, CW
   Tsai, HL
   Yeh, YS
   Wang, JY
AF Yang, I-Ping
   Yip, Kwan-Ling
   Chang, Yu-Tang
   Chen, Yen-Cheng
   Huang, Ching-Wen
   Tsai, Hsiang-Lin
   Yeh, Yung-Sung
   Wang, Jaw-Yuan
TI MicroRNAs as Predictive Biomarkers in Patients with Colorectal Cancer
   Receiving Chemotherapy or Chemoradiotherapy: A Narrative Literature
   Review
SO CANCERS
LA English
DT Review
DE microRNAs; colorectal cancer; chemoresistance; radioresistance;
   predictive biomarkers
ID CIRCULATING TUMOR-CELLS; III COLON-CANCER; EPITHELIAL-MESENCHYMAL
   TRANSITION; ADJUVANT TREATMENT; CLINICAL-OUTCOMES; RECTAL-CANCER;
   STAGE-II; DOWN-REGULATION; EARLY RELAPSE; OXALIPLATIN
AB Simple Summary Nearly two decades would be required for a cancer lesion to develop from normal colon mucosa, but most colorectal cancer (CRC) patients are at an advanced stage at presentation. Chemotherapy, targeted therapy, and radiotherapy can improve the prognosis of patients with advanced CRC, but sometimes the therapy resistance occurs, and the 5-year survival rate for patients with locally advanced CRC and with metastatic CRC (mCRC) remain poor. MicroRNAs (miRs) can regulate cancer pathways by inhibiting their target mRNA translation and triggering their degradation. MiRs can serve as predictive biomarkers for the detection of CRC or mCRC or the resistance of chemotherapy or chemoradiotherapy, and miRNA-based therapeutics may finally reach the clinical stages. Colorectal cancer (CRC) is one of the most common malignancies and is associated with high mortality rates worldwide. The underlying mechanism of tumorigenesis in CRC is complex, involving genetic, lifestyle-related, and environmental factors. Although radical resection with adjuvant FOLFOX (5-fluorouracil, leucovorin, and oxaliplatin) chemotherapy and neoadjuvant chemoradiotherapy have remained mainstays of treatment for patients with stage III CRC and locally advanced rectal cancer, respectively, the oncological outcomes of these treatments are often unsatisfactory. To improve patients' chances of survival, researchers are actively searching for new biomarkers to facilitate the development of more effective treatment strategies for CRC and metastatic CRC (mCRC). MicroRNAs (miRs), small, single-stranded, noncoding RNAs, can post-transcriptionally regulate mRNA translation and trigger mRNA degradation. Recent studies have documented aberrant miR levels in patients with CRC or mCRC, and some miRs are reportedly associated with chemoresistance or radioresistance in CRC. Herein, we present a narrative review of the literature on the roles of oncogenic miRs (oncomiRs) and tumor suppressor miRs (anti-oncomiRs), some of which can be used to predict the responses of patients with CRC to chemotherapy or chemoradiotherapy. Moreover, miRs may serve as potential therapeutic targets because their functions can be manipulated using synthetic antagonists and miR mimics.
C1 [Yang, I-Ping] Shu Zen Coll Med & Management, Dept Nursing, Kaohsiung 82144, Taiwan.
   [Yip, Kwan-Ling; Chen, Yen-Cheng; Huang, Ching-Wen; Tsai, Hsiang-Lin; Wang, Jaw-Yuan] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Colorectal Surg, Kaohsiung 80708, Taiwan.
   [Chang, Yu-Tang; Huang, Ching-Wen; Tsai, Hsiang-Lin; Wang, Jaw-Yuan] Kaohsiung Med Univ, Coll Med, Fac Med, Dept Surg, Kaohsiung 80708, Taiwan.
   [Chang, Yu-Tang] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Pediat Surg, Kaohsiung 80708, Taiwan.
   [Chen, Yen-Cheng; Wang, Jaw-Yuan] Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, Kaohsiung 80708, Taiwan.
   [Yeh, Yung-Sung] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Trauma & Surg Crit Care, 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] Pingtung Hosp, Minist Hlth & Welf, Pingtung 90054, Taiwan.
C3 Kaohsiung Medical University; Kaohsiung Medical University Hospital;
   Kaohsiung Medical University; Kaohsiung Medical University; Kaohsiung
   Medical University Hospital; Kaohsiung Medical University; Kaohsiung
   Medical University; Kaohsiung Medical University Hospital; Kaohsiung
   Medical University; Taipei Medical University; Kaohsiung Medical
   University; Kaohsiung Medical University
RP Wang, JY (corresponding author), Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Colorectal Surg, Kaohsiung 80708, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Coll Med, Fac Med, Dept Surg, Kaohsiung 80708, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, Kaohsiung 80708, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Grad Inst Med, Coll Med, Kaohsiung 80708, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Ctr Canc Res, Kaohsiung 80708, Taiwan.; Wang, JY (corresponding author), Pingtung Hosp, Minist Hlth & Welf, Pingtung 90054, Taiwan.
EM cy614112@ms14.hinet.net
RI Jaw-Yuan, Wang/AFS-8845-2022
OI Wang, Jaw-Yuan/0000-0002-7705-2621; Tsai, Hsiang-Lin/0000-0002-1645-2525
FU Ministry of Science and Technology [MOST 109-2314-B-037-046-MY3, MOST
   111-2314-B-037-070-MY3, MOST 111-2314-B-037-049, KMUH110-0M36]; Ministry
   of Health and Welfare [MOST110-2314-B-037-097]; Ministry of Health and
   Welfare [KMUH-DK(B)110004-3]; Kaohsiung Medical University (KMU)
   Hospital [KMU-TC111A04-1, S109036]; KMU Center for Cancer Research; KMU
   Office for Industry-Academic Collaboration; Taiwan Precision Medicine
   Initiative and Taiwan Biobank (Academia Sinica, Taiwan, R.O.C.); 
   [MOHW111-TDU-B-221-114014];  [KMUH110-0R37];  [KMUH110-0R38]; 
   [KMUH110-0M34];  [KMUH110-0M35]
FX This work was supported by grants from the Ministry of Science and
   Technology (MOST 109-2314-B-037-046-MY3, MOST110-2314-B-037-097, MOST
   111-2314-B-037-070-MY3, MOST 111-2314-B-037-049) and the Ministry of
   Health and Welfare (MOHW111-TDU-B-221-114014, financed by the Tobacco
   Health and Welfare Surcharge), Kaohsiung Medical University (KMU)
   Hospital (KMUH110-0R37, KMUH110-0R38, KMUH110-0M34, KMUH110-0M35,
   KMUH110-0M36, KMUH-DK(B)110004-3), the KMU Center for Cancer Research
   (KMU-TC111A04-1), and the KMU Office for Industry-Academic Collaboration
   (S109036). In addition, this study was supported by a grant from the
   Taiwan Precision Medicine Initiative and Taiwan Biobank (Academia
   Sinica, Taiwan, R.O.C.).
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NR 146
TC 8
Z9 8
U1 4
U2 17
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD MAR
PY 2023
VL 15
IS 5
AR 1358
DI 10.3390/cancers15051358
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 9T9WN
UT WOS:000947373100001
PM 36900159
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Gangrade, A
   Pathak, V
   Augelli-Szafran, CE
   Wei, HX
   Oliver, P
   Suto, M
   Buchsbaum, DJ
AF Gangrade, Abhishek
   Pathak, Vibha
   Augelli-Szafran, Corinne E.
   Wei, Han-Xun
   Oliver, Patsy
   Suto, Mark
   Buchsbaum, Donald J.
TI Preferential Inhibition of Wnt/-Catenin Signaling by Novel Benzimidazole
   Compounds in Triple-Negative Breast Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE receptor-targeted therapy; LRP6; triple-negative breast cancer; Wnt;
   -catenin signaling; benzimidazoles
ID SMALL-MOLECULE INHIBITOR; CELL-PROLIFERATION; COLON-CANCER; STEM-CELLS;
   PATHWAY ACTIVATION; DRUG-RESISTANCE; BETA-CATENIN; NICLOSAMIDE; TARGET;
   APOPTOSIS
AB Wnt/-catenin signaling is upregulated in triple-negative breast cancer (TNBC) compared to other breast cancer subtypes and normal tissues. Current Wnt/-catenin inhibitors, such as niclosamide, target the pathway nonspecifically and exhibit poor pharmacokinetics/pharmacodynamics in vivo. Niclosamide targets other pathways, including mTOR, STAT3 and Notch. Novel benzimidazoles have been developed to inhibit Wnt/-catenin signaling with greater specificity. The compounds SRI33576 and SRI35889 were discovered to produce more cytotoxicity in TNBC cell lines than in noncancerous cells. The agents also downregulated Wnt/-catenin signaling mediators LRP6, cyclin D1, survivin and nuclear active -catenin. In addition, SRI33576 did not affect mTOR, STAT3 and Notch signaling in TNBC and noncancerous cells. SRI35889 inhibited mTOR signaling less in noncancerous than in cancerous cells, while not affecting STAT3 and Notch pathways. Compounds SRI32529, SRI35357 and SRI35361 were not selectively cytotoxic against TNBC cell lines compared to MCF10A cells. While SRI32529 inhibited Wnt/-catenin signaling, the compound also mitigated mTOR, STAT3 and Notch signaling. SRI33576 and SRI35889 were identified as cytotoxic and selective inhibitors of Wnt/-catenin signaling with therapeutic potential to treat TNBC in vivo.
C1 [Gangrade, Abhishek; Buchsbaum, Donald J.] Univ Alabama Birmingham, Dept Radiat Oncol, Birmingham, AL 35294 USA.
   [Pathak, Vibha; Augelli-Szafran, Corinne E.; Wei, Han-Xun; Suto, Mark] Southern Res, Drug Discovery Div, Dept Chem, Birmingham, AL 35205 USA.
   [Oliver, Patsy] Univ Alabama Birmingham, Div Pulm Allergy & Crit Care, Birmingham, AL 35233 USA.
C3 University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham
RP Buchsbaum, DJ (corresponding author), Univ Alabama Birmingham, Dept Radiat Oncol, Birmingham, AL 35294 USA.
EM abhigan8@gmail.com; vpathak@southernresearch.org;
   caugelli-szafran@southernresearch.org; hweihml@hotmail.com;
   poliver@uab.edu; msuto@southernresearch.org; djb@uab.edu
OI Buchsbaum, Donald/0000-0003-2797-5847
FU Breast Cancer Research Foundation of Alabama; UAB Comprehensive Cancer
   Center [NCI P30CA013148]
FX Supported by Breast Cancer Research Foundation of Alabama and UAB
   Comprehensive Cancer Center support grant, NCI P30CA013148. Funds were
   received for covering the costs to publish in open access.
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NR 75
TC 37
Z9 39
U1 1
U2 7
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 MAY
PY 2018
VL 19
IS 5
AR 1524
DI 10.3390/ijms19051524
PG 17
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA GJ4BO
UT WOS:000435297000260
PM 29783777
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Abidi, A
   Gorris, MAJ
   Brennan, E
   Jongmans, MCJ
   Weijers, DD
   Kuiper, RP
   de Voer, RM
   Hoogerbrugge, N
   Schreibelt, G
   de Vries, IJM
AF Abidi, Asima
   Gorris, Mark A. J.
   Brennan, Evan
   Jongmans, Marjolijn C. J.
   Weijers, Dilys D.
   Kuiper, Roland P.
   de Voer, Richarda M.
   Hoogerbrugge, Nicoline
   Schreibelt, Gerty
   de Vries, I. Jolanda M.
TI Challenges of Neoantigen Targeting in Lynch Syndrome and Constitutional
   Mismatch Repair Deficiency Syndrome
SO CANCERS
LA English
DT Review
DE Lynch Syndrome; hereditary cancer; CMMRD; neoantigen; colorectal cancer;
   mismatch repair deficiency; targeted therapy
ID TUMOR-INFILTRATING LYMPHOCYTES; MICROSATELLITE INSTABILITY;
   COLORECTAL-CANCER; FRAMESHIFT-MUTATION; BETA2-MICROGLOBULIN MUTATIONS;
   GENOTYPIC HETEROGENEITY; DENDRITIC CELL; COLON; INACTIVATION; VACCINE
AB Simple Summary
   Lynch syndrome (LS) and constitutional mismatch repair deficiency (CMMRD) are hereditary disorders which significantly increase a person's risk of developing a variety of cancers such as colorectal, endometrial, brain and, for CMMRD also, haematological malignancies. This increased cancer risk is due to inherited mutations in specific types of DNA repair genes, which hampers repair of mispaired or damaged bases during DNA replication. As a consequence, somatic mutations rapidly accumulate and typically include insertions and deletions (indels) in microsatellites that potentially can give rise to neoantigens. These neoantigens open up avenues for neoantigen-targeting immune therapies. Here, we aim to discuss the major obstacles that are encountered in developing such a therapy, including the heterogenous tumour profile of LS and CMMRD patients which challenge the selection of suitable neoantigens and potential resistance to immune checkpoint inhibitor therapy. In addition, we give a perspective on how to overcome the encountered obstacles.
   Lynch syndrome (LS) and constitutional mismatch repair deficiency (CMMRD) are hereditary disorders characterised by a highly increased risk of cancer development. This is due to germline aberrations in the mismatch repair (MMR) genes, which results in a high mutational load in tumours of these patients, including insertions and deletions in genes bearing microsatellites. This generates microsatellite instability and cause reading frameshifts in coding regions that could lead to the generation of neoantigens and opens up avenues for neoantigen targeting immune therapies prophylactically and therapeutically. However, major obstacles need to be overcome, such as the heterogeneity in tumour formation within and between LS and CMMRD patients, which results in considerable variability in the genes targeted by mutations, hence challenging the choice of suitable neoantigens. The machine-learning methods such as NetMHC and MHCflurry that predict neoantigen- human leukocyte antigen (HLA) binding affinity provide little information on other aspects of neoantigen presentation. Immune escape mechanisms that allow MMR-deficient cells to evade surveillance combined with the resistance to immune checkpoint therapy make the neoantigen targeting regimen challenging. Studies to delineate shared neoantigen profiles across patient cohorts, precise HLA binding algorithms, additional therapies to counter immune evasion and evaluation of biomarkers that predict the response of these patients to immune checkpoint therapy are warranted.
C1 [Abidi, Asima; Gorris, Mark A. J.; Brennan, Evan; Schreibelt, Gerty; de Vries, I. Jolanda M.] Radboud Univ Nijmegen, Med Ctr, Radboud Inst Mol Life Sci, Dept Tumor Immunol, NL-6525 GA Nijmegen, Netherlands.
   [Jongmans, Marjolijn C. J.; Weijers, Dilys D.; Kuiper, Roland P.] Princess Maxima Ctr Pediat Oncol, NL-3584 CS Utrecht, Netherlands.
   [Jongmans, Marjolijn C. J.; Kuiper, Roland P.] Univ Med Ctr Utrecht, Dept Genet, NL-3584 CX Utrecht, Netherlands.
   [de Voer, Richarda M.; Hoogerbrugge, Nicoline] Radboud Univ Nijmegen, Med Ctr, Dept Human Genet, NL-6525 GA Nijmegen, Netherlands.
   [de Vries, I. Jolanda M.] Radboud Univ Nijmegen, Med Ctr, Dept Med Oncol, NL-6525 GA Nijmegen, Netherlands.
C3 Radboud University Nijmegen; Utrecht University; Utrecht University
   Medical Center; Radboud University Nijmegen; Radboud University Nijmegen
RP de Vries, IJM (corresponding author), Radboud Univ Nijmegen, Med Ctr, Radboud Inst Mol Life Sci, Dept Tumor Immunol, NL-6525 GA Nijmegen, Netherlands.; de Vries, IJM (corresponding author), Radboud Univ Nijmegen, Med Ctr, Dept Med Oncol, NL-6525 GA Nijmegen, Netherlands.
EM asima.abidi@radboudumc.nl; Mark.Gorris@radboudumc.nl;
   evan.brennan@student.ru.nl; m.c.j.jongmans-3@umcutrecht.nl;
   D.D.Weijers@prinsesmaximacentrum.nl; r.kuiper@prinsesmaximacentrum.nl;
   Richarda.deVoer@radboudumc.nl; nicoline.hoogerbrugge@radboudumc.nl;
   Gerty.Schreibelt@radboudumc.nl; Jolanda.deVries@radboudumc.nl
RI Kuiper, Roland/A-9646-2014; Gorris, Mark/D-9700-2016; de Voer,
   Richarda/P-5728-2015; hoogerbrugge, nicoline/O-1016-2013; de Vries, I.
   Jolanda M./F-5563-2010; Schreibelt, Gerty/A-1260-2016
OI hoogerbrugge, nicoline/0000-0003-2393-8141; de Vries, I. Jolanda
   M./0000-0002-8653-4040; Schreibelt, Gerty/0000-0002-0156-8365; Gorris,
   Mark/0000-0003-3621-226X; Kuiper, Roland/0000-0003-4928-3809; Weijers,
   Dilys/0009-0004-0743-0756; de Voer, Richarda M/0000-0002-8222-0343
FU Radboudumc PhD grant; KiKa Foundation [359]
FX This work was supported by a Radboudumc PhD grant and KiKa Foundation
   (project number 359).
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NR 109
TC 5
Z9 6
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 MAY
PY 2021
VL 13
IS 10
AR 2345
DI 10.3390/cancers13102345
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SI2JL
UT WOS:000654652100001
PM 34067951
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Surmeli, ZG
   Ozveren, A
   Arslan, C
   Degirmenci, M
   Karaca, B
   Uslu, R
AF Surmeli, Zeki G.
   Ozveren, Ahmet
   Arslan, Cagatay
   Degirmenci, Mustafa
   Karaca, Burcak
   Uslu, Ruchan
TI Biweekly cetuximab in combination with platinum and 5-fluorouracil in
   metastatic head and neck carcinoma
SO INDIAN JOURNAL OF CANCER
LA English
DT Article
DE Cetuximab; chemotherapy; head and neck cancer; larynx cancer; targeted
   therapy
ID CISPLATIN LV5FU2-P REGIMEN; ADVANCED COLORECTAL-CANCER; SQUAMOUS-CELL
   CARCINOMA; MULTICENTER PHASE-II; EVERY 2ND WEEK; 1ST-LINE TREATMENT;
   PLUS CETUXIMAB; TRIAL; LEUCOVORIN; FLUOROURACIL
AB BACKGROUND AND AIM: The combination of cetuximab with platinum and 5-fluorouracil (5-FU) chemotherapy prolongs survival in patients with metastatic or recurrent squamous-cell carcinoma of the head and neck (SCCHN). Biweekly (once in 2 weeks) administration of cetuximab requires fewer hospital visits and decreases treatment costs; therefore, it is more convenient both for the patients and for the healthcare providers. Here, we assessed the efficacy, safety, and tolerability of an alternative biweekly regimen of cetuximab in combination with platinum and 5-FU chemotherapy as a first-line treatment for these patients.
   METHODS AND MATERIALS: Medical records of patients with metastatic or recurrent non-nasopharyngeal SCCHN who were treated with a biweekly regimen of cetuximab (500 mg/m(2) on day 1), cisplatin (40 mg/m(2) on day 1) or carboplatin (target area under the curve 3.5 mg/ml x min on day 1), folinic acid (400 mg/m(2) on day 1), and 5-FU (400 mg/m(2) bolus on day 1 followed by continuous infusion of 2,400 mg/m(2) 5-FU over 46 h) were retrospectively reviewed. Survival estimates were calculated with the Kaplan-Meier method.
   RESULTS: In total, 60 patients were included. The median age of the patients was 60.5. The objective response rate was 53.3% (95% confidence interval [CI] = 40.7-65.9). The median progression-free survival duration was 6.8 months (95% CI = 5.5-8.1) and the median overall survival duration was 13.3 months (95% CI = 8.4-18.2). The most common grade 3 or 4 adverse events were neutropenia (28.3%) and leucopenia (13.3%). Grade 3 or 4 rash was observed in 3.3% of the patients.
   CONCLUSION: Biweekly administration of cetuximab, cisplatin, and 5-FU is an effective regimen with a favorable toxicity profile for the first-line treatment of metastatic or recurrent SCCHN. These results warrant further evaluation of this regimen in prospective trials.
C1 [Surmeli, Zeki G.] Med Pk Hosp, Dept Med Oncol, Ankara, Turkey.
   [Ozveren, Ahmet] Giresun Univ Training & Res Hosp, Dept Med Oncol, Giresun, Turkey.
   [Arslan, Cagatay] Bahcesehir Univ, Dept Internal Med & Med Oncol, Fac Med, Istanbul, Turkey.
   [Degirmenci, Mustafa] Tepecik Training & Res Hosp, Dept Med Oncol, Izmir, Turkey.
   [Karaca, Burcak; Uslu, Ruchan] Ege Univ, Dept Med Oncol, Izmir, Turkey.
C3 Medical Park Hospitals Group; Bahcesehir University; Izmir Tepecik
   Training & Research Hospital; Ege University
RP Surmeli, ZG (corresponding author), Med Pk Hosp, Dept Med Oncol, Ankara, Turkey.
EM zeki.surmeli@gmail.com
RI degirmenci, mustafa/LCE-4086-2024; Surmeli, Zeki/AAW-3349-2020; Arslan,
   Cagatay/I-1932-2016; Ozveren, Ahmet/P-4548-2017; Uslu,
   Ruchan/C-6855-2008
OI Surmeli, Zeki Gokhan/0000-0002-5087-6268; Ozveren,
   Ahmet/0000-0002-6432-5432; Uslu, Ruchan/0000-0002-9584-6134
CR [Anonymous], 1997, JAMA-J AM MED ASSOC, V277, P925
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NR 20
TC 1
Z9 1
U1 0
U2 3
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, Maharashtra, INDIA
SN 0019-509X
EI 1998-4774
J9 INDIAN J CANCER
JI Indian J. Cancer
PD JAN-MAR
PY 2019
VL 56
IS 1
BP 4
EP 8
DI 10.4103/ijc.IJC_355_18
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HR9ZR
UT WOS:000463520600002
PM 30950435
DA 2025-01-04
ER

PT J
AU Ma, R
   Xu, L
   Qu, XJ
   Che, XF
   Zhang, Y
   Fan, YB
   Li, C
   Guo, TS
   Hou, KZ
   Hu, XJ
   Drew, L
   Shen, MH
   Cheung, TN
   Liu, YP
AF Ma, Rui
   Xu, Ling
   Qu, Xiujuan
   Che, Xiaofang
   Zhang, Ye
   Fan, Yibo
   Li, Ce
   Guo, Tianshu
   Hou, Kezuo
   Hu, Xuejun
   Drew, Lisa
   Shen, Minhui
   Cheung, Tony
   Liu, Yunpeng
TI AZ304, a novel dual BRAF inhibitor, exerts anti-tumour effects in
   colorectal cancer independently of BRAF genetic status
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
ID WILD-TYPE BRAF; RAF INHIBITORS; MAPK PATHWAY; ACQUIRED-RESISTANCE;
   KINASE INHIBITORS; UP-REGULATION; COLON-CANCER; MELANOMA; VEMURAFENIB;
   CELLS
AB BACKGROUND: BRAF mutation is associated with poor clinical outcome of patients with malignant tumours, and mediates resistance to chemotherapy and targeted therapy. This study aimed to determine whether V600E mutant and wild type BRAF colorectal cancers exhibit distinct sensitivities to the dual BRAF inhibitor AZ304.
   METHODS: Kinase activity was assessed by the AlphaScreen assay. Then, MTT assay, EdU assay, colony-formation assay and Western blot were performed to evaluate the anti-tumour effects of AZ304 in vitro. In vivo efficacy was investigated by xenograft analysis and immunohistochemistry.
   RESULTS: AZ304 exerted potent inhibitory effects on both wild type and V600E mutant forms of the serine/ threonine-protein kinase BRAF, with IC50 values of 79 nM and 38 nM, respectively. By suppressing ERK phosphorylation, AZ304 effectively inhibited a panel of human cancer cell lines with different BRAF and RAS genetic statuses. In selected colorectal cancer cell lines, AZ304 significantly inhibited cell growth in vitro and in vivo, regardless of BRAF genetic status. In addition, the EGFR inhibitor Cetuximab enhanced the potency of AZ304 independently of BRAF mutational status.
   CONCLUSIONS: The BRAF inhibitor AZ304 has broad spectrum antitumour activity, which is significantly enhanced by combination with Cetuximab in colorectal cancers in vitro and in vivo.
C1 [Ma, Rui; Xu, Ling; Qu, Xiujuan; Che, Xiaofang; Zhang, Ye; Fan, Yibo; Li, Ce; Guo, Tianshu; Hou, Kezuo; Liu, Yunpeng] China Med Univ, Hosp 1, Dept Med Oncol, Shenyang 110001, Liaoning, Peoples R China.
   [Ma, Rui; Xu, Ling; Qu, Xiujuan; Che, Xiaofang; Zhang, Ye; Fan, Yibo; Li, Ce; Guo, Tianshu; Hou, Kezuo; Liu, Yunpeng] China Med Univ, Hosp 1, Key Lab Anticancer Drugs & Biotherapy Liaoning Pr, Shenyang 110001, Liaoning, Peoples R China.
   [Hu, Xuejun] China Med Univ, Hosp 1, Dept Resp Med, Shenyang 110001, Liaoning, Peoples R China.
   [Drew, Lisa; Shen, Minhui; Cheung, Tony] AstraZeneca R&D Boston, Oncol iMED, 35 Gatehouse Dr, Waltham, MA 02451 USA.
C3 China Medical University; China Medical University; China Medical
   University; AstraZeneca
RP Qu, XJ; Liu, YP (corresponding author), China Med Univ, Hosp 1, Dept Med Oncol, Shenyang 110001, Liaoning, Peoples R China.; Qu, XJ; Liu, YP (corresponding author), China Med Univ, Hosp 1, Key Lab Anticancer Drugs & Biotherapy Liaoning Pr, Shenyang 110001, Liaoning, Peoples R China.
EM xiujuanqu@yahoo.com; cmuliuyunpeng@hotmail.com
RI Xiaofang, Che/J-9430-2019; fan, yi/GYU-1036-2022
OI Qu, Xiujuan/0009-0005-9366-2314; Ma, Rui/0000-0001-5155-1230; Xu,
   Ling/0000-0001-9355-6136
FU National Science and Technology Major Project of the Ministry of Science
   and Technology of China [2017ZX09304025]; National Natural Science
   Foundation of China [81673025, 81372546]; Project for clinical ability
   construction of Chinese medicine, Science and Technology Plan Project of
   Liaoning Province [2016007010, 2015020457, 2014021069, 2014226033,
   2014225013]; Key Research and Development Programme of Shenyang
   [17-230-9-01]; National Natural Science Foundation-Outstanding Youth
   Foundation Training Project of China Medical University [YQ20160002]
FX This research was supported by National Science and Technology Major
   Project of the Ministry of Science and Technology of China (No.
   2017ZX09304025), National Natural Science Foundation of China (No.
   81673025, 81372546), Project for clinical ability construction of
   Chinese medicine, Science and Technology Plan Project of Liaoning
   Province (No. 2016007010, 2015020457, 2014021069, 2014226033,
   2014225013), The Key Research and Development Programme of Shenyang (No.
   17-230-9-01) and National Natural Science Foundation-Outstanding Youth
   Foundation Training Project of China Medical University(No. YQ20160002).
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NR 42
TC 12
Z9 12
U1 0
U2 9
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD MAY
PY 2018
VL 118
IS 11
BP 1453
EP 1463
DI 10.1038/s41416-018-0086-x
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GJ8MM
UT WOS:000435643900007
PM 29755114
OA Bronze, Green Published
DA 2025-01-04
ER

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   Zhang, Yan
   Dai, Yiwen
   Hu, Jinhang
   Zhu, Lixin
   Xu, Xiaoliang
   Yu, Yue
   Li, Huan
   Yao, Bo
   Zhou, Huixin
TI Polyelectrolyte-Mediated Nontoxic
   AgGa<i><sub>x</sub></i>In<sub>1-<i>x</i></sub>S<sub>2</sub>
   QDs/Low-Density Lipoprotein Nanoprobe for Selective 3D Fluorescence
   Imaging of Cancer Stem Cells
SO ACS APPLIED MATERIALS & INTERFACES
LA English
DT Article
DE cation exchange; quantum dots; low-density lipoprotein; colon cancer
   stem cells; selective three-dimensional imaging
ID S QUANTUM DOTS; CU-IN-S; CATION-EXCHANGE; DRUG-DELIVERY; NANOCRYSTALS;
   RECONSTITUTION; SYSTEM; AGINS2; CORE; AG2S
AB Cancer stem cells, which are a population of cancer cells sharing common properties with normal stem cells, have strong self-renewal ability and multi-lineage differentiation potential to trigger tumor proliferation, metastases, and recurrence. From this, targeted therapy for cancer stem cells may be one of the most promising strategies for comprehensive treatment of tumors in the future. We design a facile approach to establish the colon cancer stem cells-selective fluorescent probe based on the low-density lipoprotein (LDL) and the novel AgGaxIn(1-x)S2 quantum dots (AGIS QDs). The AGIS QDs with a high crystallinity are obtained for the first time via cation-exchange protocol of Ga3+ to In3+ starting from parent AgInS2 QDs. Photoluminescence peak of AGIS QDs can be turned from 502 to 719 nm by regulating the reaction conditions, with the highest quantum yield up to 37%. Subsequently, AGIS QDs-conjugated LDL nanocomposites (NCs) are fabricated, in which a cationic polyelectrolyte was used as a coupling reagent to guarantee the electrostatic self-assembly. The structural integrity and physicochemical properties of the LDL-QDs are found to be maintained in vitro, and the NCs exhibit remarkable biocompatibility. The LDL-QDs can be selectively delivered into cancer stem cells that overexpress LDL receptor, and three-dimensional imaging of cancer stem cells is realized. The results of this study not only demonstrate the versatility of nature-derived lipoprotein nanoparticles, but also confirm the feasibility of electrostatic conjugation using cationic polyelectrolyte, allowing reseachers to design nanoarchitectures for targeted diagnosis and treatment of cancer.
C1 [Song, Jiangluq; Yu, Yue; Li, Huan; Yao, Bo; Zhou, Huixin] Xidian Univ, Sch Phys & Optoelect Engn, Xian 710071, Shaanxi, Peoples R China.
   [Zhang, Yan; Zhu, Lixin] Anhui Med Univ, Cent Lab, Affiliated Hosp 1, Hefei 230022, Anhui, Peoples R China.
   [Dai, Yiwen] Anhui Med Univ, Dept Gen Surg, Hosp 2, Hefei 230601, Anhui, Peoples R China.
   [Hu, Jinhang] Shaanxi Univ Chinese Med, Shaanxi Collaborat Innovat Ctr Chinese Med Resour, Xianyang 712046, Peoples R China.
   [Xu, Xiaoliang] Chinese Acad Sci, Key Lab Strongly Coupled Quantum Matter Phys, Hefei 230026, Anhui, Peoples R China.
   [Xu, Xiaoliang] Univ Sci & Technol China, Dept Phys, Hefei 230026, Anhui, Peoples R China.
C3 Xidian University; Anhui Medical University; Anhui Medical University;
   Shaanxi University of Chinese Medicine; Chinese Academy of Sciences;
   Chinese Academy of Sciences; University of Science & Technology of
   China, CAS
RP Song, JL; Zhou, HX (corresponding author), Xidian Univ, Sch Phys & Optoelect Engn, Xian 710071, Shaanxi, Peoples R China.; Zhu, LX (corresponding author), Anhui Med Univ, Cent Lab, Affiliated Hosp 1, Hefei 230022, Anhui, Peoples R China.
EM jlqsong@mail.ustc.edu.cn; lx-zhu@163.com; hxzhou@mail.xidian.edu.cn
RI Yu, Yue/R-2141-2016
OI Zhou, Huixin/0000-0002-7909-7444; Song, Jiangluqi/0000-0003-1497-4810
FU National Natural Science Foundation of China [51801142, 61705173,
   51672003, 51872279]; Basic Research Plan of Natural Science in Shaanxi
   Province [2018JQ5022, 2017JM6079]; 111 Project [B17035]; Fundamental
   Research Funds for the Central Universities [JB180502]
FX This work was supported by the National Natural Science Foundation of
   China (Nos 51801142, 61705173, 51672003, and 51872279), Basic Research
   Plan of Natural Science in Shaanxi Province (Nos 2018JQ5022 and
   2017JM6079), 111 Project (No. B17035), and the Fundamental Research
   Funds for the Central Universities (JB180502).
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NR 50
TC 21
Z9 21
U1 3
U2 86
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 MAR 13
PY 2019
VL 11
IS 10
BP 9884
EP 9892
DI 10.1021/acsami.9b00121
PG 9
WC Nanoscience & Nanotechnology; Materials Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Materials Science
GA HP2XF
UT WOS:000461538000026
PM 30779876
DA 2025-01-04
ER

PT J
AU Pietropaolo, G
   Pugliese, D
   Armuzzi, A
   Guidi, L
   Gasbarrini, A
   Rapaccini, GL
   Wolf, FI
   Trapani, V
AF Pietropaolo, Giuseppe
   Pugliese, Daniela
   Armuzzi, Alessandro
   Guidi, Luisa
   Gasbarrini, Antonio
   Rapaccini, Gian Lodovico
   Wolf, Federica I.
   Trapani, Valentina
TI Magnesium Absorption in Intestinal Cells: Evidence of Cross-Talk between
   EGF and TRPM6 and Novel Implications for Cetuximab Therapy
SO NUTRIENTS
LA English
DT Article
DE biomarker; colorectal cancer; EGFR; hypomagnesemia; magnesium
   supplementation; monoclonal antibodies; targeted therapy
ID POOLED ANALYSIS; HYPOMAGNESEMIA; GROWTH; RISK; ANTIBODIES
AB Hypomagnesemia is very commonly observed in cancer patients, most frequently in association with therapy with cetuximab (CTX), a monoclonal antibody targeting the epithelial growth factor receptor (EGFR). CTX-induced hypomagnesemia has been ascribed to renal magnesium (Mg) wasting. Here, we sought to clarify whether CTX may also influence intestinal Mg absorption and if Mg supplementation may interfere with CTX activity. We used human colon carcinoma CaCo-2 cells as an in vitro model to study the mechanisms underlying Mg transport and CTX activity. Our findings demonstrate that TRPM6 is the key channel that mediates Mg influx in intestinal cells and that EGF stimulates such influx; consequently, CTX downregulates TRPM6-mediated Mg influx by interfering with EGF signaling. Moreover, we show that Mg supplementation does not modify either the CTX IC50 or CTX-dependent inhibition of ERK1/2 phosphorylation. Our results suggest that reduced Mg absorption in the intestine may contribute to the severe hypomagnesemia that occurs in CTX-treated patients, and Mg supplementation may represent a safe and effective nutritional intervention to restore Mg status without impairing the CTX efficacy.
C1 [Pietropaolo, Giuseppe; Wolf, Federica I.; Trapani, Valentina] Univ Cattolica Sacro Cuore, Fdn Policlin Univ A Gemelli IRCCS, Dipartimento Med & Chirurgia Traslaz, Sez Patol Gen, I-00168 Rome, Italy.
   [Pugliese, Daniela; Armuzzi, Alessandro; Guidi, Luisa; Gasbarrini, Antonio; Rapaccini, Gian Lodovico] Univ Cattolica Sacro Cuore, Fdn Policlin Univ A Gemelli IRCCS, Dipartimento Med & Chirurgia Traslaz, UOC Med Interna & Gastroenterol, I-00168 Rome, Italy.
   [Pietropaolo, Giuseppe] Sapienza Univ Roma, Fdn Cenci Bolognetti, Ist Pasteur Italia, Dipartimento Med Mol, I-00161 Rome, Italy.
C3 Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli;
   Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli;
   Sapienza University Rome; Fondazione Cenci Bolognetti
RP Wolf, FI; Trapani, V (corresponding author), Univ Cattolica Sacro Cuore, Fdn Policlin Univ A Gemelli IRCCS, Dipartimento Med & Chirurgia Traslaz, Sez Patol Gen, I-00168 Rome, Italy.
EM giuseppe.pietropaolo@uniroma1.it;
   daniela.pugliese@policlinicogemelli.it; alessandro.armuzzi@unicatt.it;
   luisa.guidi@unicatt.it; antonio.gasbarrini@unicatt.it;
   gianludovico.rapaccini@policlinicogemelli.it; federica.wolf@unicatt.it;
   valentina.trapani@unicatt.it
RI Gasbarrini, Antonio/AAB-8487-2019; Armuzzi, Alessandro/JJC-6224-2023;
   Armuzzi, Alessandro/AIC-5188-2022
OI Gasbarrini, Antonio/0000-0002-6230-1779; PIETROPAOLO,
   GIUSEPPE/0000-0002-4802-7312; Gasbarrini, Antonio/0000-0003-4863-6924;
   Armuzzi, Alessandro/0000-0003-1572-0118; Trapani,
   Valentina/0000-0002-0259-6624
FU MIUR (Italian Ministry of University and Research) [D.3.2-2015,
   D.1.2017]
FX This research was funded by MIUR (Italian Ministry of University and
   Research) D.3.2-2015 and D.1.2017.
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NR 38
TC 14
Z9 18
U1 0
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6643
J9 NUTRIENTS
JI Nutrients
PD NOV
PY 2020
VL 12
IS 11
AR 3277
DI 10.3390/nu12113277
PG 11
WC Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Nutrition & Dietetics
GA OY5SA
UT WOS:000594305300001
PM 33114586
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ye, X
   Deng, HY
   Su, M
   Liao, QJ
   Huang, D
   Liao, DF
   Xiao, ZQ
   Cao, DL
AF Ye, Xu
   Deng, Hongyu
   Su, Min
   Liao, Qianjin
   Huang, Dan
   Liao, Duan-Fang
   Xiao, Zhi-Qiang
   Cao, Deliang
TI A complex microsatellite at chromosome 7q33 as a new prognostic marker
   of colorectal cancer
SO ONCOTARGET
LA English
DT Article
DE colorectal cancer; microsatellite; polymorphisms; survival; prognostic
   marker
ID MISMATCH REPAIR GENE; COLON-CANCER; INSTABILITY; COLONOSCOPY; COLITIS;
   COMPLICATIONS; EPIDEMIOLOGY; POPULATION; MUTATIONS; LESIONS
AB Disease-specific markers are critical for early diagnosis, targeted therapy and prognostic prediction of diseases. Current study reports a complex microsatellite as a new prognostic marker of sporadic colorectal cancer. This microsatellite located at Chromosome 7q33 is composed of three tetranucleotide tandem repeats, (TTCC)(2)(TCCC)(5)(TCCT)(7), flanked by a CT-rich sequence. We analyzed polymorphisms of this microsatellite in 158 sporadic colorectal cancer, 143 matched normal adjacent tissues (NAT) and 150 health donors. Our results showed that this complex microsatellite was instable with polymorphic frequency of 77.2% in colorectal cancer, 52.4% in NAT and 54.7% in health donors (p<0.01) when compared to reference sequence. In the three tandem repeats, (TCCT)(7) site was most polymorphic accounting for over 70.0% of polymorphisms in this complex microsatellite, followed by (TTCC)(2) site for approximately 20%. Polymorphisms in (TCCC)(5) was rare. Polymorphisms at the (TCCT)(7) site were mainly insertions of 1 to 4 copies of TCCT (88.6%), and deletions occurred in about 6.4% of cases. The (TTCC)(2) site was featured with one copy TTCC insertions. Pair-wise analyses between colorectal tumors and NAT revealed that 88 of 121 (72.7%) tumors displayed expansion, contraction or both in these tetranucleotide tandem repeats when compared to NAT. A cross-analysis with clinicopathological data of 158 colorectal cancers revealed that polymorphic alterations of the microsatellite associated with less lymphatic metastasis (p<0.001), and the colorectal cancer patients with polymorphic changes in this microsatellite demonstrated better survival (n=112, p=0.0058). Together these data suggest that this complex microsatellite is a potential prognostic marker of sporadic colorectal cancer.
C1 [Ye, Xu; Xiao, Zhi-Qiang] Cent South Univ, Xiangya Hosp, Res Ctr Carcinogenesis & Targeted Therapy, Changsha 410008, Hunan, Peoples R China.
   [Ye, Xu; Xiao, Zhi-Qiang] Cent South Univ, Xiangya Hosp, Higher Educ Key Lab Canc Prote & Translat Med Hun, Changsha 410005, Hunan, Peoples R China.
   [Ye, Xu; Deng, Hongyu; Su, Min; Liao, Qianjin; Cao, Deliang] Cent South Univ, Hunan Canc Hosp, Changsha 410013, Hunan, Peoples R China.
   [Ye, Xu; Deng, Hongyu; Su, Min; Liao, Qianjin; Cao, Deliang] Cent South Univ, Affiliated Canc Hosp, Xiangya Sch Med, Changsha 410013, Hunan, Peoples R China.
   [Huang, Dan; 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 Central South University; Central South University; Central South
   University; Central South University; Hunan University of Chinese
   Medicine
RP Xiao, ZQ (corresponding author), Cent South Univ, Xiangya Hosp, Res Ctr Carcinogenesis & Targeted Therapy, Changsha 410008, Hunan, Peoples R China.; Xiao, ZQ (corresponding author), Cent South Univ, Xiangya Hosp, Higher Educ Key Lab Canc Prote & Translat Med Hun, Changsha 410005, Hunan, Peoples R China.; Cao, DL (corresponding author), Cent South Univ, Hunan Canc Hosp, Changsha 410013, Hunan, Peoples R China.; Cao, DL (corresponding author), Cent South Univ, Affiliated Canc Hosp, Xiangya Sch Med, Changsha 410013, Hunan, Peoples R China.; Cao, DL (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 zqxiao2001@hotmail.com; dlcao1998@gmail.com
RI ye, xu/HSH-7921-2023
OI Huang, Dan/0000-0003-4221-574X
FU National Natural Science Foundation of China [81472465]; National Basic
   Research Program of China [2013CB910502]; Natural Science Foundation of
   Guangxi Provence [2015GXNSFEA139003]
FX This work was supported in part by National Natural Science Foundation
   of China (81472465 to DC), National Basic Research Program of China
   (2013CB910502; to ZQX) and the Natural Science Foundation of Guangxi
   Provence (2015GXNSFEA139003 to DFL).
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NR 39
TC 0
Z9 0
U1 0
U2 5
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 OCT 24
PY 2017
VL 8
IS 51
BP 88760
EP 88769
DI 10.18632/oncotarget.21077
PG 10
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FK6AP
UT WOS:000413585600045
PM 29179473
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Masuda, M
   Sawa, M
   Yamada, T
AF Masuda, Mari
   Sawa, Masaaki
   Yamada, Tesshi
TI Therapeutic targets in the Wnt signaling pathway: Feasibility of
   targeting TNIK in colorectal cancer
SO PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
DE Colorectal cancer; Cancer stem cell; Wnt signaling; Traf2-and
   Nck-interacting kinase (TNIK); Molecular targeting therapy
ID NCK-INTERACTING KINASE; SMALL-MOLECULE INHIBITOR; WNT/BETA-CATENIN;
   BETA-CATENIN; COLON-CANCER; STEM-CELLS; HEPATOCELLULAR CARCINOMAS; APC
   MUTATIONS; CHECKPOINT KINASE; LRP6 EXPRESSION
AB The genetic and epigenetic alterations occurring during the course of multistage colorectal carcinogenesis have been extensively studied in the last few decades. One of the most notable findings is that the great majority of colorectal cancers (>80%) have mutations in the adenomatous polyposis coli (APC) tumor suppressor gene. Loss of functional APC protein results in activation of canonical Wnt/beta-catanin signaling and initiates intestinal carcinogenesis. Mutational inactivation of APC is the first genetic event, but colorectal cancer cells retain their dependency on constitutive Wnt signal activation even after accumulation of other genetic events. Accordingly, pharmacological blocking of Wnt signaling has been considered an attractive therapeutic approach for colorectal cancer. Several therapeutics targeting various molecular components of the Wnt signaling pathway, including porcupine, frizzled receptors and co-receptor, tankyrases, and cAMP response element binding protein (CREB)-binding protein (CBP), have been developed, and some of those are currently being evaluated in early-phase clinical trials. Traf2- and Nck-interacting protein kinase (TNIK) has been identified as a regulatory component of the T-cell factor-4 and beta-catenin transcriptional complex independently by two research groups. TNIK regulates Wnt signaling in the most downstream part of the pathway, and its inhibition is expected to block the signal even in colorectal cancer cells with APC gene mutation. Here we discuss some of the TNIK inhibitors under preclinical development. (C) 2015 The Authors. Published by Elsevier Inc.
C1 [Masuda, Mari; Yamada, Tesshi] Natl Canc Ctr, Div Chemotherapy & Clin Res, Res Inst, Tokyo 1040045, Japan.
   [Sawa, Masaaki] Carna Biosci Inc, Kobe, Hyogo 6500047, Japan.
C3 National Cancer Center - Japan
RP Yamada, T (corresponding author), Natl Canc Ctr, Div Chemotherapy & Clin Res, Res Inst, Tokyo 1040045, Japan.
EM tyamada@ncc.go.jp
FU Program for Promotion of Fundamental Studies in Health Sciences;
   National Cancer Center Research and Development Fund
FX We are grateful to Ms. Naoko Goto for technical assistance. This study
   was supported by the Program for Promotion of Fundamental Studies in
   Health Sciences conducted by the National Institute of Biomedical
   Innovation of Japan and by the National Cancer Center Research and
   Development Fund.
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NR 92
TC 62
Z9 71
U1 0
U2 36
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0163-7258
J9 PHARMACOL THERAPEUT
JI Pharmacol. Ther.
PD DEC
PY 2015
VL 156
BP 1
EP 9
DI 10.1016/j.pharmthera.2015.10.009
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA CZ2RP
UT WOS:000366952600001
PM 26542362
OA hybrid
DA 2025-01-04
ER

PT J
AU Khalid, AQ
   Bhuvanendran, S
   Magalingam, KB
   Ramdas, P
   Kumari, M
   Radhakrishnan, AK
AF Khalid, Ali Qusay
   Bhuvanendran, Saatheeyavaane
   Magalingam, Kasthuri Bai
   Ramdas, Premdass
   Kumari, Mangala
   Radhakrishnan, Ammu Kutty
TI Clinically Relevant Genes and Proteins Modulated by Tocotrienols in
   Human Colon Cancer Cell Lines: Systematic Scoping Review
SO NUTRIENTS
LA English
DT Review
DE vitamin E; tocotrienols; colorectal cancer; cell lines; biomarkers;
   Cytoscape; PRISMA; KEGG; STRING
ID B SIGNALING PATHWAY; COLORECTAL ADENOCARCINOMA CELLS; TRAIL-INDUCED
   APOPTOSIS; GAMMA-TOCOTRIENOL; DELTA-TOCOTRIENOL; DOWN-REGULATION;
   MICROSATELLITE INSTABILITY; UP-REGULATION; TELOMERASE ACTIVITY;
   CARCINOMA CELLS
AB The last decade has witnessed tremendous growth in tocotrienols (T3s) research, especially in the field of oncology, owing to potent anticancer property. Among the many types of cancers, colorectal cancer (CRC) is growing to become a serious global health threat to humans. Chemoprevention strategies in recent days are open to exploring alternative interventions to inhibit or delay carcinogenesis, especially with the use of bioactive natural compounds, such as tocotrienols. This scoping review aims to distil the large bodies of literature from various databases to identify the genes and their encoded modulations by tocotrienols and to explicate important mechanisms via which T3s combat CRC. For this scoping review, research papers published from 2010 to early 2021 related to T3s and human CRC cells were reviewed in compliance with the PRISMA guidelines. The study included research articles published in English, searchable on four literature databases (Ovid MEDLINE, PubMed, Scopus, and Embase) that reported differential expression of genes and proteins in human CRC cell lines following exposure to T3s. A total of 12 articles that fulfilled the inclusion and exclusion criteria of the study were short-listed for data extraction and analysis. The results from the analysis of these 12 articles showed that T3s, especially its gamma and delta analogues, modulated the expression of 16 genes and their encoded proteins that are associated with several important CRC pathways (apoptosis, transcriptional dysregulation in cancer, and cancer progression). Further studies and validation work are required to scrutinize the specific role of T3s on these genes and proteins and to propose the use of T3s to develop adjuvant or multi-targeted therapy for CRC.
C1 [Khalid, Ali Qusay; Magalingam, Kasthuri Bai; Radhakrishnan, Ammu Kutty] Monash Univ Malaysia, Jeffery Cheah Sch Med & Hlth Sci, Bandar Sunway 47500, Malaysia.
   [Bhuvanendran, Saatheeyavaane] Monash Univ Malaysia, Brain Res Inst Monash Sunway BRIMS, Jeffrey Cheah Sch Med & Hlth Sci, Jalan Lagoon Selatan, Bandar Sunway 47500, Malaysia.
   [Ramdas, Premdass] Int Med Univ, Sch Hlth Sci, Div Appl Biomed Sci & Biotechnol, Kuala Lumpur 57000, Malaysia.
   [Kumari, Mangala] Int Med Univ, Sch Med, Div Human Biol, Dept Anat, Kuala Lumpur 57000, Malaysia.
C3 Monash University; Monash University Malaysia; Monash University; Monash
   University Malaysia; International Medical University Malaysia;
   International Medical University Malaysia
RP Radhakrishnan, AK (corresponding author), Monash Univ Malaysia, Jeffery Cheah Sch Med & Hlth Sci, Bandar Sunway 47500, Malaysia.
EM ali.khalid@monash.edu; bsaatheeyavaane.bhuvanendranpillai@monash.edu;
   kasthuri.bai@monash.edu; premdass_ramdas@imu.edu.my;
   mangala_kumari@imu.edu.my; ammu.radhakrishnan@monash.edu
RI Kumari, Mangala/AAC-7875-2020; magalingam, kasthuribai/AAF-8976-2021;
   Ramdas, Premdass/M-9229-2019; Khalid, Ali/AAD-7570-2022; Pillai,
   B/ABG-8262-2020; Radhakrishnan, Ammu Kutty/F-2877-2015
OI Bhuvanendran, Saatheeyavaane/0000-0002-3889-0163; Khalid,
   Ali/0000-0003-0337-0034; Radhakrishnan, Ammu Kutty/0000-0003-2638-907X;
   Ramdas, Premdass/0000-0002-8521-7668
FU Jeffrey Cheah School of Medicine and Health Sciences, Monash University
   Malaysia and Design for Scientific Renaissance Sdn Bhd. [CNI-000044]
FX The APC was funded by Jeffrey Cheah School of Medicine and Health
   Sciences, Monash University Malaysia and Design for Scientific
   Renaissance Sdn Bhd. (Grant Code: CNI-000044).
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NR 71
TC 5
Z9 5
U1 0
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6643
J9 NUTRIENTS
JI Nutrients
PD NOV
PY 2021
VL 13
IS 11
AR 4056
DI 10.3390/nu13114056
PG 22
WC Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Nutrition & Dietetics
GA XG8EB
UT WOS:000724979900001
PM 34836311
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Homayoonfal, M
   Asemi, Z
   Yousefi, B
AF Homayoonfal, Mina
   Asemi, Zatollah
   Yousefi, Bahman
TI Targeting long non coding RNA by natural products: Implications for
   cancer therapy
SO CRITICAL REVIEWS IN FOOD SCIENCE AND NUTRITION
LA English
DT Review
DE Apoptosis; cancer therapy; long non-coding RNA (lncRNA); metastasis;
   natural product; phytochemical; proliferation
ID NF-KAPPA-B; CELL LUNG-CANCER; EPITHELIAL-MESENCHYMAL TRANSITION;
   NASOPHARYNGEAL CARCINOMA-CELLS; ARYL-HYDROCARBON RECEPTOR; NONCODING
   RNA; BREAST-CANCER; COLORECTAL-CANCER; INHIBITS PROLIFERATION;
   OVARIAN-CANCER
AB In spite of achieving substantial progress in its therapeutic strategies, cancer-associated prevalence and mortality are persistently rising globally. However, most malignant cancers either cannot be adequately diagnosed at the primary phase or resist against multiple treatments such as chemotherapy, surgery, radiotherapy as well as targeting therapy. In recent decades, overwhelming evidences have provided more convincing words on the undeniable roles of long non-coding RNAs (lncRNAs) in incidence and development of various cancer types. Recently, phytochemical and nutraceutical compounds have received a great deal of attention due to their inhibitory and stimulatory effects on oncogenic and tumor suppressor lncRNAs respectively that finally may lead to attenuate various processes of cancer cells such as growth, proliferation, metastasis and invasion. Therefore, application of phytochemicals with anticancer characteristics can be considered as an innovative approach for treating cancer and increasing the sensitivity of cancer cells to standard prevailing therapies. The purpose of this review was to investigate the effect of various phytochemicals on regulation of lncRNAs in different human cancer and evaluate their capabilities for cancer treatment and prevention.
C1 [Homayoonfal, Mina; Asemi, Zatollah] Kashan Univ Med Sci, Inst Basic Sci, Res Ctr Biochem & Nutr Metab Dis, Kashan, Iran.
   [Yousefi, Bahman] Tabriz Univ Med Sci, Mol Med Res Ctr, Tabriz, Iran.
   [Yousefi, Bahman] Tabriz Univ Med Sci, Dept Biochem, Fac Med, Tabriz, Iran.
C3 Tabriz University of Medical Science; Tabriz University of Medical
   Science
RP Asemi, Z (corresponding author), Kashan Univ Med Sci, Inst Basic Sci, Res Ctr Biochem & Nutr Metab Dis, Kashan, Iran.; Yousefi, B (corresponding author), Tabriz Univ Med Sci, Mol Med Res Ctr, Tabriz, Iran.; Yousefi, B (corresponding author), Tabriz Univ Med Sci, Dept Biochem, Fac Med, Tabriz, Iran.
EM asemi_r@yahoo.com; bahmanusefi@gmail.com
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NR 282
TC 9
Z9 9
U1 0
U2 20
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1040-8398
EI 1549-7852
J9 CRIT REV FOOD SCI
JI Crit. Rev. Food Sci. Nutr.
PD AUG 7
PY 2023
VL 63
IS 20
BP 4389
EP 4417
DI 10.1080/10408398.2021.2001785
EA NOV 2021
PG 29
WC Food Science & Technology; Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Food Science & Technology; Nutrition & Dietetics
GA M4DS7
UT WOS:000719198700001
PM 34783279
DA 2025-01-04
ER

PT J
AU Elez, E
   Argilés, G
   Tabernero, J
AF Elez, Elena
   Argiles, Guillem
   Tabernero, Josep
TI First-Line Treatment of Metastatic Colorectal Cancer: Interpreting
   FIRE-3, PEAK, and CALGB/SWOG 80405
SO CURRENT TREATMENT OPTIONS IN ONCOLOGY
LA English
DT Review
DE Colorectal cancer; Bevacizumab; Cetuximab; Panitumumab
ID PHASE-III TRIAL; CETUXIMAB PLUS IRINOTECAN; PROGRESSION-FREE SURVIVAL;
   RAS MUTATIONS; CHEMOTHERAPY; FLUOROURACIL; OXALIPLATIN; BEVACIZUMAB;
   LEUCOVORIN; PANITUMUMAB
AB The advances made in the therapeutic management of colorectal cancer (CRC) over recent years with the addition of therapies targeting angiogenesis or cell proliferation have positioned bevacizumab, cetuximab, and panitumumab as accepted first-line treatments when combined with FOLFOX or FOLFIRI for RAS wild-type (WT) metastatic CRC. The question has been raised as to the choice of targeted therapy to maximize chances of an optimal outcome. Three studies, the phase III FIRE-3 (AIO KRK-0306), the phase II PEAK, and the recently presented phase III CALGB/SWOG 80405 trial, have addressed this issue face-on, directly comparing the addition of bevacizumab versus cetuximab or panitumumab to FOLFOX/FOLFIRI in terms of efficacy outcomes. None of these studies met their primary endpoint (response rate, progression-free survival or overall survival respectively), meaning we are no closer to being able to categorically define an optimal targeted treatment in the first-line setting for patients with advanced CRC. This led to reflection over study design and further analyses, raising a number of important issues. High-sensitivity analysis of the mutational status of exons identified a population with a "pure" non-RAS-mutated profile showing benefit with anti-epidermal growth factor receptor (anti-EGFR) combinations, particularly in the context of early and greater depth of response. Coherent with a personalized therapeutic approach, the importance of performing individual high-sensitivity extended RAS testing is unequivocal and is currently a requirement in many countries to identify this all-RAS WT population, thus limiting unnecessary exposure and expense in patients unlikely to respond. These three studies, particularly the CALGB/SWOG 80405 trial, mark an important milestone in the roadmap of metastatic CRC treatment, highlighting the need for close analysis to fully exploit the available data.
C1 [Elez, Elena; Argiles, Guillem; Tabernero, Josep] Vall dHebron Inst Oncol, Barcelona 08035, Spain.
C3 Vall d'Hebron Institut d'Oncologia (VHIO)
RP Elez, E (corresponding author), Vall dHebron Inst Oncol, P Vall dHebron 119-129, Barcelona 08035, Spain.
EM meelez@vhio.net
RI Tabernero, Josep/AAG-5026-2019; Élez, Elena/AAH-2945-2019; Argiles,
   Guillem/KQU-7406-2024
OI Argiles, Guillem/0000-0002-1487-7108; Tabernero,
   Josep/0000-0002-2495-8139; Elez, Elena/0000-0002-4653-6324
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NR 32
TC 66
Z9 72
U1 0
U2 18
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1527-2729
EI 1534-6277
J9 CURR TREAT OPTION ON
JI Curr. Treat. Options Oncol.
PD NOV
PY 2015
VL 16
IS 11
AR 52
DI 10.1007/s11864-015-0369-x
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CT7WY
UT WOS:000363026900001
PM 26374340
DA 2025-01-04
ER

PT J
AU Mer, AH
   Mirzaei, Y
   Misamogooe, F
   Bagheri, N
   Bazyari, A
   Keshtkaran, Z
   Meyfour, A
   Shahedi, A
   Amirkhani, Z
   Jafari, A
   Barpour, N
   Jahandideh, S
   Rezaei, B
   Nikmanesh, Y
   Abdollahpour-Alitappeh, M
AF Mer, Ali Hussein
   Mirzaei, Yousef
   Misamogooe, Fatemeh
   Bagheri, Nader
   Bazyari, Ahmadreza
   Keshtkaran, Zahra
   Meyfour, Anna
   Shahedi, Alireza
   Amirkhani, Zahra
   Jafari, Ameneh
   Barpour, Nesa
   Jahandideh, Saeed
   Rezaei, Behzad
   Nikmanesh, Yousef
   Abdollahpour-Alitappeh, Meghdad
TI Progress of antibody-drug conjugates (ADCs) targeting c-Met in cancer
   therapy; insights from clinical and preclinical studies
SO DRUG DELIVERY AND TRANSLATIONAL RESEARCH
LA English
DT Review
DE c-Met; c-mesenchymal-epithelial transition factor; Targeted therapy;
   ADC; Antibody-drug conjugate; Immunoconjugate
ID HEPATOCYTE GROWTH-FACTOR; CELL LUNG-CANCER; TELISOTUZUMAB VEDOTIN;
   MONOCLONAL-ANTIBODIES; COLORECTAL-CANCER; FACTOR RECEPTOR;
   OVARIAN-CANCER; PHASE-II; EXPRESSION; PROTEIN
AB The cell-surface receptor tyrosine kinase c-mesenchymal-epithelial transition factor (c-Met) is overexpressed in a wide range of solid tumors, making it an appropriate target antigen for the development of anticancer therapeutics. Various antitumor c-Met-targeting therapies (including monoclonal antibodies [mAbs] and tyrosine kinases) have been developed for the treatment of c-Met-overexpressing tumors, most of which have so far failed to enter the clinic because of their efficacy and complications. Antibody-drug conjugates (ADCs), a new emerging class of cancer therapeutic agents that harness the target specificity of mAbs to deliver highly potent small molecules to the tumor with the minimal damage to normal cells, could be an attractive therapeutic approach to circumvent these limitations in patients with c-Met-overexpressing tumors. Of great note, there are currently nine c-Met-targeting ADCs being examined in different phases of clinical studies as well as eight preclinical studies for treating various solid tumors. The purpose of this study is to present a broad overview of clinical- and preclinical-stage c-Met-targeting ADCs.
C1 [Mer, Ali Hussein] Erbil Polytech Univ, Erbil Med Tech Inst, Dept Nursing, Erbil, Iraq.
   [Mirzaei, Yousef] Cihan Univ Erbil, Dept Med Biochem Anal, Erbil, Kurdistan Regio, Iraq.
   [Misamogooe, Fatemeh; Shahedi, Alireza] Larestan Univ Med Sci, Student Res Comm, Larestan, Iran.
   [Bagheri, Nader] Shahrekord Univ Med Sci, Basic Hlth Sci Inst, Cellular & Mol Res Ctr, Shahrekord 8813733450, Iran.
   [Bazyari, Ahmadreza] Shiraz Univ Med Sci, Student Res Comm, Shiraz, Iran.
   [Keshtkaran, Zahra] Shiraz Univ Med Sci, Community Based Psychiat Care Res Ctr, Sch Nursing & Midwifery, Dept Nursing, Shiraz, Iran.
   [Meyfour, Anna] Shahid Beheshti Univ Med Sci, Res Inst Gastroenterol & Liver Dis, Basic & Mol Epidemiol Gastrointestinal Disorders R, Tehran, Iran.
   [Amirkhani, Zahra] Larestan Univ Med Sci, Sch Nursing, Dept Nursing, Larestan, Iran.
   [Jafari, Ameneh] Shahid Beheshti Univ Med Sci, Prote Res Ctr, Tehran, Iran.
   [Barpour, Nesa] Univ Tabriz, Fac Nat Sci, Dept Genet, Tabriz, Iran.
   [Jahandideh, Saeed] Orchidgene Co, Dept Res & Dev, Tehran 1387837584, Iran.
   [Rezaei, Behzad] Shiraz Univ Med Sci, Laparoscopy Res Ctr, Sch Med, Dept Surg, Shiraz, Fars Province, Iran.
   [Nikmanesh, Yousef] Shiraz Univ Med Sci, Gastroenterohepatol Res Ctr, Shiraz, Iran.
   [Abdollahpour-Alitappeh, Meghdad] Larestan Univ Med Sci, Cellular & Mol Biol Res Ctr, Larestan, Iran.
C3 Erbil Polytechnic University; Cihan University-Erbil; Shahrekord
   University Medical Sciences; Shiraz University of Medical Science;
   Shiraz University of Medical Science; Shahid Beheshti University Medical
   Sciences; Shahid Beheshti University Medical Sciences; University of
   Tabriz; Shiraz University of Medical Science; Shiraz University of
   Medical Science
RP Nikmanesh, Y (corresponding author), Shiraz Univ Med Sci, Gastroenterohepatol Res Ctr, Shiraz, Iran.; Abdollahpour-Alitappeh, M (corresponding author), Larestan Univ Med Sci, Cellular & Mol Biol Res Ctr, Larestan, Iran.
EM you.nikmanesh@gmail.com; abdollahpour1983@yahoo.com
RI amirkhani, z/HJP-6998-2023; Jafari, Ameneh/ABI-3311-2020; Mirzaei,
   Yousef/AAH-5331-2020; nikmanesh, yousef/AAZ-9828-2021; keshtkaran,
   zahra/S-4980-2019
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NR 114
TC 7
Z9 7
U1 5
U2 7
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 2190-393X
EI 2190-3948
J9 DRUG DELIV TRANSL RE
JI Drug Deliv. Transl. Res.
PD NOV
PY 2024
VL 14
IS 11
BP 2963
EP 2988
DI 10.1007/s13346-024-01564-3
EA APR 2024
PG 26
WC Instruments & Instrumentation; Medicine, Research & Experimental;
   Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Instruments & Instrumentation; Research & Experimental Medicine;
   Pharmacology & Pharmacy
GA H6A8D
UT WOS:001200330400001
PM 38597995
DA 2025-01-04
ER

PT J
AU Allan, Z
   Liu, DS
   Lee, MM
   Tie, J
   Clemons, NJ
AF Allan, Zexi
   Liu, David S.
   Lee, Margaret M.
   Tie, Jeanne
   Clemons, Nicholas J.
TI A Practical Approach to Interpreting Circulating Tumor DNA in the
   Management of Gastrointestinal Cancers
SO CLINICAL CHEMISTRY
LA English
DT Review
ID METASTATIC COLORECTAL-CANCER; EGFR RECHALLENGE THERAPY; MINIMAL RESIDUAL
   DISEASE; CELL-FREE DNA; ACQUIRED-RESISTANCE; KRAS MUTATIONS; PLASMA;
   MARKER; PANITUMUMAB; BIOMARKER
AB Background There is accumulating evidence supporting the clinical use of circulating tumor DNA (ctDNA) in solid tumors, especially in different types of gastrointestinal cancer. As such, appraisal of the current and potential clinical utility of ctDNA is needed to guide clinicians in decision-making to facilitate its general applicability.Content In this review, we firstly discuss considerations surrounding specimen collection, processing, storage, and analysis, which affect reporting and interpretation of results. Secondly, we evaluate a selection of studies on colorectal, esophago-gastric, and pancreatic cancer to determine the level of evidence for the use of ctDNA in disease screening, detection of molecular residual disease (MRD) and disease recurrence during surveillance, assessment of therapy response, and guiding targeted therapy. Lastly, we highlight current limitations in the clinical utility of ctDNA and future directions.Summary Current evidence of ctDNA in gastrointestinal cancer is promising but varies depending on its specific clinical role and cancer type. Larger prospective trials are needed to validate different aspects of ctDNA clinical utility, and standardization of collection protocols, analytical assays, and reporting guidelines should be considered to facilitate its wider applicability.
C1 [Allan, Zexi; Clemons, Nicholas J.] Peter MacCallum Canc Ctr, Div Canc Res, Parkville, Vic, Australia.
   [Allan, Zexi; Liu, David S.; Lee, Margaret M.; Tie, Jeanne; Clemons, Nicholas J.] Univ Melbourne, Sir Peter MacCallum Dept Oncol, Parkville, Vic, Australia.
   [Liu, David S.] Peter MacCallum Canc Ctr, Div Canc Surg, Parkville, Vic, Australia.
   [Liu, David S.] Austin Hlth, Div Surg Anaesthesia & Procedural Med, Upper Gastrointestinal Surg Unit, Heidelberg, Vic, Australia.
   [Lee, Margaret M.; Tie, Jeanne] Walter & Eliza Hall Inst Med Res, Div Personalised Oncol, Parkville, Vic, Australia.
   [Tie, Jeanne] Peter MacCallum Canc Ctr, Dept Med Oncol, 305 Grattan St, Parkville, Vic 3000, Australia.
C3 Peter Maccallum Cancer Center; Peter Maccallum Cancer Center; University
   of Melbourne; Peter Maccallum Cancer Center; Florey Institute of
   Neuroscience & Mental Health; Austin Research Institute; Walter & Eliza
   Hall Institute; Peter Maccallum Cancer Center
RP Tie, J (corresponding author), Peter MacCallum Canc Ctr, Dept Med Oncol, 305 Grattan St, Parkville, Vic 3000, Australia.
EM Jeanne.tie@petermac.org
RI Clemons, Nicholas/AAN-6516-2020
OI Clemons, Nicholas/0000-0001-9283-9978
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NR 64
TC 2
Z9 2
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0009-9147
EI 1530-8561
J9 CLIN CHEM
JI Clin. Chem.
PD JAN 4
PY 2024
VL 70
IS 1
BP 49
EP 59
DI 10.1093/clinchem/hvad188
PG 11
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA GK1N9
UT WOS:001152473400032
PM 38175583
DA 2025-01-04
ER

PT J
AU De Mattia, E
   Bignucolo, A
   Toffoli, G
   Cecchin, E
AF De Mattia, Elena
   Bignucolo, Alessia
   Toffoli, Giuseppe
   Cecchin, Erika
TI Genetic Markers of the Host to Predict the Efficacy of Colorectal Cancer
   Targeted Therapy
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
DE Targeted agents; antiangiogenic molecules; bevacizumab; anti-EGFR
   agents; cetuximab; pharmacogenetics; polymorphism; inflammation;
   metastatic colorectal cancer
ID SINGLE-NUCLEOTIDE POLYMORPHISMS; GROWTH-FACTOR-RECEPTOR; BINDING-SITE
   POLYMORPHISM; ANTI-EGFR THERAPY; COLON-CANCER; DOUBLE-BLIND; PHASE-III;
   BEVACIZUMAB; CETUXIMAB; PATHWAY
AB The introduction of anti-EGFR (cetuximab and panitumumab) and antiangiogenic (bevacizumab, regorafeninb, ramucirumab, and aflibercept) agents in the therapeutic armamentarium of the metastatic Colorectal Cancer (CRC) has significantly improved the therapeutic efficacy and patients survival. However, despite the great improvements achieved in the patients life expectation, the high inter-individual heterogeneity in the response to the targeted agents still represent an issue for the management of advanced CRC patients. Even if the role of tumor genetic mutations as predictive markers of drug efficacy has been well-established, the contribution of the host genetic markers is still controversial. Promising results regard the germ-line immune-profile, inflammation and tumor microenvironment. Inherent variations in KRAS 3'UTR region as well as EGF/ EGFR genes were investigated as markers of cetuximab effectiveness. More recently interesting data in the field of antiEGFR agents were generated also for germ-line variants in genes involved in inflammation (e.g. COX-2, LIFR, IGF1 signaling), immune system (e.g., FCGRs, IL-1RA), and other players of the RAS signaling, including the Hippo pathway related genes (e.g. Rassf YAP, TAZ). Host genetic variants in VEGF-dependent (i.e., EGF, IGF-1, HIF1 alpha, eNOS, iNOS) and -independent (i.e., EMT cascade, EGFL7) pathways, with specific attention on inflammation and immune system-related factors (e.g., IL-8, CXCR-1/2, CXCR4-CXCL12 axis, TLRs, GADD34, PPP1R15A, ANXA11, MKNK1), were investigated as predictive markers of bevacizumab outcome, generating some promising results. In this review, we aimed to summarize the most recent literature data regarding the potential role of common and rare inhered variants in predicting which CRC patients will benefit more from a specifically targeted drug administration.
C1 [De Mattia, Elena; Bignucolo, Alessia; Toffoli, Giuseppe; Cecchin, Erika] Natl Canc Inst, Ctr Riferimento Oncol, Clin & Expt Pharmacol, Via Franco Gallini 2, I-33081 Aviano, PN, Italy.
C3 IRCCS Aviano (CRO)
RP Cecchin, E (corresponding author), Natl Canc Inst, Ctr Riferimento Oncol, Clin & Expt Pharmacol, Via Franco Gallini 2, I-33081 Aviano, PN, Italy.
EM ececchin@cro.it
RI Bignucolo, Alessia/AAZ-5587-2020; Cecchin, Erika/K-2448-2018; Toffoli,
   Giuseppe/F-6642-2018; De Mattia, Elena/F-6593-2018
OI Bignucolo, Alessia/0000-0003-4379-291X; Cecchin,
   Erika/0000-0001-7517-7490; Toffoli, Giuseppe/0000-0002-5323-4762; De
   Mattia, Elena/0000-0003-4948-8767
FU European Union's Horizon 2020 research and innovation programme [668353]
FX This project has received funding from the "European Union's Horizon
   2020 research and innovation programme" under grant agreement No.
   668353.
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NR 65
TC 9
Z9 9
U1 0
U2 12
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 2020
VL 27
IS 25
BP 4249
EP 4273
DI 10.2174/0929867326666190712151417
PG 25
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
   Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA MP3TP
UT WOS:000552129400007
PM 31298142
DA 2025-01-04
ER

PT J
AU Delgado-Ramirez, Y
   Colly, V
   Gonzalez, GV
   Leon-Cabrera, S
AF Delgado-Ramirez, Yael
   Colly, Vaneesa
   Gonzalez, Giovanni Villanueva
   Leon-Cabrera, Sonia
TI Signal transducer and activator of transcription 6 as a target in colon
   cancer therapy
SO ONCOLOGY LETTERS
LA English
DT Review
DE colon cancer; signal transducer and activator of transcription 6;
   interleukin-4; interleukin-13; signaling; targeted therapy
ID COLORECTAL-CANCER; GROWTH-FACTOR; TUMOR-GROWTH; G2964A POLYMORPHISM;
   GENE-EXPRESSION; UP-REGULATION; MOUSE MODEL; IN-VITRO; STAT6;
   INTERLEUKIN-4
AB Signal transducer and activator of transcription 6 (STAT6) is a member of the STAT family of proteins that serve key roles in the initiation of tumorigenesis and malignant transformation. STAT6 is highly expressed in several types of cancer, including breast, pancreatic, prostate and colorectal cancer. STAT6 transduces signals in response to the binding of interleukin (IL)-4 and IL-13 to their receptors and regulates the expression of genes involved in the immune response, cell survival, tumor proliferation and metastasis. Patients with colorectal cancer exhibit high STAT6 activity in the colonic epithelium, and STAT6 expression is associated with lower survival rates, lymph node metastasis, changes in the epithelial barrier function and alterations in the inflammatory response. A number of studies investigating experimental models and cancer cell lines have revealed that STAT6 is associated with tumor growth and development, as well as with increased invasion and metastasis, suggesting that STAT6 inhibition may serve as a novel therapeutic strategy in colon cancer. The present review summarizes the evidence with regard to the implications of STAT6 in cancer biology and the direct and indirect effects on colon tumor transformation. Furthermore, the current treatment strategies targeting the IL-4/IL-13/STAT6 axis in colon cancer are discussed.
C1 [Delgado-Ramirez, Yael; Colly, Vaneesa; Leon-Cabrera, Sonia] Univ Nacl Autonoma Mexico, Biomed Res Unit, Lab Oncoimmunol, Ave De los Barrios 1, Tlalnepantla 54090, Mexico.
   [Colly, Vaneesa; Gonzalez, Giovanni Villanueva; Leon-Cabrera, Sonia] Univ Nacl Autonoma Mexico, Sch Med, Fac Super Studies Iztacala, Tlalnepantla 54090, Mexico.
C3 Universidad Nacional Autonoma de Mexico; Universidad Nacional Autonoma
   de Mexico
RP Leon-Cabrera, S (corresponding author), Univ Nacl Autonoma Mexico, Biomed Res Unit, Lab Oncoimmunol, Ave De los Barrios 1, Tlalnepantla 54090, Mexico.
EM soleonca@comunidad.unam.mx
RI Leon-Cabrera, Sonia/L-6596-2019
FU Support Program for Research Projects and Technological Innovation
   (PAPIIT) [IA204218]; National Council for Science and Technology
   (CONACYT) [A1-S23944]
FX The present study was supported by grants from Support Program for
   Research Projects and Technological Innovation (PAPIIT)(grant no.
   IA204218) and National Council for Science and Technology
   (CONACYT)(grant no. A1-S23944).
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NR 67
TC 17
Z9 20
U1 2
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 JUL
PY 2020
VL 20
IS 1
BP 455
EP 464
DI 10.3892/ol.2020.11614
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA MG4OT
UT WOS:000546013100046
PM 32565970
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Cong, S
   Bai, SS
   Zhang, MH
   Bi, YF
   Wang, Y
   Jin, S
   He, H
AF Cong, Shan
   Bai, Shanshan
   Zhang, Minghao
   Bi, Yanfang
   Wang, Yu
   Jin, Shi
   He, Hui
TI A study on metabolic characteristics and metabolic markers of
   gastrointestinal tumors
SO CANCER BIOLOGY & THERAPY
LA English
DT Article
DE Gastrointestinal tumor; metabolic subtype; prognosis; drug response;
   TCGA database
ID DRUG-RESISTANCE; CANCER; BEVACIZUMAB; HETEROGENEITY; CARCINOMA; CELLS;
   IMMUNOTHERAPY; CAPECITABINE; PROGRESSION; GLYCOLYSIS
AB Tumor cells have significant heterogeneity in metabolism and are closely related to prognosis, gene mutation, and subtype. However, this association has not been demonstrated in reports of gastrointestinal tumors. In this study, we constructed four metabolic subtypes and identified four gene signatures using the expression data and clinical information of 252 metabolism-related genes from TCGA and NCBI databases for gastric adenocarcinoma (STAD) and colorectal cancer (COAD and READ). MC1 had the worst prognosis compared to other classifications. GSig1 was mainly related to drug metabolism and was the highest in MC1 with the worst prognosis, while the other subtypes were mainly related to glucose metabolism pathways. This difference also existed in other different malignant tumors. In addition, metabolic typing was associated with chemotherapeutic drug response and tumor heterogeneity, which indicated that monitoring metabolic typing could contribute to drug efficacy and gene-targeted therapy. In conclusion, we identified differences among subtypes in clinical characteristics such as prognosis and revealed the potential function of metabolic subtype in response to chemotherapeutic agents and oncogene mutations. This work highlighted the potential clinical meaning of metabolic subtype and characteristics in drug therapy and prognosis assessment of malignant tumors.
C1 [Cong, Shan; Wang, Yu; Jin, Shi; He, Hui] Dalian Med Univ, Affiliated Hosp 1, Dept Laparoscop Surg, Lianhe Rd 193, Dalian 116000, Liaoning, Peoples R China.
   [Bai, Shanshan] Dalian Med Univ, Affiliated Hosp 1, Dept Ultrasound, Dalian, Peoples R China.
   [Zhang, Minghao] Mudanjiang Med Coll, Affiliated Hongqi Hosp, Dept Vasc Intervent, Mudanjiang, Peoples R China.
   [Bi, Yanfang] Dalian Med Univ, Affiliated Hosp 1, Dept Nursing, Dalian, Liaoning, Peoples R China.
C3 Dalian Medical University; Dalian Medical University; Mudanjiang Medical
   University; Dalian Medical University
RP Jin, S; He, H (corresponding author), Dalian Med Univ, Affiliated Hosp 1, Dept Laparoscop Surg, Lianhe Rd 193, Dalian 116000, Liaoning, Peoples R China.
EM jinshi@dmu.edu.cn; hehui@dmu.edu.cn
RI Jin, Shi/KVB-2581-2024
FU Natural Science Foundation of China (NSFC) [81903964, 82174133]
FX his study was supported by the Natural Science Foundation of China (NSFC
   No.81903964 to HH; NSFC No. 82174133 to SJ
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NR 46
TC 1
Z9 1
U1 1
U2 7
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1538-4047
EI 1555-8576
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD DEC 31
PY 2023
VL 24
IS 1
AR 2255369
DI 10.1080/15384047.2023.2255369
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA R7AM2
UT WOS:001065843300001
PM 37705174
OA Green Published, gold
DA 2025-01-04
ER

PT J
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AF Buchholz, Soeren M.
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   Biggemann, Lorenz
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TI Time to Deliver on Promises: The Role of ERBB2 Alterations as Treatment
   Options for Colorectal Cancer Patients in the Era of Precision Oncology
SO JOURNAL OF PERSONALIZED MEDICINE
LA English
DT Article
DE HER2; ERBB2; colorectal cancer; molecular tumor board; genomic
   profiling; targeted therapy
ID ADJUVANT TRASTUZUMAB; OPEN-LABEL; HER2
AB Receptor tyrosine kinase erythroblastic oncogene B2 (ERBB2), also known as human epidermal growth factor receptor 2 (HER2), represents an oncogenic driver and has been effectively targeted in breast and gastric cancer. Recently, next-generation sequencing (NGS) discovered ERBB2 as a promising therapeutic target in metastatic colorectal cancer (mCRC), where it is altered in 3-5% of patients, but no therapies are currently approved for this use. Herein, we present the experience of a single center in diagnosing actionable genetic ERBB2 alterations using NGS and utilizing the latest therapeutic options. Between October 2019 and December 2022, a total of 107 patients with advanced CRC underwent molecular analysis, revealing actionable ERBB2 mutations in two patients and ERBB2 amplifications in two other patients. These findings correlated with immunohistochemical (IHC) staining. Of these four patients, two were treated with trastuzumab-deruxtecan (T-DXd). We present two exemplary cases of patients with actionable ERBB2 alterations to demonstrate the effectiveness of T-DXd in heavily pretreated ERBB2-positive mCRC patients and the need for early molecular profiling. To fully exploit the potential of this promising treatment, earlier molecular profiling and the initiation of targeted therapies are essential.
C1 [Buchholz, Soeren M.; Koenig, Ute; Reinecke, Johanna; Steuber, Benjamin; Ammer-Herrmenau, Christoph; Neesse, Albrecht; Ellenrieder, Volker; Adler, Marius; Koenig, Alexander] Univ Med Ctr Gottingen, Dept Gastroenterol Gastrointestinal Oncol & Endocr, D-37075 Gottingen, Germany.
   [Nause, Nelia; Braulke, Friederike] Univ Med Ctr Gottingen, Gottingen Comprehens Canc Ctr G CCC, D-37075 Gottingen, Germany.
   [Reuter-Jessen, Kirsten; Bohnenberger, Hanibal; Stroebel, Philipp] Univ Med Ctr Gottingen, Inst Pathol, D-37075 Gottingen, Germany.
   [Biggemann, Lorenz] Univ Med Ctr Gottingen, Inst Diagnost & Intervent Radiol, D-37075 Gottingen, Germany.
   [Adler, Marius] Univ Hosp Augsburg, Dept Gastroenterol, D-86156 Augsburg, 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 Buchholz, SM (corresponding author), Univ Med Ctr Gottingen, Dept Gastroenterol Gastrointestinal Oncol & Endocr, D-37075 Gottingen, Germany.
EM soerenmatthias.buchholz@med.uni-goettingen.de
RI Bohnenberger, Hanibal/F-2317-2013
OI Strobel, Philipp/0000-0002-8528-8060; Bohnenberger,
   Hanibal/0000-0003-1038-1030
FU Gottingen University
FX We acknowledge support by the Open Access Publication Funds of the
   Gottingen University.
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NR 37
TC 1
Z9 1
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4426
J9 J PERS MED
JI J. Pers. Med.
PD DEC
PY 2023
VL 13
IS 12
AR 1701
DI 10.3390/jpm13121701
PG 11
WC Health Care Sciences & Services; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Health Care Sciences & Services; General & Internal Medicine
GA DG2D6
UT WOS:001130801500001
PM 38138928
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Jahedi, M
   Meshkini, A
AF Jahedi, Mehrnaz
   Meshkini, Azadeh
TI Tumor tropic delivery of FU.FA@NSs using mesenchymal stem cells for
   synergistic chemo-photodynamic therapy of colorectal cancer
SO COLLOIDS AND SURFACES B-BIOINTERFACES
LA English
DT Article
DE 5-Fluorouracil (5-FU); Cerium oxide nanoparticle; Mesenchymal stem
   cell-based drug delivery; Tumor-targeting therapy; Chemo-photodynamic
   therapy
ID CERIUM OXIDE; NANOPARTICLES; 5-FLUOROURACIL; MECHANISMS; GRAPHENE; SIZE;
   PH
AB To overcome the limitations associated with the targeting abilities of nanotherapeutics and drug loading capacity of mesenchymal stem cells (MSCs), the present study relies on the combination of MSCs tumor tropism with the controlled release function of nano-based drug delivery platforms to achieve tumor-specific accumulation of chemotherapeutics with minimal off-target effects. 5-fluorouracil (5-FU)-containing ceria (CeNPs) coated calcium carbonate nanoparticles (CaNPs) were functionalized with folinic acid (FA) to develop drug-containing nanocomposites (Ca.FU.Ce.FA NCs). NCs were then conjugated with graphene oxide (GO) and decorated with silver nanoparticles (Ag degrees NPs) to form FU.FA@NS, a rationally designed drug delivery system with O2 generation capacity that alleviates tumor hypoxia for improved photodynamic therapy. Engineering of MSCs with FU. FA@NSs provided successful loading and long-term retention of therapeutics on the surface membrane with minimal changes to the functional properties of MSCs. Co-culturing of FU.FA@NS.MSCs with CT26 cells upon UVA exposure revealed enhanced apoptosis in tumor cells through ROS-mediated mitochondrial pathway. FU. FA@NSs released from MSCs were effectively taken up by CT26 cells via a clathrin-mediated endocytosis pathway and distributed their drug depots in a pH, H2O2, and UVA-stimulated fashion. Therefore, the cell-based biomimetic drug delivery platform formulated in the current study could be considered a promising strategy for targeted chemo-photodynamic therapy of colorectal cancer.
C1 [Jahedi, Mehrnaz; Meshkini, Azadeh] Ferdowsi Univ Mashhad, Fac Sci, Biochem Res Ctr, Dept Chem, Mashhad 9177948974, Iran.
   [Meshkini, Azadeh] Ferdowsi Univ Mashhad, Inst Biotechnol, Novel Diagnost & Therapeut Res Grp, Mashhad, Iran.
   [Meshkini, Azadeh] Ferdowsi Univ Mashhad, Fac Sci, Dept Chem, Mashhad 9177948974, Iran.
C3 Ferdowsi University Mashhad; Ferdowsi University Mashhad; Ferdowsi
   University Mashhad
RP Meshkini, A (corresponding author), Ferdowsi Univ Mashhad, Fac Sci, Dept Chem, Mashhad 9177948974, Iran.
EM a.meshkini@um.ac.ir
RI Jahedi, Mehrnaz/HGV-1378-2022; Meshkini, Azadeh/AAU-9654-2020
OI Jahedi, Mehrnaz/0000-0002-3255-912X; Meshkini,
   Azadeh/0000-0002-5804-7827
FU Research Council of Ferdowsi University of Mashhad [3/54161]
FX The authors appreciate the financial support for this investigation by
   the Research Council of Ferdowsi University of Mashhad (Grant No.
   3/54161) .
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NR 72
TC 7
Z9 7
U1 7
U2 22
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0927-7765
EI 1873-4367
J9 COLLOID SURFACE B
JI Colloid Surf. B-Biointerfaces
PD JUN
PY 2023
VL 226
AR 113333
DI 10.1016/j.colsurfb.2023.113333
EA MAY 2023
PG 14
WC Biophysics; Chemistry, Physical; Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biophysics; Chemistry; Materials Science
GA N9CW5
UT WOS:001039917000001
PM 37141773
DA 2025-01-04
ER

PT J
AU Wu, F
   Liu, F
   Dong, LM
   Yang, H
   He, XX
   Li, LL
   Zhao, LH
   Jin, SS
   Li, G
AF Wu, Fang
   Liu, Fang
   Dong, Lemei
   Yang, Han
   He, Xixi
   Li, Lili
   Zhao, Lihao
   Jin, Sisi
   Li, Gang
TI miR-1273g silences MAGEA3/6 to inhibit human colorectal cancer cell
   growth via activation of AMPK signaling
SO CANCER LETTERS
LA English
DT Article
DE Molecularly-targeted therapy; microRNA; Melanoma antigen A3/A6;
   AMP-activated protein kinase
ID INDUCED APOPTOSIS; PHOSPHORYLATION; AUTOPHAGY; PATHWAY; HYPOMETHYLATION;
   EXPRESSION; MICRORNAS; COMPLEXES; FAMILY
AB AMP-activated protein kinase (AMPK) is a metabolic regulator that acts to limit the growth of cancer cells. AMPK is downregulated by melanoma antigens A3/6 (MAGEA3/6), which are cancer-specific proteins that enhance the activity of specific E3 ubiquitin ligases to ubiquitinate and degrade AMP-activated protein kinase alpha 1 (AMPK alpha 1). Here, using a bioinformatic approach, we identified a microRNA, miR-1273g-3p, that is predicted to target the 3' untranslated region (UTR) of MAGEA3/6. Analyzing miR-1273g-3p expression in human colon cancer tissues, we found a reduction in miR-1273g-3p expression correlating with increased MAGEA3/6 expression and AMPK alpha 1 downregulation. Expression of miR-1273g in HT-29 cells and primary human colon cancer cells down regulated MAGEA3/6, leading to AMPK alpha 1 upregulation, inhibition of proliferation and cell apoptosis. The anti CRC activity of miR-1273g was blocked by AMPK alpha 1 knockout. MAGEA3/6 shRNA silencing mimicked and abolished miR-1273g-induced actions in HT-29 cells. In vivo, miR-1273g-or MAGEA3/6 shRNA-expressing HT-29 tumors grew significantly slower than control tumors. We propose a novel miRNA-based mechanism, whereby miR-1273g represses MAGEA3/6 expression in human CRC cells and tissues, which may provide a novel cancer-specific therapeutic.
C1 [Wu, Fang; Dong, Lemei; He, Xixi; Jin, Sisi] Wenzhou Med Univ, Dept Gastroenterol, Affiliated Hosp 1, Wenzhou, Peoples R China.
   [Liu, Fang] Nanjing Med Univ, Dept Neurosurg, Affiliated Changzhou Peoples Hosp 2, Changzhou, Peoples R China.
   [Yang, Han; Li, Lili; Zhao, Lihao; Li, Gang] Wenzhou Med Univ, Dept Chemoradiat Oncol, Affiliated Hosp 1, South Bai Xiang St, Wenzhou 325000, Zhejiang, Peoples R China.
C3 Wenzhou Medical University; Nanjing Medical University; Wenzhou Medical
   University
RP Li, G (corresponding author), Wenzhou Med Univ, Dept Chemoradiat Oncol, Affiliated Hosp 1, South Bai Xiang St, Wenzhou 325000, Zhejiang, Peoples R China.
EM ligangwzyd@163.com
FU Natural Science Foundation of Zhejiang Province [LY15H030015]; National
   Natural Science Foundation of China [81302181]
FX This project was supported by the Natural Science Foundation of Zhejiang
   Province (LY15H030015), and by National Natural Science Foundation of
   China (81302181). 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 46
TC 44
Z9 46
U1 0
U2 20
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0304-3835
EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PY 2018
VL 435
BP 1
EP 9
DI 10.1016/j.canlet.2018.07.031
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GT6WX
UT WOS:000444662700001
PM 30056111
DA 2025-01-04
ER

PT J
AU Sepulveda, AR
   Hamilton, SR
   Allegra, CJ
   Grody, W
   Cushman-Vokoun, AM
   Funkhouser, WK
   Kopetz, SE
   Lieu, C
   Lindor, NM
   Minsky, BD
   Monzon, FA
   Sargent, DJ
   Singh, VM
   Willis, J
   Clark, J
   Colasacco, C
   Rumble, RB
   Temple-Smolkin, R
   Ventura, CB
   Nowak, JA
AF Sepulveda, Antonia R.
   Hamilton, Stanley R.
   Allegra, Carmen J.
   Grody, Wayne
   Cushman-Vokoun, Allison M.
   Funkhouser, William K.
   Kopetz, Scott E.
   Lieu, Christopher
   Lindor, Noralane M.
   Minsky, Bruce D.
   Monzon, Federico A.
   Sargent, Daniel J.
   Singh, Veena M.
   Willis, Joseph
   Clark, Jennifer
   Colasacco, Carol
   Rumble, R. Bryan
   Temple-Smolkin, Robyn
   Ventura, Christina B.
   Nowak, Jan A.
TI Molecular Biomarkers for the Evaluation of Colorectal Cancer: Guideline
   From the American Society for Clinical Pathology, College of American
   Pathologists, Association for Molecular Pathology, and the American
   Society of Clinical Oncology
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID RECEPTOR MONOCLONAL-ANTIBODIES; KRAS MUTATION DETECTION; ANTI-EGFR
   THERAPY; III COLON-CANCER; K-RAS MUTATIONS; MICROSATELLITE-INSTABILITY;
   PIK3CA MUTATION; ADJUVANT CHEMOTHERAPY; 1ST-LINE TREATMENT; PTEN
   EXPRESSION
AB Purpose
   Molecular testing of colorectal cancers (CRCs) to improve patient care and outcomes of targeted and conventional therapies has been the center of many recent studies, including clinical trials. Evidence-based recommendations for the molecular testing of CRC tissues to guide epidermal growth factor receptor (EGFR) -targeted therapies and conventional chemotherapy regimens are warranted in clinical practice. The purpose of this guideline is to develop evidence-based recommendations to help establish standard molecular biomarker testing for CRC through a systematic review of the literature.
   Methods
   The American Society for Clinical Pathology (ASCP), College of American Pathologists (CAP), Association for Molecular Pathology (AMP), and the American Society of Clinical Oncology (ASCO) convened an Expert Panel to develop an evidence-based guideline to help establish standard molecular biomarker testing, guide targeted therapies, and advance personalized care for patients with CRC. A comprehensive literature search that included over 4,000 articles was conducted to gather data to inform this guideline.
   Results
   Twenty-one guideline statements (eight recommendations, 10 expert consensus opinions and three no recommendations) were established.
   Recommendations
   Evidence supports mutational testing for genes in the EGFR signaling pathway, since they provide clinically actionable information as negative predictors of benefit to anti-EGFR monoclonal antibody therapies for targeted therapy of CRC. Mutations in several of the biomarkers have clear prognostic value. Laboratory approaches to operationalize molecular testing for predictive and prognostic molecular biomarkers involve selection of assays, type of specimens to be tested, timing of ordering of tests and turnaround time for testing results. Additional information is available at: www.asco.org/CRC-markers-guideline and www.asco.org/guidelineswiki (C) 2017 by American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology, American Society of Clinical Oncology, and American Society for Investigative Pathology
C1 [Sepulveda, Antonia R.] Columbia Univ, New York, NY USA.
   [Hamilton, Stanley R.; Kopetz, Scott E.; Minsky, Bruce D.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
   [Allegra, Carmen J.] Univ Florida, Med Ctr, Gainesville, FL USA.
   [Grody, Wayne] UCLA, Los Angeles, CA USA.
   [Cushman-Vokoun, Allison M.] Univ Nebraska, Med Ctr, Omaha, NE 68182 USA.
   [Funkhouser, William K.] Univ N Carolina, Sch Med, Chapel Hill, NC USA.
   [Lieu, Christopher] Univ Colorado, Denver Sch Med, Denver, CO 80202 USA.
   [Lindor, Noralane M.] Mayo Clin, Scottsdale, AZ USA.
   [Monzon, Federico A.] Castle Biosci, Friendswood, TX USA.
   [Sargent, Daniel J.] Mayo Clin, Rochester, MN USA.
   [Singh, Veena M.] Biocept, San Diego, CA USA.
   [Willis, Joseph] Case Western Reserve Univ, Cleveland, OH USA.
   [Clark, Jennifer] Amer Soc Clin Pathologists, Washington, DC USA.
   [Colasacco, Carol; Ventura, Christina B.] Coll Amer Pathologists, Northfield, MN USA.
   [Rumble, R. Bryan] Amer Soc Clin Oncol, Alexandria, VA USA.
   [Temple-Smolkin, Robyn] Assoc Mol Pathol, Bethesda, MD USA.
   [Nowak, Jan A.] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
C3 Columbia University; University of Texas System; UTMD Anderson Cancer
   Center; State University System of Florida; University of Florida;
   University of California System; University of California Los Angeles;
   University of Nebraska System; University of Nebraska Medical Center;
   University of North Carolina; University of North Carolina Chapel Hill;
   University of North Carolina School of Medicine; University of Colorado
   System; University of Colorado Denver; University of Colorado Anschutz
   Medical Campus; Mayo Clinic; Mayo Clinic Phoenix; Mayo Clinic;
   University System of Ohio; Case Western Reserve University; College of
   American Pathologists; American Society of Clinical Oncology; Roswell
   Park Comprehensive Cancer Center
RP Sepulveda, AR (corresponding author), Amer Soc Clin Oncol, 2318 Mill Rd,Suite 800, Alexandria, VA 22314 USA.
EM guidelines@asco.org
RI Kopetz, Scott/AAC-1387-2019; Colasacco, Carol/AAA-2736-2022
OI Monzon, Federico/0000-0002-6890-9793; Kopetz, Scott/0000-0001-9647-3416;
   Temple-Smolkin, Robyn/0000-0002-5728-5436; Colasacco,
   Carol/0000-0001-7856-7531
FU Amgen; Sanofi; Biocartis; Guardant Health; Array BioPharma; Bayer;
   Genentech/Roche; MolecularMatch; Taiho Pharmaceutical; Celgene (Inst);
   Roche/Genentech (Inst)
FX Amgen, Sanofi, Biocartis, Guardant Health, Array BioPharma, Bayer,
   Genentech/Roche, MolecularMatch, Taiho PharmaceuticalCelgene (Inst),
   Roche/Genentech (Inst)
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NR 148
TC 245
Z9 253
U1 1
U2 54
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 MAY 1
PY 2017
VL 35
IS 13
BP 1453
EP +
DI 10.1200/JCO.2016.71.9807
PG 37
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ET5PD
UT WOS:000400335500012
PM 28165299
OA Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Lu, L
   Li, ZJ
   Li, LF
   Shen, J
   Zhang, L
   Li, MX
   Xiao, ZG
   Wang, JH
   Cho, CH
AF Lu, Lan
   Li, Zhi Jie
   Li, Long Fei
   Shen, Jing
   Zhang, Lin
   Li, Ming Xing
   Xiao, Zhan Gang
   Wang, Jian Hao
   Cho, Chi Hin
TI A novel vascular-targeting peptide for gastric cancer delivers low-dose
   TNFα to normalize the blood vessels and improve the anti-cancer
   efficiency of 5-fluorouracil
SO PEPTIDES
LA English
DT Article
DE Antitumor therapy; Vascular-targeting peptide; TNF alpha; Gastric
   cancer; Drug delivery
ID TUMOR-NECROSIS-FACTOR; ADVANCED SOLID TUMORS; PHAGE DISPLAY; MOUSE
   MODEL; ANTITUMOR-ACTIVITY; COLORECTAL-CANCER; DRUG-DELIVERY; ZIP CODES;
   NGR-HTNF; COMBINATION
AB Various vascular-targeted agents fused with tumor necrosis factor a (TNF alpha) have been shown to improve drug absorption into tumor tissues and enhance tumor vascular function. TCP-1 is a peptide selected through in vivo phage library biopanning against a mouse orthotopic colorectal cancer model and is a promising agent for drug delivery. This study further investigated the targeting ability of TCP-1 phage and peptide to blood vessels in an orthotopic gastric cancer model in mice and assessed the synergistic anti-cancer effect of 5-fluorouracil (5-FU) with subnanogram TNFa targeted delivered by TCP-1 peptide. In vivo phage targeting assay and in vivo colocalization analysis were carried out to test the targeting ability of TCP-1 phage/peptide. A targeted therapy for improvement of the therapeutic efficacy of 5-FU and vascular function was performed through administration of TCP-1/TNF alpha fusion protein in this model. TCP-1 phage exhibited strong homing ability to the orthotopic gastric cancer after phage injection. Immunohistochemical staining suggested that and TCP-1 phage/TCP-1 peptide could colocalize with tumor vascular endothelial cells. TCP-1/TNF alpha combined with 5-FU was found to synergistically inhibit tumor growth, induce apoptosis and reduce cell proliferation without evident toxicity. Simultaneously, subnanogram TCP-1/TNF alpha treatment normalized tumor blood vessels. Targeted delivery of low-dose TNFa by TCP-1 peptide can potentially modulate the vascular function of gastric cancer and increase the drug delivery of chemotherapeutic drugs.
C1 [Lu, Lan] Chengdu Univ, Sichuan Ind Inst Antibiot, Chengdu, Sichuan, Peoples R China.
   [Lu, Lan; Li, Zhi Jie; Li, Long Fei; Shen, Jing; Zhang, Lin; Li, Ming Xing; Xiao, Zhan Gang; Cho, Chi Hin] Southwest Med Univ, Sch Pharm, Dept Pharmacol, Lab Mol Pharmacol, Luzhou, Peoples R China.
   [Wang, Jian Hao; Cho, Chi Hin] Changzhou Univ, Sch Pharmaceut Engn & Life Sci, Changzhou, Peoples R China.
   [Cho, Chi Hin] Chinese Univ Hong Kong, Fac Med, Sch Biomed Sci, Hong Kong, Hong Kong, Peoples R China.
C3 Chengdu University; Southwest Medical University; Changzhou University;
   Chinese University of Hong Kong
RP Lu, L (corresponding author), Chengdu Univ, Sichuan Ind Inst Antibiot, Chengdu, Sichuan, Peoples R China.; Cho, CH (corresponding author), Chinese Univ Hong Kong, Fac Med, Sch Biomed Sci, Hong Kong, Hong Kong, Peoples R China.
EM eugene6251124@163.com; chcho@cuhk.edu.hk
RI Cho, Chi/C-6543-2014; LI, ZHIJIE/HJG-6926-2022; Li, 李明星/AAJ-6084-2020;
   ZHANG, Lin/O-9109-2015
OI LI, Longfei/0009-0000-7872-2175
FU National Natural Science Foundation of China [81473269]; General
   Research Fund, Hong Kong Research Grant Council [463613]; National High
   Technology Research and Development Program of China [863 Program]
   [2014AA020521]; Innovation and Technology Support Programme [ITS/212/15]
FX This work was partially supported by the National Natural Science
   Foundation of China [grant numbers 81473269]; the General Research Fund,
   Hong Kong Research Grant Council [grant numbers 463613]; the National
   High Technology Research and Development Program of China [863 Program
   2014AA020521] and the Innovation and Technology Support Programme, Tier
   3/Seed Projects [grant numbers ITS/212/15].
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NR 39
TC 5
Z9 5
U1 2
U2 30
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0196-9781
EI 1873-5169
J9 PEPTIDES
JI Peptides
PD NOV
PY 2017
VL 97
BP 54
EP 63
DI 10.1016/j.peptides.2017.09.020
PG 10
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
   Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
   Pharmacology & Pharmacy
GA FK3OS
UT WOS:000413396000007
PM 28970092
DA 2025-01-04
ER

PT J
AU Xiao, JJ
   Duan, QH
   Wang, Z
   Yan, W
   Sun, HM
   Xue, PP
   Fan, XM
   Zeng, XY
   Chen, J
   Shao, C
   Zhu, F
AF Xiao, Juanjuan
   Duan, Qiuhong
   Wang, Zhe
   Yan, Wei
   Sun, Huimin
   Xue, Peipei
   Fan, Xiaoming
   Zeng, Xiaoyu
   Chen, Juan
   Shao, Chen
   Zhu, Feng
TI Phosphorylation of TOPK at Y74, Y272 by Src increases the stability of
   TOPK and promotes tumorigenesis of colon cancer
SO ONCOTARGET
LA English
DT Article
DE TOPK; Src; colon cancer; tumorigenesis; stability
ID ORIGINATED PROTEIN-KINASE; PDZ-BINDING KINASE; COLORECTAL-CANCER;
   INDUCED APOPTOSIS; MITOTIC KINASE; CRITICAL ROLES; EXPRESSION; PBK/TOPK;
   PP60C-SRC
AB T-LAK cell-originated protein kinase (TOPK), a serine/threonine protein kinase, is highly expressed in a variety of tumors and associated with a poor prognosis of human malignancies. However, the activation mechanism of TOPK is still unrevealed. Herein, first we found that Src directly bound with and phosphorylated TOPK at Y74 and Y272 in vitro. Anti-phospho-TOPK at Y74 was prepared, the endogenous phosphorylation of TOPK at Y74 was detected in colon cancer cells, and the phosphorylation was inhibited in cells expressing low levels of Src. Subsequently, we stably transfected Y74 and Y272 double mutated TOPK (TOPK-FF) into JB6 or SW480 cells, and observed that both the anchorage-independent growth ability and tumorigenesis of TOPK-FF cells were suppressed compared with those of wild type TOPK (TOPK-WT) ex vivo and in vivo. The phosphorylation level of TOPK substrate, Histone H3 at Ser10 also decreased dramatically ex vivo or in vivo. Moreover, we showed that Src could inhibit the ubiquitination of TOPK. Transiently expressed TOPK-WT was more stable than TOPK-FF in pause and chase experiment. Endogenous TOPK was more stable in Src wild type (Src(+/+)) MEFs than in Src knockout (Src(-/-)). Taken together, our results indicate that Src is a novel upstream kinase of TOPK. The phosphorylation of TOPK at Y74 and Y272 by Src increases the stability and activity of TOPK, and promotes the tumorigenesis of colon cancer. It may provide opportunities for TOPK based prognosis and targeted therapy for colon cancer patients.
C1 [Xiao, Juanjuan; Duan, Qiuhong; Xue, Peipei; Fan, Xiaoming; Zeng, Xiaoyu; Chen, Juan; Zhu, Feng] Huazhong Univ Sci & Technol, Sch Basic Med, Dept Biochem & Mol Biol, Wuhan 430030, Hubei, Peoples R China.
   [Sun, Huimin; Shao, Chen] Fourth Mil Med Univ, Xijing Hosp, Dept Urol, Xian 710032, Shaanxi, Peoples R China.
   [Wang, Zhe; Yan, Wei] Fourth Mil Med Univ, Xijing Hosp, Dept Pathol, Xian 710032, Shaanxi, Peoples R China.
   [Xiao, Juanjuan] Hubei Univ Sci & Technol, Basic Med Coll, Lab Translat Oncol, Xianning 437100, Hubei, Peoples R China.
C3 Huazhong University of Science & Technology; Air Force Military Medical
   University; Air Force Military Medical University; Hubei University of
   Science & Technology
RP Chen, J; Zhu, F (corresponding author), Huazhong Univ Sci & Technol, Sch Basic Med, Dept Biochem & Mol Biol, Wuhan 430030, Hubei, Peoples R China.; Shao, C (corresponding author), Fourth Mil Med Univ, Xijing Hosp, Dept Urol, Xian 710032, Shaanxi, Peoples R China.
EM chenjuanlinda69@163.com; shaochen@fmmu.edu.cn; fengzhu@hust.edu.cn
RI Yan, Wei/HNR-6443-2023; ZHU, Feng/C-1303-2010
OI Zhu, Feng/0000-0003-1172-0102
FU national Natural Science Foundation of China [81472602, 81450110449,
   81570180, 81572529, 30271302]; Independent innovation project of
   Huazhong University of Science and Technology [2014TS063, 2014ZZGH013];
   Ministry of Science and Technology of People's Republic of China
   [2011DFA33110]
FX This project was supported by the national Natural Science Foundation of
   China (No. 81472602, 81450110449, 81570180, 81572529 & 30271302) and the
   Independent innovation project of Huazhong University of Science and
   Technology (No. 2014TS063&2014ZZGH013), and the major program of
   international cooperation of the Ministry of Science and Technology of
   People's Republic of China (No. 2011DFA33110).
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NR 46
TC 19
Z9 20
U1 1
U2 29
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 APR 26
PY 2016
VL 7
IS 17
BP 24483
EP 24494
DI 10.18632/oncotarget.8231
PG 12
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DO3UB
UT WOS:000377706200114
PM 27016416
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Naz, T
   Rehman, AU
   Shahzad, A
   Rasool, MF
   Saleem, Z
   Hussain, R
AF Naz, Tehnia
   Rehman, Anees ur
   Shahzad, Aleena
   Rasool, Muhammad Fawad
   Saleem, Zikria
   Hussain, Rabia
TI Impact of bevacizumab on clinical outcomes and its comparison with
   standard chemotherapy in metastatic colorectal cancer patients: a
   systematic review and meta-analysis
SO JOURNAL OF PHARMACEUTICAL POLICY AND PRACTICE
LA English
DT Article
DE Bevacizumab; CRC; efficacy; ch & iecy;moth & iecy;rapy; colorectal
   cancer; metastasis; monoclonal antibody
ID FOLFOXIRI PLUS BEVACIZUMAB; 1ST-LINE TREATMENT; INITIAL THERAPY;
   PHASE-III; EFFICACY; FOLFIRI; PROGRESSION; MFOLFOX6; TRIAL
AB Background: Advances in targeted therapies have expanded the treatment options for colorectal cancer (CRC), allowing for more tailored and effective approaches to managing the disease. In targeted therapy, Bevacizumab is a commonly prescribed anti-VEGF monoclonal antibody that has a direct anti-vascular impact in cancer patients. Vascular Endothelial Growth Factors (VEGFs), especially VEGF-A, are significant agents in promoting tumour angiogenesis. Objective: To assess the impact of adding Bevacizumab to chemotherapy on progression-free survival (PFS) and overall survival (OS) in patients with metastatic colorectal cancer. Methodology: Comprehensive searches have been performed on electronic databases such as PubMed, and Google Scholar using the following terms: colorectal cancer, adenocarcinoma, Bevacizumab, chemotherapy, and monoclonal antibody. Results: In the meta-analysis, 16 out of the 24 included studies were analysed. In the final analysis, incorporating Bevacizumab with ch & iecy;moth & iecy;rapy demonstrated favourable outcomes for OS with a hazard ratio (HR = 0.689,95%CI: 0.51-0.83, I-2 = 39%, p <0.01) and for PFS with a hazard ratio (HR = 0.77 95% CI: 0.60-0.96, I-2 = 54%, p < 0.01). The subgroup analysis of PFS, categorised by study d & iecy;sign (prosp & iecy;ctiv & iecy; vs r & iecy;trosp & iecy;ctiv & iecy;), reveals that the Hazard Ratio (HR = 0.82, 95% CI: 0.62-0.97, I-2 = 21%, p < 0.01) and for OS with a hazard ratio (HR = 0.73, 95% CI: 0.52-0.86, I-2 = 17%, p < 0.01). Conclusion: Our findings indicate that combining Bevacizumab with chemotherapy enhances clinical outcomes and results in a significant increase in PFS and OS in patients with metastatic colorectal cancer. Positive outcomes are demonstrated by a substantial 23% increase in PFS and 31% increase in OS in patients with metastatic colorectal cancer who undergo Bevacizumab in conjunction with chemotherapy.
C1 [Naz, Tehnia; Rehman, Anees ur; Shahzad, Aleena; Rasool, Muhammad Fawad; Saleem, Zikria] Bahauddin Zakariya Univ, Fac Pharm, Dept Pharm Practice, Multan, Pakistan.
   [Hussain, Rabia] Univ Sains Malaysia, Sch Pharmaceut Sci, Discipline Social & Adm Pharm, George Town 11800, Malaysia.
C3 Bahauddin Zakariya University; Universiti Sains Malaysia
RP Hussain, R (corresponding author), Univ Sains Malaysia, Sch Pharmaceut Sci, Discipline Social & Adm Pharm, George Town 11800, Malaysia.
EM rabia.hussain@usm.my
RI Rasool, Prof. Dr. Muhammad/I-6610-2013; Hussain, Rabia/AAE-7742-2020
OI Hussain, Rabia/0000-0001-8183-0855
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NR 41
TC 1
Z9 1
U1 3
U2 5
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
EI 2052-3211
J9 J PHARM POLICY PRACT
JI J. Pharm. Policy Pract.
PD DEC 31
PY 2024
VL 17
IS 1
AR 2354300
DI 10.1080/20523211.2024.2354300
PG 20
WC Health Policy & Services; Pharmacology & Pharmacy
WE Emerging Sources Citation Index (ESCI)
SC Health Care Sciences & Services; Pharmacology & Pharmacy
GA TP3S8
UT WOS:001242431000001
PM 38845624
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Reivell, V
   Hagman, H
   Haux, J
   Jorns, C
   Lindnér, P
   Taflin, H
AF Reivell, Veronica
   Hagman, Helga
   Haux, Johan
   Jorns, Carl
   Lindner, Per
   Taflin, Helena
TI SOULMATE: the Swedish study of liver transplantation for isolated
   colorectal cancer liver metastases not suitable for operation or
   ablation, compared to best established treatment-a randomized controlled
   multicenter trial
SO TRIALS
LA English
DT Article
DE Randomized controlled trial; Colorectal cancer; Liver Metastases; Liver
   transplantation; Extended criteria donors
ID HEPATOCELLULAR-CARCINOMA; HEPATIC RESECTION; RECURRENCE; CHEMOTHERAPY;
   SURVIVAL; PATTERNS; OUTCOMES; SURGERY; TUMORS
AB Background: Around one fourth of patients with colorectal cancer present themselves with distant metastases at the time of diagnosis, and one additional one fifth of the patients will develop distant metastases during the disease, most commonly in the liver.
   Surgical treatment such as liver resection or ablation, often combined with chemotherapy and targeted therapy, is the only treatment option with curative potential, but only about 20% of the patients with liver metastases are candidates for surgical intervention. Standard treatment for unresectable patients is palliative oncological therapy; however, less than 10% of these patients will achieve a 5-year survival.
   Non-randomized studies indicate that liver transplantation could be an option for selected patients with colorectal liver metastases (CRLM), which are not suitable for operation or ablation due to surgical technical reasons such as massive tumor burden and small future liver remnant, or oncological reasons, for example, early relapse after liver surgery. Since there is a shortage of donated liver grafts, it is important to select the patient group that benefit most from the treatment. Although some studies present positive results from liver transplantation of CRLM, the results must be validated in a randomized controlled trial before this new indication for liver transplantation can be introduced as a clinical routine.
   Methods: The SOULMATE study is a randomized study evaluating if liver transplantation with liver grafts, primarily from extended criteria donors, increases overall survival in patients with CRLM, not suitable for resection or ablation, in comparison with best established treatment.
   Patients will be randomized to liver transplantation (LT)+ best established treatment (BET) or to best established treatment only.
   In the SOULMATE trial, we will evaluate the use of livers from extended criteria donors to decrease the risk of prolonging waiting time for patients on the waiting list for LT.
   Discussion: The SOULMATE study has the possibility to confirm the positive results of previous studies in a randomized setting. The use of extended criteria donors will make the results transferable globally, as most countries are struggling with organ shortage.
C1 [Reivell, Veronica; Lindner, Per; Taflin, Helena] Univ Gothenburg, Transplant Inst, Inst Clin Sci, Sahlgrenska Acad, Gothenburg, Sweden.
   [Reivell, Veronica; Lindner, Per; Taflin, Helena] Sahlgrens Univ Hosp, Gothenburg, Sweden.
   [Hagman, Helga] Skanes Univ Hosp, Dept Oncol, Lund, Sweden.
   [Haux, Johan] Skaraborgs Hosp, Dept Oncol, Skovde, Sweden.
   [Jorns, Carl] Karolinska Univ Hosp, Dept Transplantat, Stockholm, Sweden.
C3 University of Gothenburg; Sahlgrenska University Hospital; Karolinska
   Institutet; Karolinska University Hospital
RP Taflin, H (corresponding author), Univ Gothenburg, Transplant Inst, Inst Clin Sci, Sahlgrenska Acad, Gothenburg, Sweden.
EM helena.taflin@vgregion.se
RI Jorns, Carl/AAE-6925-2021
OI Jorns, Carl/0000-0001-7727-8113; Taflin, Helena/0000-0002-8795-5250
FU Swedish Cancer Society; Swedish Medical Society; Swedish government;
   Region Vastra Gotaland
FX The SOULMATE trial has received financial support from the Swedish
   Cancer Society, The Swedish Medical Society, and the Swedish state under
   the agreement between the Swedish government and the county councils and
   Region Vastra Gotaland. The funding bodies provide financial support for
   the study but has no role in the design of the study, nor the
   collection, analysis, interpretation of data, or publication of results.
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NR 33
TC 6
Z9 6
U1 0
U2 4
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1745-6215
J9 TRIALS
JI Trials
PD SEP 30
PY 2022
VL 23
IS 1
AR 831
DI 10.1186/s13063-022-06778-9
PG 13
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 4Z7WI
UT WOS:000862413500005
PM 36180944
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU He, MJ
   Lin, Y
   Xu, YZ
AF He, Minjie
   Lin, Yan
   Xu, Yuzhen
TI Identification of prognostic biomarkers in colorectal cancer using a
   long non-coding RNA-mediated competitive endogenous RNA network
SO ONCOLOGY LETTERS
LA English
DT Article
DE ceRNA network; colorectal cancer; lncRNA; topology; pathogenesis;
   prognostic biomarker
ID TUMOR-SUPPRESSOR; CELL-CYCLE; MUSCLE DIFFERENTIATION; SEMAPHORIN 6B;
   CERNA NETWORK; GENE ONTOLOGY; MICRORNA; PROLIFERATION; REGULATOR;
   APOPTOSIS
AB Colorectal cancer (CRC) is a highly malignant gastrointestinal tumor accompanied by poor prognosis. Long non-coding RNA (lncRNA) plays an important role in the progression and physiology of tumors as it competes with endogenous RNAs, including miRNA and mRNA. In the present study, a multi-step computational method was used to build a CRC-related functional lncRNA-mediated competitive endogenous RNA (ceRNA) network (LMCN). lncRNAs with more degrees and betweenness centrality (BC) were screened out as hub lncRNAs. Then functional enrichment analyses of lncRNAs were carried out from the Gene Ontology (GO) and Reactome pathway databases based on the 'guilt by association' principle. As a result, lncRNAs in the LMCN displayed specific topological characteristics in accordance with the regulatory correlation of coding mRNAs in CRC pathology. HCP5, EPB41L4A-AS1, SNHG12, and LINC00649 were screened out as hub lncRNAs which were more significantly related to the development and prognosis of CRC. The hub lncRNAs in CRC were obviously involved in functions of cell cycle arrest, vacuolar transport, histone modification, and in pathways of GPCR, signaling by Rho GTPases, axon guidance pathways, meaning that they might be potential biomarkers for diagnosis, evaluation and gene-targeted therapy of CRC. Thus, the LMCN construction method could accelerate lncRNA discovery and therapeutic development in CRC.
C1 [He, Minjie] Kunming Med Univ, Dept Med Oncol, Affiliated Hosp 1, Kunming 650000, Yunnan, Peoples R China.
   [Lin, Yan] Xinjiang Med Univ, Dept Oncol, Affiliated Tradit Chinese Med Hosp, Urumqi 830000, Xinjiang, Peoples R China.
   [Xu, Yuzhen] Southeast Univ, Dept Gastrointestinal Surg, Xuzhou Hosp, Sch Med, 199 Jiefang South Rd, Xuzhou 221009, Jiangsu, Peoples R China.
C3 Kunming Medical University; Xinjiang Medical University; Southeast
   University - China
RP Xu, YZ (corresponding author), Southeast Univ, Dept Gastrointestinal Surg, Xuzhou Hosp, Sch Med, 199 Jiefang South Rd, Xuzhou 221009, Jiangsu, Peoples R China.
EM yuzhenxu12@126.com
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NR 61
TC 34
Z9 37
U1 0
U2 14
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 2019
VL 17
IS 3
BP 2687
EP 2694
DI 10.3892/ol.2019.9936
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HN9YG
UT WOS:000460555900015
PM 30854042
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Lv, XQ
   Xu, GX
AF Lv, Xiaoqun
   Xu, Guoxiong
TI Regulatory role of the transforming growth factor-β signaling pathway in
   the drug resistance of gastrointestinal cancers
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Drug resistance; Gastrointestinal cancer; Transforming growth
   factor-beta; Epithelial-mesenchymal transition; Cancer stem cells;
   MicroRNAs
ID EPITHELIAL-MESENCHYMAL TRANSITION; DEPENDENT CELLULAR CYTOTOXICITY;
   ADVANCED RECTAL-CANCER; TGF-BETA; COLORECTAL-CANCER; GASTRIC-CANCER;
   COLON-CANCER; OXALIPLATIN RESISTANCE; STEM-CELLS; PREDICTIVE MARKER
AB Gastrointestinal (GI) cancer, including esophageal, gastric, and colorectal cancer, is one of the most prevalent types of malignant carcinoma and the leading cause of cancer-related deaths. Despite significant advances in therapeutic strategies for GI cancers in recent decades, drug resistance with various mechanisms remains the prevailing cause of therapy failure in GI cancers. Accumulating evidence has demonstrated that the transforming growth factor (TGF)-beta signaling pathway has crucial, complex roles in many cellular functions related to drug resistance. This review summarizes current knowledge regarding the role of the TGF-beta signaling pathway in the resistance of GI cancers to conventional chemotherapy, targeted therapy, immunotherapy, and traditional medicine. Various processes, including epithelial-mesenchymal transition, cancer stem cell development, tumor microenvironment alteration, and microRNA biogenesis, are proposed as the main mechanisms of TGF-beta-mediated drug resistance in GI cancers. Several studies have already indicated the benefit of combining antitumor drugs with agents that suppress the TGF-beta signaling pathway, but this approach needs to be verified in additional clinical studies. Moreover, the identification of potential biological markers that can be used to predict the response to TGF-beta signaling pathway inhibitors during anticancer treatments will have important clinical implications in the future.
C1 [Lv, Xiaoqun] Fudan Univ, Jinshan Hosp, Dept Pharm, Shanghai 201508, Peoples R China.
   [Xu, Guoxiong] Fudan Univ, Jinshan Hosp, Res Ctr Clin Med, 1508 Longhang Rd, Shanghai 201508, Peoples R China.
   [Xu, Guoxiong] Fudan Univ, Dept Oncol, Shanghai Med Coll, Shanghai 200032, Peoples R China.
C3 Fudan University; Fudan University; Fudan University
RP Xu, GX (corresponding author), Fudan Univ, Jinshan Hosp, Res Ctr Clin Med, 1508 Longhang Rd, Shanghai 201508, Peoples R China.
EM guoxiong.xu@fudan.edu.cn
OI Xu, Guoxiong/0000-0002-9074-8754
FU Fourth Training Program for the Outstanding Young Talents, Jinshan
   Health Commission, China [JSYQ201904]; Key Construction Project on
   Clinical Pharmacy of Shanghai, China [2019-1229]; National Natural
   Science Foundation of China [81872121]
FX Supported by Fourth Training Program for the Outstanding Young Talents,
   Jinshan Health Commission, China, No. JSYQ201904; Key Construction
   Project on Clinical Pharmacy of Shanghai, China, No. 2019-1229; and
   National Natural Science Foundation of China, No. 81872121.
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NR 157
TC 5
Z9 6
U1 0
U2 3
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 2021
VL 13
IS 11
BP 1648
EP 1667
DI 10.4251/wjgo.v13.i11.1648
PG 20
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA XL4WF
UT WOS:000728144900007
PM 34853641
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Hagemann, IS
   Bridge, JA
   Tafe, LJ
   Hameed, MR
   Moncur, JT
   Bellizzi, AM
   Dolan, M
   Vasalos, P
   Kane, ME
   Souers, RJ
   Yemelyanova, A
AF Hagemann, Ian S.
   Bridge, Julia A.
   Tafe, Laura J.
   Hameed, Meera R.
   Moncur, Joel T.
   Bellizzi, Andrew M.
   Dolan, Michelle
   Vasalos, Patricia
   Kane, Megan E.
   Souers, Rhona J.
   Yemelyanova, Anna
TI Current Laboratory Testing Practices for Assessment of ERBB2/HER2 in
   Endometrial Serous Carcinoma and Colorectal Carcinoma
SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE
LA English
DT Article
ID OF-AMERICAN-PATHOLOGISTS; HER2 SCORING SYSTEM; GASTRIC-CANCER; PAIRED
   PRIMARY; BREAST-CANCER; SOCIETY; RECOMMENDATIONS; EXPRESSION; GUIDELINE;
   OVEREXPRESSION
AB center dot Context.-Therapy targeted at human epidermal growth factor receptor 2 (HER2; also known as ERBB2) was used initially for breast and gastroesophageal carcinoma and has more recently been adopted for endometrial serous carcinoma (ESC) and colorectal carcinoma (CRC). There is evidence that predictive biomarker testing algorithms for HER2 must be tumor type specific and that an algorithm validated for one tumor type cannot be applied to another. Objective.-To describe current laboratory practices for HER2 assessment in ESC and CRC. Design.-We surveyed laboratories participating in the 2021 College of American Pathologists (CAP) HER2 immunohistochemistry proficiency testing program. Results.-The survey was distributed to 1548 laborato-ries and returned by 1195, of which 83.5% (998) were in the United States. For ESC, 24.0% (287) of laboratories reported performing in-house testing for HER2 by immu-nohistochemical staining and/or in situ hybridization; of these, 44.3% (127) performed it reflexively on all cases of ESC. The most common criterion for evaluating HER2 was the American Society of Clinical Oncology/CAP 2018 guideline for breast carcinoma (69.0%; 194 of 281), whereas only 16.0% (45) of laboratories used guidelines specific to ESC. For CRC, 20.2% (239 of 1185) of laboratories performed in-house HER2 testing, and 82.0% of these (196) did the test only at the clinician's request. A plurality (49.4%; 115 of 233) used gastroesoph-ageal cancer guidelines when scoring CRC, 30.0% (70) used the CRC scoring system from the HERACLES trial, and 16.3% (38) used the American Society of Clinical Oncology/CAP 2018 guideline for breast carcinoma. Conclusions.-Laboratories vary in their approach to HER2 testing in ESC and CRC. Most laboratories did not report using tumor type-specific recommendations for HER2 interpretation. The lack of standardization could present a challenge to evidence-based practice when considering targeted therapy for these diseases.
C1 [Hagemann, Ian S.] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA.
   [Bridge, Julia A.] ProPath, Dallas, TX USA.
   [Bridge, Julia A.] Univ Nebraska Med Ctr, Dept Pathol & Microbiol, Omaha, NE USA.
   [Tafe, Laura J.] Dartmouth Hitchcock Med Ctr, Dept Pathol &Lab Med, Lebanon, NH USA.
   [Hameed, Meera R.] Mem Sloan Kettering Canc Ctr York, Dept Pathol, New York, NY USA.
   [Moncur, Joel T.] Joint Pathol Ctr, Off Director, Silver Spring, MD USA.
   [Bellizzi, Andrew M.] Univ Iowa, Dept Pathol, Iowa City, IA 52246 USA.
   [Dolan, Michelle] Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN USA.
   [Vasalos, Patricia; Kane, Megan E.] Coll Amer Pathologists, Proficiency Testing Dept, Northfield, IL USA.
   [Souers, Rhona J.] Coll Amer Pathologists, Biostat Dept, Northfield, IL USA.
   [Yemelyanova, Anna] Weill Cornell Med, Dept Pathol & Lab Med, New York, NY USA.
   [Hagemann, Ian S.] Washington Univ, Sch Med, 425 S Euclid Ave,Campus Box 8118, St Louis, MO 63110 USA.
C3 Washington University (WUSTL); University of Nebraska System; University
   of Nebraska Medical Center; Dartmouth College; University of Iowa;
   University of Minnesota System; University of Minnesota Twin Cities;
   College of American Pathologists; College of American Pathologists;
   Cornell University; Weill Cornell Medicine; Washington University
   (WUSTL)
RP Hagemann, IS (corresponding author), Washington Univ, Sch Med, 425 S Euclid Ave,Campus Box 8118, St Louis, MO 63110 USA.
EM hagemani@wustl.edu
RI Hagemann, Ian/ABB-2854-2021
OI Tafe, Laura/0000-0001-9613-641X
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NR 39
TC 6
Z9 6
U1 0
U2 1
PU COLL AMER PATHOLOGISTS
PI NORTHFIELD
PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 USA
SN 0003-9985
EI 1543-2165
J9 ARCH PATHOL LAB MED
JI Arch. Pathol. Lab. Med.
PD OCT
PY 2023
VL 147
IS 10
BP 1148
EP 1157
DI 10.5858/arpa.2022-0229-CP)
PG 10
WC Medical Laboratory Technology; Medicine, Research & Experimental;
   Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology; Research & Experimental Medicine;
   Pathology
GA Y9XJ0
UT WOS:001108713600006
PM 36538387
DA 2025-01-04
ER

PT J
AU Ratti, M
   Orlandi, E
   Toscani, I
   Vecchia, S
   Anselmi, E
   Hahne, JC
   Ghidini, M
   Citterio, C
AF Ratti, Margherita
   Orlandi, Elena
   Toscani, Ilaria
   Vecchia, Stefano
   Anselmi, Elisa
   Hahne, Jens Claus
   Ghidini, Michele
   Citterio, Chiara
TI Emerging Therapeutic Targets and Future Directions in Advanced Gastric
   Cancer: A Comprehensive Review
SO CANCERS
LA English
DT Review
DE metastatic gastric cancer; molecular targets; immunological targets;
   ctDNA; CAR-T cells; cancer vaccines
ID GASTROESOPHAGEAL JUNCTION CANCER; PEMBROLIZUMAB PLUS CHEMOTHERAPY;
   METASTATIC COLORECTAL-CANCER; DOUBLE-BLIND; PHASE-II; ADVANCED
   ESOPHAGEAL; SINGLE-ARM; OPEN-LABEL; ADVANCED ADENOCARCINOMA; TRASTUZUMAB
   DERUXTECAN
AB Simple Summary Metastatic gastric cancer (GC) remains a major clinical challenge due to scarce treatment options and an ominous prognosis, often diagnosed at later stages. Recent progress in identifying molecular targets and integrating immune checkpoint inhibitors with chemotherapy has transformed treatment strategies. The new classification of GC, based on immunologic and molecular markers, has drastically changed the therapeutic approach, focusing on personalized target-based treatments. This review summarizes molecular and immunological targets currently available and explores future approaches like circulating tumor DNA (ctDNA) monitoring, targeting fibroblast growth factor receptor (FGFR) and MET pathways, chimeric antigen receptor (CAR)-T cells, and cancer vaccines for their potential to improve understanding and treatment of this disease.Abstract Metastatic gastric cancer (GC) still represents a critical clinical challenge, with limited treatment options and a poor prognosis. Most patients are diagnosed at advanced stages, limiting the chances of surgery and cure. The identification of molecular targets and the possibility of combining immune checkpoint inhibitors with chemotherapy have recently reshaped the therapeutic landscape of metastatic gastric cancer. The new classification of gastric cancer, mainly based on immunologic and molecular criteria such as programmed cell death 1 (PD-1), microsatellite instability (MSI), and human epidermal growth factor receptor 2 (HER2), has made it possible to identify and differentiate patients who may benefit from immunotherapy, targeted therapy, or chemotherapy alone. All relevant and available molecular and immunological targets in clinical practice for the systemic treatment of this disease are presented. Particular attention is given to possible future approaches, including circulating tumor DNA (ctDNA) for therapeutic monitoring, new targeting agents against molecular pathways such as fibroblast growth factor receptor (FGFR) and MET, chimeric antigen receptor (CAR)-T cells, and cancer vaccines. This review aims to provide a comprehensive understanding of current targets in advanced gastric cancer and to offer valuable insights into future directions of research and clinical practice in this challenging disease.
C1 [Ratti, Margherita; Orlandi, Elena; Toscani, Ilaria; Vecchia, Stefano; Anselmi, Elisa; Citterio, Chiara] Piacenza Gen Hosp, Oncol & Hematol Dept, Via Taverna 49, I-29121 Piacenza, Italy.
   [Hahne, Jens Claus] Inst Canc Res, Div Mol Pathol, London SM2 5NG, England.
   [Ghidini, Michele] Fdn IRCCS Ca Granda Osped Maggiore Policlin, Med Oncol Unit, I-20122 Milan, Italy.
C3 Royal Marsden NHS Foundation Trust; University of London; Institute of
   Cancer Research - UK; IRCCS Ca Granda Ospedale Maggiore Policlinico
RP Ratti, M (corresponding author), Piacenza Gen Hosp, Oncol & Hematol Dept, Via Taverna 49, I-29121 Piacenza, Italy.
EM mratti.cremona@gmail.com; e.orlandi@ausl.pc.it; i.toscani@ausl.pc.it;
   s.vecchia@ausl.pc.it; e.anselmi@ausl.pc.it; hahnejen@yahoo.de;
   michele.ghidini@policlinico.mi.it; c.citterio@ausl.pc.it
RI Orlandi, Elena/HDM-2197-2022; Ghidini, Michele/I-7362-2018
OI Citterio, Chiara/0000-0002-2119-775X; Orlandi,
   Elena/0000-0002-2559-7558; Vecchia, Stefano/0000-0003-0578-0870;
   Ghidini, Michele/0000-0001-5435-1218
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NR 142
TC 2
Z9 2
U1 4
U2 4
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 15
AR 2692
DI 10.3390/cancers16152692
PG 21
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA C1N5W
UT WOS:001287100200001
PM 39123420
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Tian, YH
   Lin, J
   Tian, YM
   Zhang, GQ
   Zeng, X
   Zheng, RH
   Zhang, WJ
   Yuan, YW
AF Tian, Yunhong
   Lin, Jie
   Tian, Yunming
   Zhang, Guoqian
   Zeng, Xing
   Zheng, Ronghui
   Zhang, Weijun
   Yuan, Yawei
TI Efficacy and safety of anti-EGFR agents administered concurrently with
   standard therapies for patients with head and neck squamous cell
   carcinoma: a systematic review and meta-analysis of randomized
   controlled trials
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Review
DE randomized controlled trials; epidermal growth factor receptor; head and
   neck squamous cell carcinoma
ID METASTATIC COLORECTAL-CANCER; LOCALLY ADVANCED HEAD; PHASE-II;
   OPEN-LABEL; INDUCTION CHEMOTHERAPY; TUMOR MICROENVIRONMENT; PLUS
   RADIOTHERAPY; SURVIVAL BENEFIT; POOLED ANALYSIS; CETUXIMAB
AB Agents targeting epidermal growth factor receptor (EGFR) are used to treat head and neck squamous cell carcinoma (HNSCC); however, their efficacy and safety is poorly understood. Here we evaluated the efficacy and safety of anti-EGFR agents administered concurrently with standard therapies for HNSCC. Randomized controlled trials that evaluated addition of EGFR targeted therapy versus standard therapy alone were included. The primary outcome was overall survival (OS). Secondary outcomes were progression-free survival (PFS), overall response rate (ORR), locoregional control, and severe adverse events (SAEs, grade3). Sixteen eligible trials with 4031 patients were included. Addition of anti-EGFR regimens to standard therapy significantly improved OS of patients with HNSCC (HR=0.89; 95% CI, 0.82-0.96), with a moderately elevated rate of SAEs (RR=1.08; 95% CI, 1.03-1.13). Subgroup analysis indicated that the survival benefit was observed when cetuximab was administered concurrently with radiotherapy (RT) for stage III/IV patients (HR=0.76; 95% CI, 0.61-0.94; p=0.01), or with chemotherapy for recurrent or metastatic (R/M) HNSCC (HR=0.86; 95% CI, 0.78-0.95; p=0.005). Significantly increased ORR (RR=1.51; 95% CI 1.05-2.18) and PFS (HR=0.72; 95% CI, 0.59-0.88) were found in R/M HNSCC patients treated with anti-EGFR plus chemotherapy, while no significant improvements were found in stage III/IV patients treated with anti-EGFR plus standard therapy. In conclusion, addition of cetuximab to standard therapy may improve outcomes for R/M HNSCC patients, while causing a moderate increase in SAEs. For stage III/IV patients, anti-EGFR mAb plus RT can improve OS compared with RT alone, while replacement of chemotherapy with EGFR mAb or adding EGFR mAb to combined chemotherapy and RT did not improve outcomes.
C1 [Tian, Yunhong; Lin, Jie; Zhang, Guoqian; Zeng, Xing; Zheng, Ronghui; Zhang, Weijun; Yuan, Yawei] Guangzhou Med Univ, Affiliated Canc Hosp & Inst, Dept Radiat Oncol, Guangzhou, Guangdong, Peoples R China.
   [Tian, Yunming] Hui Zhou Municipal Cent Hosp, Dept Radiat Oncol, Guangzhou, Guangdong, Peoples R China.
C3 Guangzhou Medical University
RP Yuan, YW (corresponding author), Guangzhou Med Univ, Affiliated Canc Hosp & Inst, Dept Radiat Oncol, Guangzhou, Guangdong, Peoples R China.
EM yuanyawei2015@outlook.com
RI Ling, Jie/JJF-9995-2023; zeng, xing/GQY-6499-2022
OI Jie, Lin/0000-0002-4852-0342
FU National Natural Science Foundation of China [81502342]; Funds of
   Guangzhou key medical discipline construction project, Guangzhou Medical
   College, Guangdong Province, China [2015A23, 2016C37]
FX Grant sponsor: National Natural Science Foundation of China; Grant
   number: 81502342; Grant sponsor: Funds of Guangzhou key medical
   discipline construction project, Guangzhou Medical College, Guangdong
   Province, China; Grant numbers: 2015A23, 2016C37
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NR 43
TC 23
Z9 28
U1 0
U2 22
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 JUN 1
PY 2018
VL 142
IS 11
BP 2198
EP 2206
DI 10.1002/ijc.31157
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GC1MK
UT WOS:000429545800001
PM 29143328
OA Bronze
DA 2025-01-04
ER

PT J
AU Doble, B
   Tan, M
   Harris, A
   Lorgelly, P
AF Doble, Brett
   Tan, Marcus
   Harris, Anthony
   Lorgelly, Paula
TI Modeling companion diagnostics in economic evaluations of targeted
   oncology therapies: systematic review and methodological checklist
SO EXPERT REVIEW OF MOLECULAR DIAGNOSTICS
LA English
DT Review
DE companion diagnostics; cost-effectiveness analysis; economic evaluation;
   genomic testing; oncology; precision medicine
ID COST-EFFECTIVENESS ANALYSIS; METASTATIC COLORECTAL-CANCER; STAGE
   BREAST-CANCER; GENOMIC SCREENING-PROGRAMS; ADJUVANT TRASTUZUMAB;
   PERSONALIZED MEDICINE; LUNG-CANCER; KRAS; CETUXIMAB; CARE
AB The successful use of a targeted therapy is intrinsically linked to the ability of a companion diagnostic to correctly identify patients most likely to benefit from treatment. The aim of this study was to review the characteristics of companion diagnostics that are of importance for inclusion in an economic evaluation. Approaches for including these characteristics in model-based economic evaluations are compared with the intent to describe best practice methods. Five databases and government agency websites were searched to identify model-based economic evaluations comparing a companion diagnostic and subsequent treatment strategy to another alternative treatment strategy with model parameters for the sensitivity and specificity of the companion diagnostic (primary synthesis). Economic evaluations that limited model parameters for the companion diagnostic to only its cost were also identified (secondary synthesis). Quality was assessed using the Quality of Health Economic Studies instrument. 30 studies were included in the review (primary synthesis n = 12; secondary synthesis n = 18). Incremental cost-effectiveness ratios may be lower when the only parameter for the companion diagnostic included in a model is the cost of testing. Incorporating the test's accuracy in addition to its cost may be a more appropriate methodological approach. Altering the prevalence of the genetic biomarker, specific population tested, type of test, test accuracy and timing/sequence of multiple tests can all impact overall model results. The impact of altering a test's threshold for positivity is unknown as it was not addressed in any of the included studies. Additional quality criteria as outlined in our methodological checklist should be considered due to the shortcomings of standard quality assessment tools in differentiating studies that incorporate important test-related characteristics and those that do not. There is a need to refine methods for incorporating the characteristics of companion diagnostics into model-based economic evaluations to ensure consistent and transparent reimbursement decisions are made.
C1 [Doble, Brett; Tan, Marcus; Harris, Anthony; Lorgelly, Paula] Monash Univ, Fac Business & Econ, Ctr Hlth Econ, Clayton, Vic 3800, Australia.
   [Tan, Marcus] Deakin Univ, Fac Hlth, Deakin Strateg Res Ctr Populat Hlth, Deakin Hlth Econ, Burwood, Vic 3125, Australia.
C3 Monash University; Deakin University
RP Doble, B (corresponding author), Monash Univ, Fac Business & Econ, Ctr Hlth Econ, Room 278,Level 2,Bldg 75, Clayton, Vic 3800, Australia.
EM brett.doble@monash.edu
RI Lorgelly, Paula/B-5400-2012; harris, anthony/A-2551-2009
OI Lorgelly, Paula/0000-0002-8990-9514; Harris,
   Anthony/0000-0003-1641-3320; Doble, Brett/0000-0002-4948-8831
FU Monash University; Victorian Cancer Agency
FX B Doble is supported by research scholarships from Monash University. P
   Lorgelly is a recipient of a Victorian Government Translational Research
   Grant through the Victorian Cancer Agency. The funding sources had no
   role in the design and conduct of the study; collection, management,
   analysis and interpretation of the data; preparation, review and
   approval of the manuscript or decision to submit the manuscript for
   publication.
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   [Anonymous], MED SERV ADV COMM CO
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   [Anonymous], TECHN ASS
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NR 80
TC 22
Z9 26
U1 1
U2 25
PU TAYLOR & FRANCIS AS
PI OSLO
PA KARL JOHANS GATE 5, NO-0154 OSLO, NORWAY
SN 1473-7159
EI 1744-8352
J9 EXPERT REV MOL DIAGN
JI Expert Rev. Mol. Diagn.
PD FEB
PY 2015
VL 15
IS 2
SI SI
BP 235
EP 254
DI 10.1586/14737159.2014.929499
PG 20
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA AZ7EA
UT WOS:000348380400010
PM 25142227
DA 2025-01-04
ER

PT J
AU Tabernero, J
   Chawla, SP
   Kindler, H
   Reckamp, K
   Chiorean, EG
   Azad, NS
   Lockhart, AC
   Hsu, CP
   Baker, NF
   Galimi, F
   Beltran, P
   Baselga, J
AF Tabernero, Josep
   Chawla, Sant P.
   Kindler, Hedy
   Reckamp, Karen
   Chiorean, E. Gabriela
   Azad, Nilofer S.
   Lockhart, A. Craig
   Hsu, Cheng-Pang
   Baker, Nigel F.
   Galimi, Francesco
   Beltran, Pedro
   Baselga, Jose
TI Anticancer activity of the type I insulin-like growth factor receptor
   antagonist, ganitumab, in combination with the death receptor 5 agonist,
   conatumumab
SO TARGETED ONCOLOGY
LA English
DT Article
DE Monoclonal antibodies; Insulin-like growth factor receptor; Death
   receptor; TRAIL; Apoptosis; Targeted therapy
ID MONOCLONAL-ANTIBODY; ANTITUMOR-ACTIVITY; DOSE-ESCALATION; AMG 479;
   CANCER; APOPTOSIS; INHIBITOR; CELL; CP-751,871; RESISTANCE
AB Agents targeting the insulin-like growth factor receptor type 1 (IGF1R) have shown antitumor activity. Based on the evidence for interaction between the IGF-1 and TRAIL pathways, we hypothesized that the combination of ganitumab (monoclonal antibody to IGF1R) with the pro-apoptotic death receptor 5 agonist, conatumumab, might increase antitumor response. Ganitumab and conatumumab were tested in combination in a Colo-205 xenograft model. Part 1 of the clinical study was a phase Ib program of three doses of conatumumab (1, 3, 15 mg/kg) in combination with 18 mg/kg ganitumab to determine the maximum tolerated dose (MTD) in patients with advanced solid tumors. Part 2 was conducted in six cohorts with advanced non-small cell lung cancer (squamous or non-squamous histology), colorectal cancer, sarcoma, pancreatic cancer, or ovarian cancer, treated at the recommended doses of the combination. The combination was significantly more active in the Colo-205 xenograft model than either single agent alone (p < 0.0015). In part 1 of the clinical study, no dose-limiting toxicities were observed and the MTD of conatumumab was 15 mg/kg in combination with 18 mg/kg ganitumab. In part 2, 78 patients were treated and there were no objective responses but 28 patients (36 %) had stable disease (median 46 days, range 0-261). The combination was well-tolerated with no new toxicities. In conclusion, the combination of ganitumab and conatumumab was well-tolerated but had no objective responses in the population tested. The successful future application of this combination of antitumor mechanisms may rely on the identification of predictive biomarkers.
C1 [Tabernero, Josep] Univ Autonoma Barcelona, Vall dHebron Univ Hosp, Barcelona 08035, Spain.
   [Tabernero, Josep] Univ Autonoma Barcelona, Inst Oncol VHIO, Barcelona 08035, Spain.
   [Chawla, Sant P.] Sarcoma Oncol Ctr, Santa Monica, CA USA.
   [Kindler, Hedy] Univ Chicago, Canc Res Ctr, Chicago, IL 60637 USA.
   [Reckamp, Karen] City Hope Natl Med Ctr, Comprehens Canc Ctr Med Oncol, Duarte, CA 91010 USA.
   [Chiorean, E. Gabriela] Indiana Univ, Simon Canc Ctr, Indianapolis, IN 46204 USA.
   [Azad, Nilofer S.] John Hopkins Med Ctr, Baltimore, MD USA.
   [Lockhart, A. Craig] Washington Univ, Sch Med, St Louis, MO USA.
   [Hsu, Cheng-Pang; Galimi, Francesco; Beltran, Pedro] Amgen Inc, Thousand Oaks, CA 91320 USA.
   [Baker, Nigel F.] Amgen Ltd, Cambridge, England.
   [Baselga, Jose] Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
C3 Hospital Universitari Vall d'Hebron; Autonomous University of Barcelona;
   Vall d'Hebron Institut d'Oncologia (VHIO); Autonomous University of
   Barcelona; University of Chicago; City of Hope; Indiana University
   System; Indiana University Indianapolis; Johns Hopkins University; Johns
   Hopkins Medicine; Washington University (WUSTL); Amgen; Amgen; Amgen
   Limited; Harvard University; Massachusetts General Hospital
RP Tabernero, J (corresponding author), Univ Autonoma Barcelona, Vall dHebron Univ Hosp, Passeig Vall dHebron 119-129, Barcelona 08035, Spain.
EM jtabernero@vhio.net
RI Tabernero, Josep/AAG-5026-2019
OI Beltran, Pedro Jose/0000-0002-4103-6494; Reckamp,
   Karen/0000-0002-9213-0325; Tabernero, Josep/0000-0002-2495-8139
FU Amgen Inc., Thousand Oaks CA, USA
FX This work was sponsored by Amgen Inc., Thousand Oaks CA, USA. Wanda J.
   Krall, PhD, on behalf of Amgen Inc., and Kathryn Boorer, PhD, of Amgen
   Inc. assisted the authors in the writing of the manuscript.
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NR 50
TC 25
Z9 30
U1 0
U2 5
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 MAR
PY 2015
VL 10
IS 1
BP 65
EP 76
DI 10.1007/s11523-014-0315-z
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CE0UF
UT WOS:000351521900006
PM 24816908
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Song, Y
   Zhao, Y
   Ding, XF
   Wang, XD
AF Song, Ying
   Zhao, Yue
   Ding, Xiangfu
   Wang, Xiaodong
TI RETRACTED: microRNA-532 suppresses the PI3K/Akt signaling pathway to
   inhibit colorectal cancer progression by directly targeting IGF-1R
   (Retracted Article)
SO AMERICAN JOURNAL OF CANCER RESEARCH
LA English
DT Article; Retracted Publication
DE Colorectal cancer; microRNA-532; insulin-like growth factor 1 receptor;
   PI3K/Akt pathway
ID FACTOR-I RECEPTOR; GENE-EXPRESSION; CELL-PROLIFERATION; GASTRIC-CANCER;
   GROWTH; METASTASIS; MIGRATION; BIOMARKERS; INVASION; PREVENTION
AB Substantial evidence has shown that numerous microRNAs (miRNAs) are deregulated in colorectal cancer (CRC) and that their dysregulation is involved in CRC formation and progression. miRNA-based targeted therapy that inhibits or restores expression may be a promising therapeutic approach for anti-cancer therapy. Therefore, a comprehensive investigation of the mechanisms underlying CRC occurrence and development may help identify effective therapeutic targets for the therapy of CRC, thus improving the prognosis of patients with this disease. This study showed that miRNA-532 (miR-532) was significantly down-regulated in CRC tissues and cell lines. Low miR-532 expression strongly correlated with a ressive clinicopathological characteristics, including tumor size, lymphatic metastasis and TNM stage. Exogenous expression of miR-532 restricted cell proliferation, colony formation, migration and invasion; promoted cell apoptosis in vitro; and reduced tumor growth in vivo. Mechanistically, insulin-like growth factor 1 receptor (IGF-1R) was determined to be a novel direct target gene of miR-532 in CRC. In clinical CRC tissues, the expression of miR-532 was inversely correlated with that of IGF-1R, which was clearly over expressed in CRC tissues. Furthermore, IGF-1R silencing simulated the tumor-suppressing roles of miR-532 in CRC. Moreover, recovered IGF-1R expression antagonized the inhibitory effects of miR-532 overexpression on CRC cells. Notably, miR-532 overexpression inhibited activation of the PI3K/Akt signaling pathway in CRC, both in vitro and in vivo. These results indicate that miR-532 plays an important role in CRC development, partly by directly targeting IGF-1R and regulating the PI3K/Akt signaling pathway. Thus, the miR-532/IGF-1R axis has clinical significance in the therapy of patients with CRC.
C1 [Song, Ying; Wang, Xiaodong] Jilin Univ, Dept Digest Endoscopy, Hosp 2, 218 Ziqiang Rd, Changchun 130041, Jilin, Peoples R China.
   [Ding, Xiangfu] Jilin Univ, Dept Thyroid Surg, Hosp 2, Changchun, Jilin, Peoples R China.
   [Zhao, Yue] Jilin Univ, Dept Vasc Surg, China Japan Union Hosp, Changchun, Jilin, Peoples R China.
C3 Jilin University; Jilin University; Jilin University
RP Wang, XD (corresponding author), Jilin Univ, Dept Digest Endoscopy, Hosp 2, 218 Ziqiang Rd, Changchun 130041, Jilin, Peoples R China.
EM xia-odongwang_jilin@126.com
RI Wang, Xiaodong/V-2779-2018
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NR 45
TC 41
Z9 44
U1 0
U2 16
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 2018
VL 8
IS 3
BP 435
EP 449
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GB5PY
UT WOS:000429119500007
PM 29636999
DA 2025-01-04
ER

PT J
AU Islas, JF
   Quiroz-Reyes, AG
   Delgado-Gonzalez, P
   Franco-Villarreal, H
   Delgado-Gallegos, JL
   Garza-Treviño, EN
   Gonzalez-Villarreal, CA
AF Francisco Islas, Jose
   Quiroz-Reyes, Adriana G.
   Delgado-Gonzalez, Paulina
   Franco-Villarreal, Hector
   Luis Delgado-Gallegos, Juan
   Garza-Trevino, Elsa N.
   Gonzalez-Villarreal, Carlos A.
TI Cancer Stem Cells in Tumor Microenvironment of Adenocarcinoma of the
   Stomach, Colon, and Rectum
SO CANCERS
LA English
DT Review
DE cancer stem cells; gastrointestinal adenocarcinomas; colon cancer and
   gastric cancer
ID EPITHELIAL-MESENCHYMAL TRANSITION; GASTRIC-CANCER; MALIGNANT
   PROGRESSION; BARRETTS-ESOPHAGUS; PROGNOSTIC VALUE; DOWN-REGULATION;
   POOR-PROGNOSIS; EXPRESSION; CARCINOMA; EPIDEMIOLOGY
AB Simple Summary Gastrointestinal cancers have a high mortality rate worldwide, and the progression of the disease is related to cancer stem cells. Until now, its relationship with the microenvironment has been poorly understood. We describe the molecules and different pathways activated during this interaction and the new targeting therapies for cancer cells and microenvironment modulation. This approach could impact the way gastrointestinal cancers are managed. Gastrointestinal adenocarcinomas are one of the world's deadliest cancers. Cancer stem cells and the tissue microenvironment are highly regulated by cell and molecular mechanisms. Cancer stem cells are essential for maintenance and progression and are associated with resistance to conventional treatments. This article reviews the current knowledge of the role of the microenvironment during the primary establishment of gastrointestinal adenocarcinomas in the stomach, colon, and rectum and its relationship with cancer stem cells. We also describe novel developments in cancer therapeutics, such as targeted therapy, and discuss the advantages and disadvantages of different treatments for improving gastrointestinal cancer prognosis.
C1 [Francisco Islas, Jose; Quiroz-Reyes, Adriana G.; Delgado-Gonzalez, Paulina; Luis Delgado-Gallegos, Juan; Garza-Trevino, Elsa N.] Univ Autonoma Nuevo Leon, Sch Med, Biochem & Mol Med Dept, Monterrey 64460, Mexico.
   [Franco-Villarreal, Hector] Althian Clin Res, Monterrey 64000, Mexico.
   [Gonzalez-Villarreal, Carlos A.] Univ Monterrey, UDEM Vicerrectoria Ciencias Salud, San Pedro Garza Garcia 66238, Mexico.
C3 Universidad Autonoma de Nuevo Leon; Universidad de Monterrey;
   Tecnologico de Monterrey
RP Garza-Treviño, EN (corresponding author), Univ Autonoma Nuevo Leon, Sch Med, Biochem & Mol Med Dept, Monterrey 64460, Mexico.; Gonzalez-Villarreal, CA (corresponding author), Univ Monterrey, UDEM Vicerrectoria Ciencias Salud, San Pedro Garza Garcia 66238, Mexico.
EM carlos_glzzv@hotmail.com
RI GonzÃ¡lez Villarreal, Carlos/JBI-9934-2023; Reyes,
   Adriana/JGL-7369-2023; Islas, Jose Francisco/K-2728-2018; Delgado
   Gallegos, Juan Luis/AAJ-6221-2021
OI Islas, Jose Francisco/0000-0002-0337-9912; Gonzalez-Villarreal,
   Carlos/0000-0002-4890-1727; Garza-Trevino, Elsa N./0000-0002-1042-4603;
   Quiroz Reyes, Adriana G./0000-0002-9405-7483; Delgado Gallegos, Juan
   Luis/0000-0003-1580-0812
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NR 154
TC 3
Z9 3
U1 0
U2 12
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 16
AR 3948
DI 10.3390/cancers14163948
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 4D2HI
UT WOS:000846966800001
PM 36010940
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Datta, J
   Berk, E
   Cintolo, JA
   Xu, SW
   Roses, RE
   Czemiecki, BJ
AF Datta, Jashodeep
   Berk, Erik
   Cintolo, Jessica A.
   Xu, Shuwen
   Roses, Robert E.
   Czemiecki, Brian J.
TI Rationale for a multimodality strategy to enhance the efficacy of
   dendritic cell-based cancer immunotherapy
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE dendritic cell; immunotherapy; multimodality; adoptive cell therapy;
   targeted therapy; checkpoint inhibitor; chemotherapy; radiotherapy
ID REGULATORY T-CELLS; ANTITUMOR IMMUNITY; ADOPTIVE TRANSFER; COLON-CANCER;
   INTRATUMORAL INJECTION; ANTI-PD-1 ANTIBODY; SUPPRESSOR-CELLS; PD-1
   BLOCKADE; CUTTING EDGE; PHASE-IB
AB Dendritic cells (DC), master antigen-presenting cells that orchestrate interactions between the adaptive and innate immune arms, are increasingly utilized in cancer immunotherapy. Despite remarkable progress in our understanding of DC immunobiology, as well as several encouraging clinical applications such as DC-based sipuleucel-T for metastatic castration-resistant prostate cancer clinically effective DC-based immunotherapy as monotherapy for a majority of tumors remains a distant goal. The complex interplay between diverse molecular and immune processes that govern resistance to DC-based vaccination compels a multimodality approach, encompassing a growing arsenal of antitumor agents which target these distinct processes and synergistically enhance DC function. These include antibody-based targeted molecular therapies, immune checkpoint inhibitors, therapies that inhibit immunosuppressive cellular elements, conventional cytotoxic modalities, and immune potentiating adjuvants. It is likely that in the emerging era of "precision" cancer therapeutics, tangible clinical benefits will only be realized with a multifaceted - and - personalized approach combining DC-based vaccination with adjunctive strategies.
C1 [Datta, Jashodeep; Berk, Erik; Cintolo, Jessica A.; Xu, Shuwen; Roses, Robert E.; Czemiecki, Brian J.] Univ Penn, Div Endocrine & Oncol Surg, Dept Surg, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Czemiecki, Brian J.] Hosp Univ Penn, Rena Rowen Breast Ctr, Philadelphia, PA 19104 USA.
C3 University of Pennsylvania; University of Pennsylvania
RP Czemiecki, BJ (corresponding author), Univ Penn, Dept Surg, Perelman Sch Med, 3400 Civ Ctr Dr, Philadelphia, PA 19104 USA.
EM brian.czerniecki@uphs.upenn.edu
FU National Institutes of Health [R01 CA096997]; Pennies in Action
   Foundation
FX Work from our laboratory cited in this review was funded by National
   Institutes of Health R01 CA096997 and Pennies in Action Foundation.
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NR 131
TC 42
Z9 47
U1 2
U2 18
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 JUN 2
PY 2015
VL 6
BP 1
EP 11
AR 271
DI 10.3389/fimmu.2015.00271
PG 11
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA CL7LZ
UT WOS:000357154900001
PM 26082780
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Dokla, EME
   Abdel-Aziz, AK
   Milik, SN
   McPhillie, MJ
   Minucci, S
   Abouzid, KAM
AF Dokla, Eman M. E.
   Abdel-Aziz, Amal Kamal
   Milik, Sandra N.
   McPhillie, Martin J.
   Minucci, Saverio
   Abouzid, Khaled A. M.
TI Discovery of a benzimidazole-based dual FLT3/TrKA inhibitor targeting
   acute myeloid leukemia
SO BIOORGANIC & MEDICINAL CHEMISTRY
LA English
DT Article
DE FLT3; TrKA; Dual kinase inhibitor; Acute myeloid leukemia;
   Benzimidazole; Scaffold hopping
ID TYROSINE KINASE INHIBITOR; FLT3 INHIBITORS; IN-VITRO; T315I MUTANT; AML
   CELLS; POTENT; RESISTANCE; MUTATIONS; TRK; CYTOTOXICITY
AB FMS-like tyrosine kinase 3 (FLT3) enzyme overexpression and mutations are the most common molecular abnormalities associated with acute myeloid leukemia (AML). In addition, recent studies investigated the role of tropomyosin receptor kinase A (TrKA) enzyme fusions in promoting AML growth and survival. Based on these premises, targeting both kinases using dual inhibitors would constitute a promising therapeutic approach to target resistant AML. Guided by ligand-based design and structure simplification of the FLT3 inhibitor, quizartinib, we developed a benzimidazole-based small molecule, 4ACP, that exhibited nanomolar activity against wild-type FLT3, FLT3-Internal tandem duplications (FLT3-ITD), and FLT3-D835Y (FLT3-TKD) mutation (IC50 = 43.8, 97.2, and 92.5 nM respectively). Additionally, 4ACP demonstrated potent activity against colon cancer KM12 cell line (IC50 = 358 nM) and subsequent mechanistic deconvolution identified TrKA enzyme as a second plausible target (IC50 = 23.6 nM) for our compound. 4ACP manifested preferential antiproliferative activity against FLT3-ITD positive AML cell lines (MV4-11 IC50 = 38.8 + 10.7 nM and MOLM-13 IC50 = 54.9 + 4.1 nM), while lacking activity against FLT3-ITD negative AML cell lines. Western blot analysis confirmed 4ACP ability to downregulate ERK1/2 and mTOR signaling downstream of FLT3-ITD in AML cells. Furthermore, 4ACP prompted apoptotic and necrotic cell death and G0/G1 cell cycle arrest as indicated by cell cycle analysis.
   4ACP did not show cytotoxic effects on normal BNL and H9c2 cells and demonstrated decreased activity against c-Kit enzyme, hence, indicating lower probability of synthetic lethal toxicity and a relatively safer profile. In light of these data, 4ACP represents a novel FLT3/TrKA dual kinase inhibitor for targeted therapy of AML.
C1 [Dokla, Eman M. E.; Milik, Sandra N.; Abouzid, Khaled A. M.] Ain Shams Univ, Fac Pharm, Pharmaceut Chem Dept, Cairo 11566, Egypt.
   [Abdel-Aziz, Amal Kamal] Ain Shams Univ, Fac Pharm, Dept Pharmacol & Toxicol, Cairo 11566, Egypt.
   [Abdel-Aziz, Amal Kamal; Minucci, Saverio] European Inst Oncol IRCCS, Dept Expt Oncol, IEO, Via Adamello 16, I-20139 Milan, Italy.
   [Milik, Sandra N.; McPhillie, Martin J.] Univ Leeds, Sch Chem, Leeds LS2 9JT, W Yorkshire, England.
   [Minucci, Saverio] Univ Milan, Dept Biosci, I-20100 Milan, Italy.
   [Abouzid, Khaled A. M.] Univ Sadat City, Fac Pharm, Dept Organ & Med Chem, Sadat City 32897, Egypt.
C3 Egyptian Knowledge Bank (EKB); Ain Shams University; Egyptian Knowledge
   Bank (EKB); Ain Shams University; IRCCS European Institute of Oncology
   (IEO); University of Leeds; University of Milan; Egyptian Knowledge Bank
   (EKB); University of Sadat City
RP Dokla, EME (corresponding author), Ain Shams Univ, Fac Pharm, Pharmaceut Chem Dept, Cairo 11566, Egypt.; Minucci, S (corresponding author), European Inst Oncol IRCCS, Dept Expt Oncol, IEO, Via Adamello 16, I-20139 Milan, Italy.
EM emanelawady@pharma.asu.edu.eg; Saverio.Minucci@ico.it
RI Dokla, Eman/GLU-7635-2022; Minucci, Saverio/J-9669-2012; Abouzid,
   Khaled/S-8284-2019; Abdel-Aziz, Amal/AAA-1360-2021; Milik,
   Sandra/J-6895-2016
OI Minucci, Saverio/0000-0001-5678-536X; Abdel-Aziz, Amal
   Kamal/0000-0003-1709-1183; McPhillie, Martin/0000-0001-8264-8211; Dokla,
   Eman/0000-0002-2770-6439; Abouzid, Khaled/0000-0001-9851-5624; Milik,
   Sandra/0000-0001-6563-8265
FU Fondazione IEO-CCM; University of Leeds - Newton-Mosharafa Fund by the
   British Council
FX AKA has been awarded a fellowship from Fondazione IEO-CCM. SNM has been
   awarded a PhD scholarship at University of Leeds funded by the
   Newton-Mosharafa Fund jointly offered by the British Council and the
   Ministry of Higher Education of the Arab Republic of Egypt. We thank Dr
   Jeanine Williams (School of Chemistry, University of Leeds) for
   conducting the HPLC purity determination assays. We thank Dr. Ciro
   Mercurio (Drug Discovery Unit, IFOM) for the kind provision of
   quizartinib.
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NR 90
TC 13
Z9 13
U1 0
U2 17
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 15
PY 2022
VL 56
AR 116596
DI 10.1016/j.bmc.2021.116596
EA JAN 2022
PG 13
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry,
   Organic
WE Science Citation Index Expanded (SCI-EXPANDED); Index Chemicus (IC)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 2P4CT
UT WOS:000819692100004
PM 35033885
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Yuan, J
   Li, W
   Zhu, JX
   Deng, SL
   Tao, XJ
AF Yuan, Jian
   Li, Wen
   Zhu, Jinxiao
   Deng, Shuli
   Tao, Xuejin
TI Low expression of RECK in oral squamous cell carcinoma patients induces
   a shorter survival rate through an imbalance of RECK/MMPs
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
LA English
DT Article
DE RECK; MMP-2; MMP-9; OSCC
ID CYSTEINE-RICH PROTEIN; MATRIX METALLOPROTEINASES; COLORECTAL-CANCER;
   DOWN-REGULATION; METASTASIS; SUPPRESSOR; INVASION; GENE; P53
AB Background: RECK, as a negative MMP regulator, is extensively expressed in normal cells but decreased in tumors. In OSCC, the relationship between RECK and MMPs and the potential prognostic impact remains unclear. In this research, for the first time, we investigated the expression of RECK associated with MMPs during OSCC carcinogenesis in a large sample and its association with 5-year survival rate. Material and Methods: Immunohistochemical SP technique was applied to study the expression of RECK and MMP-2 and MMP-9 in 108 cases of OSCC and 30 normal oral mucosae. Univariate and multivariate Cox regression analysis was utilized for disease-free survival and overall survival, and analyzed by Kaplan-Meier method regarding RECK expression in patients of OSCC. Results: We found lower expression of RECK in OSCC was 51.85% (56/108) compared with 93.33% (28/30) in the control group. However, the higher expression of MMP-2 and MMP-9 was 74.07% (80/108) and 70.37% (76/108) in OSCC, respectively, compared with 20% (6/30) and 13.3% (4/30) in the control group. Furthermore, the decrease of RECK expression and the increase of MMP-2, and -9 expression were significantly correlated with the loss of histologic differentiation, the occurrence of lymphatic metastasis, and the increase of OSCC clinical stage (P<0.05). OSCC patients with a low level of RECK expression had a lower rate of 5-year survival. Conclusion: RECK may prevent metastasis and improve OSCC patients' prognosis through a RECK/MMP-2, and -9 imbalance. Furthermore, RECK is a prospective prognostic indicator and therapeutic target for cancer molecular targeting therapy. Low expression of RECK may be a significant negative prognostic predictor.
C1 [Yuan, Jian; Li, Wen; Deng, Shuli] Zhejiang Univ, Affiliated Stomatol Hosp, Dept Conservat Dent & Endodont, Sch Med, 395 Yanan Rd, Hangzhou 310006, Zhejiang, Peoples R China.
   [Yuan, Jian; Li, Wen; Deng, Shuli] Zhejiang Univ, Key Lab Oral Biomed Res Zhejiang Prov, Sch Stomatol, Hangzhou 310006, Zhejiang, Peoples R China.
   [Zhu, Jinxiao] Wuxi Childrens Hosp, Dept Stomatol, Wuxi, Jiangsu, Peoples R China.
   [Tao, Xuejin] Hua Zhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Ctr Stomatol, Wuhan 430030, Hubei, Peoples R China.
C3 Zhejiang University; Zhejiang University; Huazhong University of Science
   & Technology
RP Deng, SL (corresponding author), Zhejiang Univ, Affiliated Stomatol Hosp, Dept Conservat Dent & Endodont, Sch Med, 395 Yanan Rd, Hangzhou 310006, Zhejiang, Peoples R China.; Tao, XJ (corresponding author), Hua Zhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Ctr Stomatol, Wuhan 430030, Hubei, Peoples R China.
EM Dengshuli@zju.edu.cn; 93767345@qq.com
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NR 27
TC 9
Z9 9
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 2020
VL 13
IS 3
BP 501
EP 508
PG 8
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA KY7DT
UT WOS:000522734900018
PM 32269688
DA 2025-01-04
ER

PT J
AU Dong, LY
   Zhou, WZ
   Ni, JW
   Xiang, W
   Hu, WH
   Yu, C
   Li, HY
AF Dong, Li-Yang
   Zhou, Wei-Zhong
   Ni, Jun-Wei
   Xiang, Wei
   Hu, Wen-Hao
   Yu, Chang
   Li, Hai-Yan
TI Identifying the optimal gene and gene set in hepatocellular carcinoma
   based on differential expression and differential co-expression
   algorithm
SO ONCOLOGY REPORTS
LA English
DT Article
DE hepatocellular carcinoma; differential expression; differential
   co-expression; gene; gene set; reverse transcriptase polymerase chain
   reaction
ID PROMOTE CELLULAR GROWTH; END-BINDING PROTEIN-1; COLORECTAL-CANCER; EB1;
   INTEGRATION; NUCLEOSIDE; DISCOVERY; IMPACT; MAPRE1
AB The objective of this study was to identify the optimal gene and gene set for hepatocellular carcinoma (HCC) utilizing differential expression and differential co-expression (DEDC) algorithm. The DEDC algorithm consisted of four parts: calculating differential expression (DE) by absolute t-value in t-statistics; computing differential co-expression (DC) based on Z-test; determining optimal thresholds on the basis of Chi-squared (x(2)) maximization and the corresponding gene was the optimal gene; and evaluating functional relevance of genes categorized into different partitions to determine the optimal gene set with highest mean minimum functional information (FI) gain (Delta*(G)). The optimal thresholds divided genes into four partitions, high DE and high DC (HDE-HDC), high DE and low DC (HDE-LDC), low DE and high DC (LDE-HDC), and low DE and low DC (LDE-LDC). In addition, the optimal gene was validated by conducting reverse transcription-polymerase chain reaction (RT-PCR) assay. The optimal threshold for DC and DE were 1.032 and 1.911, respectively. Using the optimal gene, the genes were divided into four partitions including: HDE-HDC (2,053 genes), HED-LDC (2,822 genes), LDE-HDC (2,622 genes), and LDE-LDC (6,169 genes). The optimal gene was microtubule-associated protein RP/EB family member 1 (MAPRE1), and RT-PCR assay validated the significant difference between the HCC and normal state. The optimal gene set was nucleoside metabolic process (GO\GO:0009116) with Delta*(G) = 18.681 and 24 HDE-HDC partitions in total. In conclusion, we successfully investigated the optimal gene, MAPRE1, and gene set, nucleoside metabolic process, which may be potential biomarkers for targeted therapy and provide significant insight for revealing the pathological mechanism underlying HCC.
C1 [Dong, Li-Yang; Zhou, Wei-Zhong; Ni, Jun-Wei; Xiang, Wei; Hu, Wen-Hao; Yu, Chang] Wenzhou Med Univ, Dept Invas Technol, Affiliated Hosp 1, Wenzhou 325000, Zhejiang, Peoples R China.
   [Li, Hai-Yan] Wenzhou Med Univ, Dept Rehabil, Affiliated Hosp 1, 2 Xuexiang Rd, Wenzhou 325000, Zhejiang, Peoples R China.
C3 Wenzhou Medical University; Wenzhou Medical University
RP Li, HY (corresponding author), Wenzhou Med Univ, Dept Rehabil, Affiliated Hosp 1, 2 Xuexiang Rd, Wenzhou 325000, Zhejiang, Peoples R China.
EM haiyanli2016@yeah.net
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NR 47
TC 5
Z9 5
U1 0
U2 9
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 FEB
PY 2017
VL 37
IS 2
BP 1066
EP 1074
DI 10.3892/or.2016.5333
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EJ3BU
UT WOS:000393086900050
PM 28035405
OA Bronze
DA 2025-01-04
ER

PT J
AU Wang, YZ
   Thai, T
   Moore, K
   Ding, K
   McMeekin, S
   Liu, H
   Zheng, B
AF Wang, Yunzhi
   Thai, Theresa
   Moore, Kathleen
   Ding, Kai
   McMeekin, Scott
   Liu, Hong
   Zheng, Bin
TI Quantitative measurement of adiposity using CT images to predict the
   benefit of bevacizumab-based chemotherapy in epithelial ovarian cancer
   patients
SO ONCOLOGY LETTERS
LA English
DT Article
DE bevacizumab-based chemotherapy; clinical marker of prognosis;
   computer-aided detection; epithelial ovarian cancer; multivariate
   statistical data analysis; quantitative image feature analysis
ID GYNECOLOGIC-ONCOLOGY-GROUP; ENDOTHELIAL GROWTH-FACTOR;
   COLORECTAL-CANCER; VISCERAL-ADIPOSE; TARGETED THERAPY; FAT; TRIAL;
   EXPRESSION; CARCINOMA; RISK
AB The present study aims to quantitatively measure adiposity-related image features and to test the feasibility of applying multivariate statistical data analysis-based prediction models to generate a novel clinical marker and predict the benefit of epithelial ovarian cancer (EOC) patients with and without maintenance bevacizumab-based chemotherapy. A dataset involving computed tomography (CT) images acquired from 59 patients diagnosed with advanced EOC was retrospectively collected. Among them, 32 patients received maintenance bevacizumab following primary chemotherapy, while 27 did not. A computer-aided detection scheme was developed to automatically segment visceral and subcutaneous fat areas depicted on CT images of abdominal sections, and 7 adiposity-related image features were computed. Upon combining these features with the measured body mass index, multivariate data analyses were performed using three statistical models (multiple linear, logistic and Cox proportional hazards regressions) to analyze the association between the model-generated prediction results and the treatment outcome, including progression-free survival (PFS) and overall survival (OS) of the patients. The results demonstrated that applying all three prediction models yielded a significant association between the adiposity-related image features and patients' PFS or OS in the group of the patients who received maintenance bevacizumab (P<0.010), while there was no significant difference when these prediction models were applied to predict both PFS and OS in the group of patients that did not receive maintenance bevacizumab. Therefore, the present study demonstrated that the use of a quantitative adiposity-related image feature-based statistical model may generate a novel clinical marker to predict who will benefit among EOC patients receiving maintenance bevacizumab-based chemotherapy.
C1 [Wang, Yunzhi; Liu, Hong; Zheng, Bin] Univ Oklahoma, Sch Elect & Comp Engn, 1001 David L Boren Blvd, Norman, OK 73019 USA.
   [Thai, Theresa; Moore, Kathleen; Ding, Kai; McMeekin, Scott] Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK 73104 USA.
C3 University of Oklahoma System; University of Oklahoma - Norman;
   University of Oklahoma System; University of Oklahoma Health Sciences
   Center
RP Zheng, B (corresponding author), Univ Oklahoma, Sch Elect & Comp Engn, 1001 David L Boren Blvd, Norman, OK 73019 USA.
EM bin.zheng-1@ou.edu
FU Oklahoma Tobacco Settlement Endowment Trust Cancer Center Program
   (Oklahoma, OK, USA); Peggy and Charles Stephenson Cancer Center of the
   University of Oklahoma (Oklahoma, OK, ITSA) [A00-3995]
FX The present study was approved by the Institutional Review Board of the
   University of Oklahoma (Norman, OK, USA; protocol no. IRB# 4168) on
   April 9, 2014, and was supported in part by the Oklahoma Tobacco
   Settlement Endowment Trust Cancer Center Program (Oklahoma, OK, USA) and
   the Peggy and Charles Stephenson Cancer Center of the University of
   Oklahoma (Oklahoma, OK, ITSA; grant no. A00-3995).
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NR 24
TC 16
Z9 16
U1 0
U2 1
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 JUL
PY 2016
VL 12
IS 1
BP 680
EP 686
DI 10.3892/ol.2016.4648
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DR5RN
UT WOS:000379960200111
PM 27347200
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Bayle, A
   Basile, D
   Garinet, S
   Rance, B
   Laurent-Puig, P
   Blons, H
   Taieb, J
   Perkins, G
AF Bayle, Arnaud
   Basile, Debora
   Garinet, Simon
   Rance, Bastien
   Laurent-Puig, Pierre
   Blons, Helene
   Taieb, Julien
   Perkins, Geraldine
TI Next-Generation Sequencing Targeted Panel in Routine Care for Metastatic
   Colon Cancers
SO CANCERS
LA English
DT Article
DE next-generation sequencing; digestive cancer; colon cancer; oncology;
   genomics
ID NRAS MUTATIONS; RAS MUTATIONS; OPEN-LABEL; KRAS; MULTICENTER; CETUXIMAB;
   THERAPY; TUMORS
AB Simple SummaryThe place of Next-Generation-Sequencing (NGS) targeted panel in routine practice in digestive oncology should be addressed. The aim of our retrospective study was to assess the results and impact of NGS panel for metastatic colorectal cancer (mCRC) patients. In total, 210 patients with mCRC were included. Based on our findings, a major advantage of the NGS panel over single gene techniques is that, beyond the classical hotspots, it allows for an exhaustive search for molecular abnormalities in routinely recommended genes. In addition, routine NGS is a way to detect amplifications associated with resistance to anti-EGFR therapies and low-prevalence mutations in actionable genes, providing patients with the opportunity to access innovative targeted therapies. In conclusion, NGS targeted panel in mCRC is feasible in routine practice. Nevertheless, panels need to be regularly updated and in-depth studies are needed to better analyse the prognostic factors.In digestive oncology, the clinical impact of targeted next-generation sequencing (NGS) in routine practice should be addressed. In this work, we studied the impact of a 22-gene NGS amplicon-based panel with Ion Torrent Proton Sequencing, prospectively performed in routine practice. We analyzed the results of extended molecular testing, beyond RAS and BRAF, in metastatic colorectal cancer (mCRC) patients in a single-center, retrospective, observational study of consecutive mCRC patients followed up at the Georges Pompidou European Hospital between January 2016 and December 2018. Overall, 210 patients with mCRC were included. Median follow-up was 25.4 months (IQR: 14.9-39.5). The three most frequently mutated genes were: TP53 (63%), KRAS (41%) and PIK3CA (19%). A positive association was found between overall survival and performance status (PS) & GE; 2 (HR: 4.91 (1.84-13.1); p = 0.001) and differentiation (HR: 4.70 (1.51-14.6); p = 0.007) in multivariate analysis. The NGS panel enabled five patients to access a targeted therapy not currently registered for CRC. In conclusion, targeted NGS panels in mCRC are feasible in routine practice, but need to be regularly updated and in-depth studies are needed to better analyze the prognostic factors.
C1 [Bayle, Arnaud; Basile, Debora; Taieb, Julien; Perkins, Geraldine] Hop Europeen Georges Pompidou, AP HP, AP HP Ctr, Inst Canc Paris CARPEM,Dept Hepatogastroenterol &, 20 Rue Leblanc, F-75015 Paris, France.
   [Garinet, Simon; Laurent-Puig, Pierre; Blons, Helene] Hop Europeen Georges Pompidou, AP HP, AP HP Ctr, Inst Canc Paris CARPEM,Dept Biochem, F-75015 Paris, France.
   [Garinet, Simon; Laurent-Puig, Pierre; Blons, Helene; Taieb, Julien; Perkins, Geraldine] Sorbonne Univ, Univ Paris, Ctr Rech Cordeliers, INSERM, F-75015 Paris, France.
   [Rance, Bastien] Hop Europeen Georges Pompidou, AP HP, AP HP Ctr, Inst Canc Paris CARPEM,Dept Med Bioinformat, F-75015 Paris, France.
C3 Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Europeen Georges-Pompidou - APHP; Assistance
   Publique Hopitaux Paris (APHP); Universite Paris Cite; Hopital
   Universitaire Europeen Georges-Pompidou - APHP; Sorbonne Universite;
   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 Taieb, J (corresponding author), Hop Europeen Georges Pompidou, AP HP, AP HP Ctr, Inst Canc Paris CARPEM,Dept Hepatogastroenterol &, 20 Rue Leblanc, F-75015 Paris, France.; Taieb, J (corresponding author), Sorbonne Univ, Univ Paris, Ctr Rech Cordeliers, INSERM, F-75015 Paris, France.
EM arnaud.bayle@aphp.fr; debora.basile@aphp.fr; simon.garinet@aphp.fr;
   bastien.rance@aphp.fr; pierre.laurent-puig@aphp.fr;
   helene.blons@aphp.fr; jtaieb75@gmail.com; geraldine.perkins@aphp.fr
RI Basile, Debora/N-1088-2019; Garinet, Simon/HKV-6770-2023; Bayle,
   Arnaud/AGW-2758-2022; Laurent-Puig, Pierre/B-2226-2013
OI Garinet, Simon/0000-0002-2182-8793; Perkins,
   Geraldine/0000-0002-4960-2534; taieb, julien/0000-0002-9955-4753;
   basile, debora/0000-0003-1457-2272; Laurent-Puig,
   Pierre/0000-0001-8475-5459
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NR 38
TC 5
Z9 5
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 NOV
PY 2021
VL 13
IS 22
AR 5750
DI 10.3390/cancers13225750
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA XH9TM
UT WOS:000725767900001
PM 34830904
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wen, J
   Xie, Y
   Zhang, YQ
   Li, JZ
   Li, JP
   Zhang, Y
   Lu, XC
   Zhang, Y
   Liu, YK
   Liu, T
   Li, LQ
AF Wen, Jia
   Xie, Yi
   Zhang, Yingqiang
   Li, Jiazhen
   Li, Jiaping
   Zhang, Yan
   Lu, Xinchang
   Zhang, Yi
   Liu, Yongkui
   Liu, Tao
   Li, Longqing
TI MACC1 Contributes to the Development of Osteosarcoma Through Regulation
   of the HGF/c-Met Pathway and Microtubule Stability
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Article
DE MACC1; osteosarcoma; HGF/c-Met; proliferation; angiogenesis; microtubule
   stability
ID DIAGNOSIS; SURVIVAL; CANCER; ANGIOGENESIS; EXPRESSION; BREAST
AB Osteosarcoma (OS) is the most prevalent human bone malignancy, and presents a global annual morbidity of approximately five cases per million. Notably, precise and efficient targeted therapy has become the most promising strategy for the treatment of OS; however, there is still an urgent need for the identification of suitable therapeutic targets. Metastasis-associated in colon cancer 1 (MACC1) was first identified in colon tumors by differential display RT-PCR, and was shown to be involved in the regulation of colon tumor growth and metastasis through the hepatocyte growth factor (HGF)/c-Met signaling pathway. Additionally, MACC1 overexpression has been reported to induce the growth of several types of cancers, including glioblastoma multiforme and gastric cancer. However, whether MACC1 also plays a role in the progression of OS remains unclear. In this study, we found that MACC1 was highly expressed in human OS tissues, as well as in U-2OS and MG-63 cells, when compared with normal tissues and osteoblasts, respectively. Our data further indicated that MACC1 expression was correlated with several clinicopathological features of OS. Through in vitro assays, we found that MACC1 depletion markedly suppressed the proliferative ability of both OS cells and endothelial cells, and inhibited the angiogenic capacity of endothelial cells. Similarly, MACC1 depletion inhibited tumor growth, metastasis, and angiogenesis in mice. Mechanistically, we found that MACC1 could bind to the MET promoter, and enhanced the proliferation of both OS cells and endothelial cells through the HGF/c-Met signaling pathway. Furthermore, we show that MACC1 also promoted angiogenesis by regulating microtubule dynamics, thereby promoting the progression of OS. Our results indicate that MACC1 may be a new and promising therapeutic target for the treatment of OS.
C1 [Wen, Jia; Li, Jiazhen; Zhang, Yan; Lu, Xinchang; Zhang, Yi; Liu, Yongkui; Liu, Tao; Li, Longqing] Zhengzhou Univ, Affiliated Hosp 1, Dept Orthoped, Zhengzhou, Peoples R China.
   [Xie, Yi] Zhengzhou Univ, Affiliated Hosp 1, Dept Neurol, Zhengzhou, Peoples R China.
   [Li, Jiaping] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Intervent Oncol, Guangzhou, Peoples R China.
   [Zhang, Yingqiang] Sun Yat Sen Univ, Affiliated Hosp 7, Dept Intervent Radiol, Guangzhou, Peoples R China.
C3 Zhengzhou University; Zhengzhou University; Sun Yat Sen University; Sun
   Yat Sen University
RP Li, JZ (corresponding author), Zhengzhou Univ, Affiliated Hosp 1, Dept Orthoped, Zhengzhou, Peoples R China.; Li, JP (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 1, Dept Intervent Oncol, Guangzhou, Peoples R China.
EM jzhli6411@163.com; lijiaping3s@126.com
RI Jia, li/GPW-8015-2022; zhang, yi/HKV-8165-2023; Li,
   Jiazhen/HPF-9994-2023
OI Li, Longqing/0000-0002-6440-7438
FU Joint Construction Project of Henan Province; First Affiliated Hospital
   of Zhengzhou University [2018020083, 2018020114]; major scientific and
   technological project of Guangdong Province [2017B030308006]; major
   program for tackling key problems of Guangzhou City, China
   [201704020144]; National Natural Science Foundation of China (NSFC)
   [81171441]
FX This study was supported by the Joint Construction Project of Henan
   Province and the First Affiliated Hospital of Zhengzhou University (Nos.
   2018020083 and 2018020114), the major scientific and technological
   project of Guangdong Province (No. 2017B030308006), the major program
   for tackling key problems of Guangzhou City, China (No. 201704020144),
   and National Natural Science Foundation of China (NSFC) (No. 81171441).
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NR 33
TC 12
Z9 12
U1 0
U2 8
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 DEC 23
PY 2020
VL 8
AR 825
DI 10.3389/fcell.2020.00825
PG 14
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA PP6HT
UT WOS:000605962200001
PM 33425885
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Jayasinghe, C
   Simiantonaki, N
   Kirkpatrick, CJ
AF Jayasinghe, Caren
   Simiantonaki, Nektaria
   Kirkpatrick, Charles James
TI Cell type- and tumor zone-specific expression of pVEGFR-1 and its
   ligands influence colon cancer metastasis
SO BMC CANCER
LA English
DT Article
DE Colon cancer metastasis; VEGF; PlGF; VEGF-B; VEGFR-1; pVEGFR-1
ID PLACENTA GROWTH-FACTOR; COLORECTAL-CANCER; VEGF-B; FACTOR RECEPTOR-1;
   PROGNOSTIC-SIGNIFICANCE; MESENCHYMAL TRANSITION; FACTOR-I; ANGIOGENESIS;
   PROGRESSION; KINASE
AB Background: Detailed knowledge of the essential pro-angiogenic biomolecules, the vascular endothelial growth factor (VEGF) family and its receptors, in the characteristically heterogeneous tumor tissue is a pre-requisite for an effective personalized target therapy. The effects of VEGF receptors after ligand binding are mediated through receptor tyrosine autophosphorylation. We determined the relevance of the VEGFR-1 activating pathway for colon cancer (CC) metastasis.
   Methods: The expression profiles of VEGFR-1, phosphorylated (activated) VEGFR-1 (pVEGFR-1(Tyr1048), pVEGFR-1(Tyr1213) and pVEGFR-1(Tyr1333)) and the VEGFR-1 ligands (VEGF, PlGF and VEGF-B) were investigated using immunohistochemistry in different tumor compartments (intratumoral - invasive front - extratumoral), cell types (tumor cells - macro-(large and small vessels) and the microvasculature (capillaries) - inflammatory cells) in human sporadic non-metastatic, lymphogenous metastatic and haematogenous metastatic CC.
   Results: VEGF and PlGF produced by tumor cells have an autocrine affinity for their receptor VEGFR-1. Subsequent PlGF-mediated receptor activation by autophosphorylation at Tyr1048 and Tyr1213 is a potential signaling pathway, which in turn seems to protect against distant metastasis and, in regions of tumor budding, additionally against lymph node metastasis. This autocrine link could be supported by possible formation of PlGF-VEGF heterodimers and PlGF-PlGF homodimers, which are known to have anti-metastatic properties. In contrast, in order to enhance their potential for distant metastasis tumor cells produce paracrine-acting VEGF-B. VEGFR-1 activation in tumor-associated macrovasculature but not capillaries appears to affect metastatic ability. Paracrine-mediated receptor autophosphorylation at Tyr1048 and Tyr1213 in small vessels located intratumorally and along the invasive front appears to be inversely correlated with metastasis, especially distant metastasis. Additionally, macrovessels are able to produce VEGFR-1 ligands, which influence the metastatic potential. Paracrine-acting VEGF-B production by intratumorally located small vessels and autocrine-acting PlGF production by extratumorally located small vessels seem to be associated with the non-metastatic phenotype. In contrast, VEGF-B-expressing extratumoral large and small vessels correlate with distant metastasis. Lymphocyte-associated VEGFR-1 expression in the invasive front without accompanying autophosphorylation could prevent against distant metastasis possibly by acting as a decoy and scavenger receptor.
   Conclusion: VEGFR-1 and its ligands participate in vascular, tumor cell-mediated and immuno-inflammatory processes in a complex biomolecule-dependent and tumor zone-specific manner and hence could influence metastatic behavior in CC.
C1 [Jayasinghe, Caren; Simiantonaki, Nektaria; Kirkpatrick, Charles James] Johannes Gutenberg Univ Mainz, Univ Med Ctr, Inst Pathol, D-55101 Mainz, Germany.
   [Jayasinghe, Caren; Simiantonaki, Nektaria] Lab Dr Wisplinghoff, Dept Pathol, D-50931 Cologne, Germany.
C3 Johannes Gutenberg University of Mainz; University of Cologne
RP Jayasinghe, C (corresponding author), Johannes Gutenberg Univ Mainz, Univ Med Ctr, Inst Pathol, Langenbeckstr 1, D-55101 Mainz, Germany.
EM c.jayasinghe@gmx.de
OI Kirkpatrick, Charles James/0000-0002-0088-418X
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NR 42
TC 8
Z9 9
U1 0
U2 4
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD MAR 7
PY 2015
VL 15
AR 104
DI 10.1186/s12885-015-1130-3
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CF0VD
UT WOS:000352261500001
PM 25880726
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Katoh, M
AF Katoh, Masaru
TI Genomic testing, tumor microenvironment and targeted therapy of
   Hedgehog-related human cancers
SO CLINICAL SCIENCE
LA English
DT Review
ID ORAL SMOOTHENED INHIBITOR; BASAL-CELL CARCINOMAS; REGULATORY T-CELLS;
   PHASE-II TRIAL; PATHWAY INHIBITOR; SIGNALING PATHWAY; STEM-CELLS;
   ACQUIRED-RESISTANCE; ARSENIC TRIOXIDE; DRUG-RESISTANCE
AB Hedgehog signals are transduced through Patched receptors to the Smoothened (SMO)-SUFU-GLI and SMO-Gi-RhoA signaling cascades. MTOR-S6K1 and MEK-ERK signals are also transduced to GLI activators through post-translational modifications. The GLI transcription network up-regulates target genes, such as BCL2, FOXA2, FOXE1, FOXF1, FOXL1, FOXM1, GLI1, HHIP, PTCH1 and WNT2B, in a cellular context-dependent manner. Aberrant Hedgehog signaling in tumor cells leads to self-renewal, survival, proliferation and invasion. Paracrine Hedgehog signaling in the tumor microenvironment (TME), which harbors cancer-associated fibroblasts, leads to angiogenesis, fibrosis, immune evasion and neuropathic pain. Hedgehog-related genetic alterations occur frequently in basal cell carcinoma (BCC) (85%) and Sonic Hedgehog (SHH)-subgroup medulloblastoma (87%) and less frequently in breast cancer, colorectal cancer, gastric cancer, pancreatic cancer, non-small-cell lung cancer (NSCLC) and ovarian cancer. Among investigational SMO inhibitors, vismodegib and sonidegib are approved for the treatment of patients with BCC, and glasdegib is approved for the treatment of patients with acute myeloid leukemia (AML). Resistance to SMO inhibitors is caused by acquired SMO mutations, SUFU deletions, GLI2 amplification, other by-passing mechanisms of GLI activation and WNT/beta-catenin signaling activation. GLI-DNA-interaction inhibitors (glabrescione B and GANT61), GLI2 destabilizers (arsenic trioxide and pirfenidone) and a GLI-deacetylation inhibitor (4SC-202) were shown to block GLI-dependent transcription and tumorigenesis in preclinical studies. By contrast, SMO inhibitors can remodel the immunosuppressive TME that is dominated by M2-like tumor-associated macrophages (M2-TAMs), myeloid-derived suppressor cells and regulatory T cells, and thus, a Phase I/II clinical trial of the immune checkpoint inhibitor pembrolizumab with or without vismodegib in BCC patients is ongoing.
C1 [Katoh, Masaru] Natl Canc Ctr, Dept Omics Network, Chuo Ward, 5-1-1 Tsukiji, Tokyo 1040045, Japan.
C3 National Cancer Center - Japan
RP Katoh, M (corresponding author), Natl Canc Ctr, Dept Omics Network, Chuo Ward, 5-1-1 Tsukiji, Tokyo 1040045, Japan.
EM mkatoh-kkr@umin.ac.jp
OI Katoh, Masaru/0000-0003-3274-4066
FU M.K. Fund for the Knowledge-Base Project
FX This work was supported in part by a grant-in-aid from M.K. Fund for the
   Knowledge-Base Project.
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NR 218
TC 84
Z9 94
U1 4
U2 38
PU PORTLAND PRESS LTD
PI LONDON
PA 1ST FLR, 10 QUEEN STREET PLACE, LONDON, ENGLAND
SN 0143-5221
EI 1470-8736
J9 CLIN SCI
JI Clin. Sci.
PD APR 30
PY 2019
VL 133
IS 8
BP 953
EP 970
DI 10.1042/CS20180845
PG 18
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA HW5EO
UT WOS:000466712300002
PM 31036756
DA 2025-01-04
ER

PT J
AU Ma, F
   Zhu, WJ
   Guan, YF
   Yang, L
   Xia, XF
   Chen, SS
   Li, Q
   Guan, XW
   Yi, ZB
   Qian, HL
   Yi, X
   Xu, BH
AF Ma, Fei
   Zhu, Wenjie
   Guan, Yanfang
   Yang, Ling
   Xia, Xuefeng
   Chen, Shanshan
   Li, Qiao
   Guan, Xiuwen
   Yi, Zongbi
   Qian, Haili
   Yi, Xin
   Xu, Binghe
TI ctDNA dynamics: a novel indicator to track resistance in metastatic
   breast cancer treated with anti-HER2 therapy
SO ONCOTARGET
LA English
DT Article
DE circulating tumor DNA; dynamics; progression; metastatic breast cancer;
   anti-HER2 therapy
ID CIRCULATING TUMOR DNA; TYROSINE KINASE INHIBITORS; PHASE-II TRIAL;
   ACQUIRED-RESISTANCE; ACTIVATING MUTATIONS; COLORECTAL-CANCER;
   OVARIAN-CANCER; EGFR BLOCKADE; AMPLIFICATION; EVOLUTION
AB Background: Most studies utilizing circulating tumor DNA (ctDNA) to monitor disease interrogated only one or a few genes and failed to develop workable criteria to inform clinical practice. We evaluated the feasibility of detecting resistance to anti-HER2 therapy by serial gene-panel ctDNA sequencing.
   Results: Primary therapeutic resistance was identified in 6 out of 14 patients with events of progressive disease. For this subset comparison of pre- and post-treatment ctDNA assay results revealed that HER2 amplification concurred with disease progression (4/6, 66.7%). Mutations in TP53 (3/6, 50.0%) and genes implicated in the PI3K/mTOR pathway (3/6, 50.0%) were also dominant markers of resistance. Together, resistance to HER2 blockade should be indicated during treatment if any of the following situations applies: 1) recurrence or persistence of HER2 amplification in the blood; 2) emergence or >= 20% increase in the fraction of mutations in any of these resistance-related genes including TP53/PIK3CA/MTOR/PTEN. Compared with CT scans, dynamic ctDNA profiling utilizing pre-defined criteria was sensitive in identifying drug resistance (sensitivity 85.7%, specificity 55.0%), with a concordance rate up to 82.1%. Besides, the ctDNA criteria had a discriminating role in the prognosis of HER2-positive metastatic breast cancer.
   Methods: 52 plasma samples were prospectively collected from 18 patients with HER2-positive metastatic breast cancer who were treated with an oral anti-HER1/HER2 tyrosine kinase inhibitor (ClinicalTrials.gov NCT01937689). ctDNA was assayed by gene-panel target-capture next-generation sequencing.
   Conclusions: Longitudinal gene-panel ctDNA sequencing could be exploited to determine resistance and guide the precise administration of anti-HER2 targeted therapy in the metastatic setting.
C1 [Ma, Fei; Zhu, Wenjie; Chen, Shanshan; Li, Qiao; Guan, Xiuwen; Yi, Zongbi; Xu, Binghe] Chinese Acad Med Sci, Canc Hosp, Natl Canc Ctr, Dept Med Oncol, Beijing, Peoples R China.
   [Ma, Fei; Zhu, Wenjie; Chen, Shanshan; Li, Qiao; Guan, Xiuwen; Yi, Zongbi; Qian, Haili; Xu, Binghe] Peking Union Med Coll, Beijing, Peoples R China.
   [Guan, Yanfang; Yang, Ling; Yi, Xin] Geneplus Beijing, Beijing, Peoples R China.
   [Xia, Xuefeng] Weill Cornell Sch Med, Houston Methodist Res Inst, Houston, TX USA.
   [Qian, Haili] Chinese Acad Med Sci, Canc Inst Hosp, State Key Lab Mol Oncol, Beijing, 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; Houston
   Methodist; Cornell University; Chinese Academy of Medical Sciences -
   Peking Union Medical College; Cancer Institute & Hospital - CAMS
RP Xu, BH (corresponding author), Chinese Acad Med Sci, Canc Hosp, Natl Canc Ctr, Dept Med Oncol, Beijing, Peoples R China.; Xu, BH (corresponding author), Peking Union Med Coll, Beijing, Peoples R China.
EM bhxu@hotmail.com
RI Qian, Haili/H-5290-2019; Li, Ning/HJO-8544-2023; Chen,
   Shanshan/AAQ-5077-2020
OI Ma, Fei/0000-0001-9432-1902; qian, haili/0000-0003-0652-4801
FU Major Project of Beijing Municipal Science and Technology Commission
   [D161100000816004]; Beijing Hope Run Special Fund [LC2013L09]
FX The present study was funded by Major Project of Beijing Municipal
   Science and Technology Commission [D161100000816004] and Beijing Hope
   Run Special Fund [LC2013L09].
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NR 40
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Z9 78
U1 2
U2 29
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 OCT 4
PY 2016
VL 7
IS 40
BP 66020
EP 66031
DI 10.18632/oncotarget.11791
PG 12
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EB3QQ
UT WOS:000387281000115
PM 27602761
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Yang, W
   Zheng, H
   Lv, W
   Zhu, Y
AF Yang, Weiqing
   Zheng, Huifen
   Lv, Weibin
   Zhu, Yiping
TI Current status and prospect of immunotherapy for colorectal cancer
SO INTERNATIONAL JOURNAL OF COLORECTAL DISEASE
LA English
DT Review
DE Colorectal cancer; Immunotherapy; Microsatellite instability; Mismatch
   repair protein; Molecular targeting
ID MISMATCH-REPAIR-DEFICIENT; TUMOR MUTATIONAL BURDEN; MICROSATELLITE
   INSTABILITY; PD-1 BLOCKADE; OPEN-LABEL; CHECKPOINT BLOCKADE; IMMUNE;
   PEMBROLIZUMAB; CHEMOTHERAPY; NIVOLUMAB
AB PurposeColorectal cancer is the most common gastrointestinal tumor in China. While significant progress has been achieved in traditional chemotherapy, radiotherapy, and targeted therapy, the prognosis of advanced colorectal cancer is poor, and the five-year survival rate is unsatisfactory. There is an urgent need to explore new treatment modalities. In this review, we examined the latest progress of colorectal cancer immunotherapy and discussed its future prospects.MethodsWe conducted a literature review to sort out the current status of immunotherapy for different types of colorectal cancer and discussed potential combination therapy options. Results Subsequent line therapy, first-line therapy and neoadjuvant therapy for MSI-H/dMMR colorectal cancer are discussed. In addition, combination therapy options for patients with MSS/pMMR colorectal cancer are presented. Finally, current valuable biomarkers for immunotherapy are highlighted.ResultsSubsequent line therapy, first-line therapy and neoadjuvant therapy for MSI-H/dMMR colorectal cancer are discussed. In addition, combination therapy options for patients with MSS/pMMR colorectal cancer are presented. Finally, current valuable biomarkers for immunotherapy are highlighted.ConclusionThis review discussed the current status of immunotherapy for different types of colorectal cancer and biomarkers for immunotherapy.
C1 [Yang, Weiqing; Zheng, Huifen; Lv, Weibin; Zhu, Yiping] First Affiliated Hosp Wannan Med Coll, Dept Oncol, Wuhu, Peoples R China.
RP Zhu, Y (corresponding author), First Affiliated Hosp Wannan Med Coll, Dept Oncol, Wuhu, Peoples R China.
EM zhuyiping@wnmc.edu.cn
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   Wang F, 2021, CELL REP MED, V2, DOI 10.1016/j.xcrm.2021.100383
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   Xiao YP, 2015, CANCER DISCOV, V5, P16, DOI 10.1158/2159-8290.CD-14-1397
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NR 60
TC 6
Z9 7
U1 4
U2 37
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 NOV 14
PY 2023
VL 38
IS 1
DI 10.1007/s00384-023-04553-z
PG 11
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA HK2A1
UT WOS:001159317500001
PM 37962772
DA 2025-01-04
ER

PT J
AU Ogul, A
   Paydas, S
   Doran, F
   Erdogan, KE
   Tohumcuoglu, M
   Buyuksimsek, M
   Mirili, C
   Yetisir, AE
AF Ogul, Ali
   Paydas, Semra
   Doran, Figen
   Erdogan, Kivilcim Eren
   Tohumcuoglu, Mert
   Buyuksimsek, Mahmut
   Mirili, Cem
   Yetisir, Abdullah Evren
TI The effect of preferentially expressed antigen in melanoma (PRAME)
   expression status on survival in stage II and stage III colon cancer
SO JOURNAL OF BUON
LA English
DT Article
DE colon cancer; cancer testis antigen; targeted therapy
ID COLORECTAL-CANCER
AB Purpose: There are no studies showing PRAME expression in stage II and III colon adenocarcinoma. In this study, we aimed to determine the frequency of PRAME expression and the relationship with survival and clinicopathological data in stage II and III colon adenocarcinoma that need adjuvant therapy.
   Methods: Included were 81 patients with stage II and III colon cancer with adjuvant therapy without a second malignancy and systemic inflammatory diseases.
   Results: A statistically significant relationship was detected between PRAME expression and disease progression and survival (p=0.01 and p=0.003, respectively). Shorter disease-free survival (DFS) and overall survival (OS) were detected in right colon tumors in patients with lymph node metastasis, metastatic lymph node >3, N1 or N2 according to the TNM staging system, with lymphovascular invasion, perineural invasion and PRAME expression (p=0.004, p=0.023, p=0.002, p=0.004, p=0.001, p=0.006, p=0.01, respectively and p=0.009, p=0.037, p=0.001, p=0.004, p=0.003, p=0.004, p=0.006, respectively). In multivariate analysis, it was determined that right colon tumor (HR: 0.488, 95% CI, 0.201-0.998, p=0.049) and PRAME expression (HR: 0.423, 95% CI, 0.170-1.052, p=0.046) were independent risk factors for short DFS. For the OS, only the presence of PRAME expression was determined as an independent risk factor. (HR:0.332, 95%CI, 0.129-0.856, p=0.022).
   Conclusion: PRAME can be a potential target in immunotherapy in colon cancer treatment.
C1 [Ogul, Ali; Tohumcuoglu, Mert; Buyuksimsek, Mahmut; Yetisir, Abdullah Evren] Adana City Educ & Res Hosp, Dept Med Oncol, Mithat Ozsan Ave,4522 St, TR-01370 Adana, Turkey.
   [Paydas, Semra] Cukurova Univ, Dept Med Oncol, Fac Med, Adana, Turkey.
   [Doran, Figen; Erdogan, Kivilcim Eren] Cukurova Univ, Fac Med, Dept Pathol, Adana, Turkey.
   [Mirili, Cem] Erzurum Ataturk Univ, Fac Med, Dept Med Oncol, Erzurum, Turkey.
C3 Cukurova University; Cukurova University; Ataturk University
RP Ogul, A (corresponding author), Adana City Educ & Res Hosp, Dept Med Oncol, Mithat Ozsan Ave,4522 St, TR-01370 Adana, Turkey.
EM mdaliogu1@gmail.com
RI Paydas, Semra/F-3132-2018; Oğul, Ali/AAO-7285-2021; mirili,
   cem/V-4138-2018; Erdogan, Kıvılcım/D-3573-2016; Buyuksimsek,
   Mahmut/R-3412-2018
FU Cukurova University Scientific Research Fund [TSA- 2017-7947]
FX This research was supported by grant from the Cukurova University
   Scientific Research Fund (Project code: TSA- 2017-7947). 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. No writing assistance was
   utilized from any company in the production of the manuscript.
CR Al-Khadairi G, 2019, CANCERS, V11, DOI 10.3390/cancers11070984
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NR 24
TC 1
Z9 1
U1 0
U2 1
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 MAY-JUN
PY 2021
VL 26
IS 3
BP 992
EP 1001
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TC8MD
UT WOS:000668891800012
PM 34268964
DA 2025-01-04
ER

PT J
AU Wang, YR
   Meng, LB
   Su, F
   Qiu, Y
   Shi, JH
   Xu, X
   Luo, QF
AF Wang, Yi-Ran
   Meng, Ling-Bing
   Su, Fei
   Qiu, Yong
   Shi, Ji-Hua
   Xu, Xue
   Luo, Qing-Feng
TI Insights regarding novel biomarkers and the pathogenesis of primary
   colorectal carcinoma based on bioinformatic analysis
SO COMPUTATIONAL BIOLOGY AND CHEMISTRY
LA English
DT Article
DE Primary colorectal neoplasms; Biomarkers; Gene expression profiling;
   Computational biology
ID PROTEIN-INTERACTION NETWORKS; NEUROPEPTIDE-Y; CANCER STATISTICS;
   TUMOR-CELLS; ASSOCIATION; ACTIVATION; RECRUITS; THERAPY; COLON
AB Background: Biomarkers are important in the study of tumor processes for early detection and precise treatment. The biomarkers that have been previously detected are not useful for clinical application for primary colorectal carcinoma (PCRC). The aim of this study was to explore clinically valuable biomarkers of PCRC based on integrated bioinformatic analysis.
   Material and methods: Gene expression data were acquired from the GSE41258 dataset, and the differentially expressed genes were determined between PCRC and normal colorectal samples. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses were implemented via Gene Set Enrichment Analysis. A proteinprotein interaction (PPI) network was constructed. The significant modules and hub genes were screened and identified in the PPI network.
   Results: A total of 202 DEGs were identified, including 58 upregulated and 144 downregulated genes in PCRC samples compared to those in normal colorectal samples. Enrichment analysis demonstrated that the gene sets enriched in PCRC were significantly related to bicarbonate transport, regulation of sodium ion transport, potassium ion homeostasis, regulation of telomere maintenance, and other processes. A total of 10 hub genes was identified by cytoHubba: PYY, CXCL3, CXCL11, CXCL8, CXCL12, CCL20, MMP3, P2RY14, NPY1R, and CXCL1.
   Conclusion: The hub genes, such as NPY1R, P2RY14, and CXCL12, and the electrolyte disequilibrium resulting from the differential expression of genes, especially bicarbonate imbalance, may provide novel insights and evidence for the future diagnosis and targeted therapy of PCRC.
C1 [Wang, Yi-Ran; Shi, Ji-Hua; Xu, Xue; Luo, Qing-Feng] Chinese Acad Med Sci, Beijing Hosp, Natl Ctr Gerontol, Inst Geriatr Med,Dept Gastroenterol, 1 Dahua Rd, Beijing 100730, Peoples R China.
   [Meng, Ling-Bing] Chinese Acad Med Sci, Beijing Hosp, Natl Ctr Gerontol, Inst Geriatr Med,Dept Neurol, Beijing, Peoples R China.
   [Su, Fei] Chinese Acad Med Sci, Beijing Hosp, Natl Ctr Gerontol, Inst Geriatr Med,Clin Biobank, Beijing, Peoples R China.
   [Qiu, Yong] Chinese Acad Med Sci, Beijing Hosp, Natl Ctr Gerontol, Inst Geriatr Med,Dept Anesthesia, Beijing, Peoples R China.
C3 Beijing Hospital; Chinese Academy of Medical Sciences - Peking Union
   Medical College; Chinese Academy of Medical Sciences - Peking Union
   Medical College; Beijing Hospital; Beijing Hospital; Chinese Academy of
   Medical Sciences - Peking Union Medical College; Beijing Hospital;
   Chinese Academy of Medical Sciences - Peking Union Medical College
RP Luo, QF (corresponding author), Chinese Acad Med Sci, Beijing Hosp, Natl Ctr Gerontol, Inst Geriatr Med,Dept Gastroenterol, 1 Dahua Rd, Beijing 100730, Peoples R China.
EM yiransherry@qq.com; 314597690@qq.com; sufei_sh@163.com; spaceqy@163.com;
   shijihua1981@sina.com; rabbit316@sina.com; luoqf2000@126.com
RI wang, yi/KBB-3614-2024
FU Fundamental Research Funds for the Central Universities [3332019123]
FX We are thankful for the financial support of the Fundamental Research
   Funds for the Central Universities (Number: 3332019123) and the
   encouragement of Beijing Hospital.
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NR 60
TC 9
Z9 9
U1 0
U2 6
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 1476-9271
EI 1476-928X
J9 COMPUT BIOL CHEM
JI Comput. Biol. Chem.
PD APR
PY 2020
VL 85
AR 107229
DI 10.1016/j.compbiolchem.2020.107229
PG 14
WC Biology; Computer Science, Interdisciplinary Applications
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics; Computer Science
GA LG8JK
UT WOS:000528339900021
PM 32058945
OA hybrid
DA 2025-01-04
ER

PT J
AU Damaskos, C
   Valsami, S
   Spartalis, E
   Antoniou, EA
   Tomos, P
   Karamaroudis, S
   Zoumpou, T
   Pergialiotis, V
   Stergios, K
   Michaelides, C
   Kontzoglou, K
   Perrea, D
   Nikiteas, N
   Dimitroulis, D
AF Damaskos, Christos
   Valsami, Serena
   Spartalis, Eleftherios
   Antoniou, Efstathios A.
   Tomos, Periklis
   Karamaroudis, Stefanos
   Zoumpou, Theofano
   Pergialiotis, Vasilios
   Stergios, Konstantinos
   Michaelides, Constantinos
   Kontzoglou, Konstantinos
   Perrea, Despina
   Nikiteas, Nikolaos
   Dimitroulis, Dimitrios
TI Histone Deacetylase Inhibitors: A Novel Therapeutic Weapon Against
   Medullary Thyroid Cancer?
SO ANTICANCER RESEARCH
LA English
DT Review
DE HDAC; histone; inhibitors; acetylasation; epigenetics; medullary;
   thyroid; cancer; targeted; therapy; review
ID COLORECTAL-CANCER; HDAC INHIBITORS; CLINICAL-TRIALS; ACID; APOPTOSIS;
   CELLS; MECHANISMS; EXPRESSION; CARCINOMA
AB Background/Aim: Medullary thyroid cancer (MTC) is highly malignant, metastatic and recurrent, remaining generally incurable, and responsible for approximately 14% of all thyroid carcinoma-related deaths. MTC can metastasize to lymph nodes, trachea and distant organs, such as brain, lungs, liver and bones. MTC cells are resistant to chemotherapy and traditional external therapies are not showing definite clinical benefits. Scientists are trying to understand the molecular background of carcinogenesis and histone deacetylase (HDAC) seems to play a potential role to gene transcription. On the other hand, HDAC inhibitors (HDACI) hamper the HDAC action giving promising results as new anticancer drugs. The purpose of this review was to evaluate the current status of research considering the role of HDACIs in MTC treatment and to present the latest trends in MTC treatment protocols. Materials and Methods: This literature review was accomplished using the MEDLINE database. The key words/phrases were; HDACI, medullary thyroid cancer, HDACI in the therapy of neuroendocrine tumors, HDACI in MTC. Fortyone articles were selected from the total number of the search's results. Only sixteen papers focus on the use of HDACIs in the treatment of MTC. In order to extract our conclusions, we took into account some studies whose main topic does not strictly refer to the MTC but they contain noteworthy and useful information. Only English articles published up to August 2016 were assessed and used for writing this review. Results: Molecules, such as valproid acid (VPA), vorinostat, suberoyl bis-hydroxamic acid (SBHA), depsipeptide, belinostat, m-carboxycinnamic acid bis-hydroxamine (CBHA) and AB3 have shown promising antitumor effects against MTC. Conclusion: HDACIs represent a promising field for targeted therapy both for its anticancer properties, as well as for augmenting radiotherapeutic modalities. More trials are needed.
C1 [Damaskos, Christos; Antoniou, Efstathios A.; Kontzoglou, Konstantinos; Dimitroulis, Dimitrios] Univ Athens, Laiko Gen Hosp, Sch Med, Dept Propedeut Surg 2, Athens, Greece.
   [Damaskos, Christos; Spartalis, Eleftherios; Pergialiotis, Vasilios; Stergios, Konstantinos; Perrea, Despina; Nikiteas, Nikolaos] Univ Athens, Sch Med, Lab Expt Surg & Surg Res NS Christeas, Athens, Greece.
   [Valsami, Serena] Natl & Kapodistrian Athens Univ, Sch Med, Aretaie Hosp, Blood Transfus Dept, Athens, Greece.
   [Tomos, Periklis] Univ Athens, Sch Med, Attikon Gen Hosp, Dept Thorac Surg, Athens, Greece.
   [Karamaroudis, Stefanos; Zoumpou, Theofano] Univ Athens, Sch Med, Athens, Greece.
   [Stergios, Konstantinos] Princess Alexandra Hosp NHS Trust, Colorectal Dept, Gen Surg, Harlow, Essex, England.
   [Michaelides, Constantinos] Univ Athens, Sch Med, Dept Pathol 1, Athens, Greece.
C3 Laiko General Hospital; Athens Medical School; National & Kapodistrian
   University of Athens; National & Kapodistrian University of Athens;
   Athens Medical School; Athens Medical School; National & Kapodistrian
   University of Athens; Athens Medical School; University Hospital
   Attikon; National & Kapodistrian University of Athens; National &
   Kapodistrian University of Athens; Athens Medical School; Princess
   Alexandra Hospital NHS Trust; National & Kapodistrian University of
   Athens; Athens Medical School
RP Damaskos, C (corresponding author), Univ Athens, Laiko Gen Hosp, Sch Med, Dept Propedeut Surg 2, Athens, Greece.; Damaskos, C (corresponding author), Univ Athens, Sch Med, Lab Expt Surg & Surg Res NS Christeas, Athens, Greece.
EM x_damaskos@yahoo.gr
RI Stergios, Konstantinos/H-8673-2019; Spartalis, Eleftherios/W-8936-2018;
   Nikiteas, Nikolaos/A-3165-2009; VALSAMI, SERENA/AAB-4895-2020;
   Pergialiotis, Vasilios/H-3772-2019
OI Pergialiotis, Vasilios/0000-0003-4510-1633; Damaskos,
   Christos/0000-0002-5454-2564; Valsami, Serena/0000-0002-1034-6510;
   Karamaroudis, Stefanos/0000-0003-3522-2108
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NR 40
TC 31
Z9 33
U1 0
U2 11
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 OCT
PY 2016
VL 36
IS 10
BP 5019
EP 5024
DI 10.21873/anticanres.11070
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EC9SA
UT WOS:000388483300004
PM 27798860
OA Bronze
DA 2025-01-04
ER

PT J
AU Hou, B
   Li, WH
   Li, JH
   Ma, J
   Xia, P
   Liu, Z
   Zeng, QN
   Zhang, X
   Chang, DM
AF Hou, Bin
   Li, Wenhan
   Li, Jianhui
   Ma, Jia
   Xia, Peng
   Liu, Zhao
   Zeng, Qingnuo
   Zhang, Xin
   Chang, Dongmin
TI Tumor suppressor <i>LHPP</i> regulates the proliferation of colorectal
   cancer cells via the PI3K/AKT pathway
SO ONCOLOGY REPORTS
LA English
DT Article
DE colorectal cancer; LHPP; PI3K; AKT signaling pathway; proliferation
ID PROTEIN HISTIDINE PHOSPHATASE; INORGANIC PYROPHOSPHATASE; SIGNALING
   PATHWAY; PIK3CA GENE; CYCLE; 3-PHOSPHOHISTIDINE; EXPRESSION; MUTATIONS;
   NM23-H1; GROWTH
AB Colorectal cancer (CRC) is the third most commonly diagnosed cancer and the fourth leading cause of cancer-related mortality worldwide. Thus, identification of the mechanisms involved in the progression of CRC has become a crucial element of facilitating early CRC diagnosis and targeted therapy for patients with advanced CRC. Currently, Phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPP), a type of histidine phosphatase protein, has been confirmed as a tumor suppressor in hepatocellular carcinoma (HCC) and cervical cancer. However, the functions and molecular mechanisms underlying LHPP in CRC remain undefined. The present study revealed that dysregulation of LHPP was frequently observed in CRC tissues and was positively correlated with tumor severity and poor prognosis. Functional experiments demonstrated that overexpression of LHPP impeded CRC cell growth and proliferation in vitro, and was associated with a change in p53 expression and PI3K/AKT activity. In contrast, silencing of LHPP significantly promoted cell growth and proliferation by modulating the PI3K/AKT signaling pathway. Notably, the anti-CRC effects of LHPP were also observed in nude mouse in vivo experiments. Overall, the data obtained in the present study suggested that LHPP may be exploited as a diagnostic and prognostic candidate for patients with CRC.
C1 [Hou, Bin; Xia, Peng; Liu, Zhao; Zeng, Qingnuo; Zhang, Xin; Chang, Dongmin] Xi An Jiao Tong Univ, Dept Surg Oncol, Affiliated Hosp 1, 277 W Yanta Rd, Xian 710061, Shaanxi, Peoples R China.
   [Li, Wenhan; Li, Jianhui; Ma, Jia] Shaanxi Prov Peoples Hosp, Dept Surg Oncol, Xian 10068, Shaanxi, Peoples R China.
   [Li, Wenhan; Li, Jianhui; Ma, Jia] Xi An Jiao Tong Univ, Sch Med, Affiliated Hosp 3, Xian 710061, Shaanxi, Peoples R China.
C3 Xi'an Jiaotong University; Xi'an Medical University; Xi'an Jiaotong
   University
RP Chang, DM (corresponding author), Xi An Jiao Tong Univ, Dept Surg Oncol, Affiliated Hosp 1, 277 W Yanta Rd, Xian 710061, Shaanxi, Peoples R China.
EM dr_changdm@sina.com
OI , Jianhui/0000-0001-8620-3594
FU Science and Technology Foundation of Shaanxi Province
   [S2018YF-ZDSF-0102]; Shaanxi Province Key Scientific and Technological
   Innovation Team Project [2014KCT-24]
FX This research was supported by grants from the Science and Technology
   Foundation of Shaanxi Province (S2018YF-ZDSF-0102) and the Shaanxi
   Province Key Scientific and Technological Innovation Team Project
   (2014KCT-24).
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NR 43
TC 39
Z9 39
U1 0
U2 40
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 FEB
PY 2020
VL 43
IS 2
BP 536
EP 548
DI 10.3892/or.2019.7442
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KE9QU
UT WOS:000508885800015
PM 31894339
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Cornejo, KM
   Cosar, EF
   Paner, GP
   Yang, P
   Tomaszewicz, K
   Meng, XL
   Mehta, V
   Sirintrapun, SJ
   Barkan, GA
   Hutchinson, L
AF Cornejo, Kristine M.
   Cosar, Ediz F.
   Paner, Gladell P.
   Yang, Ping
   Tomaszewicz, Keith
   Meng, Xiuling
   Mehta, Vikas
   Sirintrapun, Sahussapont Joseph
   Barkan, Guliz A.
   Hutchinson, Lloyd
TI Mutational Profile Using Next-Generation Sequencing May Aid in the
   Diagnosis and Treatment of Urachal Adenocarcinoma
SO INTERNATIONAL JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE urachal; adenocarcinoma; bladder; mutation; next-generation sequencing;
   targeted therapy
ID COLORECTAL-CARCINOMA; TANKYRASE INHIBITORS; GENOMIC ALTERATIONS;
   URINARY-BLADDER; CANCER-THERAPY; BRAF MUTATIONS; KRAS; RESISTANCE;
   GROWTH; NEOPLASMS
AB Objectives. The rare urachal adenocarcinoma (UAC) of the bladder has striking morphologic and immunohistochemical overlap with colorectal adenocarcinoma (CAC) and bladder adenocarcinoma (BAC). To date, the mutational status in UAC and BAC has not been well investigated. Methods. We retrospectively evaluated 34 UACs (mucinous, n = 9; intestinal, n = 3; signet ring cell, n = 1; not otherwise specified, n = 21) and 4 BACs (n = 4). Next-generation sequencing analysis of 50 cancer "hotspot" gene mutations using the Ampliseq Cancer Hotspot Panel v2 was performed. Two UAC cases did not have adequate DNA quality with poor sequencing coverage and were excluded from the study. Results. RAS mutations were identified in 16 of 32 (50%) UACs (15 KRAS; 1 NRAS) and none of the BACs (0%). TP53 mutations were found in both UACs (18/32; 56%) and BACs (4/4; 100%). GNAS (n = 4), SMAD4 (n = 3), and BRAF (n = 1) mutations were only found in UACs. In contrast, APC (n = 2) mutations were only found in BACs. The mucinous subtype of UAC contained a SMAD4 mutation in 33% of cases (3/9), which was not identified in any other subtype (0/23; 0%) (P = .0169). The only BRAF mutation was identified in the single signet ring cell subtype of UAC. There were no other differences in the mutation profile when comparing histologic subtypes of UAC. Conclusions. In summary, UAC and BAC have overlapping but distinct mutation profiles and these differences may aid in separating these 2 entities. Next-generation sequencing to identify therapeutic targets or resistance markers may aid treatment decisions.
C1 [Cornejo, Kristine M.; Cosar, Ediz F.; Tomaszewicz, Keith; Meng, Xiuling; Hutchinson, Lloyd] Univ Massachusetts, Sch Med, UMass Mem Med Ctr, Worcester, MA 01605 USA.
   [Paner, Gladell P.] Univ Chicago, Med Ctr, Chicago, IL 60637 USA.
   [Yang, Ping] Sun Yat Sen Univ, Canc Ctr, Guangzhou, Guangdong, Peoples R China.
   [Mehta, Vikas] Mt Sinai Hosp Med Ctr, Chicago, IL USA.
   [Sirintrapun, Sahussapont Joseph] Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10021 USA.
   [Barkan, Guliz A.] Loyola Univ, Med Ctr, 2160 S 1st Ave, Maywood, IL 60153 USA.
C3 University of Massachusetts System; University of Massachusetts
   Worcester; University of Chicago; University of Chicago Medical Center;
   Sun Yat Sen University; Memorial Sloan Kettering Cancer Center; Loyola
   University Chicago
RP Cornejo, KM (corresponding author), Massachusetts Gen Hosp, Dept Pathol, 55 Fruit St,Warren 831B, Boston, MA 02114 USA.
EM Kcornejo@partners.org
RI Mehta, Vikas/J-4279-2019
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NR 49
TC 5
Z9 6
U1 0
U2 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1066-8969
EI 1940-2465
J9 INT J SURG PATHOL
JI Int. J. Surg. Pathol.
PD FEB
PY 2020
VL 28
IS 1
BP 51
EP 59
AR 1066896919872535
DI 10.1177/1066896919872535
EA SEP 2019
PG 9
WC Pathology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology; Surgery
GA JX3OX
UT WOS:000485780600001
PM 31496327
OA Bronze
DA 2025-01-04
ER

PT J
AU Huang, YY
   Zhang, S
   Hu, XQ
   Wang, XY
   Zhao, YB
   Li, ZK
AF Huang, Yingying
   Zhang, Shuai
   Hu, Xueqing
   Wang, Xiangyang
   Zhao, Yunbo
   Li, Zhongkang
TI Partial response to crizotinib
SO AME CASE REPORTS
LA English
DT Article
DE Case report; colorectal cancer (CRC); BRAF V600E; programmed cell death
   protein 1 (PD-1); circulating tumor DNA monitoring (ctDNA monitoring)
ID SUBGROUP ANALYSES; BRAF; MET; AMPLIFICATION; INHIBITION; ACTIVATION;
   CETUXIMAB; SURVIVAL; ALK
AB Background: Colorectal cancer (CRC) with the Raf murine sarcoma viral oncogene homolog B (BRAF) V600E had a relatively poor prognosis. Anaplastic lymphoma kinase (ALK) fusion and the mesenchymal-to-epithelial transition factor (MET) amplification have been recognized as potentially important therapeutic targets in non-small cell lung cancer (NSCLC). However, both of them are of extremely lower frequencies (<2%) in metastatic CRC, and few studies have mentioned the real application of their inhibitors in CRC treatment. Case Description: A 49-year-old Chinese male was diagnosed with ascending colon adenocarcinoma (cT3N+?M1) with liver metastases. The patient performed next-generation sequencing (NGS) using tissue and circulating tumor DNA (ctDNA), and the results showed a BRAF V600E mutation. He received an initial combination treatment with cetuximab, dabrafenib, and trametinib with a partial response (PR) assessment. We changed the therapy regimen on this patient several times because of the patient's intolerance to the drugs or the inefficacy of the treatment. During this period, we detected the c-MET amplification and tropomyosin 4 (TPM4)-ALK fusion by NGS after triplet targeted therapy (tislelizumab, dabrafenib, and trametinib), thus he was finally treated with programmed cell death protein 1 (PD-1) inhibitor (tislelizumab), MET/ALK inhibitor (crizotinib) plus multikinase inhibitor (regorafenib). Imageological examinations showed that PR was achieved and ctDNA sequencing results indicated a significantly reduced BRAF mutation frequency, MET amplification and TPM4-ALK fusion were undetectable. NGS analysis of peripheral blood showed a recurrence of the MET acquired resistant amplification mutation over 2 months of ongoing treatment. but the patient was assessed as PR and still under treatment of crizotinib, tislelizumab and regorafenib within good physical condition. At the last follow-up on October 2021, the patient died of symptomatic treatment fail for obstructive jaundice. The patient finally achieved 11 months overall survival. Conclusions: This study reported a co-existence of a BRAF V600E mutation, c-MET amplification and TPM4-ALK fusion in a CRC patient. Administration of crizotinib combined with regorafenib and tislelizumab obtained an obvious response. Furthermore, continuous ctDNA detection appears to be a promising technique to monitor tumor burden, which may provide better clinical decision support during the disease course.
C1 [Huang, Yingying; Zhang, Shuai; Hu, Xueqing; Zhao, Yunbo] Beijing Hosp, Natl Ctr Gerontol, Dept Oncol, 1 Dahua Rd, Beijing 100730, Peoples R China.
   [Wang, Xiangyang] Beijing Hosp, Natl Ctr Gerontol, Dept Radiol, Beijing, Peoples R China.
   [Li, Zhongkang] Geneplus Beijing, Beijing, Peoples R China.
C3 Beijing Hospital; Beijing Hospital
RP Huang, YY (corresponding author), Beijing Hosp, Natl Ctr Gerontol, Dept Oncol, 1 Dahua Rd, Beijing 100730, Peoples R China.
EM yinghh@hotmail.com
RI Zhao, Yun-Bo/F-1699-2010
OI zhongkang, li/0000-0003-1562-2438
CR Array BioPharma Inc, 2020, BRAFTOVI ENCORAFENIB
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NR 29
TC 0
Z9 0
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 2523-1995
J9 AME CASE REP
JI AME Case Rep.
PD APR 30
PY 2024
VL 8
AR 38
DI 10.21037/acr-23-155
PG 8
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA RG8G8
UT WOS:001226599600012
PM 38711893
OA gold
DA 2025-01-04
ER

PT J
AU Kovaleva, V
   Geissler, AL
   Lutz, L
   Fritsch, R
   Makowiec, F
   Wiesemann, S
   Hopt, UT
   Passlick, B
   Werner, M
   Lassmann, S
AF Kovaleva, Valentina
   Geissler, Anna-Lena
   Lutz, Lisa
   Fritsch, Ralph
   Makowiec, Frank
   Wiesemann, Sebastian
   Hopt, Ulrich T.
   Passlick, Bernward
   Werner, Martin
   Lassmann, Silke
TI Spatio-temporal mutation profiles of case-matched colorectal carcinomas
   and their metastases reveal unique <i>de novo</i> mutations in
   metachronous lung metastases by targeted next generation sequencing
SO MOLECULAR CANCER
LA English
DT Article
DE Colorectal cancer; Next generation sequencing; Metastases; FFPE
ID MICROSATELLITE INSTABILITY; CANCER; TUMORS; ASSOCIATION; BEVACIZUMAB;
   PANITUMUMAB; CONCORDANCE; BIOMARKERS; THERAPY; IMPACT
AB Background: Targeted next generation sequencing (tNGS) has become part of molecular pathology diagnostics for determining RAS mutation status in colorectal cancer (CRC) patients as predictive tool for decision on EGFR-targeted therapy. Here, we investigated mutation profiles of case-matched tissue specimens throughout the disease course of CRC, to further specify RAS-status dynamics and to identify de novo mutations associated with distant metastases.
   Methods: Case-matched formalin-fixed and paraffin-embedded (FFPE) resection specimens (n = 70; primary tumours, synchronous and/ or metachronous liver and/ or lung metastases) of 14 CRC cases were subjected to microdissection of normal colonic epithelial, primary and metastatic tumour cells, their DNA extraction and an adapted library protocol for limited DNA using the 48 gene TruSeq Amplicon Cancer Panel(TM), MiSeq sequencing and data analyses (Illumina).
   Results: By tNGS primary tumours were RAS wildtype in 5/14 and mutated in 9/14 (8/9 KRAS exon 2; 1/9 NRAS Exon 3) of cases. RAS mutation status was maintained in case-matched metastases throughout the disease course, albeit with altered allele frequencies. Case-matched analyses further identified a maximum of three sequence variants (mainly in APC, KRAS, NRAS, TP53) shared by all tumour specimens throughout the disease course per individual case. In addition, further case-matched de novo mutations were detected in synchronous and/ or metachronous liver and/ or lung metastases (e.g. in APC, ATM, FBXW7, FGFR3, GNAQ, KIT, PIK3CA, PTEN, SMAD4, SMO, STK11, TP53, VHL). Moreover, several de novo mutations were more frequent in synchronous (e.g. ATM, KIT, PIK3CA, SMAD4) or metachronous (e.g. FBXW7, SMO, STK11) lung metastases. Finally, some de novo mutations occurred only in metachronous lung metastases (CDKN2A, FGFR2, GNAS, JAK3, SRC).
   Conclusion: Together, this study employs an adapted FFPE-based tNGS approach to confirm conservation of RAS mutation status in primary and metastatic tissue specimens of CRC patients. Moreover, it identifies genes preferentially mutated de novo in late disease stages of metachronous CRC lung metastases, several of which might be actionable by targeted therapies.
C1 [Kovaleva, Valentina; Geissler, Anna-Lena; Lutz, Lisa; Werner, Martin; Lassmann, Silke] Univ Freiburg, Inst Surg Pathol, Med Ctr, Fac Med, Breisacherstr 115A, D-79106 Freiburg, Germany.
   [Kovaleva, Valentina; Geissler, Anna-Lena; Werner, Martin; Lassmann, Silke] German Canc Consortium DKTK, Heidelberg, Germany.
   [Kovaleva, Valentina; Geissler, Anna-Lena; Werner, Martin; Lassmann, Silke] German Canc Res Ctr, Heidelberg, Germany.
   [Geissler, Anna-Lena] Univ Freiburg, Fac Biol, Freiburg, Germany.
   [Fritsch, Ralph] Univ Freiburg, Med Ctr, Dept Med 1, Fac Med, Freiburg, Germany.
   [Fritsch, Ralph; Makowiec, Frank; Wiesemann, Sebastian; Hopt, Ulrich T.; Passlick, Bernward; Werner, Martin; Lassmann, Silke] Univ Freiburg, Med Ctr, Comprehens Canc Ctr Freiburg, Fac Med, Freiburg, Germany.
   [Makowiec, Frank; Hopt, Ulrich T.] Univ Freiburg, Med Ctr, Dept Gen & Visceral Surg, Fac Med, Freiburg, Germany.
   [Wiesemann, Sebastian; Passlick, Bernward] Univ Freiburg, Med Ctr, Dept Thorac Surg, Fac Med, Freiburg, Germany.
   [Lassmann, Silke] Univ Freiburg, BIOSS Ctr Biol Signaling Studies, Freiburg, Germany.
C3 University of Freiburg; Helmholtz Association; German Cancer Research
   Center (DKFZ); Helmholtz Association; German Cancer Research Center
   (DKFZ); University of Freiburg; University of Freiburg; University of
   Freiburg; University of Freiburg; University of Freiburg; University of
   Freiburg
RP Lassmann, S (corresponding author), Univ Freiburg, Inst Surg Pathol, Med Ctr, Fac Med, Breisacherstr 115A, D-79106 Freiburg, Germany.; Lassmann, S (corresponding author), German Canc Consortium DKTK, Heidelberg, Germany.; Lassmann, S (corresponding author), German Canc Res Ctr, Heidelberg, Germany.; Lassmann, S (corresponding author), Univ Freiburg, Med Ctr, Comprehens Canc Ctr Freiburg, Fac Med, Freiburg, Germany.; Lassmann, S (corresponding author), Univ Freiburg, BIOSS Ctr Biol Signaling Studies, Freiburg, Germany.
EM silke.lassmann@uniklinik-freiburg.de
RI Fritsch, Ralph/Q-8836-2019
OI Makowiec, Frank/0000-0003-0012-3775; Fritsch, Ralph/0000-0001-9639-3213
FU German Cancer Consortium (DKTK); Mushett Family Foundation (Chester, New
   Jersey, USA)
FX This study was funded by the German Cancer Consortium (DKTK, grants to
   MW and SL) and in part by the Mushett Family Foundation (Chester, New
   Jersey, USA).
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NR 34
TC 41
Z9 42
U1 0
U2 9
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD OCT 18
PY 2016
VL 15
AR 63
DI 10.1186/s12943-016-0549-8
PG 19
WC Biochemistry & Molecular Biology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA DZ2PU
UT WOS:000385684500001
PM 27756406
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Rodrigues, P
   Bangali, H
   Hammoud, A
   Mustafa, YF
   Al-Hetty, HRAK
   Alkhafaji, AT
   Deorari, MM
   Al-Taee, MM
   Zabibah, RS
   Alsalamy, A
AF Rodrigues, Paul
   Bangali, Harun
   Hammoud, Ahmad
   Mustafa, Yasser Fakri
   Al-Hetty, Hussein Riyadh Abdul Kareem
   Alkhafaji, Adnan Taan
   Deorari, Maha Medha
   Al-Taee, Muataz Mohammed
   Zabibah, Rahman S.
   Alsalamy, Ali
TI COX 2-inhibitors; a thorough and updated survey into combinational
   therapies in cancers
SO MEDICAL ONCOLOGY
LA English
DT Review
DE Cancer; COX-2; COX-2 inhibitor; Combinational therapy
ID CARBONIC-ANHYDRASE INHIBITION; ENDOTHELIAL GROWTH-FACTOR; BREAST-CANCER;
   COLON-CANCER; COLORECTAL-CANCER; PROSTAGLANDIN E-2; CYCLOOXYGENASE-2
   INHIBITORS; INTESTINAL POLYPOSIS; SELECTIVE INHIBITORS;
   PANCREATIC-CANCER
AB Cyclooxygenase (COX) enzymes are pivotal in inflammation and cancer development. COX-2, in particular, has been implicated in tumor growth, angiogenesis, and immune evasion. Recently, COX-2 inhibitors have arisen as potential therapeutic agents in cancer treatment. In addition, combining COX inhibitors with other treatment modalities has demonstrated the potential to improve therapeutic efficacy. This review aims to investigate the effects of COX inhibition, both alone and in combination with other methods, on signaling pathways and carcinogenesis in various cancers. In this study, a literature search of all major academic databases was conducted (PubMed, Scholar google), including the leading research on the mechanisms of COX-2, COX-2 inhibitors, monotherapy with COX-2 inhibitors, and combining COX-2-inhibitors with chemotherapeutic agents in tumors. The study encompasses preclinical and clinical evidence, highlighting the positive findings and the potential implications for clinical practice. According to preclinical studies, multiple signaling pathways implicated in tumor cell proliferation, survival, invasion, and metastasis can be suppressed by inhibiting COX. In addition, combining COX inhibitors with chemotherapy drugs, targeted therapies, immunotherapies, and miRNA-based approaches has enhanced anti-tumor activity. These results suggest that combination therapy has the potential to overcome resistance mechanisms and improve treatment outcomes. However, caution must be exercised when selecting and administering combination regimens. Not all combinations of COX-2 inhibitors with other drugs result in synergistic effects; some may even have unfavorable interactions. Therefore, personalized approaches that consider the specific characteristics of the cancer and the medications involved are crucial for optimizing therapeutic strategies. In conclusion, as monotherapy or combined with other methods, COX inhibition bears promise in modulating signaling pathways and inhibiting carcinogenesis in various cancers. Additional studies and well-designed clinical trials are required to completely elucidate the efficacy of COX inhibition and combination therapy in enhancing cancer treatment outcomes. This narrative review study provides a detailed summary of COX-2 monotherapy and combination targeted therapy in cancer treatment.
C1 [Rodrigues, Paul; Bangali, Harun] King Khalid Univ, Coll Comp Sci, Dept Comp Engn, Abha, Saudi Arabia.
   [Hammoud, Ahmad] Bauman Moscow State Tech Univ, Dept Med & Tech Informat Technol, Moscow, Russia.
   [Hammoud, Ahmad] Gulf Univ Sci & Technol, Dept Math & Nat Sci, Mishref Campus, Mubarak Al Abdullah, Kuwait.
   [Mustafa, Yasser Fakri] Univ Mosul, Coll Pharm, Dept Pharmaceut Chem, Mosul 41001, Iraq.
   [Al-Hetty, Hussein Riyadh Abdul Kareem] Univ Anbar, Coll Educ Pure Sci, Dept Biol, Ramadi, Iraq.
   [Alkhafaji, Adnan Taan] Al Ayen Univ, Coll Med, Cardiol Dept, Thi Qar, Iraq.
   [Deorari, Maha Medha] Uttaranchal Univ, Uttaranchal Inst Pharmaceut Sci, Dehra Dun, India.
   [Al-Taee, Muataz Mohammed] AL Nisour Univ Coll, Dept Med Labs Technol, Baghdad, Iraq.
   [Zabibah, Rahman S.] Islamic Univ, Coll Med Tech, Najaf, Iraq.
   [Alsalamy, Ali] Imam Jaafar Al Sadiq Univ, Coll Tech Engn, Al Muthanna 66002, Iraq.
C3 King Khalid University; Bauman Moscow State Technical University;
   University of Mosul; University of Anbar; Al-Ayen University;
   Uttaranchal University; Al-Nisour University College; Islamic University
   College; Imam Jaa'far al-Sadiq University
RP Hammoud, A (corresponding author), Bauman Moscow State Tech Univ, Dept Med & Tech Informat Technol, Moscow, Russia.; Hammoud, A (corresponding author), Gulf Univ Sci & Technol, Dept Math & Nat Sci, Mishref Campus, Mubarak Al Abdullah, Kuwait.; Al-Hetty, HRAK (corresponding author), Univ Anbar, Coll Educ Pure Sci, Dept Biol, Ramadi, Iraq.
EM hammoud.a@mail.ru; hussin.riyadh@uoanbar.edu.iq
RI Al-Heety, Hussein/ACI-5584-2022; Mustafa, Yasser Fakri/D-1589-2019;
   Hammoud, Ahmad/AAD-1981-2022
OI Riyadh Abdul Kareem Al-Hetty, Hussein/0000-0002-4861-9377; Riyadh,
   Hussein/0009-0006-9585-3381; Mustafa, Yasser Fakri/0000-0002-0926-7428;
   , Hussein/0009-0005-1965-8755
FU Deanship of Scientific Research, King Khalid University [RGP2/420/44];
   Deanship of Scientific Research at King Khalid University
FX The authors extend their appreciation to the Deanship of Scientific
   Research at King Khalid University for funding this work through a large
   group Research Project under grant number RGP2/420/44.
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NR 129
TC 9
Z9 9
U1 4
U2 12
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 JAN 2
PY 2024
VL 41
IS 1
AR 41
DI 10.1007/s12032-023-02256-7
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EF9D8
UT WOS:001137616900001
PM 38165473
DA 2025-01-04
ER

PT J
AU Yao, HJ
   Luo, LX
   Li, R
   Zhao, YL
   Zhang, L
   Pesic, M
   Cai, L
   Li, L
AF Yao, Hongjuan
   Luo, Liaoxin
   Li, Rui
   Zhao, Yelin
   Zhang, Li
   Pesic, Milica
   Cai, Lin
   Li, Liang
TI New insight into the role of SMAD4 mutation/deficiency in the prognosis
   and therapeutic resistance of pancreatic ductal adenocarcinomas
SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
LA English
DT Review
DE SMAD4 mutation/deficiency; Pancreatic ductal adenocarcinoma (PDAC);
   Prognosis; Therapeutic resistance; Clinical implementation
ID TGF-BETA; DOWN-REGULATION; COLON-CANCER; IN-VITRO; MESENCHYMAL
   TRANSITION; TUMOR MICROENVIRONMENT; IMMUNE EVASION; POOR-PROGNOSIS;
   CELL-GROWTH; EXPRESSION
AB Pancreatic ductal adenocarcinoma (PDAC) patients have an unfavorable prognosis and disappointing treatment outcomes because of late diagnosis, high chemotherapy resistance, ineffective adjuvant chemotherapy, unavailable molecular targeted therapy, and profound immunosuppressive effects in the tumor microenvironment (TME). There are a variety of critical driver proteins, such as KRAS, TP53, PTEN and SMAD4, putatively involved in PDAC etiology. Current knowledge of their molecular mechanisms is still limited. SMAD4 gene alterations in similar to 55 % of patients emphasize its key role in PDAC progression, metastasis, resistance and immunity. Despite extensive studies on the TGF-beta/SMAD pathway, the impact of SMAD4 mutation/deficiency on PDAC prognosis and treatment, especially its mechanism in drug resistance, has not yet been elucidated. This review summarizes the latest advances in the effect of SMAD4 deficiency on the prognosis and therapeutic resistance of PDAC patients. It might be a predictive and prognostic biomarker or therapeutic target to achieve the desired clinical benefits. Moreover, we discuss potential strategies to implement targeted therapies in terms of SMAD4 genetic status.
C1 [Yao, Hongjuan; Li, Rui; Zhao, Yelin; Zhang, Li; Li, Liang] Chinese Acad Med Sci & Peking Union Med Coll CAMS, Inst Med Biotechnol, State Key Lab Resp Hlth & Multimorbid, NHC Key Lab Biotechnol Microbial Drugs,Dept Oncol, 1 Tiantan Xili, Beijing 100050, Peoples R China.
   [Luo, Liaoxin; Cai, Lin] Wenzhou Med Univ, Sch Pharmaceut Sci, Wenzhou 325000, Peoples R China.
   [Pesic, Milica] Univ Belgrade, Dept Neurobiol, Natl Inst Republ Serbia, Inst Biol Res Sinisa Stankovic, Despota Stefana 142, Belgrade 11060, Serbia.
C3 Wenzhou Medical University; University of Belgrade
RP Li, L (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll CAMS, Inst Med Biotechnol, State Key Lab Resp Hlth & Multimorbid, NHC Key Lab Biotechnol Microbial Drugs,Dept Oncol, 1 Tiantan Xili, Beijing 100050, Peoples R China.; Cai, L (corresponding author), Wenzhou Med Univ, Sch Pharmaceut Sci, Wenzhou 325000, Peoples R China.
EM cailin@wmu.edu.cn; llsophia2011@foxmail.com
FU CAMS Innovation Fund for Medical Sciences [CIFMS 2021-1-I2M-026, CIFMS
   2023-I2M-2-001]; Innovation Team and Talents Cultivation Program of the
   National Administration of Traditional Chinese Medicine
   [ZYYCXTD-C-202205]; Belt and Road Innovative " Talents Exchange Foreign
   Experts Project [DL2022194002L]
FX This work was supported by the CAMS Innovation Fund for Medical Sciences
   (CIFMS 2021-1-I2M-026, CIFMS 2023-I2M-2-001) , the Innovation Team and
   Talents Cultivation Program of the National Administration of
   Traditional Chinese Medicine (ZYYCXTD-C-202205) and the " Belt and Road
   Innovative " Talents Exchange Foreign Experts Project (DL2022194002L) .
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NR 132
TC 1
Z9 1
U1 1
U2 1
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0304-419X
EI 1879-2561
J9 BBA-REV CANCER
JI Biochim. Biophys. Acta-Rev. Cancer
PD NOV
PY 2024
VL 1879
IS 6
AR 189220
DI 10.1016/j.bbcan.2024.189220
PG 12
WC Biochemistry & Molecular Biology; Biophysics; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Oncology
GA O1Q9I
UT WOS:001368968700001
PM 39571764
DA 2025-01-04
ER

PT J
AU Jaafar, RF
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   Faraj, W
AF Jaafar, Rola F.
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   Ataya, Karim
   Hassanieh, Joelle
   Ard, Natasha
   Faraj, Walid
TI Receptor-Interacting Serine/Threonine-Protein Kinase-2 as a Potential
   Prognostic Factor in Colorectal Cancer
SO MEDICINA-LITHUANIA
LA English
DT Article
DE colorectal cancer; inflammatory pathways; NFKB; RIPK2
ID KAPPA-B; INFLAMMATION; EXPRESSION; DISEASE; INNATE; RIPK2; GENE
AB Background and objectives: Receptor-interacting serine/threonine-protein kinase-2 (RIPK2) is an important mediator in different pathways in the immune and inflammatory response system. RIPK2 was also shown to play different roles in different cancer types; however, in colorectal cancer (CRC), its role is not well established. This study aims at identifying the role of RIPK2 in CRC progression and survival. Materials and methods: Data of patients and mRNA protein expression level of genes associated with CRC (RIPK2, tumor necrosis factor (TNF), TRAF1, TRAF7, KLF6, interlukin-6 (Il6), interlukin-8 (Il8), vascular-endothelial growth factor A (VEGFA), MKI67, TP53, nuclear factor-kappa B (NFKB), NFKB2, BCL2, XIAP, and RELA) were downloaded from the PrognoScan online public database. Patients were divided between low and high RIPK2 expression and different CRC characteristics were studied between the two groups. Survival curves were evaluated using a Kaplan-Meier estimator. The Pearson correlation was used to study the correlation between RIPK2 and the other factors. Statistical analysis was carried out using SPSS version 25.0. The Human Protein Atlas was also used for the relationship between RIPK2 expression in CRC tissues and survival. Differences were considered statistically significant at p < 0.05. Results: A total of 520 patients were downloaded from the PrognoScan database, and RIPK2 was found to correlate with MKI67, TRAF1, KLF6, TNF, Il6, Il8, VEGFA, NFKB2, BCL2, and RELA. High expression of RIPK2 was associated with high expression of VEGFA (p < 0.01) and increased mortality (p < 0.01). Conclusions: In this study, RIPK2 is shown to be a potential prognostic factor in CRC; however, more studies are needed to assess and verify its potential role as a prognostic marker and in targeted therapy.
C1 [Jaafar, Rola F.; Ibrahim, Zeid; Hassanieh, Joelle; Faraj, Walid] Amer Univ Beirut, Med Ctr, Dept Surg, Beirut 11072020, Lebanon.
   [Ataya, Karim; Faraj, Walid] Amer Univ Beirut, Med Ctr, Dept Gen Surg, Div Liver Transplantat Hepatobiliary & Pancreat S, Beirut 11072020, Lebanon.
   [Ard, Natasha] Amer Univ Beirut, Med Ctr, Fac Med, Dept Gen Med, Beirut 11072020, Lebanon.
C3 American University of Beirut; American University of Beirut; American
   University of Beirut
RP Faraj, W (corresponding author), Amer Univ Beirut, Med Ctr, Dept Surg, Beirut 11072020, Lebanon.; Faraj, W (corresponding author), Amer Univ Beirut, Med Ctr, Dept Gen Surg, Div Liver Transplantat Hepatobiliary & Pancreat S, Beirut 11072020, Lebanon.
EM rj29@aub.edu.lb; iz13@aub.edu.lb; ka71@aub.edu.lb; jh91@aub.edu.lb;
   noa09@aub.edu.lb; wf07@aub.edu.lb
RI Jaafar, Rola/AFB-0063-2022; Jaafar, Rola/X-9979-2018
OI Jaafar, Rola/0000-0001-9477-7678; Hassaniyeh, Joelle/0000-0002-0465-7355
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NR 37
TC 11
Z9 12
U1 1
U2 11
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 JUL
PY 2021
VL 57
IS 7
AR 709
DI 10.3390/medicina57070709
PG 9
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA TO2TZ
UT WOS:000676772200001
PM 34356990
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Mauri, G
   Valtorta, E
   Cerea, G
   Amatu, A
   Schirru, M
   Marrapese, G
   Fiorillo, V
   Recchimuzzo, P
   Cavenago, IS
   Bonazzina, EF
   Motta, V
   Lauricella, C
   Veronese, S
   Tosi, F
   Maiolani, M
   Rospo, G
   Truini, M
   Bonoldi, E
   Christiansen, J
   Potts, SJ
   Siena, S
   Sartore-Bianchi, A
AF Mauri, Gianluca
   Valtorta, Emanuele
   Cerea, Giulio
   Amatu, Alessio
   Schirru, Michele
   Marrapese, Giovanna
   Fiorillo, Vincenzo
   Recchimuzzo, Patrizia
   Cavenago, Ivana Stella
   Bonazzina, Erica Francesca
   Motta, Valentina
   Lauricella, Calogero
   Veronese, Silvio
   Tosi, Federica
   Maiolani, Martina
   Rospo, Giuseppe
   Truini, Mauro
   Bonoldi, Emanuela
   Christiansen, Jason
   Potts, Steven J.
   Siena, Salvatore
   Sartore-Bianchi, Andrea
TI TRKA expression and<i> NTRK1</i> gene copy number across solid tumours
SO JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article
ID IN-SITU HYBRIDIZATION; INHIBITOR ENTRECTINIB; PROTOONCOGENE PRODUCT;
   TARGETED THERAPY; RECEPTOR; IMMUNOHISTOCHEMISTRY; REARRANGEMENTS;
   RESISTANCE; MUTATIONS; CARCINOMA
AB Aims Neurotrophic Tropomyosin Kinase Receptor 1 (NTRK1) gene encodes for the protein Tropomyosin-related kinase A (TRKA). Deregulated activity of TRKA has been shown to have oncogenic potentiaL We present here the results of an immunohistochemical (IHC) observational cohort study of TRKA expression together with gene copy number (GCN) assessment in various solid tumours.
   Methods Formalin-fixed, paraffin-embedded consecutive samples of different tumour types were tested for TRKA expression. Samples showing TRKA IHC staining in at least 10% of cells were analysed by fluorescence in situ hybridisation to assess NTRK1 gene rearrangements and/or individual GCN gain. All patients underwent this molecular assessment within the phase I ALKA-001 clinical trial.
   Results 1043 samples were tested and annotation for histology was available in 1023. Most of the samples were colorectal adenocarcinoma (CRC) (n=550, 52.7%) and lung adenocarcinoma (n=312, 29.9%). 24 samples (2.3%) were biliary tract carcinoma (BTC). Overall, 17 (1.6%) samples were characterised by TRKA IHC expression (four weak, eight moderate, five strong): 9/17 lung adenocarcinoma, 3/17 CRC, 3/17 BTC, 1/17 thyroid cancer and 1/17 cancer of unknown primary. Of these, 1/17 with strong TRKA IHC staining displayed NTRK1 gene rearrangement and 15/17 NTRK1 GCN gain by FISH. No correlation was found between intensity of TRKA IHC staining and number of copies of NTRK1.
   Conclusions TRKA expression can be found in 1.6% of solid tumours and can be paralleled by NTRK1 gene rearrangements or mostly GCN gain. The prognostic and translational therapeutic impact of the latter remains to be established.
C1 [Mauri, Gianluca; Valtorta, Emanuele; Cerea, Giulio; Amatu, Alessio; Schirru, Michele; Marrapese, Giovanna; Fiorillo, Vincenzo; Recchimuzzo, Patrizia; Cavenago, Ivana Stella; Bonazzina, Erica Francesca; Motta, Valentina; Lauricella, Calogero; Veronese, Silvio; Tosi, Federica; Maiolani, Martina; Truini, Mauro; Bonoldi, Emanuela; Siena, Salvatore; Sartore-Bianchi, Andrea] Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, Milan, Italy.
   [Mauri, Gianluca; Tosi, Federica; Maiolani, Martina; Siena, Salvatore; Sartore-Bianchi, Andrea] Univ Milan, Dipartimento Ematol & Oncoematol, Milan, Italy.
   [Valtorta, Emanuele; Fiorillo, Vincenzo; Recchimuzzo, Patrizia; Cavenago, Ivana Stella; Motta, Valentina; Lauricella, Calogero; Veronese, Silvio; Truini, Mauro; Bonoldi, Emanuela] Grande Osped Metropolitano Niguarda, Div Pathol, Dept Lab Med, Milan, Italy.
   [Rospo, Giuseppe] IRCCS, Candiolo Canc Inst FPO, Turin, Italy.
   [Christiansen, Jason; Potts, Steven J.] Ignyta Inc, San Diego, CA USA.
C3 University of Milan; IRCCS Fondazione del Piemonte per l'Oncologia
RP Sartore-Bianchi, A (corresponding author), Univ Milan, Niguarda Canc Ctr, I-20162 Milan, Italy.
EM andrea.sartorebianchi@ospedaleniguarda.it
RI Rospo, Giuseppe/AAC-4523-2020; Sartore-Bianchi, Andrea/AAB-9848-2019;
   TOSI, FEDERICA MARIA/AIA-1174-2022; SIENA, SALVATORE/AAC-5806-2019
OI Rospo, Giuseppe/0000-0002-1757-9085; Mauri,
   Gianluca/0000-0002-7646-0973; Sartore-Bianchi,
   Andrea/0000-0003-0780-0409; VALTORTA, EMANUELE/0000-0002-5087-6233;
   SIENA, SALVATORE/0000-0002-2681-2846; TOSI, FEDERICA
   MARIA/0000-0001-6146-7411
FU grant 'Terapia Molecolare dei Tumori' by Fondazione Oncologia Niguarda;
   Associazione Italiana Ricerca Cancro grant AIRC 5 x mille Project
   [51000]; AIRC Investigator Grant Project [20685]; AIRC 5 x mille project
   [21091]; CORDIS Community Research and Development Information Service,
   grant MoTriColor, Horizon 2020 Project [635342]
FX The molecular screening for NTRK1 was performed within the phase I
   ALKA-001 clinical trial funded by Ignyta, Inc. The study was partly
   supported by the grant 'Terapia Molecolare dei Tumori' by Fondazione
   Oncologia Niguarda; Associazione Italiana Ricerca Cancro grant AIRC 5 x
   mille Project ID 51000 Special Program Molecular Clinical Oncology; AIRC
   Investigator Grant Project ID 20685; AIRC 5 x mille project ID Project
   21091; CORDIS Community Research and Development Information Service,
   grant MoTriColor, Horizon 2020 Project ID 635342.
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NR 41
TC 13
Z9 15
U1 0
U2 7
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0021-9746
EI 1472-4146
J9 J CLIN PATHOL
JI J. Clin. Pathol.
PD OCT
PY 2018
VL 71
IS 10
BP 926
EP 931
DI 10.1136/jclinpath-2018-205124
PG 6
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA GV4QG
UT WOS:000446084700018
PM 29802225
DA 2025-01-04
ER

PT J
AU Lian, J
   Wang, R
   Wang, X
   Pang, XY
   Xu, BJ
   Tang, SL
   Shao, JY
   Lu, HB
AF Lian, Jie
   Wang, Ren
   Wang, Xin
   Pang, Xiangyi
   Xu, Benjie
   Tang, Shuli
   Shao, Jiayue
   Lu, Haibo
TI Irinotecan plus raltitrexed as second-line chemotherapy for metastatic
   colorectal cancer: A retrospective study
SO ONCOLOGY LETTERS
LA English
DT Article
DE metastatic colorectal cancer; raltitrexed; irinotecan; chemotherapy;
   prognosis
ID PHASE-II TRIAL; 1ST-LINE CHEMOTHERAPY; THERAPY; BEVACIZUMAB; STANDARD;
   SURVIVAL; FOLFIRI; XELOX
AB The present study evaluated the efficiency, prognostic factors for and the safety of irinotecan combined with raltitrexed (TOMIRI) in patients with metastatic colorectal cancer (CRC). Outcome data of patients who received TOMIRI as first-, second- and third- or later-line treatment regimens were assessed to compare the efficacy of this regimen. Progression-free survival (PFS), overall survival (OS), objective response rate (ORR) and disease control rate (DCR) were evaluated for each group. Kaplan-Meier curves and univariate and multivariate analyses were performed to evaluate efficacy. From January 2017 to December 2019, TOMIRI was administered as a first-line treatment in 23 patients, second-line treatment in 164 patients and third- or later-line treatment in 18 patients. Irinotecan and 5-fluorouracil (FOLFIRI) was administered to another 50 patients, who served as the control group. The median PFS was 9, 7 and 6 months and the median OS was 37, 21 and 17 months for first-, second- and third- or later-line treatments, respectively. The ORRs of the included patients were 21.7, 13.4 and 11.1%, respectively, and the DCRs were 91.3, 81.7 and 66.7%, respectively. Compared with FOLFIRI, TOMIRI as a second-line chemotherapy treatment was associated with longer survival of the patients with CRC. Further analysis demonstrated that pathologic tumor-node-metastasis category, carcinoembryonic antigen, carbohydrate antigen 19-9, treatment cycles, targeted therapy, treatment of local metastases and first-line PFS were prognostic factors for second-line treatment. Among these, the number of treatment cycles was of vital importance. Hepatic dysfunction was the most commonly reported grade 1-2 (55.1%) and grade 3-4 (7.3%) adverse event. Neutropenia (12.2%), thrombocytopenia (10.2%), anemia (27.3%), proteinuria (38.1%) and hematuria (21.0%) were also common grade 1-2 adverse events. In conclusion, TOMIRI may be recommended as an effective and safe second-line treatment for metastatic CRC in the clinic.
C1 [Lian, Jie; Wang, Ren; Wang, Xin; Pang, Xiangyi; Xu, Benjie; Tang, Shuli; Shao, Jiayue; Lu, Haibo] Harbin Med Univ Canc Hosp, Dept Outpatient Chemotherapy, 150 Haping Rd, Harbin 150040, Heilongjiang, Peoples R China.
C3 Harbin Medical University
RP Lu, HB (corresponding author), Harbin Med Univ Canc Hosp, Dept Outpatient Chemotherapy, 150 Haping Rd, Harbin 150040, Heilongjiang, Peoples R China.
EM luhaibo@hrbmu.edu.cn
RI Shao, Jiayue/GZA-6552-2022
FU National Natural Science Foundation of China
FX Not applicable.
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NR 25
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 409
DI 10.3892/ol.2024.14542
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YL8K4
UT WOS:001268732700001
PM 38988448
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Hao, Y
   Baker, D
   ten Dijke, P
AF Hao, Yang
   Baker, David
   ten Dijke, Peter
TI TGF--Mediated Epithelial-Mesenchymal Transition and Cancer Metastasis
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE EMT; lncRNA; metastasis; miRNA; SMAD; TGF-; targeted therapy; tumor
   microenvironment
ID LONG NONCODING RNA; GROWTH-FACTOR-BETA; CELL LUNG-CANCER; COMPETING
   ENDOGENOUS RNA; BREAST-CANCER; REGULATORY NETWORK; TUMOR-SUPPRESSOR;
   PROSTATE-CANCER; DOWN-REGULATION; COLON-CANCER
AB Transforming growth factor (TGF-) is a secreted cytokine that regulates cell proliferation, migration, and the differentiation of a plethora of different cell types. Consistent with these findings, TGF- plays a key role in controlling embryogenic development, inflammation, and tissue repair, as well as in maintaining adult tissue homeostasis. TGF- elicits a broad range of context-dependent cellular responses, and consequently, alterations in TGF- signaling have been implicated in many diseases, including cancer. During the early stages of tumorigenesis, TGF- acts as a tumor suppressor by inducing cytostasis and the apoptosis of normal and premalignant cells. However, at later stages, when cancer cells have acquired oncogenic mutations and/or have lost tumor suppressor gene function, cells are resistant to TGF--induced growth arrest, and TGF- functions as a tumor promotor by stimulating tumor cells to undergo the so-called epithelial-mesenchymal transition (EMT). The latter leads to metastasis and chemotherapy resistance. TGF- further supports cancer growth and progression by activating tumor angiogenesis and cancer-associated fibroblasts and enabling the tumor to evade inhibitory immune responses. In this review, we will consider the role of TGF- signaling in cell cycle arrest, apoptosis, EMT and cancer cell metastasis. In particular, we will highlight recent insights into the multistep and dynamically controlled process of TGF--induced EMT and the functions of miRNAs and long noncoding RNAs in this process. Finally, we will discuss how these new mechanistic insights might be exploited to develop novel therapeutic interventions.
C1 [Hao, Yang; Baker, David; ten Dijke, Peter] Leiden Univ, Med Ctr, Dept Cell & Chem Biol, Einthovenweg 20, NL-2300 RC Leiden, Netherlands.
   [Hao, Yang; Baker, David; ten Dijke, Peter] Leiden Univ, Med Ctr, Oncode Inst, Einthovenweg 20, NL-2300 RC Leiden, Netherlands.
C3 Leiden University - Excl LUMC; Leiden University; Leiden University
   Medical Center (LUMC); Leiden University; Leiden University Medical
   Center (LUMC); Leiden University - Excl LUMC
RP ten Dijke, P (corresponding author), Leiden Univ, Med Ctr, Dept Cell & Chem Biol, Einthovenweg 20, NL-2300 RC Leiden, Netherlands.
EM Y.Hao@lumc.nl; D.A.Baker@lumc.nl; p.ten_dijke@lumc.nl
RI Hao, Yang/ABZ-0348-2022; ten Dijke, Peter/AAG-4660-2021
OI Hao, Yang/0000-0003-2708-530X; ten Dijke, Peter/0000-0002-7234-342X
FU Cancer Genomics Centre Netherlands (CGC.nl); CSC scholarship
FX Our studies on TGF-beta signaling in cancer are supported by Cancer
   Genomics Centre Netherlands (CGC.nl). YH is supported by CSC
   scholarship.
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NR 263
TC 763
Z9 828
U1 5
U2 127
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 JUN 1
PY 2019
VL 20
IS 11
AR 2767
DI 10.3390/ijms20112767
PG 34
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA IE8OX
UT WOS:000472634100161
PM 31195692
OA gold, Green Published, Green Submitted
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Shi, Y
   Shan, SF
   Li, CH
   Song, XJ
   Zhang, CX
   Chen, JY
   You, J
   Xiong, JY
AF Shi, Ying
   Shan, Shufang
   Li, Chenghui
   Song, Xuejiao
   Zhang, Chaoxiong
   Chen, Jiayi
   You, Jia
   Xiong, Jingyuan
TI Application of the Tumor Site Recognizable and Dual-Responsive
   Nanoparticles for Combinational Treatment of the Drug-Resistant
   Colorectal Cancer
SO PHARMACEUTICAL RESEARCH
LA English
DT Article
DE combination therapy; drug resistance; dual redox responsible;
   nanoparticles; tumor-homing peptide
ID PHOTODYNAMIC THERAPY; PHOTOCHEMICAL INTERNALIZATION; P-GLYCOPROTEIN;
   DELIVERY; RELEASE; PACLITAXEL; PRINCIPLES; NEUROPILIN; TARIQUIDAR;
   EFFICACY
AB PurposeCombination of PCI and chemotherapy represents a promising strategy for combating drug resistance of cancer. However, poor solubility of photosensitizers and unselectively released drugs at unwanted sites significantly impaired the treatment efficacy. Therefore, in the present study, we aimed to develop a nano-platform which could efficiently co-entrapping photosensitizers and chemotherapeutics for active targeting therapy of drug resistant cancers.MethodsTwo pro-drugs were respectively developed by covalently linking the Ce6 with each other via the GSH-sensitive linkage and the PTX with mPEG-PLA-COOH through the ROS sensitive-linker. The dual-responsive nanoparticles (PNP-Ce6) was developed by emulsion/solvent evaporation method and further modified with tLyp-1 peptides. Physicochemical properties of nanoparticles were determined by the TEM and DLC. Cellular uptake assay was investigated with the Ce6 acting as the fluorescent probe and cell growth was studied by the MTT experiment. In vivo tumor targeting and anti-tumor assay was investigated on the colorectal cancer-bearing mice.ResultsThe developed tPNP-Ce6 were stable enough under the normal physiological conditions. However, free Ce6 and PTX were completely released when exposed the tPNP-Ce6 to the redox environment. Excellent tumor-targeting drug delivery was achieved by the tPNP-Ce6, which in turn resulted in satisfactory anit-tumor effect. Of great importance, super inhibition effect on tumor progress was achieved by the combination therapy when compared with the group only received with chemotherapy..ConclusionThe results obtained in the present study indicated that the developed tPNP-Ce6 may have great potential in enhancing the therapeutic efficacy of drug-resistant colorectal cancer. Left: Targeting delivery of drug to tumor site by the tumor recognizable and dual-responsive nanoparticles and penetrating into tumor inner via the mediation of irradiation. Right: Nanoparticle distribution within tumor tissues with green represents the blood vessels stained with CD31, blue signal represents the cell nuclei stained with DAPI and red shows fluorescence of Ce6 as the indicator of the nanoparticles.
C1 [Shi, Ying; Shan, Shufang; Li, Chenghui; Song, Xuejiao; Zhang, Chaoxiong; Chen, Jiayi; You, Jia; Xiong, Jingyuan] Sichuan Univ, West China Sch Publ Hlth, Hlth Food Evaluat Res Ctr, 16 Renminnan Rd 3rd Sect, Chengdu 610041, Sichuan, Peoples R China.
   [Shi, Ying; Shan, Shufang; Li, Chenghui; Song, Xuejiao; Zhang, Chaoxiong; Chen, Jiayi; You, Jia; Xiong, Jingyuan] Sichuan Univ, West China Hosp 4, 16 Renminnan Rd 3rd Sect, Chengdu 610041, Sichuan, Peoples R China.
C3 Sichuan University; Sichuan University
RP You, J; Xiong, JY (corresponding author), Sichuan Univ, West China Sch Publ Hlth, Hlth Food Evaluat Res Ctr, 16 Renminnan Rd 3rd Sect, Chengdu 610041, Sichuan, Peoples R China.; You, J; Xiong, JY (corresponding author), Sichuan Univ, West China Hosp 4, 16 Renminnan Rd 3rd Sect, Chengdu 610041, Sichuan, Peoples R China.
EM jiayou_scu2014@163.com; jzx0004@tigermail.auburn.edu
RI Xiong, Jingyuan/JEO-7171-2023; Chen, Jiayi/GZM-5106-2022
OI Xiong, Jingyuan/0000-0001-9354-862X
FU Sichuan University Talent Introduction Start-up Fund; Public Health and
   Preventive Medicine Provincal Experiment Teaching Center at Sichuan
   University; Food Safety Monitoring and Risk Assessment Key Laboratory of
   Sichuan Province
FX This work was supported by Sichuan University Talent Introduction
   Start-up Fund (Jingyuan Xiong) and also the Public Health and Preventive
   Medicine Provincal Experiment Teaching Center at Sichuan University, as
   well as the Food Safety Monitoring and Risk Assessment Key Laboratory of
   Sichuan Province.
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U2 58
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0724-8741
EI 1573-904X
J9 PHARM RES-DORDR
JI Pharm. Res.
PD MAR 25
PY 2020
VL 37
IS 4
DI 10.1007/s11095-020-02791-2
PG 14
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA KX9PJ
UT WOS:000522207000002
PM 32215748
DA 2025-01-04
ER

PT J
AU Steinke-Lange, V
   de Putter, R
   Holinski-Feder, E
   Claes, KBM
AF Steinke-Lange, Verena
   de Putter, Robin
   Holinski-Feder, Elke
   Claes, Kathleen B. M.
TI Somatic mosaics in hereditary tumor predisposition syndromes
SO EUROPEAN JOURNAL OF MEDICAL GENETICS
LA English
DT Article
DE Tumor predisposition syndromes; Somatic mosaicism
ID FAMILIAL ADENOMATOUS POLYPOSIS; MISMATCH-REPAIR DEFICIENCY; LI-FRAUMENI
   SYNDROME; COLORECTAL-CANCER; NEUROFIBROMATOSIS TYPE-1; CLONAL
   HEMATOPOIESIS; GONOSOMAL MOSAICISM; FREQUENT CAUSE; LYNCH SYNDROME;
   DE-NOVO
AB Historically, it is estimated that 5-10% of cancer patients carry a causative genetic variant for a tumor predisposition syndrome. These conditions have high clinical relevance as they are actionable regarding risk-specific surveillance, predictive genetic testing, reproductive options, and - in some cases - risk reducing surgery or targeted therapy. Every individual is born with on average 0.5-1 exonic mosaic variants prevalent in single or multiple tissues. Depending on the tissues affected, mosaic conditions can abrogate the clinical phenotype of a tumor predisposition syndrome and can even go unrecognized, because it can be impossible or difficult to detect them with routine genetic testing in blood/leucocytes. On the other hand, it is estimated that at least 4% of presumed de novo variants are the result of low-level mosaicism (variant allele frequency <10%) in a parent, while around 7% are true mosaic variants with a higher variant allele frequency, which can sometimes be confused for heterozygous variants. Clonal hematopoiesis however can simulate a mosaic tumor predisposition in genetic diagnostics and has to be taken into account, especially for TP53 variants.
   Depending on the technique, variant allele frequencies of 2-3% can be detected for single nucleotide variants by next generation sequencing, copy number variants with variant allele frequencies of 5-30% can be detected by array-based technologies or MLPA.
   Mosaic tumor predisposition syndromes are more common than previously thought and may often remain undiagnosed. The clinical suspicion and diagnostic procedure for several cases with mosaic tumor predisposition syndromes are presented.
C1 [Steinke-Lange, Verena; Holinski-Feder, Elke] MGZ Med Genet Ctr, Bayerstr 3-5, D-80335 Munich, Germany.
   [Steinke-Lange, Verena; Holinski-Feder, Elke] Klinikum Univ Munchen, Arbeitsgrp Erbl Gastrointestinale Tumore, Med Klin & Poliklin 4, Campus Innenstadt, Munich, Germany.
   [de Putter, Robin; Claes, Kathleen B. M.] Ghent Univ Hosp, Ctr Med Genet, Ghent, Belgium.
   [Claes, Kathleen B. M.] Univ Ghent, CRIG Canc Res Inst Ghent, Ghent, Belgium.
   [Claes, Kathleen B. M.] Univ Ghent, Dept Biomol Med, Ghent, Belgium.
C3 University of Munich; Ghent University; Ghent University Hospital; Ghent
   University; Ghent University
RP Steinke-Lange, V (corresponding author), MGZ Med Genet Ctr, Bayerstr 3-5, D-80335 Munich, Germany.
EM verena.steinke-lange@mgz-muenchen.de
RI Claes, Kathleen/AFR-6830-2022
OI Steinke-Lange, Verena/0000-0001-8491-3234
FU European Reference Network on Genetic Tumour Risk Syndromes (ERN
   GENTURIS) [739547]; European Union
FX This research is supported (not financially) by the European Reference
   Network on Genetic Tumour Risk Syndromes (ERN GENTURIS) - Project ID No
   739547. ERN GENTURIS is partly co-funded by the European Union within
   the framework of the Third Health Programme "ERN-2016-Framework
   Partnership Agreement 2017-2021".
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NR 66
TC 7
Z9 8
U1 0
U2 3
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1769-7212
EI 1878-0849
J9 EUR J MED GENET
JI Eur. J. Med. Genet.
PD DEC
PY 2021
VL 64
IS 12
AR 104360
DI 10.1016/j.ejmg.2021.104360
EA OCT 2021
PG 9
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA WN5NT
UT WOS:000711814800010
PM 34655802
DA 2025-01-04
ER

PT J
AU Cho, J
AF Cho, Jeonghee
TI Mechanistic insights into differential requirement of receptor
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SO BMB REPORTS
LA English
DT Review
DE cetuximab; Dimerization; EGFR; erlotinib; Mig6
ID EPIDERMAL-GROWTH-FACTOR; CELL LUNG-CANCER; EXTRACELLULAR DOMAIN;
   CRYSTAL-STRUCTURE; CETUXIMAB RESISTANCE; ACQUIRED-RESISTANCE; NEGATIVE
   REGULATOR; ERBB RECEPTORS; KINASE DOMAIN; MUTATIONS
AB The epidermal growth factor receptor (EGFR), a member of the ErbB family (EGFR, ErbB2, ErbB3 and ErbB4), plays a crucial role in regulating various cellular responses such as proliferation, differentiation, and survival. As a result, aberrant activation of EGFR, mostly mediated through different classes of genomic alterations occurring within EGFR, is closely associated with the pathogenesis of numerous human cancers including lung adenocarcinoma, glioblastoma, and colorectal cancer. Thus, specific suppression of oncogenic activity of mutant EGFR with its targeted drugs has been routinely used in the clinic as a very effective anti-cancer strategy in treating a subset of tumors driven by such oncogenic EGFR mutants. However, the clinical efficacy of EGFR-targeted therapy does not last long due to several resistance mechanisms that emerge in the patients following the drug treatment. Thus, there is an urgent need for the development of novel therapeutic tactics specifically targeting mutant EGFR with the focus on the unique biological features of various mutant EGFR. Regarding this point, our review specifically emphasizes the recent findings about distinct requirements of receptor dimerization and autophosphorylation, which are critical steps for enzymatic activation of EGFR and signaling cascades, respectively, among wildtype and mutant EGFR and further discuss their clinical significance. In addition, the molecular mechanisms regulating EGFR dimerization and enzymatic activity by a key negative feedback inhibitor Mig6 as well as the clinical use for developing potential novel drugs targeting it are described in this review.
C1 [Cho, Jeonghee] Dankook Univ, Dept Nanobiomed Sci, Cheonan 31116, South Korea.
C3 Dankook University
RP Cho, J (corresponding author), Dankook Univ, Dept Nanobiomed Sci, Cheonan 31116, South Korea.
EM jeonghee.cho@dankook.ac.kr
OI Cho, Jeonghee/0000-0003-4422-6266
FU National Research Foundation of Korea (NRF) - Korea government (MEST)
   [NRF-2016R1A2B2011100, NRF-2019R1H1A 2079880, NRF-2019R1A4A1028268]
FX These works were in part supported by the National Research Foundation
   of Korea (NRF) grant funded by the Korea government (MEST)
   (NRF-2016R1A2B2011100, NRF-2019R1H1A 2079880 and NRF-2019R1A4A1028268).
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NR 72
TC 7
Z9 9
U1 0
U2 6
PU KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
PI SEOUL
PA KOREA SCIENCE & TECHNOLOGY CENTER, # 801,  635-4 , YEOKSAM-DONG,
   KANGNAM-KU, SEOUL, 135-703, SOUTH KOREA
SN 1976-6696
EI 1976-670X
J9 BMB REP
JI BMB Rep.
PD MAR 31
PY 2020
VL 53
IS 3
BP 133
EP 141
DI 10.5483/BMBRep.2020.53.3.025
PG 9
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA LL4AW
UT WOS:000531499200002
PM 32172728
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Chi, JL
   Li, HC
   Zhou, Z
   Izquierdo-Ferrer, J
   Xue, YF
   Wavelet, CM
   Schiltz, GE
   Zhang, B
   Cristofanilli, M
   Lu, XH
   Bahar, I
   Wan, Y
AF Chi, Junlong (Jack)
   Li, Hongchun
   Zhou, Zhuan
   Izquierdo-Ferrer, Javier
   Xue, Yifan
   Wavelet, Cindy M.
   Schiltz, Gary E.
   Zhang, Bin
   Cristofanilli, Massimo
   Lu, Xinghua
   Bahar, Ivet
   Wan, Yong
TI A novel strategy to block mitotic progression for targeted therapy
SO EBIOMEDICINE
LA English
DT Article
DE Cdc20 PROTAC; Cdc20-APC/C; Mitotic regulation; Ubiquitination and
   anticancer therapy
ID E3 UBIQUITIN LIGASE; ANAPHASE-PROMOTING COMPLEX; PROTEIN-DEGRADATION;
   COLORECTAL-CANCER; SMALL MOLECULES; BREAST-CANCER; CELL-DEATH; CDC20;
   OVEREXPRESSION; POLYMORPHISMS
AB Background: Blockade of mitotic progression is an ideal approach to induce mitotic catastrophe that suppresses cancer cell expansion. Cdc20 is a critical mitotic factor governing anaphase initiation and the exit from mitosis through recruiting substrates to APC/C for degradation. Results from recent TCGA (The Cancer Genome Atlas) and pathological studies have demonstrated a pivotal oncogenic role for Cdc20-APC/C in tumor progression as well as drug resistance. Thus, deprivation of the mitotic role for Cdc20-APC/C by either inhibition of Cdc20-APC/C activity or elimination of Cdc20 protein via induced protein degradation emerges as an effective therapeutic strategy to control cancer.
   Methods: We designed a proteolysis targeting chimera, called CP5V, which comprises a Cdc20 ligand and VHL binding moiety bridged by a PEG5 linker that induces Cdc20 degradation. We characterized the effect of CP5V in destroying Cdc20, arresting mitosis, and inhibiting tumor progression by measuring protein degradation, 3D structure dynamics, cell cycle control, tumor cell killing and tumor inhibition using human breast cancer xenograft mouse model. Findings:
   Results from our study demonstrate that CP5V can specifically degrade Cdc20 by linking Cdc20 to the VHL/VBC complex for ubiquitination followed by proteasomal degradation. Induced degradation of Cdc20 by CP5V leads to significant inhibition of breast cancer cell proliferation and resensitization of Taxol-resistant cell lines. Results based on a human breast cancer xenograft mouse model show a significant role for CP5V in suppressing breast tumor progression.
   Interpretation: CP5V-mediated degradation of Cdc20 could be an effective therapeutic strategy for antimitotic therapy. (c) 2019 The Author(s). Published by Elsevier B.V.
C1 [Chi, Junlong (Jack); Zhou, Zhuan; Wavelet, Cindy M.; Wan, Yong] Northwestern Univ, Dept Obstet & Gynecol, Feinberg Sch Med, Evanston, IL 60208 USA.
   [Schiltz, Gary E.; Wan, Yong] Northwestern Univ, Dept Pharmacol, Feinberg Sch Med, Evanston, IL 60208 USA.
   [Chi, Junlong (Jack); Zhou, Zhuan; Wavelet, Cindy M.; Schiltz, Gary E.; Wan, Yong] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Feinberg Sch Med, Evanston, IL 60208 USA.
   [Wan, Yong] Northwestern Univ, Chem Life Proc Inst, Evanston, IL 60208 USA.
   [Chi, Junlong (Jack)] Northwestern Univ, Dept Biomed Engn, Evanston, IL 60208 USA.
   [Li, Hongchun; Bahar, Ivet] Univ Pittsburgh, Dept Computat & Syst Biol, Sch Med, Pittsburgh, PA 15260 USA.
   [Izquierdo-Ferrer, Javier; Schiltz, Gary E.] Northwestern Univ, Ctr Mol Innovat & Drug Discovery, Evanston, IL 60208 USA.
   [Xue, Yifan; Lu, Xinghua] Univ Pittsburgh, Dept Biomed Informat, Sch Med, Pittsburgh, PA 15260 USA.
   [Zhang, Bin; Cristofanilli, Massimo] Northwestern Univ, Dept Med Hematol & Oncol, Robert H Lurie Comprehens Canc Ctr, Feinberg Sch Med, Evanston, IL 60208 USA.
   [Li, Hongchun] Chinese Acad Sci, Shenzhen Inst Adv Technol, Res Ctr Comp Aided Drug Discovery, Shenzhen 518055, Guangdong, Peoples R China.
C3 Northwestern University; Feinberg School of Medicine; Northwestern
   University; Feinberg School of Medicine; Northwestern University;
   Feinberg School of Medicine; Ann & Robert H. Lurie Children's Hospital
   of Chicago; Robert H. Lurie Comprehensive Cancer Center; Northwestern
   University; Northwestern University; Pennsylvania Commonwealth System of
   Higher Education (PCSHE); University of Pittsburgh; Northwestern
   University; Pennsylvania Commonwealth System of Higher Education
   (PCSHE); University of Pittsburgh; Robert H. Lurie Comprehensive Cancer
   Center; Ann & Robert H. Lurie Children's Hospital of Chicago;
   Northwestern University; Feinberg School of Medicine; Chinese Academy of
   Sciences; Shenzhen Institute of Advanced Technology, CAS
RP Wan, Y (corresponding author), Lurie Med Res Ctr, 303 East Super, Chicago, IL 60611 USA.
EM yong.wan@northwestern.edu
RI Li, Hongchun/AAN-9504-2020; Zheng, Zhou/JJD-0602-2023; CHI,
   Junlong/AAB-7840-2022; Bahar, Ivet/AAH-2921-2020
OI CHI, Junlong/0000-0002-2650-8756; Zhou, Zhuan/0000-0002-9683-5760; Li,
   Hongchun/0000-0002-3446-2962
FU Northwestern University Zell scholar fund; National Institutes of Health
   (NIH) [P41 GM103712, P30 CA060553]; Chicago Biomedical Consortium;
   Searle Funds at The Chicago Community Trust (ChemCore)
FX This work was supported by Northwestern University Zell scholar fund
   (YW), National Institutes of Health (NIH) grant #P41 GM103712 (IB), P30
   CA060553 (ChemCore) and Chicago Biomedical Consortium with support from
   The Searle Funds at The Chicago Community Trust (ChemCore).
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NR 54
TC 36
Z9 42
U1 1
U2 27
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2352-3964
J9 EBIOMEDICINE
JI EBioMedicine
PD NOV
PY 2019
VL 49
BP 40
EP 54
DI 10.1016/j.ebiom.2019.10.013
PG 15
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA JO1SC
UT WOS:000497363700017
PM 31669221
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU You, HL
   Liu, TT
   Weng, SW
   Chen, CH
   Wei, YC
   Eng, HL
   Huang, WT
AF You, Huey-Ling
   Liu, Ting-Ting
   Weng, Shao-Wen
   Chen, Chang-Han
   Wei, Yu-Ching
   Eng, Hock-Liew
   Huang, Wan-Ting
TI Association of IRS2 overexpression with disease progression in
   intrahepatic cholangiocarcinoma
SO ONCOLOGY LETTERS
LA English
DT Article
DE intrahepatic cholangiocarcinoma; IRS2; epithelial-mesenchymal
   transition; disease progression; disease-free survival
ID FACTOR-I RECEPTOR; MAMMARY-TUMOR METASTASIS; BREAST-CANCER;
   COLORECTAL-CANCER; PROSTATE-CANCER; INSULIN-RECEPTOR-SUBSTRATE-1 IRS-1;
   HEPATOCELLULAR-CARCINOMA; MESENCHYMAL TRANSITION; GROWTH-FACTORS; IGF-IR
AB Insulin receptor substrate 2 (IRS2) is a candidate driver oncogene frequently amplified in cancer and is positively associated with IRS2 expression. The overexpression of IRS2 has been suggested to promote tumor metastasis. However, its function in intrahepatic cholangiocarcinoma (iCCA) has not been investigated extensively. The present study examined 86 cases of iCCA to analyze IRS2 expression and its correlation with clinicopathological characteristics using immunohistochemical assays. Three stable cell lines overexpressing IRS2 were established. The mobility potential of cells was compared in the basal condition and following manipulation using cell migration and invasion assays. Epithelial-mesenchymal transition (EMT)-associated proteins were assessed by western blotting. IRS2 was overexpressed in 29 iCCA cases (33.7%) and was significantly more frequent in cases with large tumor size (P=0.033), classified as an advanced stage by the American Joint Committee on Cancer (P=0.046). In comparison with the control cells, the three IRS2-overexpressing iCCA cell lines exhibited a statistically significant increase in mobility potential. Expression analysis of EMT markers demonstrated decreased epithelial marker levels and increased mesenchymal marker levels in IRS2-overexpressing cells compared with their corresponding control cells. The results of the present study indicate that IRS2 overexpression is characterized by a large tumor size and advanced tumor stage in iCCA, and that it may increase tumor mobility potential by regulating EMT pathways. Therefore, it is a valuable predictive indicator of metastasis and may provide a novel direction for targeted therapy in iCCA.
C1 [You, Huey-Ling; Huang, Wan-Ting] Kaohsiung Chang Gung Mem Hosp, Dept Lab Med, 123 Ta Pei Rd, Kaohsiung 83301, Taiwan.
   [You, Huey-Ling; Huang, Wan-Ting] Chang Gung Univ, Coll Med, 123 Ta Pei Rd, Kaohsiung 83301, Taiwan.
   [You, Huey-Ling; Huang, Wan-Ting] Fooyin Univ, Dept Med Lab Sci & Biotechnol, Kaohsiung 83102, Taiwan.
   [Liu, Ting-Ting; Eng, Hock-Liew; Huang, Wan-Ting] Kaohsiung Chang Gung Mem Hosp, Dept Pathol, Kaohsiung 83301, Taiwan.
   [Weng, Shao-Wen] Kaohsiung Chang Gung Mem Hosp, Dept Internal Med, Kaohsiung 83301, Taiwan.
   [Chen, Chang-Han] Kaohsiung Chang Gung Mem Hosp, Inst Translat Res Biomed, Kaohsiung 83301, Taiwan.
   [Wei, Yu-Ching] Kaohsiung Med Univ Hosp, Dept Pathol, Kaohsiung Municipal Ta Tung Hosp, Kaohsiung 80708, Taiwan.
C3 Chang Gung Memorial Hospital; Chang Gung University; Fooyin University;
   Chang Gung Memorial Hospital; Chang Gung Memorial Hospital; Chang Gung
   Memorial Hospital; Kaohsiung Medical University; Kaohsiung Municipal
   Ta-Tung Hospital; Kaohsiung Medical University Hospital
RP Huang, WT (corresponding author), Kaohsiung Chang Gung Mem Hosp, Dept Lab Med, 123 Ta Pei Rd, Kaohsiung 83301, Taiwan.; Huang, WT (corresponding author), Chang Gung Univ, Coll Med, 123 Ta Pei Rd, Kaohsiung 83301, 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 Ministry of Science and Technology, Taiwan [MOST 104-2320-B-182A-010,
   MOST 105-2320-B-182A-016]; Chang Gung Memorial Hospital [CMRPG8C0591-2,
   CMRPG8E1471-2, CMRPG8B1251-3, CMRPG8D1321, CMRPG8E0921]
FX The study was supported by the Ministry of Science and Technology,
   Taiwan (grant nos. MOST 104-2320-B-182A-010 and MOST
   105-2320-B-182A-016) and Chang Gung Memorial Hospital (grant nos.
   CMRPG8C0591-2, CMRPG8E1471-2, CMRPG8B1251-3, CMRPG8D1321 and
   CMRPG8E0921). The funders had no role in the manuscript design, data
   collection and analysis, decision to publish, or preparation of the
   manuscript.
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NR 35
TC 7
Z9 7
U1 0
U2 2
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 OCT
PY 2018
VL 16
IS 4
BP 5505
EP 5511
DI 10.3892/ol.2018.9284
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GU1BU
UT WOS:000444990700182
PM 30250623
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Klinghammer, K
   Otto, R
   Raguse, JD
   Albers, AE
   Tinhofer, I
   Fichtner, I
   Leser, U
   Keilholz, U
   Hoffmann, J
AF Klinghammer, Konrad
   Otto, Raik
   Raguse, Jan-Dirk
   Albers, Andreas E.
   Tinhofer, Ingeborg
   Fichtner, Iduna
   Leser, Ulf
   Keilholz, Ulrich
   Hoffmann, Jens
TI Basal subtype is predictive for response to cetuximab treatment in
   patient- derived xenografts of squamous cell head and neck cancer
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE head and neck cancer; patient-derived xenograft; molecular subtype;
   cetuximab; EGFR
ID GENE-EXPRESSION; GENOMIC CHARACTERIZATION; MUTATIONAL LANDSCAPE;
   COLORECTAL-CANCER; CARCINOMA; HPV; METAANALYSIS; INHIBITOR; RECURRENT;
   TRIAL
AB Cetuximab is the single targeted therapy approved for the treatment of head and neck cancer (HNSCC). Predictive biomarkers have not been established and patient stratification based on molecular tumor profiles has not been possible. Since EGFR pathway activation is pronounced in basal subtype, we hypothesized this activation could be a predictive signature for an EGFR directed treatment. From our patient-derived xenograft platform of HNSCC, 28 models were subjected to Affymetrix gene expression studies on HG U133 + 2.0. Based on the expression of 821 genes, the subtype of each of the 28 models was determined by integrating gene expression profiles through centroid-clustering with previously published gene expression data by Keck et al. The models were treated in groups of 5-6 animals with docetaxel, cetuximab, everolimus, cis-or carboplatin and 5-fluorouracil. Response was evaluated by comparing tumor volume at treatment initiation and after 3 weeks of treatment (RTV). Tumors distributed over the 3 signature-defined subtypes: 5 mesenchymal/inflamed phenotype (MS), 15 basal type (BA), 8 classical type (CL). Cluster analysis revealed a strong correlation between response to cetuximab and the basal subtype. RTV MS 3.32 vs. BA 0.78 (MS vs. BA, unpaired t-test, p 0.0002). Cetuximab responders were distributed as following: 1/5 in MS, 5/8 in CL and 13/15 in the BA group. Activity of classical chemotherapies did not differ between the subtypes. In conclusion basal subtype was associated with response to EGFR directed therapy in head and neck squamous cell cancer patient-derived xenografts.
C1 [Klinghammer, Konrad] Charite, Dept Hematol & Oncol, Hindenburgdamm 30, D-12200 Berlin, Germany.
   [Otto, Raik; Leser, Ulf] Humboldt Univ, WBI, Berlin, Germany.
   [Raguse, Jan-Dirk] Charite, Dept Maxilliofacial Surg, Berlin, Germany.
   [Albers, Andreas E.] Charite, Dept ENT, Berlin, Germany.
   [Tinhofer, Ingeborg] Charite, Dept Radiooncol & Radiotherapy, Berlin, Germany.
   [Fichtner, Iduna; Hoffmann, Jens] Expt Pharmacol & Oncol GmbH, Berlin, Germany.
   [Keilholz, Ulrich] Charite, Ctr Comprehens Canc, Berlin, Germany.
C3 Berlin Institute of Health; Free University of Berlin; Humboldt
   University of Berlin; Charite Universitatsmedizin Berlin; Humboldt
   University of 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; Berlin Institute of Health;
   Free University of Berlin; Humboldt University of Berlin; Charite
   Universitatsmedizin Berlin
RP Klinghammer, K (corresponding author), Charite, Dept Hematol & Oncol, Hindenburgdamm 30, D-12200 Berlin, Germany.
EM konrad.klinghammer@charite.de
RI Klinghammer, Konrad/CAE-9956-2022; Albers, Andreas/AAP-4669-2021
OI Tinhofer-Keilholz, Ingeborg/0000-0002-0512-549X; Hoffmann,
   Jens/0000-0003-3880-1658; Klinghammer, Konrad/0000-0001-6425-4833;
   Albers, Andreas E./0000-0001-5614-9873
FU Wilhelm-Sander Stiftung; Charite - Universitatsmedizin Berlin; Berlin
   Institute of Health
FX Grant sponsors: The Wilhelm-Sander Stiftung; The Charite -
   Universitatsmedizin Berlin and the Berlin Institute of Health
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NR 29
TC 24
Z9 24
U1 0
U2 2
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 SEP 15
PY 2017
VL 141
IS 6
BP 1215
EP 1221
DI 10.1002/ijc.30808
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FB1WK
UT WOS:000405934300013
PM 28560858
OA Bronze
DA 2025-01-04
ER

PT J
AU Xie, YL
   Chen, HM
   Fang, JY
AF Xie, Yile
   Chen, Huimin
   Fang, Jing-Yuan
TI Amino acid metabolism-based molecular classification of colon
   adenocarcinoma<i>via in silico</i> analysis
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE amino acid metabolism; colon adenocarcinoma; classification; prognosis;
   immune signature; therapy
ID R/BIOCONDUCTOR PACKAGE; COLORECTAL-CANCER; PATHWAY; GENOMICS; MUTATION;
   SERINE; CELLS; BRAF
AB Amino acid metabolism is closely related to the occurrence and development of colon adenocarcinoma (COAD). Studies on the relationship between COAD and the expression of amino acid metabolism are still rare. Based on in silico analysis, we used 358 amino acid metabolism-related genes (AAMRGs) to determine the amino acid metabolism characteristics and then classified COAD into two distinct subtypes, namely AA1 and AA2. Then we analyzed the clinical characteristics, somatic mutation landscape, transcriptome profile, metabolism signatures, immune infiltration, and therapy sensitivity of these two subtypes. The AA1 subtype had inferior overall survival and was characterized by lower amino acid metabolic activity, higher tumor mutation burden, and higher immune cell infiltration, while AA2 displayed higher metabolic activity and relatively better survival. Furthermore, the AA1 subtype was likely to benefit from irinotecan in chemotherapy and immune checkpoint blockade therapy including programmed cell death protein-1 (PD-1) and cytotoxic T-lymphocyte-associated protein-4 (CTLA-4) immune checkpoint inhibitor but was resistant to targeted therapy cetuximab. The AA2 subtype showed higher sensitivity to 5-fluorouracil and oxaliplatin. To provide perspectives on cell-specific metabolism for further investigation, we explored metabolic activity in different cell types including lymphocytes, mast cells, myeloid cells stromal cells, and epithelial cells via colorectal cancer single-cell data. Additionally, to assist in clinical decision-making and prognosis prediction, a 60-AAMRG-based classifier was generated and validated in an independent cohort.
C1 [Xie, Yile; Chen, Huimin; Fang, Jing-Yuan] Shanghai Jiao Tong Univ, Renji Hosp, Shanghai Inst Digest Dis, Sch Med,State Key Lab Oncogen & Related Genes,Key, Shanghai, Peoples R China.
C3 Shanghai Jiao Tong University
RP Chen, HM; Fang, JY (corresponding author), Shanghai Jiao Tong Univ, Renji Hosp, Shanghai Inst Digest Dis, Sch Med,State Key Lab Oncogen & Related Genes,Key, Shanghai, Peoples R China.
EM huimin.chan@foxmail.com
RI FANG, Jing-Yuan/JOZ-1388-2023
OI Xie, Yile/0000-0001-6810-9465
FU National Key R&D Program of China; National Natural Science Foundation
   of China;  [2020YFA0509200];  [81830081];  [31970718];  [81972203]
FX Funding This project was supported in part by grants from the National
   Key R&D Program of China (2020YFA0509200), and the National Natural
   Science Foundation of China (81830081, 31970718, 81972203).
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NR 69
TC 3
Z9 3
U1 0
U2 7
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 20
PY 2022
VL 13
AR 1018334
DI 10.3389/fimmu.2022.1018334
PG 13
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 5Y1DP
UT WOS:000879030800001
PM 36341436
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Corcoran, RB
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AF Corcoran, Ryan B.
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   Jaeger, Savina
   Bettinger, Severine
   Mookerjee, Bijoyesh
   Rangwala, Fatima
   Van Cutsem, Eric
TI Combined BRAF, EGFR, and MEK Inhibition in Patients with
   &ITBRAF&IT<SUP>V600E</SUP>-Mutant Colorectal Cancer
SO CANCER DISCOVERY
LA English
DT Article
ID ACQUIRED-RESISTANCE; MICROSATELLITE INSTABILITY; RAF INHIBITORS;
   TARGETED THERAPY; POOLED ANALYSIS; MAPK PATHWAY; COLON-CANCER;
   OPEN-LABEL; DABRAFENIB; MUTATIONS
AB Although BRAF inhibitor monotherapy yields response rates > 50% in BRAF(V600)-mutant melanoma, only approximately 5% of patients with BRAF(V600E) colorectal cancer respond. Preclinical studies suggest that the lack of efficacy in BRAF(V600E) colorectal cancer is due to adaptive feedback reactivation of MAPK signaling, often mediated by EGFR. This clinical trial evaluated BRAF and EGFR inhibition with dabrafenib (D) + panitumumab (P) +/- MEK inhibition with trametinib (T) to achieve greater MAPK suppression and improved efficacy in 142 patients with BRAF(V600E) colorectal cancer. Confirmed response rates for D+P, D+T+P, and T+P were 10%, 21%, and 0%, respectively. Pharmacodynamic analysis of paired pretreatment and on-treatment biopsies found that efficacy of D+T+P correlated with increased MAPK suppression. Serial cell-free DNA analysis revealed additional correlates of response and emergence of KRAS and NRAS mutations on disease progression. Thus, targeting adaptive feedback pathways in BRAF(V600E) colorectal cancer can improve efficacy, but MAPK reactivation remains an important primary and acquired resistance mechanism.
   SIGNIFICANCE: This trial demonstrates that combined BRAF + EGFR +MEK inhibition is tolerable, with promising activity in patients with BRAF(V600E) colorectal cancer. Our findings highlight the MAPK pathway as a critical target in BRAF(V600E) colorectal cancer and the need to optimize strategies inhibiting this pathway to overcome both primary and acquired resistance. (C) 2018 AACR.
C1 [Corcoran, Ryan B.] Harvard Med Sch, Massachusetts Gen Hosp, Canc Ctr, Boston, MA 02129 USA.
   [Corcoran, Ryan B.] Harvard Med Sch, Dept Med, Boston, MA 02129 USA.
   [Andre, Thierry] Hop St Antoine, Paris, France.
   [Andre, Thierry] Sorbonne Univ, Paris, France.
   [Atreya, Chloe E.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
   [Schellens, Jan H. M.] Netherlands Canc Inst, Amsterdam, Netherlands.
   [Yoshino, Takayuki] Natl Canc Ctr Hosp East, Chiba, Japan.
   [Bendell, Johanna C.] Sarah Cannon Res Inst Tennessee Oncol, Nashville, TN USA.
   [Hollebecque, Antoine] Inst Gustave Roussy, Villejuif, France.
   [McRee, Autumn J.] Univ N Carolina, Chapel Hill, NC USA.
   [Siena, Salvatore] Univ Milan, Grande Osoped Metropolitano Niguarda, Niguarda Canc Ctr, Milan, Italy.
   [Siena, Salvatore] Univ Milan, Dept Oncol & Hematooncoll, Milan, Italy.
   [Middleton, Gary] Univ Birmingham, Birmingham, W Midlands, England.
   [Middleton, Gary] Univ Hosp, Birmingham, W Midlands, England.
   [Muro, Kei] Aichi Canc Ctr Hosp, Nagoya, Aichi, Japan.
   [Gordon, Michael S.] Pinnacle Oncol Hematol, Scottsdale, AZ USA.
   [Tabernero, Josep] Vall dHebron Univ Hosp, Barcelona, Spain.
   [Yaeger, Rona] Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10021 USA.
   [O'Dwyer, Peter J.] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
   [Humblet, Yves] St Luc Univ Hosp, Brussels, Belgium.
   [De Vos, Filip] Univ Med Ctr Utrecht, Dept Med Oncol, Utrecht, Netherlands.
   [Jung, A. Scott] Amgen Inc, Thousand Oaks, CA USA.
   [Brase, Jan C.; Bettinger, Severine] Novartis Pharma AG, Basel, Switzerland.
   [Jaeger, Savina] Novartis Inst Biomed Res, Cambridge, MA USA.
   [Mookerjee, Bijoyesh; Rangwala, Fatima] Novartis Pharmaceut, E Hanover, NJ USA.
   [Van Cutsem, Eric] Univ Hosp Leuven, Leuven, Belgium.
   [Van Cutsem, Eric] Katholieke Univ Leuven, Leuven, Belgium.
C3 Harvard University; Massachusetts General Hospital; Harvard Medical
   School; Harvard University; Harvard Medical School; Assistance Publique
   Hopitaux Paris (APHP); Sorbonne Universite; Hopital Universitaire
   Saint-Antoine - APHP; Sorbonne Universite; University of California
   System; University of California San Francisco; Netherlands Cancer
   Institute; National Cancer Center - Japan; Sarah Cannon Research
   Institute; Tennessee Oncology; UNICANCER; Gustave Roussy; University of
   North Carolina; University of North Carolina Chapel Hill; University of
   Milan; University of Milan; University of Birmingham; University of
   Birmingham; Aichi Cancer Center; Hospital Universitari Vall d'Hebron;
   Memorial Sloan Kettering Cancer Center; University of Pennsylvania;
   Universite Catholique Louvain; Cliniques Universitaires Saint-Luc;
   Utrecht University; Utrecht University Medical Center; Amgen; Novartis;
   Novartis; Novartis USA; Novartis; Novartis USA; KU Leuven; University
   Hospital Leuven; KU Leuven
RP Corcoran, RB (corresponding author), Harvard Med Sch, 149 13th St,7th Floor, Boston, MA 02129 USA.
EM rbcorcoran@partners.org
RI Schellens, Jan/O-8444-2016; Tabernero, Josep/AAG-5026-2019; André,
   Thierry/N-8830-2017; SIENA, SALVATORE/AAC-5806-2019; Van+Cutsem,
   Eric/ABE-1762-2021; Hollebecque, Antoine/M-2695-2013
OI De Vos, Filip/0000-0002-9082-5991; Brase, Jan
   Christoph/0000-0002-1325-2528; Andre, Thierry/0000-0002-5103-7095;
   SIENA, SALVATORE/0000-0002-2681-2846; Tabernero,
   Josep/0000-0002-2495-8139; Middleton, Gary/0000-0001-5695-3474;
   Hollebecque, Antoine/0000-0003-2869-7551
FU GlaxoSmithKline; Damon Runyon Clinical Investigator Award; NIH/NCI [P50
   CA127003, R01CA208437]; Stand Up To Cancer (SU2C) Colorectal Cancer
   Dream Team Translational Research Grant [SU2C-AACR-DT22-17]; Novartis
   Pharmaceuticals Corporation
FX This study was supported by GlaxoSmithKline. As of March 2, 2015,
   dabrafenib and trametinib are assets of Novartis AG. R.B. Corcoran
   acknowledges support from a Damon Runyon Clinical Investigator Award and
   NIH/NCI P50 CA127003 and R01CA208437. This research was supported by a
   Stand Up To Cancer (SU2C) Colorectal Cancer Dream Team Translational
   Research Grant (Grant Number: SU2C-AACR-DT22-17). Stand Up To Cancer
   (SU2C) is a program of the Entertainment Industry Foundation. Research
   grants are administered by the American Association for Cancer Research,
   the scientific partner of SU2C. The authors acknowledge Yiquin Yan for
   biomarker statistical analyses, Kohinoor Dasgupta for clinical
   statistical analyses, and Ilona Tala for biomarker sample collection.
   Medical writing assistance was provided by William Fazzone, PhD
   (ArticulateScience LLC), funded by Novartis Pharmaceuticals Corporation.
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NR 49
TC 423
Z9 448
U1 5
U2 54
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 APR
PY 2018
VL 8
IS 4
BP 428
EP 443
DI 10.1158/2159-8290.CD-17-1226
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GB4PL
UT WOS:000429042800024
PM 29431699
OA Green Accepted, Green Submitted, Green Published, Bronze
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Tabernero, J
   Velez, L
   Trevino, TL
   Grothey, A
   Yaeger, R
   Van Cutsem, E
   Wasan, H
   Desai, J
   Ciardiello, F
   Yoshino, T
   Gollerkeri, A
   Maharry, K
   Christy-Bittel, J
   Kopetz, S
AF Tabernero, J.
   Velez, L.
   Trevino, T. L.
   Grothey, A.
   Yaeger, R.
   Van Cutsem, E.
   Wasan, H.
   Desai, J.
   Ciardiello, F.
   Yoshino, T.
   Gollerkeri, A.
   Maharry, K.
   Christy-Bittel, J.
   Kopetz, S.
TI Management of adverse events from the treatment of encorafenib plus
   cetuximab for patients with <i>BRAF</i> V600E-mutant metastatic
   colorectal cancer: insights from the BEACON CRC study
SO ESMO OPEN
LA English
DT Review
DE encorafenib; cetuximab; CRC; metastatic colorectal cancer; adverse
   events
ID MUTATIONS; INHIBITORS; GENE
AB Colorectal cancer is the second leading cause of cancer deaths worldwide, with a 5-year relative survival of 14% in patients with metastatic colorectal cancer (mCRC). Patients with BRAF V600E mutations, which occur in similar to 10%-15% of patients with mCRC, have a poorer prognosis compared with those with wild-type BRAF tumours. The combination of the BRAF inhibitor encorafenib with the epidermal growth factor receptor inhibitor cetuximab currently represents the only chemotherapy-free targeted therapy approved in the USA and Europe for previously treated patients with BRAF V600E-mutated mCRC. As a class, BRAF inhibitors are associated with dermatologic, gastrointestinal, and renal events, as well as pyrexia and secondary skin malignancies. Adverse event (AE) profiles of specific BRAF inhibitors vary, however, and are affected by the specific agents given in combination. In patients with mCRC, commonly reported AEs of cetuximab monotherapy include infusion reactions and dermatologic toxicities. Data from the phase III BEACON CRC study indicate that the combination of encorafenib with cetuximab has a distinct safety profile. Here we review the most frequently reported AEs that occurred with this combination in BEACON CRC and best practices for managing and mitigating AEs that require more than standard supportive care.
C1 [Tabernero, J.; Velez, L.] Med Oncol Dept, Vall dHebron Hosp Campus, Barcelona, Spain.
   [Tabernero, J.; Velez, L.] Vall dHebron Inst Oncol VHIO, UVIC UCC, IOB Quiron, Barcelona, Spain.
   [Trevino, T. L.; Kopetz, S.] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
   [Grothey, A.] OneOncology, West Canc Ctr & Res Inst, Germantown, TN USA.
   [Yaeger, R.] Mem Sloan Kettering Canc Ctr, Dept Med, 1275 York Ave, New York, NY 10021 USA.
   [Van Cutsem, E.] Univ Hosp Gasthuisberg Leuven, Digest Oncol Dept, Leuven, Belgium.
   [Van Cutsem, E.] Katholieke Univ Leuven, Leuven, Belgium.
   [Wasan, H.] Hammersmith Hosp, Dept Canc Med, London, England.
   [Desai, J.] Royal Melbourne Hosp, Dept Med Oncol, Parkville, Vic, Australia.
   [Desai, J.] Peter MacCallum Canc Ctr, Walter & Aliza Hall Inst, Parkville, Vic, Australia.
   [Ciardiello, F.] Univ Campania, Dept Precis Med, Naples, Italy.
   [Yoshino, T.] Natl Canc Ctr Hosp East, Dept Gastroenterol & Gastrointestinal Oncol, Kashiwa, Chiba, Japan.
   [Gollerkeri, A.; Maharry, K.; Christy-Bittel, J.] Pfizer Inc, New York, NY USA.
C3 Vall d'Hebron Institut d'Oncologia (VHIO); Universitat de Vic -
   Universitat Central de Catalunya (UVic-UCC); University of Texas System;
   UTMD Anderson Cancer Center; Memorial Sloan Kettering Cancer Center; KU
   Leuven; University Hospital Leuven; KU Leuven; Imperial College London;
   Melbourne Health; Royal Melbourne Hospital; Peter Maccallum Cancer
   Center; Universita della Campania Vanvitelli; National Cancer Center -
   Japan; Pfizer
RP Tabernero, J (corresponding author), Vall dHebron Univ Hosp HUVH, Med Oncol Dept, Vall dHebron Inst Oncol VHIO, P Vall dHebron 119-129, Barcelona 08035, Spain.
EM jtabernero@vhio.net
RI Desai, Jayesh/AAV-1237-2021; Van+Cutsem, Eric/ABE-1762-2021
OI Wasan, Harpreet/0000-0002-6268-2030; Desai, Jayesh/0000-0003-4246-9344;
   Yoshino, Takayuki/0000-0002-0489-4756; Grothey,
   Axel/0000-0002-9341-6499; Van Cutsem, Eric/0000-0002-6372-1230
FU Array BioPharma; ONO Pharmaceutical, Japan; Pierre Fabre, France; Cancer
   Center Core [P30 CA 008748]; Pfizer
FX This work was supported by Array BioPharma in collaboration with Merck
   KGaA Darmstadt, Germany (for sites outside of North America), ONO
   Pharmaceutical, Japan, and Pierre Fabre, France. Array BioPharma was
   acquired by Pfizer in July 2019. This work was also supported by the
   Cancer Center Core [grant number P30 CA 008748] to MSKCC. Medical
   writing/editorial support was provided by Namiko Abe, PhD, and Alyson
   Bexfield, PhD, of Caudex, New York, and was funded by Pfizer.
CR André F, 2017, CANCER DISCOV, V7, P818, DOI 10.1158/2159-8290.CD-17-0151
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NR 33
TC 15
Z9 15
U1 1
U2 3
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2059-7029
J9 ESMO OPEN
JI ESMO Open
PD DEC
PY 2021
VL 6
IS 6
DI 10.1016/j.esmoop.2021.100328
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 2P7MV
UT WOS:000819921100002
PM 34896698
OA Green Published
DA 2025-01-04
ER

PT J
AU Baker, K
   O'Donnell, C
   Bendix, M
   Keogh, S
   Byrne, J
   O'Riordain, M
   Neary, P
   Houston, A
   Brint, E
AF Baker, Kevin
   O'Donnell, Charlotte
   Bendix, Maura
   Keogh, Samuel
   Byrne, James
   O'Riordain, Michael
   Neary, Peter
   Houston, Aileen
   Brint, Elizabeth
TI IL-36 signalling enhances a pro-tumorigenic phenotype in colon cancer
   cells with cancer cell growth restricted by administration of the IL-36R
   antagonist
SO ONCOGENE
LA English
DT Article
ID ULCERATIVE-COLITIS; EXPRESSION; INTERLEUKIN-36; RECEPTOR; FAMILY; ROLES
AB The IL-36 cytokines are a recently described subset of the IL-1 family of cytokines, shown to play a role in the pathogenesis of intestinal diseases such as Inflammatory Bowel Disease (IBD). Given the link between IBD and colitis -associated cancer, as well as the involvement of other IL-1 family members in intestinal tumorigenesis, the aim of this work was to investigate whether IL-36 cytokines play a role in the pathogenesis of colon cancer. Whilst research to date has focused on the role of IL-36 family members in augmenting the immune response to induce tumour rejection, very little remains known about IL-36R signalling in tumour cells in this context. In this study we demonstrate that expression of IL-36 family member mRNA and protein are significantly increased in colorectal cancer tissue compared to adjacent non-tumour. In vitro assays showed stimulation of colon cancer cell lines with IL-36R agonists resulted in the activation of the pro-tumorigenic phenotypes of increased cellular migration, invasion and proliferation in both 2D and 3D models. In addition, the IL-36 cytokines induced strong expression of pro-inflammatory chemokines in both human and murine cell lines. Intraperitoneal injection of IL-36Ra significantly reduced tumour burden using the subcutaneous CT26 tumour model in syngeneic Balb/mice, and this was associated with a decrease in Ki-67 expression by tumour cells in the IL-36Ra- treated group relative to untreated, suggesting the inhibition of the pro-proliferative signalling of IL-36 agonists resulted in the decreased tumour size. Moreover, colon cancer cells lacking the IL-36R also showed reduced tumour growth and reduced Ki-67 expression in vivo. Taken together, this data suggests that targeting IL-36R signalling may be a useful targeted therapy for colorectal cancer patients with IL-36R(+) tumour cells.
C1 [Baker, Kevin; Bendix, Maura; Keogh, Samuel; Byrne, James; Brint, Elizabeth] Univ Coll Cork, Dept Pathol, Cork, Ireland.
   [Baker, Kevin; Houston, Aileen; Brint, Elizabeth] Univ Coll Cork, APC Microbiome Ireland, Cork, Ireland.
   [O'Donnell, Charlotte; Houston, Aileen] Univ Coll Cork, Dept Med, Cork, Ireland.
   [Bendix, Maura] Univ Coll Cork, Canc Res UCC, Cork, Ireland.
   [O'Riordain, Michael] Mercy Univ Hosp, Cork, Ireland.
   [Neary, Peter] Waterford Univ Hosp, Waterford, Ireland.
C3 University College Cork; University College Cork; University College
   Cork; University College Cork; University College Cork
RP Brint, E (corresponding author), Univ Coll Cork, Dept Pathol, Cork, Ireland.; Brint, E (corresponding author), Univ Coll Cork, APC Microbiome Ireland, Cork, Ireland.
EM e.brint@ucc.ie
RI Houston, Aileen/ABF-2473-2020
OI Brint, Elizabeth/0000-0001-9214-149X; Bendix, Maura/0000-0001-8883-2677;
   Houston, Aileen/0000-0003-1362-5256
FU Government of Ireland [GOIPG/2018/2974]; IReL Consortium
FX This work was funded by a grant from the Government of Ireland
   postgraduate scholarship scheme GOIPG/2018/2974. Open Access funding
   provided by the IReL Consortium.
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   Yang W, ADV SCI, V2022
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NR 41
TC 10
Z9 10
U1 2
U2 9
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD MAY 6
PY 2022
VL 41
IS 19
BP 2672
EP 2684
DI 10.1038/s41388-022-02281-2
EA APR 2022
PG 13
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 1A5QI
UT WOS:000777275200001
PM 35365751
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Staderini, F
   Cianchi, F
   Badii, B
   Skalamera, 
   Fiorenza, G
   Foppa, C
   Qirici, E
   Perigli, G
AF Staderini, F.
   Cianchi, F.
   Badii, B.
   Skalamera, I
   Fiorenza, G.
   Foppa, C.
   Qirici, E.
   Perigli, G.
TI A unique presentation of a renal clear cell carcinoma with atypical
   metastases
SO INTERNATIONAL JOURNAL OF SURGERY CASE REPORTS
LA English
DT Article
DE Kidney cancer; Renal clear cell carcinoma; Metastases; Nephrectomy;
   Metastasectomy; Targeted therapies
ID PROGNOSTIC-FACTORS; CANCER
AB INTRODUCTION: Renal cancer is a relatively common neoplasia with renal clear cell carcinoma being the most frequent histological type. This tumor has a strong tendency to metastasize virtually to all organs. Today, new diagnostic tools allow physicians to distinguish between those patients with "incidental findings" and those with advanced metastatic disease.
   PRESENTATION OF CASE: A 70-year-old male with multiple indolent subcutaneous masses underwent colonoscopy after a positive fecal screening test for colorectal carcinoma. A rectal lesion was discovered but biopsy was negative. CT scan revealed advanced renal cancer involving the peritoneal cavity, retroperitoneum and lung. Biopsy of subcutaneous masses confirmed the suspected metastases. The patient underwent surgery (an open left nephrectomy with rectosigmoid resection and metastases debulking) because of a high risk of bowel obstruction and increasing anemia. After three years of multi-targeted therapy and follow-up, the patient is still asymptomatic and in good general condition.
   DISCUSSION: Treatment of metastatic renal cancer is still controversial even if more than 30% of patients have metastasis at the time of diagnosis. Recently introduced targeted therapies are encouraging but still present problems with side effects and an unlimited period of efficacy. Although there is no consensus, several studies and guidelines consider metastasectomy to be a valid option.
   CONCLUSION: Recent series highlight surgery as a key-point in the management of advanced renal clear cell carcinoma. Our case demonstrates the validity of a surgical strategy supported by a multidisciplinary approach. (C) 2015 The Authors. Published by Elsevier Ltd. on behalf of Surgical Associates Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
C1 [Staderini, F.; Cianchi, F.; Badii, B.; Skalamera, I; Fiorenza, G.; Foppa, C.; Qirici, E.; Perigli, G.] Univ Florence, Unit Gen & Endocrine Surg, Dept Surg & Translat Med, Florence, Italy.
C3 University of Florence
RP Staderini, F (corresponding author), Univ Florence, Unit Gen & Endocrine Surg, Dept Surg & Translat Med, Florence, Italy.
EM staderini.fabio@gmail.com
RI Staderini, Fabio/AAM-4423-2020; Foppa, Caterina/AAC-2327-2020
OI CIANCHI, FABIO/0000-0002-6936-8693; Foppa, Caterina/0000-0001-9920-0368;
   Staderini, Fabio/0000-0002-2438-2563
CR Alt AL, 2011, CANCER-AM CANCER SOC, V117, P2873, DOI 10.1002/cncr.25836
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NR 19
TC 12
Z9 12
U1 0
U2 2
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 2210-2612
J9 INT J SURG CASE REP
JI Int. J. Surg. Case Rep.
PY 2015
VL 11
BP 29
EP 32
DI 10.1016/j.ijscr.2015.03.009
PG 4
WC Surgery
WE Emerging Sources Citation Index (ESCI)
SC Surgery
GA CR1GA
UT WOS:000361071700008
PM 25911241
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Díaz-Díaz, A
   Roca-Lema, D
   Casas-Pais, A
   Romay, G
   Colombo, G
   Concha, A
   Graña, B
   Figueroa, A
AF Diaz-Diaz, Andrea
   Roca-Lema, Daniel
   Casas-Pais, Alba
   Romay, Gabriela
   Colombo, Giovanni
   Concha, Angel
   Grana, Begona
   Figueroa, Angelica
TI Heat Shock Protein 90 Chaperone Regulates the E3 Ubiquitin-Ligase Hakai
   Protein Stability
SO CANCERS
LA English
DT Article
DE Hsp90 chaperone; E3 ubiquitin-ligase Hakai; targeted therapy; colon
   cancer
ID HSP90 CHAPERONE; ANNEXIN A2; CANCER; DEGRADATION; PLASTICITY; INHIBITOR;
   CELLS; ASSOCIATION; COMPLEX; BINDING
AB The E3 ubiquitin-ligase Hakai binds to several tyrosine-phosphorylated Src substrates, including the hallmark of the epithelial-to-mesenchymal transition E-cadherin, and signals for degradation of its specific targets. Hakai is highly expressed in several human cancers, including colon cancer, and is considered as a drug target for cancer therapy. Here, we report a link between Hakai and the heat shock protein 90 (Hsp90) chaperone complex. Hsp90 participates in the correct folding of its client proteins, allowing them to maintain their stability and activity. Hsp90 inhibitors specifically interfere with the association with its Hsp90 client proteins, and exhibit potent anti-cancer properties. By immunoprecipitation, we present evidence that Hakai interacts with Hsp90 chaperone complex in several epithelial cells and demonstrate that is a novel Hsp90 client protein. Interestingly, by overexpressing and knocking-down experiments with Hakai, we identified Annexin A2 as a Hakai-regulated protein. Pharmacological inhibition of Hsp90 with geldanamycin results in the degradation of Hakai in a lysosome-dependent manner. Interestingly, geldanamycin-induced Hakai degradation is accompanied by an increased expression of E-cadherin and Annexin A2. We also show that geldanamycin suppresses cell motility at least in part through its action on Hakai expression. Taken together, our results identify Hakai as a novel Hsp90 client protein and shed light on the regulation of Hakai stability. Our results open the possibility to the potential use of Hsp90 inhibitors for colorectal cancer therapy through its action on Hakai client protein of Hsp90.
C1 [Diaz-Diaz, Andrea; Roca-Lema, Daniel; Casas-Pais, Alba; Romay, Gabriela; Figueroa, Angelica] Univ Coruna UDC, CHUAC, Inst Invest Biomed A Coruna INIBIC, Epithelial Plast & Metastasis Grp, La Coruna 15006, Spain.
   [Colombo, Giovanni] CNR Palermo, IRIB, Via Ugo La Malfa 153, I-90146 Palermo, Italy.
   [Concha, Angel] Univ Coruna UDC, CHUAC, Inst Invest Biomed A Coruna INIBIC, Pathol Dept, La Coruna 15006, Spain.
   [Concha, Angel] Univ Coruna UDC, CHUAC, Inst Invest Biomed A Coruna INIBIC, A Coruna Biobank, La Coruna 15006, Spain.
   [Grana, Begona] Univ Coruna UDC, CHUAC, Inst Invest Biomed A Coruna INIBIC, Clin Oncol Grp, La Coruna 15006, Spain.
C3 Universidade da Coruna; Instituto de Investigacion Biomedica de A Coruna
   (INIBIC); Complejo Hospitalario Universitario A Coruna; Consiglio
   Nazionale delle Ricerche (CNR); Istituto Ricerca l'Innovazione Biomedica
   (IRIB-CNR); Universidade da Coruna; Instituto de Investigacion Biomedica
   de A Coruna (INIBIC); Complejo Hospitalario Universitario A Coruna;
   Complejo Hospitalario Universitario A Coruna; Universidade da Coruna;
   Instituto de Investigacion Biomedica de A Coruna (INIBIC); Complejo
   Hospitalario Universitario A Coruna; Universidade da Coruna; Instituto
   de Investigacion Biomedica de A Coruna (INIBIC)
RP Figueroa, A (corresponding author), Univ Coruna UDC, CHUAC, Inst Invest Biomed A Coruna INIBIC, Epithelial Plast & Metastasis Grp, La Coruna 15006, Spain.
EM andrea.diaz.diaz@sergas.es; Daniel.roca.lema@sergas.es;
   alba.casas.pais@sergas.es; Gabriela.Romay.Cousido@sergas.es;
   giovanni.colombo@community.unipa.it; angel.concha.lopez@sergas.es;
   Begona.Grana.Suarez@sergas.es; Angelica.Figueroa.Conde-Valvis@sergas.es
RI Figueroa, Angelica/ABD-7705-2020; Figueroa, PhD, Angelica/K-1266-2014
OI Casas-Pais, Alba/0000-0002-4880-7298; Concha Lopez,
   Angel/0009-0007-9757-1051; Colombo, Giovanni/0000-0002-7138-7551;
   Figueroa, PhD, Angelica/0000-0001-5530-5213
FU Plan Estatal I + D + I 2013 2016; Instituto de Salud Carlos III (ISCIII,
   Spain) under Fondo Europeo de Desarrollo Regional (FEDER) "A way of
   Making Europe" [PI13/00250, PI18/00121]; "la Caixa" Foundation
   [100010434, LCF/TR/CI19/52460016]; Seed project (NEODIANAR) from
   Conselleria de Cultura, Educacion y Ordenacion Universitaria from Xunta
   de Galicia; PRIS3 project-ACIS from Xunta de Galicia; I.M.Q. San Rafael
   Foundation from A Coruna; FPU contract from Ministerio de Educacion,
   Cultura y Deporte from Spain [FPU014/02837]; Axencia Galega de
   Innovacion (GAIN)-Conselleria de Economia, Empleo e Industria from Xunta
   de Galicia, Spain [IN606A-2017/013]; Profesor Novoa Santos Foundation;
   Diputacion A Coruna
FX This work has been supported by Plan Estatal I + D + I 2013 2016,
   co-funded by the Instituto de Salud Carlos III (ISCIII, Spain) under
   grant agreements PI13/00250 and PI18/00121 by Fondo Europeo de
   Desarrollo Regional (FEDER) "A way of Making Europe". The project
   leading to these results has received funding from "la Caixa" Foundation
   (ID 100010434) under the agreement (LCF/TR/CI19/52460016). Also
   supported by Seed project (NEODIANAR) from Conselleria de Cultura,
   Educacion y Ordenacion Universitaria, by PRIS3 project-ACIS, both from
   Xunta de Galicia and by I.M.Q. San Rafael Foundation from A Coruna,.
   A.D-D has been supported by FPU contract (FPU014/02837) from Ministerio
   de Educacion, Cultura y Deporte from Spain; A.C-P Casas-Pais by a
   predoctoral contract (IN606A-2017/013) from Axencia Galega de Innovacion
   (GAIN)-Conselleria de Economia, Empleo e Industria from Xunta de
   Galicia, Spain and D.R-L was supported by Profesor Novoa Santos
   Foundation and by Diputacion A Coruna.
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NR 47
TC 12
Z9 12
U1 1
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 215
DI 10.3390/cancers12010215
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KQ3KZ
UT WOS:000516826700215
PM 31952268
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Xiao, HJ
   Guo, YP
   Liu, HM
   Liu, YS
   Wang, YM
   Li, CQ
   Císar, J
   Skoda, D
   Kuritka, I
   Guo, L
   Sedlarík, V
AF Xiao, Haijun
   Guo, Yiping
   Liu, Hongmei
   Liu, Yushi
   Wang, Yumin
   Li, Changqing
   Cisar, Jaroslav
   Skoda, David
   Kuritka, Ivo
   Guo, Li
   Sedlarik, Vladimir
TI Structure-based design of charge-conversional drug self-delivery systems
   for better targeted cancer therapy
SO BIOMATERIALS
LA English
DT Article
DE Irinotecan; Curcumin; Charge conversion; Self-delivery; Targeting
   therapy; Diarrhea
ID CELLULAR UPTAKE; CURCUMIN; CYTOTOXICITY; FORMULATIONS; BINDING
AB Various design and fabrication strategies of carrier-based drug delivery systems have been quickly established and applied for cancer therapy in recent years. These systems contribute greatly to current cancer treatments but further development needs to be made to eliminate obstacles such as low drug loading capacity and severe side effects. To achieve better drug delivery, we propose an innovative strategy for the construction of easy manufactured drug self-delivery systems based on molecular structures, which can be used for the co-delivery of curcuminoids and all the nitrogen-containing derivatives of camptothecin for better targeted cancer therapy with minimized side effects. The formation mechanism investigation demonstrates that the rigid planar structures of camptothecin derivatives and curcuminoids with relevant leaving hydrogens make it possible for them to be assembled into nanoparticles under suitable conditions. These nanoparticles show stabilized particle sizes (100 nm) under various conditions and tunable surface charges which increase from around -10 mV in a normal physiological condition (pH 7.4) to +40 mV under acidic tumor environments. In addition, in vivo mice experiments have demonstrated that, compared to irinotecan (a derivative of camptothecin) itself, the co-delivered irinotecan curcumin nanoparticles exhibited significantly enhanced lung and gallbladder targeting, improved macrophage-clearance escape and ameliorated colorectal cancer treatment with an eradication of life-threatening diarrhea, bringing hope for better targeted chemotherapy and clinical translation. Lastly, the strategy of structure based design of drug self-delivery systems may inspire more research and discoveries of similar self-delivered nano systems for wider pharmaceutical applications.
C1 [Xiao, Haijun; Wang, Yumin; Cisar, Jaroslav; Skoda, David; Kuritka, Ivo; Sedlarik, Vladimir] Tomas Bata Univ Zlin, Ctr Polymer Syst, Zlin 76001, Czech Republic.
   [Guo, Yiping; Li, Changqing] Univ Calif, Quantitat & Syst Biol Program, Merced, CA 95343 USA.
   [Liu, Hongmei; Liu, Yushi; Guo, Li] Chengdu Univ Tradit Chinese Med, Sch Pharm, Chengdu 611137, Peoples R China.
   [Li, Changqing] Univ Calif, Dept Bioengn, Merced, CA 95343 USA.
   [Guo, Li] Chengdu Univ Tradit Chinese Med, State Key Lab Characterist Chinese Med Resources, Chengdu 611137, Peoples R China.
C3 Tomas Bata University Zlin; University of California System; University
   of California Merced; Chengdu University of Traditional Chinese
   Medicine; University of California System; University of California
   Merced; Chengdu University of Traditional Chinese Medicine
RP Sedlarík, V (corresponding author), Tomas Bata Univ Zlin, Ctr Polymer Syst, Zlin 76001, Czech Republic.; Guo, L (corresponding author), Chengdu Univ Tradit Chinese Med, Sch Pharm, Chengdu 611137, Peoples R China.
EM guoli@cdutcm.edu.cn; sedlarik@utb.cz
RI Skoda, David/U-4258-2019; 刘, Capsula/JJD-6028-2023; Wang,
   Yu-Min/JMQ-5055-2023; Chen, Chien-Jen/N-4723-2019; Guo,
   Yiping/HQZ-2987-2023; Liu, Hermine/AAG-6494-2019; Kuritka,
   Ivo/J-2285-2016; Sedlarik, Vladimir/H-6362-2012; Skoda,
   David/A-3586-2015
OI Guo, Li/0000-0002-7445-5257; Kuritka, Ivo/0000-0002-1016-5170; Wang,
   Yu-Min/0000-0002-3615-658X; Sedlarik, Vladimir/0000-0002-7843-0719; Guo,
   Yiping/0000-0002-5989-2125; Xiao, Haijun/0000-0001-5349-3580; Skoda,
   David/0000-0002-3787-1956
FU Ministry of Education, Youth and Sports of the Czech Republic [LO 1504];
   Internal Grant Agency of the Tomas Bata University in Zlin
   [IGA/CPS/2017/005, IGA/CPS/2018/003, IGA/CPS/2019/006]; Fund for
   Fostering Talents in Basic Science of the National Natural Science
   Foundation of China [J1310034-18]; Quantitative and Systems Biology
   program, University of California, Merced, United States
FX We express our great appreciation to Jiayi Sun at Innovative Institute
   of Chinese Medicine and Pharmacy, Chengdu University of Traditional
   Chinese Medicine, for the assistance with confocal laser scanning
   microscopy, Haojie Fei at Centre of Polymer Systems, Tomas Bata
   University in Zlin, for the help with scanning electron microscopy,
   Juanru Liu at School of Pharmacy, Chengdu University of Traditional
   Chinese Medicine, for the assistance during in vitro evaluation and all
   the technicians who helped us during this research. This work was
   cofunded by the Ministry of Education, Youth and Sports of the Czech
   Republic [Grant No. LO 1504]; Internal Grant Agency of the Tomas Bata
   University in Zlin [Grant No. IGA/CPS/2017/005, Grant No.
   IGA/CPS/2018/003, Grant No. IGA/CPS/2019/006]; Fund for Fostering
   Talents in Basic Science of the National Natural Science Foundation of
   China [J1310034-18] and graduate student summer fellowship of
   Quantitative and Systems Biology program, University of California,
   Merced, United States.
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NR 46
TC 37
Z9 40
U1 6
U2 119
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0142-9612
EI 1878-5905
J9 BIOMATERIALS
JI Biomaterials
PD FEB
PY 2020
VL 232
AR 119701
DI 10.1016/j.biomaterials.2019.119701
PG 14
WC Engineering, Biomedical; Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Materials Science
GA KN3NS
UT WOS:000514748200008
PM 31901505
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Zhou, BQ
   Apata, CO
   Zhou, YF
   Jiang, L
   Pei, QM
AF Zhou, Bin-qian
   Apata, Charles Omotomide
   Zhou, Yi-fan
   Jiang, Long
   Pei, Qi-ming
TI Noise and noise propagation in transition cascade of colonic cells with
   four coupled feedback regulations
SO PHYSICA A-STATISTICAL MECHANICS AND ITS APPLICATIONS
LA English
DT Article
DE Noise; Noise propagation; Noise amplification; Coupled feedback; Colonic
   cells
ID STOCHASTIC GENE-EXPRESSION; NEGATIVE FEEDBACK; COLORECTAL-CANCER;
   DEGRADATION; IMPACT; RISK
AB Noise and noise propagation are vital in various biological processes. In a phenotypic transition cascade of colonic cells, there are three compartments: stem cells (SCs), transit-amplifying cells (TACs), and fully differentiated cells (FDCs). Instead of pure linear feedback (L) or pure saturation feedback (S) in regulating SCs and TACs differentiation, four coupled feedbacks including LL, LS, SL, and SS are considered to compare the impacts of different feedbacks on noise and noise propagation of cells. Rather than LL feedback and LS feedback, SL feedback and SS feedback have obvious advantages: Firstly, the characteristics of cells steady states changing with the parameter are more consistent with the tumor development. Secondly, as long as the key parameter is adjusted reasonably, the strong correlation between any two fluctuations of cells can be effectively utilized or avoided. Finally, although there is no direct interaction between SCs and FDCs, the noise in SCs can propagate to FDCs by TACs. And the transmitted noise from upstream cells can cause the large total noise of downstream cells even the number of downstream cells is large. The strong correlation and noise propagation between upstream and downstream cells may be the theoretical basis of the targeted therapy, which can achieve dual or even triple-drug targeted anti-tumor therapy by acting on different targets in the upstream or downstream pathways. Therefore, SL feedback or SS feedback may be a better choice for SCs and TACs to adjust their differentiation rather than LL feedback and LS feedback. This work is an extension and application of the elementary fluctuation theory of statistical physics in life system. (C) 2021 Elsevier B.V. All rights reserved.
C1 [Zhou, Bin-qian; Apata, Charles Omotomide; Zhou, Yi-fan; Jiang, Long; Pei, Qi-ming] Yangtze Univ, Sch Phys & Optoelect Engn, Jingzhou 434023, Peoples R China.
C3 Yangtze University
RP Pei, QM (corresponding author), Yangtze Univ, Sch Phys & Optoelect Engn, Jingzhou 434023, Peoples R China.
EM qmpei@yangtzeu.edu.cn
OI Pei, Qiming/0000-0002-9468-2879; Zhou, Binqian/0000-0002-7369-781X
FU National Natural Science Foundation of China [11605014]
FX This work was supported by the National Natural Science Foundation of
   China under Grant No. 11605014 (to Q.-m. P).
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PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0378-4371
EI 1873-2119
J9 PHYSICA A
JI Physica A
PD JAN 1
PY 2022
VL 585
AR 126429
DI 10.1016/j.physa.2021.126429
EA SEP 2021
PG 14
WC Physics, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Physics
GA WC0CV
UT WOS:000703932500031
DA 2025-01-04
ER

PT J
AU De Falco, V
   Poliero, L
   Vitello, PP
   Ciardiello, D
   Vitale, P
   Zanaletti, N
   Giunta, EF
   Terminiello, M
   Caputo, V
   Carlino, F
   Di Liello, R
   Ventriglia, A
   Famiglietti, V
   Martinelli, E
   Morgillo, F
   Orditura, M
   De Vita, F
   Fasano, M
   Napolitano, S
   Martini, G
   Della Corte, CM
   Franco, R
   Altucci, L
   Ciardiello, F
   Troiani, T
AF De Falco, Vincenzo
   Poliero, Luca
   Vitello, Pietro Paolo
   Ciardiello, Davide
   Vitale, Pasquale
   Zanaletti, Nicoletta
   Giunta, Emilio Francesco
   Terminiello, Marinella
   Caputo, Vincenza
   Carlino, Francesca
   Di Liello, Raimondo
   Ventriglia, Anna
   Famiglietti, Vincenzo
   Martinelli, Erika
   Morgillo, Floriana
   Orditura, Michele
   De Vita, Ferdinando
   Fasano, Morena
   Napolitano, Stefania
   Martini, Giulia
   Della Corte, Carminia Maria
   Franco, Renato
   Altucci, Lucia
   Ciardiello, Fortunato
   Troiani, Teresa
TI Feasibility of next-generation sequencing in clinical practice: results
   of a pilot study in the Department of Precision Medicine at the
   University of Campania 'Luigi Vanvitelli'
SO ESMO OPEN
LA English
DT Article
ID TARGETED THERAPY; CANCER MEDICINE; UTILITY; DNA
AB Background The emerging role of next-generation sequencing (NGS) targeted panels is revolutionising our approach to cancer patients, providing information on gene alterations helpful for diagnosis and clinical decision, in a short time and with acceptable costs.
   Materials and methods In this work, we evaluated the clinical application of FoundationOne CDx test, a hybrid capture-based NGS. This test identifies alterations in 324 genes, tumour mutational burden and genomic signatures as microsatellite instability. The decision to obtain the NGS assay for a particular patient was done according to investigator's choice.
   Results Overall, 122 tumour specimens were analysed, of which 84 (68.85%) succeeded. The success rate was influenced by type of specimen formalin-fixed paraffin embedded (FFPE block vs FFPE slides), by origin of the sample (surgery vs biopsy) and by time of fixation (<5 years vs >= 5 years). The most frequent subgroups of effective reports derived from colorectal cancer (25 samples), non-small-cell lung cancer (16 samples), ovarian cancer (10 samples), biliary tract cancer (9 samples), breast cancer (7 samples), gastric cancer (7 samples). The most frequent alterations found in whole population referred to TP53 (45.9%), KRAS (19.6%) and APC (13.9%). Furthermore, we performed an analysis of patients in whom this comprehensive genomic profiling (CGP) had a relevance for the patient's disease.
   Conclusions On our opinion, CGP could be proposed in clinical practice in order to select patients that could most benefit from the analysis proposed, like patients with good performance status without any available treatments or with unexpected resistance to a therapy.
C1 [De Falco, Vincenzo; Poliero, Luca; Vitello, Pietro Paolo; Ciardiello, Davide; Vitale, Pasquale; Zanaletti, Nicoletta; Giunta, Emilio Francesco; Terminiello, Marinella; Caputo, Vincenza; Carlino, Francesca; Di Liello, Raimondo; Ventriglia, Anna; Famiglietti, Vincenzo; Martinelli, Erika; Morgillo, Floriana; Orditura, Michele; De Vita, Ferdinando; Fasano, Morena; Napolitano, Stefania; Martini, Giulia; Della Corte, Carminia Maria; Altucci, Lucia; Ciardiello, Fortunato; Troiani, Teresa] Univ Campania Luigi Vanvitelli, Dept Precis Med, Med Oncol, Naples, Campania, Italy.
   [Franco, Renato] Univ Campania Luigi Vanvitelli, Dept Mental Phys Hlth & Prevent Med, Naples, Italy.
C3 Universita della Campania Vanvitelli; Universita della Campania
   Vanvitelli
RP Troiani, T (corresponding author), Univ Campania Luigi Vanvitelli, Dept Precis Med, Med Oncol, Naples, Campania, Italy.
EM troiani.teresa@yahoo.it
RI Franco, Rafael/C-3694-2015; De Falco, Vincenzo/AAP-5495-2021; Altucci,
   Lucia/S-8031-2019; Ciardiello, Davide/AAC-4613-2022; Martini,
   Giulia/AIB-8246-2022; Giunta, Emilio/AAC-3434-2022; Della Corte,
   Carminia/ABE-1377-2021; Vitiello, Pietro Paolo/HKN-2581-2023;
   Napolitano, Stefania/AIB-9708-2022
OI Napolitano, Stefania/0000-0003-3504-8349; Vitiello, Pietro
   Paolo/0000-0002-4060-7662; DI LIELLO, RAIMONDO/0000-0003-4511-7969;
   Giunta, Emilio Francesco/0000-0002-5383-4469; De Falco,
   Vincenzo/0000-0003-0261-0382; martinelli, erika/0000-0002-7108-0971;
   Della Corte, Carminia Maria/0000-0002-3396-8099; MARTINI,
   Giulia/0000-0003-4093-2681
FU Regione Campania Cancer Research Campaign I-Cure Grant
FX This research was funded within Regione Campania Cancer Research
   Campaign I-Cure Grant to F.C.
CR [Anonymous], [No title captured]
   [Anonymous], [No title captured]
   [Anonymous], [No title captured]
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NR 39
TC 13
Z9 13
U1 0
U2 3
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
IS 2
AR e000675
DI 10.1136/esmoopen-2020-000675
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LF9YI
UT WOS:000527768100018
PM 32234730
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Mitra, D
   Clark, JW
   Shih, HA
   Oh, KS
   Brastianos, PK
   Wo, JY
   Strickland, MR
   Curry, WT
   Parikh, AR
   Corcoran, RB
   Ryan, DP
   Iafrate, AJ
   Borger, DR
   Lennerz, JK
   Hong, TS
AF Mitra, Devarati
   Clark, Jeffrey W.
   Shih, Helen A.
   Oh, Kevin S.
   Brastianos, Priscilla K.
   Wo, Jennifer Y.
   Strickland, Matthew R.
   Curry, William T.
   Parikh, Aparna R.
   Corcoran, Ryan B.
   Ryan, David P.
   Iafrate, A. John
   Borger, Darrell R.
   Lennerz, Jochen K.
   Hong, Theodore S.
TI Enrichment of <i>HER2</i> Amplification in Brain Metastases from Primary
   Gastrointestinal Malignancies
SO ONCOLOGIST
LA English
DT Article
DE HER2; Brain metastases; Gastrointestinal cancer; Biomarker
ID BREAST-CANCER PATIENTS; PROGNOSTIC-FACTORS; GASTROESOPHAGEAL
   ADENOCARCINOMA; GENOMIC CHARACTERIZATION; OVEREXPRESSION; ESOPHAGEAL;
   THERAPY; LAPATINIB; CARCINOMA
AB Background In nongastric gastrointestinal (GI) cancers, HER2-positive (HER2+) disease is not common. In breast cancer, HER2 status is associated with increased risk of brain metastases and response to HER2-targeted therapy. The purpose of this project was to compare HER2 status in GI cancer brain metastases versus matched prior sites of disease in order to determine if HER2+ disease is more common intracranially. Materials and Methods We identified 28 patients with GI cancer who had craniotomy for brain metastases between 1999 and 2017 with intracranial metastatic tissue available at Massachusetts General Hospital. Twenty-four patients also had tissue from a prior site of disease. Fluorescence in situ hybridization (FISH) and immunohistochemistry (IHC) for HER2 were performed on all samples. A tumor was defined as HER2+ if it had 3+ staining by IHC or amplification by FISH. Results A prior site of disease (including intracranial metastases) was HER2+ for 13% of evaluable patients: 3 of 11 patients with colorectal cancer and no patients with esophageal or pancreatic cancer. The most recent brain metastases were HER2+ for 32% of patients: 2 of 3 esophageal squamous cell carcinomas, 3 of 10 esophageal adenocarcinomas (ACs), 3 of 14 colorectal ACs, and 1 of 1 pancreatic AC. Only 37.5% of patients with HER2+ brain metastasis had concordant HER2+ prior tissue (kappa = 0.38, p = .017). Conclusion In this cohort of patients with GI cancer with brain metastases, HER2+ status was more common intracranially compared with prior sites of disease. These findings suggest that testing HER2 in patients with GI cancer with brain metastases may lead to additional therapeutic options, regardless of HER2 status in previously examined tissue.
C1 [Mitra, Devarati; Shih, Helen A.; Oh, Kevin S.; Wo, Jennifer Y.; Hong, Theodore S.] Massachusetts Gen Hosp, Dept Radiat Oncol, 55 Fruit St, Boston, MA 02114 USA.
   [Clark, Jeffrey W.; Brastianos, Priscilla K.; Strickland, Matthew R.; Parikh, Aparna R.; Corcoran, Ryan B.; Ryan, David P.] Massachusetts Gen Hosp, Dept Hematol Oncol, Boston, MA 02114 USA.
   [Curry, William T.] Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02114 USA.
   [Iafrate, A. John; Lennerz, Jochen K.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
   [Borger, Darrell R.] Massachusetts Gen Hosp, Biomarker Lab, Boston, MA 02114 USA.
C3 Harvard University; Massachusetts General Hospital; Harvard University;
   Massachusetts General Hospital; Harvard University; Massachusetts
   General Hospital; Harvard University; Massachusetts General Hospital;
   Harvard University; Massachusetts General Hospital
RP Hong, TS (corresponding author), Massachusetts Gen Hosp, Dept Radiat Oncol, 55 Fruit St, Boston, MA 02114 USA.
EM tshong1@mgh.harvard.edu
RI Wo, Jennifer/Y-6074-2018; Oh, Kevin/HKE-2536-2023; Shih,
   Helen/O-7653-2017
OI Shih, Helen/0000-0003-1550-9726; Brastianos,
   Priscilla/0000-0003-4470-8425
CR Abu Hejleh T, 2012, WORLD J GASTRO ONCOL, V4, P103, DOI 10.4251/wjgo.v4.i5.103
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NR 45
TC 17
Z9 17
U1 0
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 FEB
PY 2019
VL 24
IS 2
BP 193
EP 201
DI 10.1634/theoncologist.2018-0152
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HL7OM
UT WOS:000458930900014
PM 30373904
OA Bronze, Green Published
DA 2025-01-04
ER

PT J
AU Bear, HD
   Tang, G
   Rastogi, P
   Geyer, CE
   Zoon, CK
   Kidwell, KM
   Robidoux, A
   Baez-Diaz, L
   Brufsky, AM
   Mehta, RS
   Fehrenbacher, L
   Young, JA
   Senecal, FM
   Gaur, R
   Margolese, RG
   Adams, PT
   Gross, HM
   Costantino, JP
   Paik, S
   Swain, SM
   Mamounas, EP
   Wolmark, N
AF Bear, Harry D.
   Tang, Gong
   Rastogi, Priya
   Geyer, Charles E., Jr.
   Zoon, Christine K.
   Kidwell, Kelley M.
   Robidoux, Andre
   Baez-Diaz, Luis
   Brufsky, Adam M.
   Mehta, Rita S.
   Fehrenbacher, Louis
   Young, James A.
   Senecal, Francis M.
   Gaur, Rakesh
   Margolese, Richard G.
   Adams, Paul T.
   Gross, Howard M.
   Costantino, Joseph P.
   Paik, Soonmyung
   Swain, Sandra M.
   Mamounas, Eleftherios P.
   Wolmark, Norman
TI The Effect on Surgical Complications of Bevacizumab Added to Neoadjuvant
   Chemotherapy for Breast Cancer: NRG Oncology/NSABP Protocol B-40
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Article
ID WOUND-HEALING COMPLICATIONS; ADJUVANT BEVACIZUMAB; COLORECTAL-CANCER;
   LIVER METASTASES; TARGETED THERAPY; NAB-PACLITAXEL; SURGERY;
   ANGIOGENESIS; PHASE-3; TRIAL
AB NRG Oncology/NSABP trial B-40 tested the impact of adding bevacizumab (bev) to neoadjuvant chemotherapy for operable breast cancer. Secondary endpoints included rates of surgical complications after surgery in patients who did or did not receive bev.
   A total of 1206 women with HER2-negative operable breast cancer were randomly assigned to receive one of three different docetaxel-plus-anthracycline-based regimens, without or with bev (15 mg/kg every 3 weeks) for the first 6 of 8 cycles and for 10 doses postoperatively. Surgical complications were assessed from date of surgery through 24 months following study entry.
   Early surgical complications were significantly more frequent in the bev group (25.4 vs. 18.9%; trend test p = 0.008), but most were grade 1-2. Early noninfectious wound dehiscences were infrequent and not significantly different (5.4 vs. 3.1%; trend test p = 0.15). Long-term noninfectious wound complications were significantly higher for patients receiving bev (11.8 vs. 5.1%; trend test p = 0.0007), but the incidence of grade 3 wound dehiscence was low in both groups (< 1%). Among 193 patients undergoing expander or implant reconstructions, 19 (19.6%) of 97 in the bev-receiving group versus 10 (10.4%) of 96 in the non-bev group had grade 3 complications (Pearson, p = 0.11).
   Overall, adding bev increased surgical complications, but most serious complications were not significantly increased. In particular, the need for surgical intervention in patients undergoing breast reconstruction with prosthetic implants was higher with bev but was not statistically significantly different. With precautions, bev can be used safely perioperatively in patients undergoing surgery for breast cancer.
C1 [Bear, Harry D.; Tang, Gong; Rastogi, Priya; Geyer, Charles E., Jr.; Kidwell, Kelley M.; Robidoux, Andre; Baez-Diaz, Luis; Brufsky, Adam M.; Mehta, Rita S.; Fehrenbacher, Louis; Young, James A.; Senecal, Francis M.; Gaur, Rakesh; Margolese, Richard G.; Adams, Paul T.; Gross, Howard M.; Costantino, Joseph P.; Paik, Soonmyung; Swain, Sandra M.; Mamounas, Eleftherios P.; Wolmark, Norman] NRG Oncol, Pittsburgh, PA 19103 USA.
   [Bear, Harry D.; Tang, Gong; Rastogi, Priya; Geyer, Charles E., Jr.; Kidwell, Kelley M.; Robidoux, Andre; Baez-Diaz, Luis; Brufsky, Adam M.; Mehta, Rita S.; Fehrenbacher, Louis; Young, James A.; Senecal, Francis M.; Gaur, Rakesh; Margolese, Richard G.; Adams, Paul T.; Gross, Howard M.; Costantino, Joseph P.; Paik, Soonmyung; Swain, Sandra M.; Mamounas, Eleftherios P.; Wolmark, Norman] NSABP, Pittsburgh, PA 15212 USA.
   [Bear, Harry D.; Geyer, Charles E., Jr.; Zoon, Christine K.] Virginia Commonwealth Univ, Massey Canc Ctr, Richmond, VA USA.
   [Tang, Gong; Kidwell, Kelley M.; Costantino, Joseph P.] Univ Pittsburgh, Pittsburgh, PA USA.
   [Rastogi, Priya] Univ Pittsburgh, Canc Inst, Sch Med, Pittsburgh, PA USA.
   [Kidwell, Kelley M.] Univ Michigan, Sch Publ Hlth, Dept Biostat, Ann Arbor, MI 48109 USA.
   [Robidoux, Andre] CHUM, Montreal, PQ, Canada.
   [Baez-Diaz, Luis] San Juan MBCCOP, San Juan, PR USA.
   [Brufsky, Adam M.] Univ Pittsburgh, Magee Womens Hosp, Pittsburgh, PA 15213 USA.
   [Mehta, Rita S.] Univ Calif Irvine, Chao Family Comprehens Canc Ctr, Sch Med, Orange, CA 92668 USA.
   [Fehrenbacher, Louis] Kaiser Permanente Oncol Clin Trials, Vallejo, CA USA.
   [Young, James A.] Colorado Canc Res Program, CCOP, Colorado Springs, CO USA.
   [Senecal, Francis M.] North West Med Specialties, CCOP, Tacoma, WA USA.
   [Gaur, Rakesh] Kansas City Clin Oncol Program, Kansas City, MO USA.
   [Margolese, Richard G.] McGill Univ, Jewish Gen Hosp, Montreal, PQ, Canada.
   [Adams, Paul T.] Genesys Reg Med Ctr, Grand Blanc, MI USA.
   [Gross, Howard M.] Dayton CCOP, Dayton, OH USA.
   [Paik, Soonmyung] Yonsei Univ, Coll Med, Severance Biomed Sci Inst, Seoul, South Korea.
   [Paik, Soonmyung] Yonsei Univ, Coll Med, Dept Med Oncol, Seoul, South Korea.
   [Swain, Sandra M.] Washington Hosp Ctr, Washington Canc Inst, Washington, DC 20010 USA.
   [Swain, Sandra M.] Georgetown Univ, Med Ctr, Washington, DC 20007 USA.
   [Mamounas, Eleftherios P.] Orlando Hlth, UF Hlth Canc Ctr, Orlando, FL USA.
   [Wolmark, Norman] Allegheny Hlth Network Canc Inst, Pittsburgh, PA USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); University
   of Pittsburgh; National Surgical Adjuvant Breast & Bowel Project;
   Pennsylvania Commonwealth System of Higher Education (PCSHE); University
   of Pittsburgh; National Surgical Adjuvant Breast & Bowel Project;
   Virginia Commonwealth University; Pennsylvania Commonwealth System of
   Higher Education (PCSHE); University of Pittsburgh; Pennsylvania
   Commonwealth System of Higher Education (PCSHE); University of
   Pittsburgh; University of Michigan System; University of Michigan;
   Universite de Montreal; Pennsylvania Commonwealth System of Higher
   Education (PCSHE); University of Pittsburgh; University of California
   System; University of California Irvine; Kaiser Permanente; McGill
   University; Yonsei University; Yonsei University Health System; Yonsei
   University; Yonsei University Health System; MedStar Washington Hospital
   Center; Georgetown University
RP Bear, HD (corresponding author), NRG Oncol, Pittsburgh, PA 19103 USA.; Bear, HD (corresponding author), NSABP, Pittsburgh, PA 15212 USA.; Bear, HD (corresponding author), Virginia Commonwealth Univ, Massey Canc Ctr, Richmond, VA USA.
EM harry.bear@vcuhealth.org
RI Geyer, Charles/AGY-0119-2022; Brufsky, Adam/AAE-7470-2020
OI Paik, Soonmyung/0000-0001-9688-6480; Brufsky, Adam/0000-0001-8080-7960;
   Swain, Sandra/0000-0002-1320-3830; Kidwell, Kelley
   M/0000-0002-1717-4483; , Gong/0000-0002-6247-4338
FU National Cancer Institute, Department of Health and Human Services,
   Public Health Service [U10-CA-108068, U10-CA-180822, NCI-44066-26,
   UG1CA-189867, UM1-CA-189869, UGI-CA-189853]; Genentech, Inc.
FX This work was supported by National Cancer Institute, Department of
   Health and Human Services, Public Health Service Grants: U10-CA-108068,
   U10-CA-180822, NCI-44066-26(AR); UG1CA-189867, UM1-CA-189869(HDB), and
   UGI-CA-189853(RG) (NCORPs); and by Genentech, Inc., a full member of the
   Roche Group of companies; Roche Laboratories Inc.; Lilly Research
   Laboratories, a division of Eli Lilly & Company; and Precision
   Therapeutics, Inc. The authors also thank participating member sites as
   well as patients enrolled in the study.
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NR 38
TC 8
Z9 10
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9265
EI 1534-4681
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD JUL
PY 2017
VL 24
IS 7
BP 1853
EP 1860
DI 10.1245/s10434-016-5662-9
PG 8
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA EW4GC
UT WOS:000402459000016
PM 27864694
OA Green Accepted, Green Submitted
DA 2025-01-04
ER

PT J
AU Shirjang, S
   Mansoori, B
   Mohammad, A
   Shajari, N
   Duijf, PHG
   Najaf, S
   Gaballu, FA
   Nofouzi, K
   Baradaran, B
AF Shirjang, Solmaz
   Mansoori, Behzad
   Mohammad, Ali
   Shajari, Neda
   Duijf, Pascal H. G.
   Najaf, Souzan
   Gaballu, Fereydoon Abedi
   Nofouzi, Katayoon
   Baradaran, Behzad
TI miR-330 Regulates Colorectal Cancer Oncogenesis by Targeting BACH1
SO ADVANCED PHARMACEUTICAL BULLETIN
LA English
DT Article
DE miR-330; BACH1; MMP9; CXCR4; VEGFR; Proliferation; Colorectal cancer
ID MICRO-RNA; CHROMOSOME INSTABILITY; EXPRESSION PROFILES; SIGNALING
   PATHWAY; MASTER REGULATOR; CELLS; PROGNOSIS; GENES; CXCR4;
   OVEREXPRESSION
AB Purpose: Based on WHO report, colorectal cancer (CRC) is the second cause of death among patients with cancer worldwide. Dysregulation of miRNAs expressions has been demonstrated in different human cancers, especially CRC. Studies have shown that miR-330 could act as both TS-miR and/or oncomiR in different types of cancers. BACH1 is also identified as a transcription factor, which is involved in ontogenesis. In this study, we evaluated the CRC suppression via silencing of BACH1 by small silencer molecule called miR-330.
   Methods: Firstly, we analyzed the BACH1, miR-330-3p and miR-330-5p expressions according to the colon adenocarcinoma (COAD) and rectal adenocarcinoma (READ) project established from a patient of the colon and rectal cancer patients in The Cancer Genome Atlas (TCGA) database. The targeting of BACH1 via miR-330 in human CRC cells was evaluated by Vejnar bioinformatics methods, and confirmed by qRT-PCR and western blot analysis. Proliferation was performed by MTT assay. The MMP9, CXCR4, and VEGFR proteins were measured by western blotting.
   Results: The analysis of BACH1, miR-330-3p, and miR-330-5p expressions according to the COAD and READ projects showed that BACH1 was overexpressed, but miR-330-3p and miR-330-5p were reduced in CRC tumors compared to normal controls. The miR-330 induction prevented proliferation of CRC cell by targeting BACH1 mRNA, which represses MMP9, C-X-C chemokine receptor type 4 (CXCR4), and vascular endothelial growth factor receptor (VEGFR) proteins expressions.
   Conclusion: Our results suggested that BACH1 is a potential target for miR-330 in CRC cells. The miR-330 induction inhibits CRC cells proliferation by suppressing BACH1 expression in posttranscriptional level. It was suggested that targeting of BACH1 via miRNA such as miR-330 could be a valid strategy in the field of CRC targeted therapy via modulating the oncogenic signaling pathway.
C1 [Shirjang, Solmaz; Mansoori, Behzad; Mohammad, Ali; Najaf, Souzan; Gaballu, Fereydoon Abedi; Baradaran, Behzad] Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran.
   [Mansoori, Behzad] Tabriz Univ Med Sci, Student Res Comm, Tabriz, Iran.
   [Mansoori, Behzad] Univ Southern Denmark, Inst Mol Med, Dept Canc & Inflammat Res, Odense, Denmark.
   [Shajari, Neda] Shiraz Univ Med Sci, Sch Med, Dept Immunol, Shiraz, Iran.
   [Duijf, Pascal H. G.] Univ Queensland, Diamantina Inst, Translat Res Inst, Brisbane, Qld, Australia.
   [Nofouzi, Katayoon] Univ Tabriz, Fac Vet Med, Dept Pathobiol, Tabriz, Iran.
C3 Tabriz University of Medical Science; Tabriz University of Medical
   Science; University of Southern Denmark; Shiraz University of Medical
   Science; University of Queensland; University of Tabriz
RP Baradaran, B (corresponding author), Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran.
EM baradaranb@tbzmed.ac.ir
RI Nofouzi, Katayoon/AAK-8130-2021; Mansoori, Behzad/T-2720-2017; Gaballu,
   Fereydoon/AAM-8731-2021; Arshad, Muhammad/A-4201-2013; Duijf,
   Pascal/KRO-8849-2024; Shirjang, Solmaz/K-2426-2019; Baradaran,
   Behzad/AAQ-5177-2020; Duijf, Pascal/E-7110-2012
OI baradaran, behzad/0000-0002-8642-6795; Shajari,
   Neda/0009-0005-8060-0472; Duijf, Pascal/0000-0001-8646-9843; Shirjang,
   Solmaz/0000-0003-2303-8645
FU Iran national science foundation [93041394]
FX This work was financially supported by the Iran national science
   foundation [grant number 93041394].
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NR 46
TC 22
Z9 22
U1 2
U2 8
PU TABRIZ UNIV MEDICAL SCIENCES & HEALTH SERVICES
PI TABRIZ
PA DANESHGHAH ST, TABRIZ, REPUBLIC ISLAMIC 51664-14766, IRAN
SN 2228-5881
EI 2251-7308
J9 ADV PHARM BULL
JI Adv. Pharm. Bull.
PY 2020
VL 10
IS 3
BP 444
EP 451
DI 10.34172/apb.2020.054
PG 8
WC Pharmacology & Pharmacy
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA LN2BN
UT WOS:000532749000014
PM 32665904
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Guo, SC
   Zheng, SL
   Liu, ML
   Wang, GD
AF Guo, Shanchun
   Zheng, Shilong
   Liu, Mingli
   Wang, Guangdi
TI Novel Anti-Cancer Stem Cell Compounds: A Comprehensive Review
SO PHARMACEUTICS
LA English
DT Review
DE targeted therapy; Notch; Wnt/beta-catenin; ALDH; compound
ID NF-KAPPA-B; TRANS-RETINOIC ACID; LUNG-CANCER STEM;
   EPITHELIAL-MESENCHYMAL TRANSITION; WNT/BETA-CATENIN PATHWAY; WNT
   SIGNALING PATHWAY; BREAST-CANCER; COLORECTAL-CANCER; ALDEHYDE
   DEHYDROGENASE; MAMMARY-GLAND
AB Cancer stem cells (CSCs) possess a significant ability to renew themselves, which gives them a strong capacity to form tumors and expand to encompass additional body areas. In addition, they possess inherent resistance to chemotherapy and radiation therapies used to treat many forms of cancer. Scientists have focused on investigating the signaling pathways that are highly linked to the ability of CSCs to renew themselves and maintain their stem cell properties. The pathways encompassed are Notch, Wnt/beta-catenin, hedgehog, STAT3, NF-kappa B, PI-3K/Akt/mTOR, sirtuin, ALDH, MDM2, and ROS. Recent studies indicate that directing efforts towards CSC cells is essential in eradicating the overall cancer cell population and reducing the likelihood of tumor metastasis. As our comprehension of the mechanisms that stimulate CSC activity, growth, and resistance to chemotherapy advances, the discovery of therapeutic drugs specifically targeting CSCs, such as small-molecule compounds, holds the potential to revolutionize cancer therapy. This review article examines and analyzes the novel anti-CSC compounds that have demonstrated effective and selective targeting of pathways associated with the renewal and stemness of CSCs. We also discussed their special drug metabolism and absorption mechanisms. CSCs have been the subject of much study in cancer biology. As a possible treatment for malignancies, small-molecule drugs that target CSCs are gaining more and more attention. This article provides a comprehensive review of the current state of key small-molecule compounds, summarizes their recent developments, and anticipates the future discovery of even more potent and targeted compounds, opening up new avenues for cancer treatment.
C1 [Guo, Shanchun; Zheng, Shilong; Wang, Guangdi] Xavier Univ Louisiana, RCMI Canc Res Ctr, New Orleans, LA 70125 USA.
   [Guo, Shanchun; Zheng, Shilong; Wang, Guangdi] Xavier Univ Louisiana, Dept Chem, New Orleans, LA 70125 USA.
   [Liu, Mingli] Morehouse Sch Med, Dept Biochem & Immunol, Atlanta, GA 30310 USA.
C3 Xavier University of Louisiana; Xavier University of Louisiana;
   Morehouse School of Medicine
RP Guo, SC; Wang, GD (corresponding author), Xavier Univ Louisiana, RCMI Canc Res Ctr, New Orleans, LA 70125 USA.; Guo, SC; Wang, GD (corresponding author), Xavier Univ Louisiana, Dept Chem, New Orleans, LA 70125 USA.
EM sguo@xula.edu; szheng@xula.edu; mliu@msm.edu; gwang@xula.edu
RI Z, Shilong/H-3746-2019
OI Guo, Shanchun/0000-0002-3593-3738; zheng, shilong/0000-0002-6244-2408
FU National Institute of Minority Health and Health Disparities (NIMHD)
   [U54MD007595]; NIH/NIGMS [SC1 GM144021]
FX This study was funded by National Institute of Minority Health and
   Health Disparities (NIMHD), U54MD007595 (G. Wang), and NIH/NIGMS SC1
   GM144021 (ML).
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NR 227
TC 0
Z9 0
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1999-4923
J9 PHARMACEUTICS
JI Pharmaceutics
PD AUG
PY 2024
VL 16
IS 8
AR 1024
DI 10.3390/pharmaceutics16081024
PG 27
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA E8H9L
UT WOS:001305367800001
PM 39204369
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Heinrich, K
   Miller-Phillips, L
   Ziemann, F
   Hasselmann, K
   Rühlmann, K
   Flach, M
   Biro, D
   von Bergwelt-Baildon, M
   Holch, J
   Herold, T
   von Baumgarten, L
   Greif, PA
   Jeremias, I
   Wuerstlein, R
   Casuscelli, J
   Spitzweg, C
   Seidensticker, M
   Renz, B
   Corradini, S
   Baumeister, P
   Goni, E
   Tufman, A
   Jung, A
   Kumbrink, J
   Kirchner, T
   Klauschen, F
   Metzeler, KH
   Heinemann, V
   Westphalen, CB
AF Heinrich, Kathrin
   Miller-Phillips, Lisa
   Ziemann, Frank
   Hasselmann, Korbinian
   Ruehlmann, Katharina
   Flach, Madeleine
   Biro, Dorottya
   von Bergwelt-Baildon, Michael
   Holch, Julian
   Herold, Tobias
   von Baumgarten, Louisa
   Greif, Philip A.
   Jeremias, Irmela
   Wuerstlein, Rachel
   Casuscelli, Jozefina
   Spitzweg, Christine
   Seidensticker, Max
   Renz, Bernhard
   Corradini, Stefanie
   Baumeister, Philipp
   Goni, Elisabetta
   Tufman, Amanda
   Jung, Andreas
   Kumbrink, Joerg
   Kirchner, Thomas
   Klauschen, Frederick
   Metzeler, Klaus H.
   Heinemann, Volker
   Westphalen, C. Benedikt
TI Lessons learned: the first consecutive 1000 patients of the
   CCCMunich<SUP>LMU</SUP> Molecular Tumor Board
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Article
DE Precision oncology; Personalized medicine; Molecular tumor board;
   Targeted therapy; Comprehensive genomic profiling
ID PRECISION ONCOLOGY; OPEN-LABEL; CANCERS; EFFICACY; SELPERCATINIB;
   MULTICENTER; MEDICINE; THERAPY; IMPACT
AB Purpose In 2016, the University of Munich Molecular Tumor Board (MTB) was implemented to initiate a precision oncology program. This review of cases was conducted to assess clinical implications and functionality of the program, to identify current limitations and to inform future directions of these efforts. Methods Charts, molecular profiles, and tumor board decisions of the first 1000 consecutive cases (01/2016-03/2020) were reviewed. Descriptive statistics were applied to describe relevant findings. Results Of the first 1000 patients presented to the MTB; 914 patients received comprehensive genomic profiling. Median age of patients was 56 years and 58% were female. The most prevalent diagnoses were breast (16%) and colorectal cancer (10%). Different types of targeted or genome-wide sequencing assays were used; most of them offered by the local department of pathology. Testing was technically successful in 88%. In 41% of cases, a genomic alteration triggered a therapeutic recommendation. The fraction of patients receiving a tumor board recommendation differed significantly between malignancies ranging from over 50% in breast or biliary tract to less than 30% in pancreatic cancers. Based on a retrospective chart review, 17% of patients with an MTB recommendation received appropriate treatment. Conclusion Based on these retrospective analyses, patients with certain malignancies (breast and biliary tract cancer) tend to be more likely to have actionable variants. The low rate of therapeutic implementation (17% of patients receiving a tumor board recommendation) underscores the importance of meticulous follow-up for these patients and ensuring broad access to innovative therapies for patients receiving molecular tumor profiling.
C1 [Heinrich, Kathrin; Miller-Phillips, Lisa; Ziemann, Frank; Hasselmann, Korbinian; von Bergwelt-Baildon, Michael; Holch, Julian; Herold, Tobias; Greif, Philip A.; Heinemann, Volker; Westphalen, C. Benedikt] Univ Hosp, LMU Munich, Dept Med 3, Marchioninistr 15, D-81377 Munich, Germany.
   [Heinrich, Kathrin; Miller-Phillips, Lisa; Ziemann, Frank; Hasselmann, Korbinian; Ruehlmann, Katharina; Flach, Madeleine; Biro, Dorottya; von Bergwelt-Baildon, Michael; Holch, Julian; Herold, Tobias; Greif, Philip A.; Wuerstlein, Rachel; Casuscelli, Jozefina; Spitzweg, Christine; Seidensticker, Max; Renz, Bernhard; Corradini, Stefanie; Baumeister, Philipp; Goni, Elisabetta; Tufman, Amanda; Jung, Andreas; Kumbrink, Joerg; Kirchner, Thomas; Klauschen, Frederick; Metzeler, Klaus H.; Heinemann, Volker; Westphalen, C. Benedikt] Univ Hosp, LMU Munich, Comprehens Canc Ctr CCC Munich LMU, Marchioninistr 15, D-81377 Munich, Germany.
   [Heinrich, Kathrin; von Baumgarten, Louisa; Westphalen, C. Benedikt] Ludwig Maximilians Univ Munchen, Dept Neurol, Munich, Germany.
   [von Baumgarten, Louisa; Westphalen, C. Benedikt] Ludwig Maximilians Univ Munchen, Comprehens Canc Ctr CCC Munich LMU, Munich, Germany.
   [Jeremias, Irmela] German Ctr Environm Hlth HMGU, Helmholtz Ctr Munich, Dept Apoptosis Hematopoiet Stem Cells, Munich, Germany.
   [Wuerstlein, Rachel] Ludwig Maximilians Univ Munchen, Univ Hosp, Dept Obstet & Gynecol, Munich, Germany.
   [Casuscelli, Jozefina] Univ Hosp, LMU Munich, Dept Urol, Munich, Germany.
   [Spitzweg, Christine] Univ Hosp, LMU Munich, Dept Med 5, Munich, Germany.
   [Seidensticker, Max] Univ Hosp, LMU Munich, Dept Radiol, Munich, Germany.
   [Renz, Bernhard] Univ Hosp, LMU Munich, Dept Gen Visceral & Transplantat Surg, Munich, Germany.
   [Corradini, Stefanie] Univ Hosp, LMU Munich, Dept Radiat Oncol, Munich, Germany.
   [Baumeister, Philipp] Univ Hosp, LMU Munich, Dept Otorhinolaryngol Head & Neck Surg, Munich, Germany.
   [Goni, Elisabetta] Univ Hosp, LMU Munich, Dept Med 2, Munich, Germany.
   [Tufman, Amanda] Univ Hosp, LMU Munich, Dept Med 5, Munich, Germany.
   [Jung, Andreas; Kumbrink, Joerg; Kirchner, Thomas; Klauschen, Frederick] Ludwig Maximilians Univ LMU, Inst Pathol, Munich, Germany.
   [Metzeler, Klaus H.] Univ Hosp Leipzig, Dept Hematol Cell Therapy & Hemostaseol, Leipzig, Germany.
C3 University of Munich; University of Munich; University of Munich;
   University of Munich; Helmholtz Association; Helmholtz-Center Munich -
   German Research Center for Environmental Health; University of Munich;
   University of Munich; University of Munich; University of Munich;
   University of Munich; University of Munich; University of Munich;
   University of Munich; University of Munich; University of Munich;
   Leipzig University
RP Heinrich, K; Westphalen, CB (corresponding author), Univ Hosp, LMU Munich, Dept Med 3, Marchioninistr 15, D-81377 Munich, Germany.; Heinrich, K; Westphalen, CB (corresponding author), Univ Hosp, LMU Munich, Comprehens Canc Ctr CCC Munich LMU, Marchioninistr 15, D-81377 Munich, Germany.; Heinrich, K; Westphalen, CB (corresponding author), Ludwig Maximilians Univ Munchen, Dept Neurol, Munich, Germany.; Westphalen, CB (corresponding author), Ludwig Maximilians Univ Munchen, Comprehens Canc Ctr CCC Munich LMU, Munich, Germany.
EM Kathrin.Heinrich@med.uni-muenchen.de; cwestpha@med.lmu.de
RI Renz, Bernhard/AGE-4868-2022; Jeremias, Irmela/C-6090-2015; Corradini,
   Stefanie/HLP-6817-2023; Greif, Philipp/J-4432-2016; Metzeler,
   Klaus/C-2118-2009; Herold, Tobias/AAD-1072-2019; Klauschen,
   Frederick/C-5637-2015
OI Metzeler, Klaus/0000-0003-3920-7490; Westphalen,
   Benedikt/0000-0002-5310-3754; Jeremias, Irmela/0000-0003-1773-7677;
   Herold, Tobias/0000-0002-9615-9432; Klauschen,
   Frederick/0000-0002-9131-2389; Greif, Philipp/0000-0002-3744-7936; Renz,
   Bernhard W./0000-0001-9574-8051
FU Projekt DEAL
FX Open Access funding enabled and organized by Projekt DEAL. The authors
   declare that no funds, grants, or other support were received during the
   preparation of this manuscript.
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NR 45
TC 27
Z9 28
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 MAY
PY 2023
VL 149
IS 5
BP 1905
EP 1915
DI 10.1007/s00432-022-04165-0
EA JUL 2022
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA D4DL4
UT WOS:000825374300001
PM 35796778
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Netterberg, I
   Karlsson, MO
   Terstappen, LWMM
   Koopman, M
   Punt, CJA
   Friberg, LE
AF Netterberg, Ida
   Karlsson, Mats O.
   Terstappen, Leon W. M. M.
   Koopman, Miriam
   Punt, Cornelis J. A.
   Friberg, Lena E.
TI Comparing Circulating Tumor Cell Counts with Dynamic Tumor Size Changes
   as Predictor of Overall Survival: A Quantitative Modeling Framework
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID CLINICAL VALIDITY; PROGRESSION-FREE; TREATED PATIENTS; CANCER;
   CHEMOTHERAPY; ONCOLOGY; BEVACIZUMAB; KINETICS; EFFICACY; METRICS
AB Purpose: Quantitative relationships between treatment-induced changes in tumor size and circulating tumor cell (CTC) counts, and their links to overall survival (OS), are lacking. We present a population modeling framework identifying and quantifying such relationships, based on longitudinal data collected in patients with metastatic colorectal cancer (mCRC) to evaluate the value of tumor size and CTC counts as predictors of OS.
   Experimental Design: A pharmacometric approach (i.e., population pharmacodynamic modeling) was used to characterize the changes in tumor size and CTC count and evaluate them as predictors of OS in 451 patients with mCRC treated with chemotherapy and targeted therapy in a prospectively randomized phase III study (CAIRO2).
   Results: A tumor size model of tumor quiescence and drug resistance was used to characterize the tumor size time-course, and was, in addition to the total normalized dose (i.e., of all administered drugs) in a given cycle, related to the CTC counts through a negative binomial model (CTC model). Tumor size changes did not contribute additional predictive value when themean CTC count was a predictor of OS. Treatment reduced the typical mean count from 1.43 to 0.477 (HR = 3.94). The modeling framework was applied to explore whether dose modifications (increased and reduced) would result in a CTC count below 1/7.5 mL after 1 to 2 weeks of treatment.
   Conclusions: Time-varying CTC counts can be useful for early predicting OS in patients with mCRC, and may therefore have potential for model-based treatment individualization. Although tumor size was connected to CTC, its link to OS was weaker.
C1 [Netterberg, Ida; Karlsson, Mats O.; Friberg, Lena E.] Uppsala Univ, Dept Pharmaceut Biosci, Uppsala, Sweden.
   [Terstappen, Leon W. M. M.] Univ Twente, Fac Sci & Technol, Dept Med Cell BioPhys, Enschede, Netherlands.
   [Koopman, Miriam] Univ Utrecht, Univ Med Ctr Utrecht, Dept Med Oncol, Utrecht, Netherlands.
   [Punt, Cornelis J. A.] Univ Amsterdam, Amsterdam Univ Med Ctr, Dept Med Oncol, Amsterdam, Netherlands.
C3 Uppsala University; University of Twente; Utrecht University; Utrecht
   University Medical Center; University of Amsterdam
RP Friberg, LE (corresponding author), Uppsala Univ, Box 591, S-75124 Uppsala, Sweden.
EM lena.friberg@farmbio.uu.se
RI Friberg, Lena/AAW-5888-2021; terstappen, leon/O-4923-2018
OI Friberg, Lena/0000-0002-2979-679X; Terstappen, Leon/0000-0001-5944-3787
FU Swedish Cancer Society [CAN 2017/626]
FX The authors acknowledge all patients and investigators who contributed
   to the CAIRO2 study. The analysis was funded by the Swedish Cancer
   Society (CAN 2017/626).
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NR 50
TC 8
Z9 9
U1 1
U2 5
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 SEP 15
PY 2020
VL 26
IS 18
BP 4892
EP 4900
DI 10.1158/1078-0432.CCR-19-2570
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA NT3DN
UT WOS:000572826000021
PM 32527941
OA Green Submitted, Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Wtorek, K
   Dlugosz, A
   Janecka, A
AF Wtorek, Karol
   Dlugosz, Angelika
   Janecka, Anna
TI Drug resistance in topoisomerase-targeting therapy
SO POSTEPY HIGIENY I MEDYCYNY DOSWIADCZALNEJ
LA English
DT Review
DE drug efflux; gene mutations; doxorubicin; camptothecin; siRNA
ID COLON-CANCER CELLS; MULTIDRUG-RESISTANCE; ABC-TRANSPORTERS;
   BREAST-CANCER; DNA TOPOISOMERASES; II-ALPHA; ANTIPROLIFERATIVE ACTIVITY;
   CAMPTOTHECIN RESISTANCE; SINGLE MUTATION; EXPRESSION
AB Drug resistance is a well-known phenomenon that occurs when initially responsive to chemotherapy cancer cells become tolerant and elude further effectiveness of anticancer drugs. Based on their mechanism of action, anticancer drugs can be divided into cytotoxic-based agents and target-based agents. An important role among the therapeutics of the second group is played by drugs targeting topoisomerases, nuclear enzymes critical to DNA function and cell survival. These enzymes are cellular targets of several groups of anticancer agents which generate DNA damage in rapidly proliferating cancer cells. Drugs targeting topoisomerase I are mostly analogs of camtothecin, a natural compound isolated from the bark of a tree growing in China. Drugs targeting topoisomerase II are divided into poisons, such as anthracycline antibiotics, whose action is based on intercalation between DNA bases, and catalytic inhibitors that block topoisomerase II at different stages of the catalytic cycle. Unfortunately, chemotherapy is often limited by the induction of drug resistance. Identifying mechanisms that promote drug resistance is critical for the improvement of patient prognosis. Cancer drug resistance is a complex phenomenon that may be influenced by many factors. Here we discuss various mechanisms by which cancer cells can develop resistance to topoisomerase-directed drugs, which include enhanced drug efflux, mutations in topoisomerase genes, hypophosphorylation of topoisomerase II catalytic domain, activation of NF-kappa B transcription factor and drug inactivation. All these events may lead to the ineffective induction of cancer cell death. Attempts at circumventing drug resistance through the inhibition of cellular efflux pumps, use of silencing RNAs or inhibition of some important mechanisms, which can allow cancer cells to survive therapy, are also presented.
C1 [Wtorek, Karol; Dlugosz, Angelika; Janecka, Anna] Med Univ Lodz, Dept Biomol Chem, Mazowiecka 6-8, PL-92215 Lodz, Poland.
C3 Medical University Lodz
RP Janecka, A (corresponding author), Med Univ Lodz, Dept Biomol Chem, Mazowiecka 6-8, PL-92215 Lodz, Poland.
EM anna.janecka@umed.lodz.pl
OI Dlugosz-Pokorska, Angelika/0000-0003-4932-6186; Wtorek,
   Karol/0000-0002-3567-6962
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NR 107
TC 5
Z9 5
U1 1
U2 17
PU POLISH ACAD SCIENCES, INST IMMUNOL & EXP THERAPY
PI WROCLAW
PA RUDOLF WEIGL 12, WROCLAW, 53-114, POLAND
SN 0032-5449
EI 1732-2693
J9 POSTEP HIG MED DOSW
JI Postep. Hig. Med. Dosw.
PD DEC 21
PY 2018
VL 72
BP 1073
EP 1083
DI 10.5604/01.3001.0012.8131
PG 11
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA HF8OA
UT WOS:000454500600001
OA gold
DA 2025-01-04
ER

PT J
AU Ngema, LM
   Adeyemi, SA
   Marimuthu, T
   Choonara, YE
AF Ngema, Lindokuhle M.
   Adeyemi, Samson A.
   Marimuthu, Thashree
   Choonara, Yahya E.
TI A review on engineered magnetic nanoparticles in Non-Small-Cell lung
   carcinoma targeted therapy
SO INTERNATIONAL JOURNAL OF PHARMACEUTICS
LA English
DT Review
DE Non-small-cell lung carcinoma; Chemotherapy; Conjugated linoleic acid;
   Nanotechnology; Angiogenesis
ID CONJUGATED LINOLEIC-ACID; IRON-OXIDE NANOPARTICLES; COLON-CANCER CELLS;
   DRUG-DELIVERY; DIENOIC DERIVATIVES; IN-VITRO; MATRIX METALLOPROTEINASES;
   1ST-LINE TREATMENT; GROWTH; CHEMOTHERAPY
AB There are growing appeals for the design of efficacious treatment options for non-small-cell lung carcinoma (NSCLC) as it accrues to similar to 85% cases of lung cancer. Although platinum-based doublet chemotherapy has been the main therapeutic intervention in NSCLC management, this leads to myriad of problems including intolerability to the doublet regimens and detrimental side effects due to high doses. A new approach is therefore needed and warrants the design of targeted drug delivery systems that can halt tumor proliferation and metastasis by targeting key molecules, while exhibiting minimal side effects and toxicity. This review aims to explore the rational design of magnetic nanoparticles for the development of tumor-targeting systems for NSCLC. In the review, we explore the anticancer merits of conjugated linoleic acid (CLA) and provide a concise incursion into its application for the invention of functionalized magnetic nanoparticles in the targeted treatment of NSCLC. Recent nanoparticle-based targeted chemotherapies for targeting angiogenesis biomarkers in NSCLC will also be reviewed to further highlight versatility of magnetic nanoparticles. These developments through molecular tuning at the nanoscale and supported by comprehensive pre-clinical studies could lead to the establishment of precise nanosystems for tumor-homing cancer therapy.
C1 [Ngema, Lindokuhle M.; Adeyemi, Samson A.; Marimuthu, Thashree; Choonara, Yahya E.] Univ Witwatersrand, Sch Therapeut Sci, Dept Pharm & Pharmacol, Wits Adv Drug Delivery Platform Res Unit,Fac Hlth, 7 York Rd, ZA-2193 Parktown, South Africa.
C3 University of Witwatersrand
RP Choonara, YE (corresponding author), Univ Witwatersrand, Sch Therapeut Sci, Dept Pharm & Pharmacol, Wits Adv Drug Delivery Platform Res Unit,Fac Hlth, 7 York Rd, ZA-2193 Parktown, South Africa.
EM yahya.choonara@wits.ac.za
RI Adeyemi, Samson/ABE-4356-2021; Choonara, Yahya/B-2955-2013; Marimuthu,
   Thashree/Q-6605-2018
OI Choonara, Yahya/0000-0002-3889-1529; Marimuthu,
   Thashree/0000-0003-1487-5273; Adeyemi, Samson/0000-0002-4813-904X;
   Ngema, Lindokuhle/0000-0003-4547-4392
FU National Research Foundation (NRF) of South Africa, Pretoria
FX This work is dedicated to Prof. Viness Pillay who passed away on the
   24th July 2020. The National Research Foundation (NRF) of South Africa,
   Pretoria is recognised for their financial support for this work.
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NR 196
TC 12
Z9 12
U1 3
U2 18
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 SEP 5
PY 2021
VL 606
AR 120870
DI 10.1016/j.ijpharm.2021.120870
EA JUL 2021
PG 12
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA UK8TV
UT WOS:000692239100007
PM 34245844
DA 2025-01-04
ER

PT J
AU Yu, YY
   Guo, MZ
   Wei, Y
   Yu, S
   Li, H
   Wang, Y
   Xu, XJ
   Cui, YH
   Tian, JW
   Liang, L
   Peng, K
   Liu, TS
AF Yu, Yiyi
   Guo, Mengzhou
   Wei, Ye
   Yu, Shan
   Li, Hong
   Wang, Yan
   Xu, Xiaojing
   Cui, Yuehong
   Tian, Jiawen
   Liang, Li
   Peng, Ke
   Liu, Tianshu
TI FoxO3a confers cetuximab resistance in RAS wild-type metastatic
   colorectal cancer through c-Myc
SO ONCOTARGET
LA English
DT Article
DE cetuximab resistance; FoxO3a; c-Myc; RAS; colorectal cancer
ID TRANSCRIPTION FACTORS; CELLS; METABOLISM; EXPRESSION; AXIS; PROGRESSION;
   ACTIVATION; MUTATIONS; GROWTH
AB Resistance to epidermal growth factor receptor (EGFR) targeted monoclonal antibody therapy represents a clinical challenge in patients suffered from RAS wild-type (WT) metastatic colorectal cancer (mCRC). However, the molecular mechanisms and key factors conferring this resistance are largely unknown. Forkhead transcription factors of the O class 3a (FoxO3a), an important regulator of cell survival, has been reported with dual functions in tumor recently. In this study, we found that FoxO3a was highly expressed in cetuximab resistant CRC tissues compared with cetuximab sensitive tissues. We therefore further analyzed its function in induced cetuximab resistant RAS-WT CRC cells (Caco2-CR) and intrinsic resistant cells with BRAF mutation (HT29). We found that FoxO3a was significantly up-regulated in Caco2-CR as well as in cetuximab treated HT29 cells. Knockdown of FoxO3a could sensitize these cells to cetuximab treatment with reduced cell proliferation and migration ability. Further, biochemical experiments demonstrated that FoxO3a directly bind to c-Myc promoter and activated the transcription of the c-Myc gene, thus participated in regulating of c-Myc downstream genes, including ACO2, LARS2, MRPL12 and PKM2 in these resistant cells. Moreover, knockdown of c-Myc elevated cell apoptosis to cetuximab treatment and suppressed cell proliferation and migration ability consistently. Altogether, our study indicates that FoxO3a might be a key regulator in cetuximab resistance through up-regulating c-Myc in colorectal cancer targeted therapy.
C1 [Yu, Yiyi; Guo, Mengzhou; Yu, Shan; Li, Hong; Wang, Yan; Xu, Xiaojing; Cui, Yuehong; Tian, Jiawen; Liang, Li; Peng, Ke; Liu, Tianshu] Fudan Univ, Zhong Shan Hosp, Dept Med Oncol, Shanghai, Peoples R China.
   [Wei, Ye] Fudan Univ, Zhong Shan Hosp, Dept Gen Surg, Shanghai, Peoples R China.
C3 Fudan University; Fudan University
RP Liu, TS (corresponding author), Fudan Univ, Zhong Shan Hosp, Dept Med Oncol, Shanghai, Peoples R China.
EM liu.tianshu@zs-hospital.sh.cn
RI xu, xiaojing/C-2759-2014; yu, yiyi/HMP-5697-2023; Liu,
   Tianshu/H-6879-2019
OI Liang, Li/0000-0002-1694-380X
FU National Natural Science Foundation of China [81602038]; Shanghai
   Science and Technology Commission [14ZR1406500]
FX This research is supported by:1. The project 81602038 from National
   Natural Science Foundation of China (www.nsfc.gov.cn).2. Shanghai
   Science and Technology Commission (14ZR1406500).
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NR 34
TC 19
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 DEC 6
PY 2016
VL 7
IS 49
BP 80888
EP 80900
DI 10.18632/oncotarget.13105
PG 13
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EE8LO
UT WOS:000389877500064
PM 27825133
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Howlader, N
   Forjaz, G
   Mooradian, MJ
   Meza, R
   Kong, CY
   Cronin, KA
   Mariotto, AB
   Lowy, DR
   Feuer, EJ
AF Howlader, Nadia
   Forjaz, Goncalo
   Mooradian, Meghan J.
   Meza, Rafael
   Kong, Chung Yin
   Cronin, Kathleen A.
   Mariotto, Angela B.
   Lowy, Douglas R.
   Feuer, Eric J.
TI The Effect of Advances in Lung-Cancer Treatment on Population Mortality
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID NON-HODGKIN-LYMPHOMA; OPEN-LABEL; COLORECTAL-CANCER; PROSTATE-CANCER;
   PHASE-III; TRENDS; DOCETAXEL; NIVOLUMAB; ADENOCARCINOMA; MULTICENTER
AB Lung-cancer incidence has been decreasing in part because of a decrease in smoking. However, the decline in population-based mortality from non-small-cell lung cancer has been greater than can be accounted for by cancer screening and a decrease in cancer incidence. Evidence indicates that advances in treatment account for the acceleration in decreased mortality.
   Background Lung cancer is made up of distinct subtypes, including non-small-cell lung cancer (NSCLC) and small-cell lung cancer (SCLC). Although overall mortality from lung cancer has been declining in the United States, little is known about mortality trends according to cancer subtype at the population level because death certificates do not record subtype information. Methods Using data from Surveillance, Epidemiology, and End Results (SEER) areas, we assessed lung-cancer mortality and linked deaths from lung cancer to incident cases in SEER cancer registries. This allowed us to evaluate population-level mortality trends attributed to specific subtypes (incidence-based mortality). We also evaluated lung-cancer incidence and survival according to cancer subtype, sex, and calendar year. Joinpoint software was used to assess changes in incidence and trends in incidence-based mortality. Results Mortality from NSCLC decreased even faster than the incidence of this subtype, and this decrease was associated with a substantial improvement in survival over time that corresponded to the timing of approval of targeted therapy. Among men, incidence-based mortality from NSCLC decreased 6.3% annually from 2013 through 2016, whereas the incidence decreased 3.1% annually from 2008 through 2016. Corresponding lung cancer-specific survival improved from 26% among men with NSCLC that was diagnosed in 2001 to 35% among those in whom it was diagnosed in 2014. This improvement in survival was found across all races and ethnic groups. Similar patterns were found among women with NSCLC. In contrast, mortality from SCLC declined almost entirely as a result of declining incidence, with no improvement in survival. This result correlates with limited treatment advances for SCLC in the time frame we examined. Conclusions Population-level mortality from NSCLC in the United States fell sharply from 2013 to 2016, and survival after diagnosis improved substantially. Our analysis suggests that a reduction in incidence along with treatment advances - particularly approvals for and use of targeted therapies - is likely to explain the reduction in mortality observed during this period.
C1 [Howlader, Nadia; Forjaz, Goncalo; Cronin, Kathleen A.; Mariotto, Angela B.; Feuer, Eric J.] NCI, Surveillance Res Program, Div Canc Control & Populat Sci, 9609 Med Ctr Dr,Rm 4E532, Bethesda, MD 20892 USA.
   [Lowy, Douglas R.] NCI, Off Director, Bethesda, MD 20892 USA.
   [Mooradian, Meghan J.; Kong, Chung Yin] Harvard Med Sch, Massachusetts Gen Hosp, Boston, MA 02115 USA.
   [Meza, Rafael] Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
   (NCI); National Institutes of Health (NIH) - USA; NIH National Cancer
   Institute (NCI); Harvard University; Massachusetts General Hospital;
   Harvard Medical School; University of Michigan System; University of
   Michigan
RP Howlader, N (corresponding author), NCI, Surveillance Res Program, Div Canc Control & Populat Sci, 9609 Med Ctr Dr,Rm 4E532, Bethesda, MD 20892 USA.
EM howladern@mail.nih.gov
RI Kong, Chang/A-6559-2017; Mariotto, Angela/K-3090-2014
OI Kong, Chung Yin/0000-0001-6431-7830
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NR 38
TC 1004
Z9 1073
U1 15
U2 143
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD AUG 13
PY 2020
VL 383
IS 7
BP 640
EP 649
DI 10.1056/NEJMoa1916623
PG 10
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA NE7HD
UT WOS:000562771200011
PM 32786189
OA Bronze, Green Accepted
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Karabulut, M
   Afsar, CU
   Alis, H
   Oran, E
   Karabulut, S
   Akarsu, C
   Sahbaz, NA
   Gümüsoglu, AY
   Bilgin, E
   Aykan, NF
AF Karabulut, Mehmet
   Afsar, Cigdem Usul
   Alis, Halil
   Oran, Ebru
   Karabulut, Senem
   Akarsu, Cevher
   Sahbaz, Nuri Alper
   Gumusoglu, Alpen Yahya
   Bilgin, Elif
   Aykan, Nuri Faruk
TI Evaluation of epidermal growth factor receptor serum levels and their
   association with clinicopathological characteristics in patients with
   colorectal cancer
SO MOLECULAR AND CLINICAL ONCOLOGY
LA English
DT Article
DE epidermal growth factor receptor; serum; diagnostic; clinicopathological
   characteristics; colorectal cancer
ID TUMOR-MARKERS; EGFR; LIGANDS; BIOMARKERS; GUIDELINES; PROGNOSIS; CEA
AB Colorectal cancer (CRC) is a major public health concern and one of the leading causes of cancer-related mortality worldwide. The aim of the present study was to determine the serum epidermal growth factor receptor (sEGFR) levels in healthy volunteers and patients with CRC, to determine the association between tumor marker levels and clinicopathological findings, and investigate its prognostic value. A total of 140 patients with CRC were enrolled in the present study. Pre-treatment sEGFR levels were determined using ELISA. A total of 140 age- and sex-matched healthy controls were included in the analysis. The median age of patients was 60 years (range, 24-84 years); the majority of the tumor localization was to the colon (n=81, 58%). The median follow-up time was 14 months, while 43 (31%) patients experienced disease progression and 31 (22%) succumbed to the disease. A total of 81 patients (58%) were in the early stages of disease (stage II and III), and 42% of the patients had stage IV disease. The estimated 2-year overall and 1-year progression-free survival rates for the whole patient group were 70% [95% confidence interval (CI): 58.8-81.2] and 26.2% (95% CI: 12.9-39.5), respectively. The number of patients who received neoadjuvant treatment was 37. Of the patients who were administered palliative treatment, 24 received oxaliplatin, whereas 22 received irinotecan and 9 received fluorouracil/capecitabine. A total of 36 and 15 of the patients who received targeted therapy were administered bevacizumab and cetuximab, respectively. Of the 55 patients with metastatic disease who received palliative chemotherapy (CTx), 31% were CTx-responsive. The baseline median sEGFR levels were significantly higher in patients with CRC compared with the healthy control group (P=0.002). In addition, established clinical variables, including no surgical resection, metastatic stage, higher pathological tumor stage, poorer regression score (3-4) and higher lactate dehydrogenase levels, were found to be associated with higher sEGFR levels (P=0.03, P=0.009, P=0.05, P=0.05 and P=0.05, respectively). The results of the present study did not reveal statistically significant associations between sEGFR concentrations and overall and progression-free survival rates. In conclusion, sEGFR concentrations may be diagnostic markers in patients with CRC; however, their predictive and prognostic values were not determined.
C1 [Karabulut, Mehmet; Alis, Halil; Oran, Ebru; Akarsu, Cevher; Sahbaz, Nuri Alper; Gumusoglu, Alpen Yahya] Istanbul Bakirkoy Dr Sadi Konuk Educ & Res Hosp, Clin Gen Surg, TR-34147 Istanbul, Turkey.
   [Afsar, Cigdem Usul] Bakirkoy Acibadem Hosp, Clin Med Oncol, 1 Halit Ziya Usakligil Cd, TR-34140 Istanbul, Turkey.
   [Karabulut, Senem] Istanbul Bakirkoy Dr Sadi Konuk Educ & Res Hosp, Clin Med Oncol, TR-34147 Istanbul, Turkey.
   [Bilgin, Elif] Istanbul Univ, Inst Oncol, Dept Basic Oncol, TR-34093 Istanbul, Turkey.
   [Aykan, Nuri Faruk] Istanbul Univ, Inst Oncol, Dept Med Oncol, TR-34093 Istanbul, Turkey.
C3 Bakirkoy Dr. Sadi Konuk Research & Training Hospital; Acibadem Hospitals
   Group; Bakirkoy Dr. Sadi Konuk Research & Training Hospital; Istanbul
   University; Istanbul University
RP Afsar, CU (corresponding author), Bakirkoy Acibadem Hosp, Clin Med Oncol, 1 Halit Ziya Usakligil Cd, TR-34140 Istanbul, Turkey.
EM cigdemusul@yahoo.com
RI Alis, Halil/AAJ-6721-2020; Sahbaz, Nuri Alper/LWJ-3392-2024; Şen,
   Ebru/ABB-6373-2021; Afsar, Cigdem/C-3436-2015; karabulut,
   senem/AAT-3594-2020; Bilgin, Elif/A-6543-2018; Aykan, Nuri
   Faruk/I-6425-2019
OI Bilgin, Elif/0000-0003-0077-7939; Aykan, Nuri Faruk/0000-0002-5472-3218
CR Arteaga CL, 2001, J CLIN ONCOL, V19, p32S
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NR 26
TC 2
Z9 2
U1 0
U2 0
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 NOV
PY 2017
VL 7
IS 5
BP 787
EP 797
DI 10.3892/mco.2017.1405
PG 11
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA VH8DK
UT WOS:000455354600013
PM 29142750
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU García-Solano, J
   Turpin, MC
   Torres-Moreno, D
   Huertas-López, F
   Tuomisto, A
   Mäkinen, MJ
   Conesa, A
   Conesa-Zamora, P
AF Garcia-Solano, Jose
   Turpin, Maria C.
   Torres-Moreno, Daniel
   Huertas-Lopez, Francisco
   Tuomisto, Anne
   Makinen, Markus J.
   Conesa, Ana
   Conesa-Zamora, Pablo
TI Two histologically colorectal carcinomas subsets from the serrated
   pathway show different methylome signatures and diagnostic biomarkers
SO CLINICAL EPIGENETICS
LA English
DT Article
DE Colorectal cancer; Methylome; Serrated; Immune response; Microsatellite
   instability; Epigenetics; Colon carcinogenesis; CD14; HLA-DOA
ID LIVER-TRANSPLANT REJECTION; MICROSATELLITE INSTABILITY; CANCER;
   ADENOCARCINOMA; METHYLATION; EXPRESSION; MUTATIONS; GENES; TIME; KRAS
AB BackgroundAltered methylation patterns are driving forces in colorectal carcinogenesis. The serrated adenocarcinoma (SAC) and sporadic colorectal carcinoma showing histological and molecular features of microsatellite instability (hmMSI-H) are two endpoints of the so-called serrated pathological route sharing some characteristics but displaying a totally different immune response and clinical outcome. However, there are no studies comparing the methylome of these two subtypes of colorectal carcinomas. The methylation status of 450,000 CpG sites using the Infinium Human Methylation 450 BeadChip array was investigated in 48 colorectal specimens, including 39 SACs and 9 matched hmMSI-H.ResultsMicroarray data comparing SAC and hmMSI-H showed an enrichment in functions related to morphogenesis, neurogenesis, cytoskeleton, metabolism, vesicle transport and immune response and also significant differential methylation of 1540 genes, including CD14 and HLA-DOA which were more methylated in hmMSI-H than in SAC and subsequently validated at the CpG, mRNA and protein level using pyrosequencing, quantitative polymerase chain reaction (qPCR) and immunohistochemistry.ConclusionsThese results demonstrate particular epigenetic regulation patterns in SAC which may help to define key molecules responsible for the characteristic weak immune response of SAC and identify potential targets for treating SAC, which lacks molecular targeted therapy.
C1 [Garcia-Solano, Jose; Torres-Moreno, Daniel] Santa Lucia Gen Univ Hosp, Dept Pathol, C Mezquita S-N, Cartagena 30202, Spain.
   [Garcia-Solano, Jose; Conesa-Zamora, Pablo] Catholic Univ Murcia UCAM, Fac Ciencias Salud, Murcia, Spain.
   [Garcia-Solano, Jose; Conesa-Zamora, Pablo] IMIB, Murcia, Spain.
   [Turpin, Maria C.] Univ Francisco de Vitoria, Fac Expt Sci, Carretera Pozuelo Majadahonda Km 1-800, Madrid 28223, Spain.
   [Huertas-Lopez, Francisco; Conesa, Ana] Univ Florida, Inst Food & Agr Sci, Microbiol & Cell Sci Dept, Gainesville, FL 32611 USA.
   [Tuomisto, Anne; Makinen, Markus J.] Univ Oulu, Dept Pathol, Canc & Translat Med Res Inst, Oulu, Finland.
   [Tuomisto, Anne; Makinen, Markus J.] Univ Oulu, Med Res Ctr, Oulu, Finland.
   [Tuomisto, Anne; Makinen, Markus J.] Oulu Univ Hosp, Oulu, Finland.
   [Conesa, Ana] CIPF, Genom Gene Express Lab, Valencia, Spain.
   [Conesa, Ana] Univ Florida, Inst Food & Agr Sci, Genet Inst, Gainesville, FL 32611 USA.
   [Conesa-Zamora, Pablo] Santa Lucia Gen Univ Hosp, Dept Clin Chem, C Mezquita S-N, Cartagena 30202, Spain.
C3 Universidad Catolica de Murcia; Universidad Francisco de Vitoria; State
   University System of Florida; University of Florida; University of Oulu;
   University of Oulu; University of Oulu; Prince Felipe Research Center;
   State University System of Florida; University of Florida
RP Conesa-Zamora, P (corresponding author), Catholic Univ Murcia UCAM, Fac Ciencias Salud, Murcia, Spain.; Conesa-Zamora, P (corresponding author), IMIB, Murcia, Spain.
EM pablo.conesa@carm.es
RI Conesa-Zamora, Pablo/S-1408-2019; Conesa, Ana/A-9559-2014; Turpin
   Sevilla, Maria del Carmen/H-8312-2017
OI Conesa-Zamora, Pablo/0000-0003-0190-3044; Conesa,
   Ana/0000-0001-9597-311X; Huertas-Lopez, Francisco/0000-0002-9467-9645;
   Turpin Sevilla, Maria del Carmen/0000-0002-3187-7409
FU Instituto de Salud Carlos III, Ministerio de Sanidad, Spain; FEDER funds
   [PI12-1232, PI15-0626]
FX This work was supported by a grant from Instituto de Salud Carlos III,
   Ministerio de Sanidad, Spain, and FEDER funds (refs: PI12-1232 and
   PI15-0626).
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NR 35
TC 11
Z9 11
U1 0
U2 4
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1868-7083
J9 CLIN EPIGENETICS
JI Clin. Epigenetics
PD NOV 9
PY 2018
VL 10
AR 141
DI 10.1186/s13148-018-0571-3
PG 12
WC Oncology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Genetics & Heredity
GA HA0EH
UT WOS:000449879400001
PM 30413173
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Tang, TY
   Nichetti, F
   Kaplan, B
   Lonardi, S
   Pietrantonio, F
   Salvatore, L
   Vivaldi, C
   Rimassa, L
   de Braud, F
   Rizzato, MD
   Pavlick, D
   Chu, RY
   De Armas, AD
   Sharaf, R
   Sokol, E
   Ahnert, JR
   Ross, JS
   Javle, M
   Niger, M
AF Tang, Tin-Yun
   Nichetti, Federico
   Kaplan, Ben
   Lonardi, Sara
   Pietrantonio, Filippo
   Salvatore, Lisa
   Vivaldi, Caterina
   Rimassa, Lorenza
   de Braud, Filippo
   Rizzato, Mario Domenico
   Pavlick, Dean
   Chu, Randy
   De Armas, Anaemy Danner
   Sharaf, Radwa
   Sokol, Ethan
   Ahnert, Jordi Rodon
   Ross, Jeffrey S.
   Javle, Milind
   Niger, Monica
TI Comparative Genomic Analysis and Clinical Outcomes of
   <i>BRAF</i>-mutated Advanced Biliary Tract Cancers
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID METASTATIC COLORECTAL-CANCER; SIGNALING PATHWAY; MUTATIONS;
   TUMORIGENESIS
AB Purpose: BRAF mutations are rare in biliary tract cancers (BTC), but are of interest given the recent developments in targeted therapy for BTC. We investigated the clinical outcomes in a cohort of BRAF-mutant advanced BTC treated with first-line chemotherapy. Furthermore, we investigated the genomic landscape of BRAF class I, II, and III mutations in the intrahepatic cholangiocarcinoma (iCCA) subgroup of BTC. Experimental Design: We analyzed two nonoverlapping cohorts. We examined the genomic landscape of BRAF-mutated iCCA in a "genomic cohort" [187 class I, 82 class II, 113 class III BRAF mutants and 8,026 wildtype (WT)]. We also analyzed median progression-free survival (PFS) and overall survival (OS) on first-line chemotherapy in a separate multi-institutional "clinical cohort" of patients with BTC (including iCCA and extrahepatic cholangiocarcinoma (eCCA) and gallbladder cancer; 41 class I, 32 class II+III BRAF mutants and 1,042 WT). Results: In the entire BTC clinical cohort, the median PFS was shorter for class I [HR, 2.11 (P < 0.001)] and class II+III [HR, 1.72 (P = 0.007)] as compared with BRAF WT. OS was also shorter in class I [HR, 2.04 (P = 0.011)] and class II+III [HR, 1.86 (P = 0.002)] as compared with BRAF WT. In the iCCA subgroup, class I alterations were mutually exclusive with FGFR2, IDH1/2, ERBB2, and KRAS mutations. Class II+III mutations appear to be mutually exclusive with FGFR2 and KRAS. Conclusions: In BTC, all classes of BRAF mutations are associated with a worse prognosis. BRAF mutations occur in 5% of iCCA subgroup and may be mutually exclusive with other targetable mutations.
C1 [Tang, Tin-Yun] Univ Texas MD Anderson Canc Ctr, Div Canc Med, Houston, TX 77030 USA.
   [Nichetti, Federico; Pietrantonio, Filippo; de Braud, Filippo; Niger, Monica] Fdn IRCCS Ist Nazl Tumori, Med Oncol Dept, Milan, Italy.
   [Nichetti, Federico] Natl Ctr Tumor Dis NCT, Mol Diagnost Program, Computat Oncol, Heidelberg, Germany.
   [Nichetti, Federico] German Canc Res Ctr, Heidelberg, Germany.
   [Kaplan, Ben; Pavlick, Dean; Sharaf, Radwa; Sokol, Ethan; Ross, Jeffrey S.] Fdn Med, Cambridge, MA USA.
   [Lonardi, Sara; Rizzato, Mario Domenico] Veneto Inst Oncol IOV IRCCS, Dept Oncol, Padua, Italy.
   [Salvatore, Lisa] Fdn Policlin Univ Agostino Gemelli, Comprehens Canc Ctr, Oncol Med, IRCCS, Rome, Italy.
   [Vivaldi, Caterina] Azienda Osped Univ Pisana, Azienda Ospedaliero Universitaria Pisana, Pisa, Italy.
   [Rimassa, Lorenza] Humanitas Univ, Dept Biomed Sci, Milan, Italy.
   [Rimassa, Lorenza] IRCCS Humanitas Res Hosp, Human Canc Ctr, Med Oncol & Hematol Unit, Milan, Italy.
   [de Braud, Filippo] Univ Milan, Dept Oncol & Hemato Oncol, Milan, Italy.
   [Rizzato, Mario Domenico] Univ Padua, Dept Surg Oncol & Gastroenterol, Padua, Italy.
   [Chu, Randy; De Armas, Anaemy Danner] Univ Texas MD Anderson Canc Ctr, Dept Genom Med, Houston, TX USA.
   [Ahnert, Jordi Rodon; Javle, Milind] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
   [Ahnert, Jordi Rodon] Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapeut, Houston, TX 77030 USA.
   [Ross, Jeffrey S.] Upstate Med Univ, Dept Pathol, Syracuse, NY USA.
   [Ross, Jeffrey S.] Upstate Med Univ, Dept Urol, Syracuse, NY USA.
   [Ross, Jeffrey S.] Upstate Med Univ, Dept Med Oncol, Syracuse, NY USA.
   [Javle, Milind] Univ Texas MD Anderson Canc Ctr, 1515 Holcombe Blvd, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; Fondazione
   IRCCS Istituto Nazionale Tumori Milan; Helmholtz Association; German
   Cancer Research Center (DKFZ); Ruprecht Karls University Heidelberg;
   Helmholtz Association; German Cancer Research Center (DKFZ); Foundation
   Medicine; IRCCS Istituto Oncologico Veneto (IOV); Catholic University of
   the Sacred Heart; IRCCS Policlinico Gemelli; University of Pisa; Azienda
   Ospedaliero Universitaria Pisana; Humanitas University; University of
   Milan; University of Padua; University of Texas System; UTMD Anderson
   Cancer Center; University of Texas System; UTMD Anderson Cancer Center;
   University of Texas System; UTMD Anderson Cancer Center; State
   University of New York (SUNY) System; State University of New York
   (SUNY) Upstate Medical Center; State University of New York (SUNY)
   System; State University of New York (SUNY) Upstate Medical Center;
   State University of New York (SUNY) System; State University of New York
   (SUNY) Upstate Medical Center; University of Texas System; UTMD Anderson
   Cancer Center
RP Javle, M (corresponding author), Univ Texas MD Anderson Canc Ctr, 1515 Holcombe Blvd, Houston, TX 77030 USA.
EM mjavle@mdanderson.org
RI Niger, Monica/AAC-2452-2022; Nichetti, Federico/AAG-3984-2020; Rizzato,
   Mario/AAI-5958-2021; de Braud, Filippo Guglielmo Maria/B-9997-2017;
   Pietrantonio, Filippo/C-2180-2017; Salvatore, Lisa/L-7746-2019; Lonardi,
   Sara/F-4228-2014; Rimassa, Lorenza/N-4884-2016
OI Nichetti, Federico/0000-0001-8044-4207; de Braud, Filippo Guglielmo
   Maria/0000-0003-0103-730X; Rizzato, Mario Domenico/0000-0002-8322-2842;
   Vivaldi, Caterina/0000-0001-9307-2326; Pietrantonio,
   Filippo/0000-0002-8530-8420; Salvatore, Lisa/0000-0003-3864-0719;
   Lonardi, Sara/0000-0002-7593-8138; Tang, Tin-Yun/0000-0003-2030-9518;
   Rimassa, Lorenza/0000-0001-9957-3615
FU Italian Ministry of Health - Ricerca Finalizzata, Progetto
   [GR-2019-12368903]; Italian Ministry of Health - Ricerca Finalizzata
FX S. Lonardi is funded by Italian Ministry of Health - Ricerca
   Finalizzata, Progetto (GR-2019-12368903); M.D. Rizzato is also funded by
   Italian Ministry of Health - Ricerca Finalizzata, Progetto
   (GR-2019-12368903).
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NR 50
TC 4
Z9 5
U1 0
U2 2
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 DEC 1
PY 2023
VL 29
IS 23
BP 4853
EP 4862
DI 10.1158/1078-0432.CCR-23-1926
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GR4D4
UT WOS:001154376400027
PM 37773629
DA 2025-01-04
ER

PT J
AU Chu, TQ
   Li, R
   Shao, MH
   Ye, JY
   Han, BH
AF Chu, Tian-qing
   Li, Rong
   Shao, Min-hua
   Ye, Jun-yi
   Han, Bao-hui
TI <i>RAD18</i> polymorphisms are associated with platinum-based
   chemotherapy toxicity in Chinese patients with non-small cell lung
   cancer
SO ACTA PHARMACOLOGICA SINICA
LA English
DT Article
DE NSCLC; platinum-based chemotherapy; RAD18 polymorphisms;
   gastrointestinal toxicity; hematological toxicity
ID DNA-POLYMERASE-ETA; TRANSLESION SYNTHESIS; GENETIC POLYMORPHISMS;
   COLORECTAL-CANCER; STRUCTURAL BASIS; POL-ETA; REPAIR; DAMAGE; UBIQUITIN;
   RESISTANCE
AB Aim: Although targeted therapy is very efficient for lung cancer, traditional platinum-based chemotherapies are still the principal strategy in the absence of positive biomarkers. The aim of the present study is to evaluate the contribution of RAD18 polymorphisms to platinum-chemotherapy response and its potential side effects in Chinese patients with non-small cell lung cancer (NSCLC).
   Methods: A total of 1021 Chinese patients with histological diagnosis of advanced NSCLC were enrolled. Treatment responses were classified into 4 categories (complete response, partial response, stable disease and progressive disease). Gastrointestinal and hematological toxicity incidences were assessed twice a week during the first-line treatment. Ten RAD18 SNPs were genotyped. A logistic regression model was utilized to analyze the associations between RAD18 SNPs and treatment response or toxicity.
   Results: Among the 10 SNPs tested, none was significantly correlated with the treatment response in a combined cohort. For gastrointestinal toxicity incidences, rs586014 was significantly associated with an increased risk of grade 3 or 4 gastrointestinal toxicity in non-smokers and in the combined cohort; rs654448 and rs618784 were significantly associated with gastrointestinal toxicity in non-smokers; rs6763823 was significantly associated with gastrointestinal toxicity in smokers. For hematological toxicity incidences, rs586014, rs654448 and rs618784 were significantly associated with hematologic toxicity in non-smokers; rs6763823 and rs9880051 were significantly associated with leukocytopenia in smokers.
   Conclusion: RAD18 polymorphisms are correlated with the side effects of platinum-chemotherapy in Chinese patients with advanced NSCLC.
C1 [Chu, Tian-qing; Li, Rong; Shao, Min-hua; Han, Bao-hui] Shanghai Jiao Tong Univ, Shanghai Chest Hosp, Dept Pulm Med, Shanghai 200030, Peoples R China.
   [Ye, Jun-yi] Fudan Univ, Inst Biomed Sci, Shanghai 200032, Peoples R China.
C3 Shanghai Jiao Tong University; Fudan University
RP Han, BH (corresponding author), Shanghai Jiao Tong Univ, Shanghai Chest Hosp, Dept Pulm Med, Shanghai 200030, Peoples R China.
EM hbhxkyy@126.com
OI Li, Rong/0000-0003-3971-1670
FU National Natural Science Foundation of China [81302004]; Shanghai Jiao
   Tong University Grant for Interdisciplinary Research on Medicine and
   Engineering [YG2013MS12]; Major and Key Program of Technology
   Development Foundation of Shanghai Chest Hospital [2014YZDC10101];
   Program of Study Foundation of Chinese Society of Clinical
   Oncology(CSCO) [Y-S2015-007]; Western Medicine Guide Project of Shanghai
   Committee of Science and Technology Foundation [16411964700]
FX This work was supported by the National Natural Science Foundation of
   China (Grant No 81302004), Shanghai Jiao Tong University Grant for
   Interdisciplinary Research on Medicine and Engineering (Grant No
   YG2013MS12), the Major and Key Program of Technology Development
   Foundation of Shanghai Chest Hospital (Grant No 2014YZDC10101), the
   Program of Study Foundation of Chinese Society of Clinical
   Oncology(CSCO) (Grant No Y-S2015-007), and the Western Medicine Guide
   Project of Shanghai Committee of Science and Technology Foundation
   (Grant No 16411964700).
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   Zhang YB, 2000, MOL CELL BIOL, V20, P7099, DOI 10.1128/MCB.20.19.7099-7108.2000
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NR 49
TC 9
Z9 10
U1 0
U2 5
PU NATURE PUBL GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1671-4083
EI 1745-7254
J9 ACTA PHARMACOL SIN
JI Acta Pharmacol. Sin.
PD NOV
PY 2016
VL 37
IS 11
BP 1490
EP 1498
DI 10.1038/aps.2016.100
PG 9
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA EB9ZC
UT WOS:000387755900011
PM 27665847
OA Bronze, Green Published
DA 2025-01-04
ER

PT J
AU Chen, Y
   Ling, CR
   Xu, YS
   Liu, JJ
   Tang, WZ
AF Chen, Yi
   Ling, Chunrun
   Xu, Yansong
   Liu, Junjie
   Tang, Weizhong
TI Evaluation of Diagnostic and Prognostic Value of hsa_circ_0084927 and
   Analysis of Associated ceRNA Network in Colorectal Cancer
SO INTERNATIONAL JOURNAL OF GENERAL MEDICINE
LA English
DT Article
DE circRNAs; ceRNAs; biomarker; colon adenocarcinoma; prognosis
ID E3 LIGASE ITCH; CIRCULAR RNAS; GROWTH; PROGRESSION; METASTASIS;
   MIGRATION; INVASION; VEGF
AB Object: This study aims to analyze the differentially expressed circRNA in colon adenocarcinoma (COAD) and evaluate its diagnostic and prognostic value. Analyze associated circRNA-miRNA-mRNA network in COAD.
   Methods and Materials: Real-time quantitative PCR (RT-PCR) was used to verify differentially expressed circRNA in COAD tissues and cells; Receiver operator characteristic (ROC) and Cox regression analysis were used to evaluating its diagnostic and prognostic value; Meanwhile we conducted CCK-8, invasion, and migration experiments in cell lines to explore the function of circRNA. In addition, a competitive endogenous RNA (ceRNA) network was established using bioinformatics methods to explore its prognostic value and potential functional mechanisms.
   Results: Our study found that hsa_circ_0084927 is highly expressed in COAD tissues and cell lines. Plasma hsa_circ_0084927 can be used as a diagnostic marker for COAD patients; hsacirc_0084927 can promote the proliferation, migration and invasion of COAD cells. In addition, we effectively constructed a ceRNA: network has_circ_0084927/miR-106b-5p/VEGFA. The ceRNA network indicates that hsacirc_0084927 may affect the prognosis of COAD through the regulation of cell cycle, apoptosis and other pathways.
   Conclusion: Our research results indicate that hsa_circ_0084927 has a cancer-promoting effect and may be used as a circulating tumor marker for COAD prognosis. In addition, this study proposes a new ceRNA network to provide new insights for the targeted therapy of COAD.
C1 [Chen, Yi; Tang, Weizhong] Guangxi Med Univ, Dept Gastrointestinal Surg, Canc Hosp, Nanning 530021, Guangxi Zhuang, Peoples R China.
   [Chen, Yi; Tang, Weizhong] Guangxi Clin Res Ctr Colorectal Canc, Nanning 530021, Guangxi Zhuang, Peoples R China.
   [Ling, Chunrun] Peoples Hosp Guangxi Zhuang Autonomous Reg, Dept Colorectal & Anal Surg, Nanning, Guangxi Zhuang, Peoples R China.
   [Xu, Yansong] Guangxi Med Univ, Emergency, Affiliated Hosp 1, Nanning 530021, Peoples R China.
   [Liu, Junjie] Guangxi Med Univ, Dept Ultrasound, Canc Hosp, Nanning 530021, Guangxi Zhuang, Peoples R China.
C3 Guangxi Medical University; Guangxi Medical University; Guangxi Medical
   University
RP Tang, WZ (corresponding author), Guangxi Med Univ, Dept Gastrointestinal Surg, Canc Hosp, Nanning 530021, Guangxi Zhuang, Peoples R China.; Tang, WZ (corresponding author), Guangxi Clin Res Ctr Colorectal Canc, Nanning 530021, Guangxi Zhuang, Peoples R China.; Liu, JJ (corresponding author), Guangxi Med Univ, Dept Ultrasound, Canc Hosp, Nanning 530021, Guangxi Zhuang, Peoples R China.
EM 907870351@qq.com; tangweizhong0771@163.com
FU Innovation Project of Guangxi Graduate Education [YCBZ2021050]; National
   Natural Science Foundation of China [81973533]; Guangxi Science and
   Technology Project [AD19245197, 2019AC03004]; 2019 Guangxi University
   High-level Innovation Team; Project of Outstanding Scholars Program
FX This research was supported by the following projects: (1) Innovation
   Project of Guangxi Graduate Education (YCBZ2021050) ; (2) National
   Natural Science Foundation of China (81973533) ; (3) Guangxi Science and
   Technology Project (AD19245197) ; and (4) 2019 Guangxi University
   High-level Innovation Team and the Project of Outstanding Scholars
   Program, and Guangxi Science and Technology Project (2019AC03004) .
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NR 41
TC 3
Z9 4
U1 0
U2 9
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 2022
VL 15
BP 4357
EP 4377
DI 10.2147/IJGM.S355043
PG 21
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 1A5AK
UT WOS:000791769200003
PM 35493197
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Emery, CM
   Monaco, KA
   Wang, P
   Balak, M
   Freeman, A
   Meltzer, J
   Delach, SM
   Rakiec, D
   Ruddy, DA
   Korn, JM
   Haling, J
   Acker, MG
   Caponigro, G
AF Emery, Caroline M.
   Monaco, Kelli-Ann
   Wang, Ping
   Balak, Marissa
   Freeman, Alyson
   Meltzer, Jodi
   Delach, Scott M.
   Rakiec, Daniel
   Ruddy, David A.
   Korn, Joshua M.
   Haling, Jacob
   Acker, Michael G.
   Caponigro, Giordano
TI BRAF-inhibitor Associated MEK Mutations Increase RAF-Dependent and
   -Independent Enzymatic Activity
SO MOLECULAR CANCER RESEARCH
LA English
DT Article
ID ACQUIRED-RESISTANCE; METASTATIC MELANOMA; PATHWAY ALTERATIONS; CONFER
   RESISTANCE; KINASE ACTIVATION; COLORECTAL-CANCER; TARGETED THERAPY;
   V600E MUTATION; PROTEIN-KINASE; CELL-LINE
AB Alterations in MEK1/2 occur in cancers, both in the treatment naive state and following targeted therapies, most notably BRAF and MEK inhibitors in BRAF-V600E-mutant melanoma and colorectal cancer. Efforts were undertaken to understand the effects of these mutations, based upon protein structural location, and MEK1/2 activity. Two categories of MEK1/2 alterations were evaluated, those associated with either the allosteric pocket or helix-A. Clinically, MEK1/2 alterations of the allosteric pocket are rare and we demonstrate that they confer resistance to MEK inhibitors, while retaining sensitivity to BRAF inhibition. Most mutations described in patients fall within, or are associated with, helix-A. Mutations in this region reduce sensitivity to both BRAF and MEK inhibition and display elevated phospho-ERK1/2 levels, independent from increases in phospho-MEK1/2. Bio-chemical experiments with a representative helix-A variant, MEK1-Q56P, reveal both increased catalytic efficiency of the activated enzyme, and phosphorylation-independent activity relative to wild-type MEK1. Consistent with these findings, MEK1/2 alterations in helix A retain sensitivity to downstream antagonism via pharmacologic inhibition of ERK1/2. This work highlights the importance of classifying mutations based on structural and phenotypic consequences, both in terms of pathway signaling output and response to pharmacologic inhibition. (C) 2017 AACR.
C1 [Emery, Caroline M.; Monaco, Kelli-Ann; Wang, Ping; Balak, Marissa; Freeman, Alyson; Meltzer, Jodi; Delach, Scott M.; Rakiec, Daniel; Ruddy, David A.; Korn, Joshua M.; Acker, Michael G.; Caponigro, Giordano] Novartis Inst Biomed Res, Oncol Dis Area, Cambridge, MA 02139 USA.
   [Haling, Jacob] Novartis Res Fdn, Genom Inst, Oncol Pharmacol, San Diego, CA USA.
   [Emery, Caroline M.] BioMed Valley Discoveries, Kansas City, MO USA.
C3 Novartis; Novartis USA; Novartis; Novartis USA
RP Caponigro, G (corresponding author), Novartis Inst Biomed Res, 250 Massachusetts Ave, Cambridge, MA 02139 USA.
EM giordano.caponigro@novartis.com
OI Acker, Michael/0000-0002-3565-9601
FU Novartis Institutes for BioMedical Research
FX This research was funded by The Novartis Institutes for BioMedical
   Research.
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NR 52
TC 16
Z9 18
U1 1
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1541-7786
EI 1557-3125
J9 MOL CANCER RES
JI Mol. Cancer Res.
PD OCT
PY 2017
VL 15
IS 10
BP 1431
EP 1444
DI 10.1158/1541-7786.MCR-17-0211
PG 14
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FI7FD
UT WOS:000412161400013
PM 28655712
DA 2025-01-04
ER

PT J
AU Yee, NS
   Lengerich, EJ
   Schmitz, KH
   Maranki, JL
   Gusani, NJ
   Tchelebi, L
   Mackley, HB
   Krok, KL
   Baker, MJ
   de Boer, C
   Yee, JD
AF Yee, Nelson S.
   Lengerich, Eugene J.
   Schmitz, Kathryn H.
   Maranki, Jennifer L.
   Gusani, Niraj J.
   Tchelebi, Leila
   Mackley, Heath B.
   Krok, Karen L.
   Baker, Maria J.
   de Boer, Claire
   Yee, Julian D.
TI Frontiers in Gastrointestinal Oncology: Advances in Multi-Disciplinary
   Patient Care
SO BIOMEDICINES
LA English
DT Article
DE gastrointestinal oncology; pancreatic carcinoma; hepatocellular
   carcinoma; biliary tract carcinoma; gastric carcinoma; colorectal
   carcinoma; stereotactic body radiation therapy; liver transplant;
   targeted therapy; psychosocial support
ID HEPATOCELLULAR-CARCINOMA; PANCREATIC-CANCER; COLORECTAL-CARCINOMA;
   AMERICAN SOCIETY; RISK-FACTORS; DIAGNOSIS; EXERCISE;
   CHOLANGIOPANCREATOSCOPY; MULTICENTER; MANAGEMENT
AB Cancers of the digestive system remain highly lethal; therefore, the care of patients with malignant diseases of the digestive tract requires the expertise of providers from multiple health disciplines. Progress has been made to advance the understanding of epidemiology and genetics, diagnostic and screening evaluation, treatment modalities, and supportive care for patients with gastrointestinal cancers. At the Multi-Disciplinary Patient Care in Gastrointestinal Oncology conference at the Hershey Country Club in Hershey, Pennsylvania on 29 September 2017, the faculty members of the Penn State Health Milton S. Hershey Medical Center presented a variety of topics that focused on this oncological specialty. In this continuing medical education-certified conference, updates on the population sciences including health disparities and resistance training were presented. Progress made in various diagnostic evaluation and screening procedures was outlined. New developments in therapeutic modalities in surgical, radiation, and medical oncology were discussed. Cancer genetic testing and counseling and the supportive roles of music and arts in health and cancer were demonstrated. In summary, this disease-focused medical conference highlighted the new frontiers in gastrointestinal oncology, and showcase the multi-disciplinary care provided at the Penn State Cancer Institute.
C1 [Yee, Nelson S.] Penn State Univ, Coll Med, Div Hematol Oncol,Expt Therapeut Program,Penn Sta, Dept Med,Penn State Hlth Milton S Hershey Med Ctr, Hershey, PA 17033 USA.
   [Lengerich, Eugene J.; Schmitz, Kathryn H.] Penn State Univ, Populat Sci Program, Penn State Canc Inst, Dept Publ Hlth Sci, Hershey, PA 17033 USA.
   [Maranki, Jennifer L.; Krok, Karen L.] Penn State Univ, Coll Med, Div Gastroenterol & Hepatol, Dept Med,Penn State Hlth Milton S Hershey Med Ctr, Hershey, PA 17033 USA.
   [Gusani, Niraj J.] Penn State Univ, Coll Med, Div Gen Surg & Surg Oncol, Dept Surg,Penn State Hlth Milton S Hershey Med Ct, Hershey, PA 17033 USA.
   [Tchelebi, Leila] Penn State Univ, Coll Med, Dept Radiol, Penn State Hlth Milton S Hershey Med Ctr, Hershey, PA 17033 USA.
   [Mackley, Heath B.] Penn State Univ, Coll Med, Dept Radiol Med & Pediat, Penn State Hlth Milton S Hershey Med Ctr, Hershey, PA 17033 USA.
   [Baker, Maria J.] Penn State Univ, Coll Med, Dept Med, Penn State Hlth Milton S Hershey Med Ctr,Penn Sta, Hershey, PA 17033 USA.
   [de Boer, Claire] Penn State Univ, Coll Med, Ctr Stage Arts Hlth, Penn State Hlth Milton S Hershey Med Ctr,Dept Hum, Hershey, PA 17033 USA.
   [Yee, Julian D.] Penn State Univ, Coll Liberal Arts, State Coll, PA 16801 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 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
   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 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 Commonwealth System of
   Higher Education (PCSHE); Pennsylvania State University
RP Yee, NS (corresponding author), Penn State Univ, Coll Med, Div Hematol Oncol,Expt Therapeut Program,Penn Sta, Dept Med,Penn State Hlth Milton S Hershey Med Ctr, Hershey, PA 17033 USA.
EM nyee@pennstatehealth.psu.edu; elengeri@phs.psu.edu;
   kschmitz@phs.psu.edu; jmaranki@pennstatehealth.psu.edu;
   ngusani@pennstatehealth.psu.edu; ltchelebi@pennstatehealth.psu.edu;
   hmackley@pennstatehealth.psu.edu; kkrok@pennstatehealth.psu.edu;
   mbaker@pennstatehealth.psu.edu; cdeboer@pennstatehealth.psu.edu;
   jdy133@psu.edu
RI Schmitz, Kathryn/HOA-7861-2023; Gusani, Niraj/C-8171-2013
OI , Leila/0000-0002-4789-449X; Schmitz, Kathryn H./0000-0003-2400-2935;
   Krok, Karen/0000-0001-5849-5251; Gusani, Niraj/0000-0002-7695-5108
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NR 58
TC 7
Z9 7
U1 0
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD JUN
PY 2018
VL 6
IS 2
AR 64
DI 10.3390/biomedicines6020064
PG 16
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 GK8PN
UT WOS:000436489000028
PM 29865163
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Jiang, HP
   Kang, BX
   Huang, XM
   Yan, YC
   Wang, S
   Ye, YJ
   Shen, ZL
AF Jiang, Hongpeng
   Kang, Boxi
   Huang, Xinmei
   Yan, Yichao
   Wang, Shan
   Ye, Yingjiang
   Shen, Zhanlong
TI Cancer IgG, a potential prognostic marker, promotes colorectal cancer
   progression
SO CHINESE JOURNAL OF CANCER RESEARCH
LA English
DT Article
DE Cancer IgG; colorectal cancer; E-cadherin; prognosis
ID IMMUNOGLOBULIN-G; GROWTH; EXPRESSION; INVASION; CATENIN; BINDING; GENE;
   ASSOCIATION; MIGRATION; PROTEINS
AB Objective: Currently, no satisfactory targets for colorectal cancer or markers for immunotherapy and diagnosis and prognosis are available. Immunoglobulin G (IgG) is widely expressed in many cancers, and it promotes cancer progression. This study explored the role of cancer-derived IgG (CIgG) in colorectal cancer.
   Methods: First, using a monoclonal antibody to CIgG, we examined the expression levels of CIgG in colorectal cancer cell lines by western blot and immunofluorescence analyses and in tissue specimens by immunohistochemistry. Second, the variable region gene was amplified by nested polymerase chain reaction (PCR), and PCR products were sequenced and analyzed. Third, we investigated the effect of CIgG on colorectal cancer cells by cell proliferation, wound healing, migration and invasion assays, and colony formation assay. Fourth, we performed in vivo tumorigenicity experiments to explore the effect of CIgG on tumorigenicity. Finally, we used RNA-seq analysis and co-immunoprecipitation experiments to further clarify possible mechanisms of CIgG.
   Results: We found that CIgG is widely expressed in colorectal cancer cells, and the overexpression of CIgG indicates significantly poor colorectal cancer prognosis. Furthermore, CIgG knockdown significantly inhibits the proliferation, migration and invasion ability of cells, and tumor growth in vivo. RNA-seq analysis indicated that CIgG knockdown results primarily in changes in expression of apical junction and epithelial-mesenchymal transition-related genes. CIgG may be involved in colorectal cancer invasion and metastasis through interacting with E-cadherin.
   Conclusions: CIgG is a potential human oncogene in colorectal cancer and that it has potential for application as a novel target in targeted therapy and a marker for prognostic evaluation.
C1 [Jiang, Hongpeng; Wang, Shan; Ye, Yingjiang; Shen, Zhanlong] Peking Univ, Beijing Key Lab Colorectal Canc Diag & Treatment, Dept Surg Gastroenterol, Lab Surg Oncol,Peoples Hosp, Beijing 100044, Peoples R China.
   [Kang, Boxi] Peking Univ, Sch Life Sci, Beijing 100871, Peoples R China.
   [Huang, Xinmei] Peking Univ, Sch Basic Med Sci, Dept Immunol, Beijing 100191, Peoples R China.
   [Yan, Yichao] Peking Univ, Int Hosp, Dept Surg Gastroenterol, Beijing 102206, Peoples R China.
C3 Peking University; Peking University; Peking University; Peking
   University
RP Ye, YJ; Shen, ZL (corresponding author), Peking Univ, Beijing Key Lab Colorectal Canc Diag & Treatment, Dept Surg Gastroenterol, Lab Surg Oncol,Peoples Hosp, Beijing 100044, Peoples R China.
EM yeyingjiang@pkuph.edu.cn; shenlong1977@163.com
RI Wang, Jianye/KFA-4087-2024
OI Shen, Zhanlong/0000-0002-6897-5125; Kang, Boxi/0000-0002-0276-0519
FU National Natural Science Foundation of China [8157101395]; Beijing
   Natural Science Foundation [7182171]
FX This present study was supported by grants from the National Natural
   Science Foundation of China (No. 8157101395) and Beijing Natural Science
   Foundation (No. 7182171).
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NR 35
TC 18
Z9 20
U1 2
U2 20
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 JUN
PY 2019
VL 31
IS 3
BP 499
EP 510
DI 10.21147/j.issn.1000-9604.2019.03.12
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IF7SG
UT WOS:000473283600012
PM 31354219
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Liu, JJ
   Xie, H
AF Liu, Junjia
   Xie, Hao
TI BRAF Non-V600 Mutations in Metastatic Colorectal Cancer
SO CANCERS
LA English
DT Review
DE BRAF non-V600 mutation; colorectal cancer; targeted therapy;
   heterogeneity
ID 1ST-LINE TREATMENT; KRAS MUTATIONS; COLON-CANCER; WILD-TYPE; RAF;
   SURVIVAL; VEMURAFENIB; INHIBITION; ACTIVATION; GENOMICS
AB Simple Summary Metastatic Colorectal cancer (CRC) is an aggressive and complex disease influenced by gene changes, including BRAF mutations. While previous work has largely spotlighted the BRAF V600 mutation, there remains much to uncover about its lesser-studied non-V600 counterparts. Through examining their characteristics, clinical relevance, and emerging treatment possibilities, this review bridges some knowledge gaps and paints a clearer picture of the BRAF non-V600 mutations. By understanding these intricacies, healthcare professionals and researchers can be better equipped to explore targeted treatments, potentially enhancing care for metastatic CRC patients.Abstract Colorectal cancer (CRC) is the third leading cause of cancer-related deaths in the United States. Despite advancements in detection and therapeutic options, patients with metastatic CRC continue to face poor survival rates. The heterogeneity of oncogenic alterations, including BRAF mutations, poses a substantial challenge in identifying optimal treatment approaches. Notably, BRAF non-V600 mutations, encompassing class II and class III mutations, exhibit the distinct patterns of the signaling pathways and responses to targeted therapies compared to BRAF V600 mutations (class I). Nevertheless, the current classification system may underestimate the complexity and heterogeneity of BRAF-mutant CRC. Ongoing clinical trials are actively investigating targeted therapies for BRAF non-V600 mutations, but they are being confronted with patient recruitment obstacles due to the genetic diversity of these alterations. Continued research is needed to refine mutation subtyping, identify effective treatment strategies, and improve outcomes for patients with BRAF non-V600-mutant CRC. Enhancing our understanding and management of this specific subgroup of CRC is crucial for developing personalized treatment approaches and advancing patient care. This manuscript provides a comprehensive overview of the recent advances in and perspectives on BRAF non-V600 alterations in colorectal cancer, including relevant ongoing clinical trials.
C1 [Liu, Junjia] Albert Einstein Coll Med, Bronx, NY 10461 USA.
   [Xie, Hao] Mayo Clin, Dept Oncol, Rochester, MN 55905 USA.
C3 Yeshiva University; Montefiore Medical Center; Albert Einstein College
   of Medicine; Mayo Clinic
RP Xie, H (corresponding author), Mayo Clin, Dept Oncol, Rochester, MN 55905 USA.
EM junjia.liu@einsteinmed.edu; xie.hao@mayo.edu
RI xie, hao/KWU-8636-2024
OI Xie, Hao/0000-0002-9640-4055
FU Mayo Clinic Department of Oncology FORIT award; Morton Funger Clinician
   Career Development Fund Award in Colon Cancer Research
FX This research was funded by Mayo Clinic Department of Oncology FORIT
   award, Norma Lee, and Morton Funger Clinician Career Development Fund
   Award in Colon Cancer Research for Hao Xie.
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TC 1
Z9 2
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 SEP
PY 2023
VL 15
IS 18
AR 4604
DI 10.3390/cancers15184604
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA S7XQ3
UT WOS:001073265700001
PM 37760573
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Hua, HJ
   He, WG
   Chen, N
   He, YJ
   Wu, GS
   Ye, F
   Zhou, XL
   Li, YD
   Ding, YF
   Zhong, WX
   Teng, LS
   Jiang, WQ
   Sheng, QS
AF Hua, Hanju
   He, Wenguang
   Chen, Nan
   He, Yinjun
   Wu, Guosheng
   Ye, Feng
   Zhou, Xile
   Li, Yandong
   Ding, Yongfeng
   Zhong, Weixiang
   Teng, Lisong
   Jiang, Weiqin
   Sheng, Qinsong
TI Genomic and transcriptomic analysis of MSI-H colorectal cancer patients
   with targetable alterations identifies clinical implications for
   immunotherapy
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE MSI-H cancer; targetable alterations; TME (tumor microenvironment);
   immunotherapy; GEP
ID MICROSATELLITE INSTABILITY; INHIBITOR ENTRECTINIB; BRAF; TRK; MUTATIONS;
   EFFICACY; FEATURES; THERAPY; FUSIONS; SAFETY
AB IntroductionTargetable alterations such as BRAFV600E mutation and NTRK fusion are enriched in microsatellite instability-high (MSI-H) colorectal cancer (CRC). MSI-H with targetable alterations (MSI-H altered) might present unique opportunities for both targeted therapy and immunotherapy. We systematically evaluated the molecular characteristics and immune-related features of MSI-H altered and MSI-H without targetable alterations (MSI-H wt) CRC patients in our study. MethodsAmong 1938 continuously enrolled CRC patients, 126 patients with MSI-H status (6.50%) were included in this retrospective study. Genomic and transcriptomic data were investigated by next-generation sequencing (NGS) and gene expression profiling (GEP), respectively. ResultsBRAFV600E, NTRK1, and FGFR2 mutations were the most frequent targetable alterations in MSI-H CRC patients. The MSI-H altered phenotype was significantly associated with older age (p< 0.001), right side (p=0.024) and females (p= 0.036). No lynch syndrome (LS) patients were identified in MSI-H altered group. The tumor mutational burden (TMB), and tumor neoantigen burden (TNB) of MSI-H altered and wt subgroups were comparable (p<0.05). Subsequently, transcriptomic study analysis further revealed MSI-H altered CRC patients were linked to an immune-active tumor microenvironment with higher levels of Teff IFN-gamma, CYT, and MERCK 18 signatures, and lower levels of the IPRES gene signature, EMT and TGF Beta signatures. In addition, case study supported MSI-H CRC patient harboring targetable alterations might also achieved a long-term disease-free survival benefit from immunotherapy. DiscussionOur study preliminary revealed MSI-H altered as a novel subtype of MSI-H CRC patients with unique molecular signatures and immune-active tumor microenvironment. Given the accessibility of immune checkpoint inhibitors (ICIs) treatment, our results might provide clinical evidence for immunotherapy in MSI-H CRC patients with targetable alterations.
C1 [Hua, Hanju; Wu, Guosheng; Ye, Feng; Zhou, Xile; Li, Yandong; Jiang, Weiqin; Sheng, Qinsong] Zhejiang Univ, Affiliated Hosp 1, Dept Colorectal Surg, Hangzhou, Peoples R China.
   [He, Wenguang] Zhejiang Univ, Affiliated Hosp 1, Dept Radiol, Sch Med, Hangzhou, Peoples R China.
   [Chen, Nan] Yuyao Hosp Tradit Chinese Med, Dept Colorectal Surg, Yuyao, Peoples R China.
   [He, Yinjun] Zhejiang Univ, Coll Med, Hangzhou, Peoples R China.
   [Ding, Yongfeng] Zhejiang Univ, Affiliated Hosp 1, Coll Med, Dept Med Oncol, Hangzhou, Peoples R China.
   [Zhong, Weixiang] Zhejiang Univ, Affiliated Hosp 1, Coll Med, Dept Pathol, Hangzhou, Peoples R China.
   [Teng, Lisong] Zhejiang Univ, Affiliated Hosp 1, Coll Med, Dept Surg Oncol, Hangzhou, Peoples R China.
C3 Zhejiang University; Zhejiang University; Zhejiang University; Zhejiang
   University; Zhejiang University; Zhejiang University
RP Jiang, WQ; Sheng, QS (corresponding author), Zhejiang Univ, Affiliated Hosp 1, Dept Colorectal Surg, Hangzhou, Peoples R China.; Teng, LS (corresponding author), Zhejiang Univ, Affiliated Hosp 1, Coll Med, Dept Surg Oncol, Hangzhou, Peoples R China.
EM lsteng@zju.edu.cn; weiqinjiang@zju.edu.cn; shengqinsong@zju.edu.cn
RI Wu, George/JCE-1302-2023
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NR 47
TC 6
Z9 6
U1 3
U2 8
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 9
PY 2023
VL 13
AR 974793
DI 10.3389/fimmu.2022.974793
PG 15
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 8B2FH
UT WOS:000916744100001
PM 36700211
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Tu, SH
   Hsieh, YC
   Huang, LC
   Lin, CY
   Hsu, KW
   Hsieh, WS
   Chi, WM
   Lee, CH
AF Tu, Shih-Hsin
   Hsieh, Yi-Chen
   Huang, Li-Chi
   Lin, Chun-Yu
   Hsu, Kai-Wen
   Hsieh, Wen-Shyang
   Chi, Wei-Ming
   Lee, Chia-Hwa
TI A rapid and quantitative method to detect human circulating tumor cells
   in a preclinical animal model
SO BMC CANCER
LA English
DT Article
DE Cancer metastasis; Circulating tumor cells; Quantitative PCR; In vivo
   bioluminescent imaging system
ID CANCER METASTASIS; PERIPHERAL-BLOOD; COLORECTAL-CANCER; PCR DETECTION;
   RT-PCR; LUNG; SURVIVAL; BREAST; GENES; PROGRESSION
AB Background: As cancer metastasis is the deadliest aspect of cancer, causing 90% of human deaths, evaluating the molecular mechanisms underlying this process is the major interest to those in the drug development field. Both therapeutic target identification and proof-of-concept experimentation in anti-cancer drug development require appropriate animal models, such as xenograft tumor transplantation in transgenic and knockout mice. In the progression of cancer metastasis, circulating tumor cells (CTCs) are the most critical factor in determining the prognosis of cancer patients. Several studies have demonstrated that measuring CTC-specific markers in a clinical setting (e.g., flow cytometry) can provide a current status of cancer development in patients. However, this useful technique has rarely been applied in the real-time monitoring of CTCs in preclinical animal models.
   Methods: In this study, we designed a rapid and reliable detection method by combining a bioluminescent in vivo imaging system (IVIS) and quantitative polymerase chain reaction (QPCR)-based analysis to measure CTCs in animal blood. Using the IVIS Spectrum CT System with 3D-imaging on orthotropic-developed breast-tumor-bearing mice.
   Results: In this manuscript, we established a quick and reliable method for measuring CTCs in a preclinical animal mode. The key to this technique is the use of specific human and mouse GUS primers on DNA/RNA of mouse peripheral blood under an absolute qPCR system. First, the high sensitivity of cancer cell detection on IVIS was presented by measuring the luciferase carried MDA-MB-231 cells from 5 to 5x10(11) cell numbers with great correlation (R-2 = 0.999). Next, the MDA-MB-231 cell numbers injected by tail vein and their IVIS radiance signals were strongly corrected with qPCR-calculated copy numbers (R-2 > 0.99). Furthermore, by applying an orthotropic implantation animal model, we successfully distinguished xenograft tumor-bearing mice and control mice with a significant difference (p < 0.001), whereas IVIS Spectrum-CT 3D-visualization showed that blood of mice with lung metastasis contained more than twice the CTC numbers than ordinary tumor-bearing mice. We demonstrated a positive correlation between lung metastasis status and CTC numbers in peripheral mouse blood.
   Conclusion: Collectively, the techniques developed for this study resulted in the integration of CTC assessments into preclinical models both in vivo and ex vivo, which will facilitate translational targeted therapy in clinical practice.
C1 [Tu, Shih-Hsin] Taipei Med Univ, Coll Med, Sch Med, Dept Surg, Taipei, Taiwan.
   [Tu, Shih-Hsin] Cathay Gen Hosp, Dept Surg, Div Breast Surg, Taipei, Taiwan.
   [Tu, Shih-Hsin] Taipei Med Univ, Breast Med Ctr, Taipei, Taiwan.
   [Tu, Shih-Hsin] Taipei Med Univ, Taipei Canc Ctr, Taipei, Taiwan.
   [Tu, Shih-Hsin; Hsieh, Yi-Chen; Lee, Chia-Hwa] Taipei Med Univ, Comprehens Canc Ctr, Taipei, Taiwan.
   [Hsieh, Yi-Chen] Taipei Med Univ, Coll Med Sci & Technol, PhD Program Neural Regenerat Med, Taipei, Taiwan.
   [Huang, Li-Chi] Cathay Gen Hosp, Dept Endocrinol, Taipei, Taiwan.
   [Lin, Chun-Yu] Natl Chiao Tung Univ, Inst Bioinformat & Syst Biol, Hsinchu, Taiwan.
   [Hsu, Kai-Wen] China Med Univ, Res Ctr Tumor Med Sci, Taichung, Taiwan.
   [Hsieh, Wen-Shyang; Chi, Wei-Ming; Lee, Chia-Hwa] Taipei Med Univ, Shuang Ho Hosp, Dept Lab Med, Taipei, Taiwan.
   [Lee, Chia-Hwa] Taipei Med Univ, Coll Med Sci & Technol, Sch Med Lab Sci & Biotechnol, Taipei, Taiwan.
C3 Taipei Medical University; Cathay General Hospital; Taipei Medical
   University; Taipei Medical University; Taipei Medical University; Taipei
   Medical University; Cathay General Hospital; National Yang Ming Chiao
   Tung University; China Medical University Taiwan; Taipei Medical
   University; Shuang Ho Hospital; Taipei Medical University
RP Lee, CH (corresponding author), Taipei Med Univ, Comprehens Canc Ctr, Taipei, Taiwan.; Lee, CH (corresponding author), Taipei Med Univ, Shuang Ho Hosp, Dept Lab Med, Taipei, Taiwan.
EM chlee@tmu.edu.tw
RI Lin, Chun-Yu/AFK-1793-2022; Tang, Chih/O-5212-2015
OI Tu, Shih-Hsin/0000-0002-4106-8146; Hsu, Kai-Wen/0000-0002-9736-8869;
   Lin, Chun-Yu/0000-0003-2901-2681
FU Taipei Medical University [TMU102-AE1-B10]; Cathay Medical Center
   [CGH-MR-A10209]; Ministry of Science and Technology
   [102-2320-B-038-039-MY3]; National Research Program for
   Biopharmaceuticals (NRPB) [MOHW103-TDU-PB-211-112,024]; Health and
   Welfare Surcharge of Tobacco Products; Ministry of Health and Welfare
   [MOHW105-TDU-B-212-134007, MOHW105-TDU-B-212-134001]
FX This study was supported by Taipei Medical University, grant
   TMU102-AE1-B10 for Dr. Lee; Cathay Medical Center, grant CGH-MR-A10209
   for Dr. Tu; the Ministry of Science and Technology, grant
   102-2320-B-038-039-MY3 for Dr. Lee; and the National Research Program
   for Biopharmaceuticals (NRPB), grant MOHW103-TDU-PB-211-112,024 for Dr.
   Wu, and the Health and Welfare Surcharge of Tobacco Products, Ministry
   of Health and Welfare to the Comprehensive Cancer Center of Taipei
   Medical University (MOHW105-TDU-B-212-134007, MOHW105-TDU-B-212-134001).
   None of the funding bodies were involved in in the design of the study
   and collection, analysis, and interpretation of data and in writing the
   manuscript.
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NR 27
TC 16
Z9 16
U1 0
U2 22
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD JUN 23
PY 2017
VL 17
AR 440
DI 10.1186/s12885-017-3419-x
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EY7QO
UT WOS:000404186500001
PM 28645267
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Iwasaki, M
   Naito, K
   Endo, T
   Hijikata, Y
   Mizuno, M
   Hoshimaru, M
   Hida, K
AF Iwasaki, Motoyuki
   Naito, Kentaro
   Endo, Toshiki
   Hijikata, Yasukazu
   Mizuno, Masaki
   Hoshimaru, Minoru
   Hida, Kazutoshi
CA Neurospinal Soc Japan
   Takami, T
TI Impact of surgical treatment for intramedullary spinal cord metastasis
   on neurological function and survival: A multicenter retrospective study
   by the Neurospinal Society of Japan
SO JOURNAL OF CLINICAL NEUROSCIENCE
LA English
DT Article
DE Intramedullary spinal cord metastasis; Myelotomy; Neurological function;
   Posterolateral sulcus; Survival
ID RENAL-CELL CARCINOMA; TUMORS; RESECTION
AB Background: This retrospective multicenter study aimed to analyze the characteristics and surgical outcomes of intramedullary spinal cord metastasis (ISCM) and to discuss the controversy regarding its surgical indications. Methods: This study included 29 ISCM patients who underwent surgery between 2009 and 2020. Biopsy cases were excluded from analysis. For functional and neurological functional assessments, Karnofsky Performance Status (KPS, %) and modified McCormick Scale (MMS, 5-grade scale) scores were determined before and after surgery. Patients were divided into two groups: a mild-to-moderate disability group with preoperative MMS grades 1 to 3, and a severe disability group with preoperative MMS grades 4 to 5. Results: The mean preoperative KPS was 45.9, and the mean duration from symptom onset to surgical intervention was 1 month. The ISCM was located in the cervical spine in 10 cases and the thoracic spine in 19 cases. The access route (myelotomy) for ISCM removal was via the posterior median sulcus in 9 cases and via the posterior lateral sulcus in 11 cases, while others were not recorded. The degree of removal was gross total resection in 20 patients (69%), subtotal resection in 0 patients, and partial removal in 9 patients (31%). No significant complications related to the surgical procedures were recorded. Postoperative adjuvant therapy included radiotherapy in 17 patients (58.6%) and chemotherapy or molecular targeted therapy in 13 patients (44.8%). Pathological findings of ISCM showed that colorectal cancer was the most common in 9 cases, followed by lung cancer in 7, renal cell carcinoma in 5, and breast cancer in 2. Twenty-one of the 29 patients (72.4%) were confirmed to have survived 6 months after surgery: 8 of the 10 patients (80%) in the mild-to-moderate disability group and 13 of the 19 patients (68.4%) in the severe disability group. At 6 months after surgery, 3 of the 8 patients (38%) in the mild-to-moderate group were able to maintain or improve their function. Eleven of the 13 patients (85%) in the severe disability group maintained their function despite being severely disabled. Conclusions: This study suggests that surgical treatment can maintain or improve neurological function in a limited number of patients with ISCM, although it had minimal impact on improving the survival rate after surgery.
C1 [Iwasaki, Motoyuki] Hokkaido Univ, Dept Neurosurg, Sapporo, Japan.
   [Naito, Kentaro] Osaka Metropolitan Univ, Dept Neurosurg, Grad Sch Med, Osaka, Japan.
   [Endo, Toshiki] Tohoku Med & Pharmaceut Univ, Div Neurosurg, Sendai, Japan.
   [Hijikata, Yasukazu] Kitasuma Hosp, Spine & Low Back Pain Ctr, Kobe, Japan.
   [Mizuno, Masaki] Mie Univ, Dept Minimum Invas Neurospinal Surg, Tsu, Mie, Japan.
   [Hoshimaru, Minoru] Katano Hosp, Shinaikai Spine Ctr, Katano, Japan.
   [Hida, Kazutoshi] Sapporo Azabu Neurosurg Hosp, Dept Neurosurg, Sapporo, Japan.
   [Neurospinal Soc Japan] Osaka Med & Pharmaceut Univ, Dept Neurosurg, Osaka, Japan.
   [Iwasaki, Motoyuki] Hokkaido Univ, Dept Neurosurg, North 15 West 7,Kita Ku, Sapporo, Japan.
C3 Hokkaido University; Osaka Metropolitan University; Tohoku Medical &
   Pharmaceutical University; Mie University; Osaka Medical &
   Pharmaceutical University; Hokkaido University
RP Iwasaki, M (corresponding author), Hokkaido Univ, Dept Neurosurg, North 15 West 7,Kita Ku, Sapporo, Japan.
EM jzesso801@med.hokudai.ac.jp
RI Hijikata, Yasukazu/HTP-2755-2023
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NR 44
TC 1
Z9 1
U1 0
U2 1
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 0967-5868
EI 1532-2653
J9 J CLIN NEUROSCI
JI J. Clin. Neurosci.
PD NOV
PY 2023
VL 117
BP 27
EP 31
DI 10.1016/j.jocn.2023.09.013
EA SEP 2023
PG 5
WC Clinical Neurology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA T9VP9
UT WOS:001081392600001
PM 37740999
DA 2025-01-04
ER

PT J
AU Provenzano, L
   Gwee, YX
   Conca, V
   Lonardi, S
   Bozzarelli, S
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   Ambrosini, M
   Vetere, G
   Carullo, M
   Guaglio, M
   Battaglia, L
   Zhao, JJ
   Chia, DKA
   Yong, WP
   Tan, PT
   So, J
   Kim, G
   Shabbir, A
   Ong, CAJ
   Casella, F
   Cremolini, C
   Bencivenga, M
   Sundar, R
   Pietrantonio, F
AF Provenzano, Leonardo
   Gwee, Yong Xiang
   Conca, Veronica
   Lonardi, Sara
   Bozzarelli, Silvia
   Tamburini, Emiliano
   Passardi, Alessandro
   Zaniboni, Alberto
   Tosi, Federica
   Aprile, Giuseppe
   Nasca, Vincenzo
   Boccaccino, Alessandra
   Ambrosini, Margherita
   Vetere, Guglielmo
   Carullo, Martina
   Guaglio, Marcello
   Battaglia, Luigi
   Zhao, Joseph Jonathan
   Chia, Daryl Kai Ann
   Yong, Wei Peng
   Tan, Patrick
   So, Jimmy
   Kim, Guowei
   Shabbir, Asim
   Ong, Chin-Ann Johnny
   Casella, Francesco
   Cremolini, Chiara
   Bencivenga, Maria
   Sundar, Raghav
   Pietrantonio, Filippo
TI Unveiling the prognostic significance of malignant ascites in advanced
   gastrointestinal cancers: a marker of peritoneal carcinomatosis burden
SO THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
LA English
DT Article
DE chemotherapy; gastric cancer; intraperitoneal chemotherapy; medical
   oncology; precision oncology; prognostic biomarker; systemic treatment;
   targeted therapy
ID HYPERTHERMIC INTRAPERITONEAL CHEMOTHERAPY; METASTATIC COLORECTAL-CANCER;
   CYTOREDUCTIVE SURGERY; GASTRIC-CANCER; OPEN-LABEL; MULTICENTER;
   BEVACIZUMAB; EXPRESSION; PHASE-3; PATTERN
AB Background: Ascites is common in advanced gastrointestinal cancers with peritoneal metastases (PM) and negatively impacts patient survival. No study to date has specifically evaluated the relationship between ascites, PM and survival outcomes in metastatic colorectal cancer (mCRC) and metastatic gastric cancer (mGC). Objectives: This study aims to investigate and elucidate the relationship between malignant ascites, PM and survival outcomes in both mCRC and mGC patients. Design: This is a retrospective analysis of prospectively collected clinical trial data of mCRC and mGC patients with PM. Methods: We performed two pooled analyses, firstly of two Italian randomized trials enrolling patients with mCRC eligible for systemic therapy (TRIBE2; VALENTINO), and secondly of gastric cancer and peritoneal metastasis (GCPM) patients who underwent bi-directional therapeutic treatment comprising systemic and peritoneal-directed therapies. Results: Of 900 mCRC patients, 39 (4.3%) had PM with malignant ascites. Compared to the group without PM, median progression-free and overall survival were significantly inferior in the ascites group (hazard ratio (HR) for progression-free survival (PFS) 1.68, 95% confidence interval (CI): 1.21-2.35, p = 0.007; HR for overall survival (OS) 2.14, 95% CI: 1.57-3.01, p < 0.001), but not in the group of PM without ascites (HR for PFS 1.10, 95% CI: 0.91 - 1.34; HR for OS 1.04, 95% CI: 0.84 - 1.30). Of 170 patients with GCPM, those with ascites had higher median Peritoneal Cancer Index scores (23 vs 9, p < 0.001). Median OS was significantly inferior among those with ascites compared to those without (13.0 vs 21.0 months, HR 1.71, 95% CI: 1.16-2.52, p = 0.007). Conclusion: Ascites identifies a subgroup of patients with PM and poor outcomes, for whom tailored research are needed.
C1 [Provenzano, Leonardo; Conca, Veronica; Ambrosini, Margherita; Pietrantonio, Filippo] Fdn IRCCS Ist Nazl Tumori, Med Oncol Dept, Via GVenezian 1, I-20133 Milan, Italy.
   [Gwee, Yong Xiang; Zhao, Joseph Jonathan; Yong, Wei Peng; Sundar, Raghav] Natl Univ Canc Inst, Dept Haematol Oncol, 1E Kent Ridge Rd, Singapore 119228, Singapore.
   [Yong, Wei Peng; Tan, Patrick; So, Jimmy; Sundar, Raghav] Singapore Gastr Canc Consortium, Singapore, Singapore.
   [Tan, Patrick; Sundar, Raghav] Duke NUS, Canc & Stem Cell Biol Program, Med Sch, Singapore 165897, Singapore.
   [So, Jimmy; Sundar, Raghav] Natl Univ Singapore, Yong Loo Lin Sch Med, Singapore, Singapore.
   [Bencivenga, Maria; Sundar, Raghav] Natl Univ Singapore, N Inst Hlth 1, Singapore, Singapore.
   [Conca, Veronica; Boccaccino, Alessandra; Cremolini, Chiara] Univ Pisa, Dept Translat Res & New Technol Med, Pisa, Italy.
   [Lonardi, Sara] Veneto Inst Oncol IOV IRCCS, Med Oncol Unit 3, I-35128 Padua, Italy.
   [Bozzarelli, Silvia] IRCCS Human Res Hosp, Human Canc Ctr, Med Oncol & Hematol Unit, Milan, Italy.
   [Tamburini, Emiliano] Cardinale G Pan Hosp, Cardiol Unit, Tricase, Italy.
   [Boccaccino, Alessandra] IRCCS, Ist Romagnolo Studio Tumori IRST Dino Amadori, Dept Med Oncol, Meldola, Italy.
   [Zaniboni, Alberto] Ist Ospedaliero Fdn Poliambulanza, Dept Unit Allergol Clin Immunol & Resp Dis, Brescia, Italy.
   [Tosi, Federica] ASST Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, Hematol & Oncol, Milan, Italy.
   [Aprile, Giuseppe] San Bortolo Gen Hosp, Dept Oncol, Azienda ULSS8, Vicenza, Italy.
   [Vetere, Guglielmo; Cremolini, Chiara] Univ Hosp Pisa, Unity Oncol, Pisa, Italy.
   [Guaglio, Marcello; Battaglia, Luigi] Fdn IRCCS Ist Nazl Tumori, Colorectal Surg, Milan, Italy.
   [Chia, Daryl Kai Ann; So, Jimmy; Kim, Guowei; Shabbir, Asim] Natl Univ Singapore Hosp, Univ Surg Cluster, Dept Surg, Singapore, Singapore.
   [Yong, Wei Peng; Tan, Patrick] Natl Univ Singapore, Canc Sci Inst Singapore, Singapore, Singapore.
   [Tan, Patrick] Agcy Sci Technol & Res, Genome Inst Singapore, Singapore, Singapore.
   [Tan, Patrick] SingHealth Duke NUS Inst Precis Med, Natl Heart Ctr, Singapore, Singapore.
   [Tan, Patrick] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Physiol, Singapore, Singapore.
   [So, Jimmy; Kim, Guowei; Shabbir, Asim] Natl Univ, Div Surg Oncol, Canc Inst, Singapore, Singapore.
   [So, Jimmy; Kim, Guowei; Shabbir, Asim] Natl Univ Hlth Syst, Singapore, Singapore.
   [Ong, Chin-Ann Johnny] Natl Canc Ctr Singapore, Div Surg & Surg Oncol, Dept Sarcoma Peritoneal & Rare Tumors SPRinT, Singapore, Singapore.
   [Casella, Francesco] Verona Univ Hosp, Upper GI Surg Unit, Verona, Italy.
   [Bencivenga, Maria] Univ Verona, Dept Surg Dent Pediat & Gynaecol, Upper GI Surg Unit, Verona, Italy.
C3 Fondazione IRCCS Istituto Nazionale Tumori Milan; National University of
   Singapore; National University of Singapore; National University of
   Singapore; National University of Singapore; University of Pisa; IRCCS
   Istituto Oncologico Veneto (IOV); ULSS 8 Berica; Ospedale San Bortolo di
   Vicenza; University of Pisa; Azienda Ospedaliero Universitaria Pisana;
   Fondazione IRCCS Istituto Nazionale Tumori Milan; National University of
   Singapore; National University of Singapore; Agency for Science
   Technology & Research (A*STAR); A*STAR - Genome Institute of Singapore
   (GIS); National Heart Centre Singapore; National University of
   Singapore; National University of Singapore; National University of
   Singapore; National Cancer Centre Singapore (NCCS); University of
   Verona; Azienda Ospedaliera Universitaria Integrata Verona; University
   of Verona
RP Pietrantonio, F (corresponding author), Fdn IRCCS Ist Nazl Tumori, Med Oncol Dept, Via GVenezian 1, I-20133 Milan, Italy.; Sundar, R (corresponding author), Natl Univ Canc Inst, Dept Haematol Oncol, 1E Kent Ridge Rd, Singapore 119228, Singapore.
EM raghav.sundar@yale.edu; filippo.pietrantonio@istitutotumori.mi.it
RI Tamburini, Emiliano/LQJ-8211-2024; Bencivenga, Maria/AAR-1122-2020;
   Lonardi, Sara/F-4228-2014; Cremolini, Chiara/AAC-1889-2019; Guaglio,
   Marcello/I-2770-2017; TOSI, FEDERICA MARIA/AIA-1174-2022; Ambrosini,
   Margherita/ABF-8196-2021; passardi, alessandro/AAH-4786-2019
OI passardi, alessandro/0000-0002-7099-240X
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NR 37
TC 0
Z9 0
U1 1
U2 1
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 17588359241289517
DI 10.1177/17588359241289517
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA L0V5I
UT WOS:001347987400001
PM 39502404
DA 2025-01-04
ER

PT J
AU Alyami, MH
   Musallam, AA
   Ibrahim, TM
   Mahdy, MA
   Elnahas, HM
   Aldeeb, RA
AF Alyami, Mohammad H.
   Musallam, Abeer A.
   Ibrahim, Tarek M.
   Mahdy, Mahmoud A.
   Elnahas, Hanan M.
   Aldeeb, Reem A.
TI The Exploitation of pH-Responsive Eudragit-Coated Mesoporous Silica
   Nanostructures in the Repurposing of Terbinafine Hydrochloride for
   Targeted Colon Cancer Inhibition: Design Optimization, In Vitro
   Characterization, and Cytotoxicity Assessment
SO PHARMACEUTICS
LA English
DT Article
DE terbinafine hydrochloride; drug repurposing; pH-responsive mesoporous
   silica nanostructures; Eudragit; DiSupLo technique; targeted therapy;
   colon cancer
ID DRUG-DELIVERY; ENHANCED SOLUBILITY; NANOPARTICLES; DISSOLUTION;
   STRATEGIES; RELEASE
AB Targeted drug delivery is achieving great success in cancer therapy due to its potential to deliver drugs directly to the action site. Terbinafine hydrochloride (TER) is a broad-spectrum anti-fungal drug that has been found to have some potential anti-tumor effects in the treatment of colon cancer. We aimed here to design and develop pH-sensitive Eudragit (Eud)-coated mesoporous silica nanostructures (MSNs) to control drug release in response to changes in pH. The diffusion-supported loading (DiSupLo) technique was applied for loading TER into the MSNs. The formulation was optimized by a D-optimal design, which permits the concurrent assessment of the influence of drug/MSN%, coat concentration, and MSN type on the drug entrapment efficiency (EE) and its release performance. The optimal formula displayed a high EE of 96.49%, minimizing the release in pH 1.2 to 16.15% and maximizing the release in pH 7.4 to 78.09%. The cytotoxicity of the optimal formula on the colon cancer cells HT-29 was higher than it was with TER alone by 2.8-fold. Apoptosis in cancer cells exposed to the optimum formula was boosted as compared to what it was with the plain TER by 1.2-fold and it was more efficient in arresting cells during the G0/G1 and S stages of the cell cycle. Accordingly, the repurposing of TER utilizing Eud/MSNs is a promising technique for targeted colon cancer therapy.
C1 [Alyami, Mohammad H.] Najran Univ, Coll Pharm, Dept Pharmaceut, Najran 66462, Saudi Arabia.
   [Musallam, Abeer A.; Aldeeb, Reem A.] Misr Univ Sci & Technol, Coll Pharmaceut Sci & Drug Mfg, Dept Pharmaceut, 6th of October City 12582, Egypt.
   [Ibrahim, Tarek M.; Mahdy, Mahmoud A.; Elnahas, Hanan M.] Zagazig Univ, Fac Pharm, Dept Pharmaceut, Zagazig 44519, Egypt.
C3 Najran University; Egyptian Knowledge Bank (EKB); Misr University for
   Science & Technology; Egyptian Knowledge Bank (EKB); Zagazig University
RP Musallam, AA (corresponding author), Misr Univ Sci & Technol, Coll Pharmaceut Sci & Drug Mfg, Dept Pharmaceut, 6th of October City 12582, Egypt.
EM aber.abdelaziz@must.edu.eg
RI Ibrahim, Tarek/AAJ-4321-2020
OI A. Aldeeb, Reem/0000-0002-7717-3925; M Elnahas,
   Hanan/0000-0002-9148-3276; Musallam, Abeer A./0000-0002-2956-0736;
   Ibrahim, Tarek/0000-0002-9415-4267
FU Deanship of Scientific Research (DSR) at Najran University; Deanship of
   Scientific Research at Najran University
FX The authors are thankful to the Deanship of Scientific Research at
   Najran University for funding this work under the General Research
   Funding program.
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NR 61
TC 1
Z9 1
U1 1
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1999-4923
J9 PHARMACEUTICS
JI Pharmaceutics
PD DEC
PY 2023
VL 15
IS 12
AR 2677
DI 10.3390/pharmaceutics15122677
PG 23
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA EA7H1
UT WOS:001136242100001
PM 38140018
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Stachowiak, M
   Szymanski, M
   Ornoch, A
   Jancewicz, I
   Rusetska, N
   Chrzan, A
   Demkow, T
   Siedlecki, JA
   Sarnowski, TJ
   Sarnowska, E
AF Stachowiak, Malgorzata
   Szymanski, Michal
   Ornoch, Anna
   Jancewicz, Iga
   Rusetska, Natalia
   Chrzan, Alicja
   Demkow, Tomasz
   Siedlecki, Janusz A.
   Sarnowski, Tomasz J.
   Sarnowska, Elzbieta
TI SWI/SNF chromatin remodeling complex and glucose metabolism are
   deregulated in advanced bladder cancer
SO IUBMB LIFE
LA English
DT Article
DE AMPK; bladder cancer; chromatin remodeling; glucose metabolism; SWI; SNF
   complex
ID BREAST-CANCER; UROTHELIAL CARCINOMA; GENE-EXPRESSION; DOWN-REGULATION;
   E-CADHERIN; BASAL; IDENTIFICATION; SURVIVAL; SUBTYPES; TARGETS
AB Bladder cancer (BC) is a frequently diagnosed malignancy affecting predominantly adult and elderly populations. It is expected that due to the longer life time, BC will become even more frequent in the future; thus in consequence, it will represent serious health problem of older society part. The treatment of advanced BC is mostly ineffective due to its very aggressive behavior. So far, no effective targeted therapy is used for BC treatment. Here, we found that BC is characterized by lower protein levels of BRM, INI1, and BAF155 main subunits of SWI/SNF chromatin remodeling complex (CRC) which is involved in global control of gene expression and influences various important cellular processes like: cell cycle control, apoptosis, DNA repair, etc. Moreover, the expression of SMARCA2, a BRM encoding gene, strongly correlated with BC metastasis and expression of such metabolic genes as PKM2 and PRKAA1. Furthermore, the analysis of T24 and 5637 commonly used BC cell lines revealed different expression levels of metabolic genes including FBP1 gene encoding Frutose-1,6-Bisphosphatase, an enzyme controlling glycolysis flux and gluconeogenesis. The tested BC cell lines exhibited various molecular and metabolic alterations as well as differential glucose uptake, growth rate, and migration potential. We have shown that BRM subunit is involved in the transcriptional control of genes encoding metabolic enzymes. Moreover, we found that the FBP1 expression level and the SWI/SNF CRCs may serve as markers of molecular subtypes of BC. Collectively, this study may provide a new knowledge about the molecular and metabolic BC subtypes which likely will be of high importance for the clinic in the future.
C1 [Stachowiak, Malgorzata; Ornoch, Anna; Jancewicz, Iga; Rusetska, Natalia; Siedlecki, Janusz A.; Sarnowska, Elzbieta] Maria Sklodowska Curie Natl Res Inst Oncol, Dept Mol & Translat Oncol, Warsaw, Poland.
   [Szymanski, Michal; Demkow, Tomasz] Maria Sklodowska Curie Natl Res Inst Oncol, Dept Urooncol, Warsaw, Poland.
   [Chrzan, Alicja] Maria Sklodowska Curie Natl Res Inst Oncol, Dept Pathol, Warsaw, Poland.
   [Sarnowski, Tomasz J.] Polish Acad Sci, Inst Biochem & Biophys, Warsaw, Poland.
C3 Polish Academy of Sciences; Institute of Biochemistry & Biophysics -
   Polish Academy of Sciences
RP Sarnowski, TJ (corresponding author), Pawinskiego 5A Str, PL-02106 Warsaw, Poland.; Sarnowska, E (corresponding author), Roentgena 5 Str, PL-02781 Warsaw, Poland.
EM tsarn@ibb.waw.pl; elasarn@coi.pl
RI Stachowiak, Małgorzata/ABA-1572-2021; Jancewicz, Iga/AAB-4191-2020
OI Sarnowska, Elzbieta/0000-0001-7723-1198; Siedlecki,
   Janusz/0000-0003-4889-5416; Rusetska, Natalia/0000-0001-7496-2489;
   Chrzan, Alicja/0000-0002-3460-7105; Sarnowski,
   Tomasz/0000-0002-3805-2039; Jancewicz, Iga/0000-0002-4978-709X; ,
   Malgorzata/0000-0002-0151-2417; Szymanski, Michal
   Daniel/0000-0003-0161-4189
FU Polish Ministry of Sciences and Higher Education [0139/DIA/2017/46,
   0229/DIA/2015/44]; Polish National Science Center (NCN)
   [UMO-2014/13/B/NZ2/01187, UMO-2014/15/B/NZ5/03532,
   UMO-2018/02/X/NZ5/00792]
FX Polish Ministry of Sciences and Higher Education, Grant/Award Numbers:
   Diamond Grant 0139/DIA/2017/46 (MS), Diamond Grant 0229/DIA/2015/44
   (IJ); Polish National Science Center (NCN), Grant/Award Numbers:
   UMO-2014/13/B/NZ2/01187 (TJS), UMO-2014/15/B/NZ5/03532 (JAS),
   UMO-2018/02/X/NZ5/00792 (MSz)
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NR 35
TC 13
Z9 13
U1 1
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1521-6543
EI 1521-6551
J9 IUBMB LIFE
JI IUBMB Life
PD JUN
PY 2020
VL 72
IS 6
SI SI
BP 1175
EP 1188
DI 10.1002/iub.2254
EA FEB 2020
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA LP9ND
UT WOS:000514240500001
PM 32073734
OA Green Accepted, Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Hoang, T
   Sohn, DK
   Kim, BC
   Cha, Y
   Kim, J
AF Hoang, Tung
   Sohn, Dae Kyung
   Kim, Byung Chang
   Cha, Yongjun
   Kim, Jeongseon
TI Efficacy and Safety of Systemic Treatments Among Colorectal Cancer
   Patients: A Network Meta-Analysis of Randomized Controlled Trials
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE network meta-analysis; colorectal cancer; metastasis; chemotherapy;
   targeted therapy
ID PHASE-II TRIAL; UNRESECTABLE LIVER METASTASES; CETUXIMAB PLUS
   IRINOTECAN; 1ST-LINE TREATMENT; WILD-TYPE; 2ND-LINE TREATMENT; FOLINIC
   ACID; OPEN-LABEL; OXALIPLATIN XELOX; ELDERLY-PATIENTS
AB Background: Systemic treatments, namely, either monotherapy or combination therapy, are commonly administered to patients with advanced or metastatic colorectal cancer (CRC). This study aimed to provide the complete efficacy and safety profiles and ranking of systemic therapies for the treatment of unresectable advanced or metastatic CRC. Methods: We searched PubMed, Embase, the Cochrane Library, and ClinicalTrials.gov from inception until June 30, 2021, and also the bibliographies of relevant studies. Randomized controlled trials comparing two or more treatments, namely, at least capecitabine, 5-fluorouracil, leucovorin, irinotecan, bevacizumab, cetuximab, oxaliplatin, or panitumumab were investigated. A network meta-analysis using the Bayesian approach was performed to compare the efficacy and safety of treatments. The surface under the cumulative ranking curve (SUCRA) was calculated for the probability of each treatment as the most effective. The overall response rate (ORR), disease control rate (DCR), overall survival (OS), progression-free survival (PFS), adverse events (AEs) grade >= 3, and serious adverse events (SAEs) were evaluated. Results: One hundred two publications with 36,147 participants were assigned to 39 different treatments. Among 11 treatments with full information on six outcomes, FOLFIRI/FOLFOX/FOLFOXIRI + bevacizumab significantly improved both the ORR and DCR, compared to FOLFIRI. Although FOLFOX and FOLFIRI/FOLFOX + cetuximab significantly prolonged both OS and PFS, treatments were comparable in terms of AEs grade >= 3 and SAEs. The top highest SUCRA values were observed in the FOLFOXIRI + panitumumab group for ORR (96%) and DCR (99%), FOLFIRI + bevacizumab + panitumumab group for OS (62%) and PFS (54%), and FOLFOXIRI + bevacizumab group for AEs grade >= 3 (59%) and SAEs (59%) outcomes. Conclusions: These findings suggest an available range of systemic treatment therapies with different efficacy and safety profiles with patients. Further investigations of the side effects and mutation status are required to confirm our findings. Systematic Review Registrationhttps://www.crd.york.ac.uk/prospero/, identifier CRD42019127772
C1 [Hoang, Tung; Kim, Jeongseon] Natl Canc Ctr, Dept Canc Biomed Sci, Grad Sch Canc Sci & Policy, Goyang, South Korea.
   [Sohn, Dae Kyung; Kim, Byung Chang; Cha, Yongjun] Res Inst & Hosp, Ctr Colorectal Canc, Natl Canc Ctr, Goyang, South Korea.
C3 National Cancer Center - Korea (NCC); National Cancer Center - Korea
   (NCC)
RP Kim, J (corresponding author), Natl Canc Ctr, Dept Canc Biomed Sci, Grad Sch Canc Sci & Policy, Goyang, South Korea.
EM jskim@ncc.re.kr
RI KIM, JEONGSEON/AAA-4643-2022; Hoang, Tung/ABG-7027-2020
OI Hoang, Tung/0000-0001-6653-3406; Cha, Yongjun/0000-0001-5651-7939
FU National Cancer Center [1710882, 2210990]
FX This work was supported by grants from the National Cancer Center (Nos.
   1710882 and 2210990).
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NR 128
TC 8
Z9 8
U1 0
U2 9
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 9
PY 2022
VL 11
AR 756214
DI 10.3389/fonc.2021.756214
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZH6JN
UT WOS:000761042800001
PM 35223449
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Jin, L
   Hu, WY
   Li, T
   Sun, HH
   Kang, DX
   Piao, LZ
AF Jin, Lan
   Hu, Wuyun
   Li, Teng
   Sun, Honghua
   Kang, Dongxu
   Piao, Longzhen
TI Case report and literature review: PET/CT in the evaluation of response
   to treatment of liver metastasis from colorectal cancer with DEBIRI-TACE
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE colorectal liver metastases; DEBIRI-TACE; FDG PET; CT; irinotecan;
   prognosis; case report
ID DRUG-ELUTING BEADS; HEPATIC INTRAARTERIAL INJECTION;
   HEPATOCELLULAR-CARCINOMA; CRITERIA; THERAPY; CHEMOTHERAPY; PERCIST;
   RECIST
AB BackgroundIrinotecan-loaded drug-eluting beads transarterial chemoembolization (DEBIRI-TACE) is a safe and effective therapeutic option for unresectable colorectal liver metastases (CRLM). The evaluation of treatment response after DEBIRI-TACE is very important for assessing the patient's condition. At present, the Response Evaluation Criteria in Solid Tumors (RECIST) with the tumor size obtained by CT and/or MRI and PET Response Criteria in Solid Tumors (PERCIST) based on fluorodeoxyglucose-positron emission tomography/computed tomography (FDG PET/CT) are used for evaluating the response to therapy of solid tumors; however, their value in the assessment of treatment response after DEBIRI-TACE remains unclear. Case presentationA 52-year-old male with unresectable simultaneous CRLM was treated in the Affiliated Hospital of Yanbian University with DEBIRI-TACE combined with systemic chemotherapy and targeted therapy. Carcinoembryonic antigen levels decreased by 82.50% after 27 days of treatment. At 6 weeks post-surgery, FDG-PET/CT showed that the maximum standardized uptake value (SUVmax) of intrahepatic lesions was reduced to 62.14%. Abdominal MRI revealed that the sum of target lesion diameters was less than 30% that at baseline. PERCIST indicated partial metabolic response, whereas RECIST suggested stable disease. ConclusionFDG PET/CT-based PERCIST may be accurate in determining treatment response and evaluating patient prognosis after DEBIRI-TACE in unresectable CRLM.
C1 [Jin, Lan; Hu, Wuyun; Li, Teng; Sun, Honghua; Kang, Dongxu; Piao, Longzhen] Yanbian Univ, Dept Oncol, Affiliated Hosp, Yanji, Peoples R China.
C3 Yanbian University
RP Kang, DX; Piao, LZ (corresponding author), Yanbian Univ, Dept Oncol, Affiliated Hosp, Yanji, Peoples R China.
EM jerryk0202@163.com; Plz1978@126.com
CR Akinwande O, 2017, SURG ONCOL, V26, P268, DOI 10.1016/j.suronc.2017.05.003
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NR 20
TC 0
Z9 0
U1 0
U2 1
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 2
PY 2023
VL 13
AR 1015976
DI 10.3389/fonc.2023.1015976
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 9Y0DE
UT WOS:000950134900001
PM 36937414
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhao, FN
   Liu, YL
   Tan, FS
   Tang, L
   Du, ZY
   Mou, J
   Zhou, G
   Yuan, CF
AF Zhao, Fangnan
   Liu, Yuling
   Tan, Fangshun
   Tang, Lu
   Du, Zhuoying
   Mou, Jie
   Zhou, Gang
   Yuan, Chengfu
TI MIR4435-2HG: A Tumor-associated Long Non-coding RNA
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Review
DE LncRNA; MIR4435-2HG; tumor; biomarkers; therapeutic target; diagnosis
ID UP-REGULATION; CANCER; PROLIFERATION; MIGRATION; LNCRNA; METASTASIS;
   INVASION
AB Background: It is well known that the changes in the expression level of LncRNA can affect the progression of tumors, which has caused a great upsurge of research in recent years. Several LncRNAs have been identified to affect a series of cancers and can promote tumor growth, migration, and invasion. In this \nreview, we aim to clarify the pathophysiological functions of LncRNA MIR4435-2 HG in multiple tumors. Methods: By searching the literature through PubMed, this paper summarizes the relationship between MIR4435-2HG and tumor and its role in the occurrence and development of cancer and also explains the specific molecular mechanism of the effect of MIR4435-2HG on cancer. Results: MIR4435-2HG can function as an oncogene in a variety of cancers. The expression level was reported to be abnormally elevated in a series of cancers, consisting of melanoma, gastric cancer, head and neck squamous cell carcinoma, oral squamous cell carcinoma, lung cancer, cervical cancer, prostate carcinoma, ovarian cancer, breast cancer, hepatocellular carcinoma, clear cell renal cell carcinoma malignant, glioma, and colorectal cancer. Moreover, MIR4435-2HG is related to the poor prognosis of a variety of cancers. MIR4435-2HG can also affect tumor proliferation, invasion, and apoptosis. In addition, MIR4435-2HG can also enhance the metabolic function of myeloid dendritic cells of elite HIV-1 controllers. Conclusion: MIR4435-2HG affects the development of a variety of cancers. It can act as a clinical marker for early tumor diagnosis and affects tumor-targeted therapy.
C1 [Zhao, Fangnan; Liu, Yuling; Tan, Fangshun; Tang, Lu; Du, Zhuoying; Mou, Jie; Yuan, Chengfu] China Three Gorges Univ, Third Grade Pharmacol Lab Tradit Chinese Med, State Adm Tradit Chinese Med, Yichang 443002, Peoples R China.
   [Zhao, Fangnan; Liu, Yuling; Tan, Fangshun; Tang, Lu; Du, Zhuoying; Mou, Jie; Yuan, Chengfu] China Three Gorges Univ, Med Coll, 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.
   [Yuan, Chengfu] China Three Gorges Univ, Hubei Key Lab Tumor Microenvironm & Immunotherapy, Yichang 443002, Peoples R China.
C3 China Three Gorges University; China Three Gorges University; China
   Three Gorges University; China Three Gorges University
RP Zhou, G (corresponding author), China Three Gorges Univ, Coll Tradit Chinese Med, Yichang 443002, Peoples R China.; Yuan, CF (corresponding author), China Three Gorges Univ, Hubei Key Lab Tumor Microenvironm & Immunotherapy, Yichang 443002, Peoples R China.
EM 13661880@qq.com; yuancf46@ctgu.edu.cn
RI Du, Zhuoying/HJY-2279-2023; Tan, Fangshun/HTN-4756-2023
OI Tan, Fangshun/0000-0002-0175-2533; Zhao, fangnan/0000-0002-2255-3103;
   Du, Zhuoying/0000-0001-8924-8421; Mou, Jie/0000-0001-6159-5739
FU National Natural Science Foundation of China [81974528, 82174035,
   81773959]; Hubei Province Natural Science Foundation in China
   [2021CFA015]; central government guides the special funds for the
   development of local science and technology [2020ZYYD016]; Health
   commission of Hubei Province scientific research project in China
   [WJ2019H527]
FX The work was supported by grants from the National Natural Science
   Foundation of China (Grant No. 81974528 to C.F. Yuan, No. 82174035 to
   C.F. Yuan, and No. 81773959 to C.F. Yuan), the innovational group
   project of Hubei Province Natural Science Foundation in China (Grant No.
   2021CFA015 to C.F. Yuan), and central government guides the special
   funds for the development of local science and technology (Grant No.
   2020ZYYD016 to C.F. Yuan), and Health commission of Hubei Province
   scientific research project in China (Grant No. WJ2019H527 to C.F.
   Yuan).
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NR 46
TC 3
Z9 3
U1 0
U2 4
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1381-6128
EI 1873-4286
J9 CURR PHARM DESIGN
JI Curr. Pharm. Design
PY 2022
VL 28
IS 25
BP 2043
EP 2051
DI 10.2174/1381612828666220607100228
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 4J6LP
UT WOS:000851376200002
PM 35674305
DA 2025-01-04
ER

PT J
AU Coussy, F
   Lallemand, F
   Vacher, S
   Schnitzler, A
   Chemlali, W
   Caly, M
   Nicolas, A
   Richon, S
   Meseure, D
   El Botty, R
   De-Plater, L
   Fuhrmann, L
   Dubois, T
   Roman-Roman, S
   Dangles-Marie, V
   Marangoni, E
   Bièche, I
AF Coussy, F.
   Lallemand, F.
   Vacher, S.
   Schnitzler, A.
   Chemlali, W.
   Caly, M.
   Nicolas, A.
   Richon, S.
   Meseure, D.
   El Botty, R.
   De-Plater, L.
   Fuhrmann, L.
   Dubois, T.
   Roman-Roman, S.
   Dangles-Marie, V.
   Marangoni, E.
   Bieche, I.
TI Clinical value of R-spondins in triple-negative and metaplastic breast
   cancers
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE triple-negative and metaplastic breast cancers; R-spondins;
   Wnt/beta-catenin pathway; prognosis; targeted therapy
ID MAMMARY EPITHELIAL-CELLS; BETA-CATENIN; COLORECTAL-CANCER; SIGNALING
   PATHWAY; PROGNOSTIC VALUE; PROSTATE-CANCER; WNT; TUMORIGENESIS;
   CARCINOMAS; EXPRESSION
AB Background: RSPO ligands, activators of the Wnt/beta-catenin pathway, are overexpressed in different cancers. The objective of this study was to investigate the role of RSPOs in breast cancer (BC).
   Methods: Expression of RSPO and markers of various cancer pathways were measured in breast tumours and cell lines by qRT-PCR. The effect of RSPO on the Wnt/beta-catenin pathway activity was determined by luciferase assay, western blotting, and qRT-PCR. The effect of RSPO2 inhibition on proliferation was determined by using RSPO2 siRNAs. The effect of IWR-1, an inhibitor of the Wnt/beta-catenin pathway, was examined on the growth of an RSPO2-positive patient-derived xenograft (PDX) model of metaplastic triple-negative BC.
   Results: We detected RSPO2 and RSPO4 overexpression levels in BC, particularly in triple-negative BC (TNBC), metaplastic BC, and triple-negative cell lines. Various mechanisms could account for this overexpression: presence of fusion transcripts involving RSPO, and amplification or hypomethylation of RSPO genes. Patients with RSPO2-overexpressing tumours have a poorer metastasis-free survival (P = 3.6 x 10(-4)). RSPO2 and RSPO4 stimulate Wnt/beta-catenin pathway activity. Inhibition of RSPO expression in a TN cell line inhibits cell growth, and IWR-1 significantly inhibits the growth of an RSPO2-overexpressing PDX.
   Conclusions: RSPO overexpression could therefore be a new prognostic biomarker and therapeutic target for TNBC.
C1 [Coussy, F.; Lallemand, F.; Vacher, S.; Schnitzler, A.; Chemlali, W.; Bieche, I.] Inst Curie, Dept Genet, Unit Pharmacogen, 26 Rue Ulm, F-75005 Paris, France.
   [Caly, M.; Nicolas, A.; Meseure, D.; Fuhrmann, L.] Inst Curie, Dept Biopathol, 26 Rue Ulm, F-75005 Paris, France.
   [Richon, S.] Inst Curie, Res Ctr, CNRS, UMR 144, 26 Rue Ulm, F-75005 Paris, France.
   [El Botty, R.; De-Plater, L.; Dangles-Marie, V.; Marangoni, E.] Inst Curie, Dept Translat Res, Lab Preclin Invest, 26 Rue Ulm, F-75005 Paris, France.
   [Dubois, T.] Inst Curie, Dept Translat Res, Breast Canc Biol Grp, 26 Rue Ulm, F-75005 Paris, France.
   [Roman-Roman, S.] Inst Curie, Dept Translat Res, 26 Rue Ulm, F-75005 Paris, France.
   [Dangles-Marie, V.] Univ Paris 05, Sorbonne Paris Cite, F-75006 Paris, France.
   [Bieche, I.] Univ Paris 05, EA7331, 4 Ave Observ, F-75006 Paris, France.
C3 UNICANCER; Universite PSL; Institut Curie; UNICANCER; Universite PSL;
   Institut Curie; Centre National de la Recherche Scientifique (CNRS);
   CNRS - National Institute for Biology (INSB); Universite PSL; UNICANCER;
   Institut Curie; Sorbonne Universite; UNICANCER; Universite PSL; Institut
   Curie; UNICANCER; Universite PSL; Institut Curie; UNICANCER; Universite
   PSL; Institut Curie; Universite Paris Cite; Universite Paris Cite
RP Bièche, I (corresponding author), Inst Curie, Dept Genet, Unit Pharmacogen, 26 Rue Ulm, F-75005 Paris, France.; Bièche, I (corresponding author), Univ Paris 05, EA7331, 4 Ave Observ, F-75006 Paris, France.
EM ivan.bieche@curie.fr
RI Marangoni, Elisabetta/GSO-3945-2022; Bieche, Ivan/O-7399-2017;
   Roman-Roman, Sergio/K-9993-2014; Dubois, Thierry/D-2852-2017
OI EL BOTTY, Rania/0000-0002-8885-4304; Bieche, Ivan/0000-0002-2430-5429;
   VACHER, Sophie/0000-0002-0042-6023; Meseure, Didier/0000-0001-6730-6686;
   Marangoni, Elisabetta/0000-0002-3337-6448; Roman-Roman,
   Sergio/0000-0001-6459-2613; Dubois, Thierry/0000-0003-4739-6164
FU Fondation pour la Recherche Medicale [DEA20130727212]; Agence Nationale
   de la Recherche (Programme Investissements d'Avenir-Institut Carnot)
   [ANR-11CARN-008-01]; GEFLUC, Les Entreprises contre le Cancer [2014
   59/188]; Ligue Nationale de lutte Contre le Cancer; Canceropole
   Ile-de-France
FX We thank Dr Shinji Takada for donating mouse fibroblast L cells
   producing Wnt-3a and L cells stably transfected with the pGKneo plasmid.
   This work was supported by a medical-scientific grant from the Fondation
   pour la Recherche Medicale (DEA20130727212; to CF), by the Agence
   Nationale de la Recherche (Programme Investissements d'Avenir-Institut
   Carnot ANR-11CARN-008-01), and GEFLUC, Les Entreprises contre le Cancer
   (Grant 2014 59/188). This work was also supported by the Ligue Nationale
   de lutte Contre le Cancer and the Canceropole Ile-de-France. We thank
   the staff of Institut Curie-Rene Huguenin Hospital for their assistance
   in specimen collection and patient care and the in vivo Experiment
   Platform-Institut Curie managed by Isabelle Grandjean.
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NR 49
TC 32
Z9 34
U1 2
U2 10
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD JUN 6
PY 2017
VL 116
IS 12
BP 1595
EP 1603
DI 10.1038/bjc.2017.131
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EW9GQ
UT WOS:000402825200013
PM 28472820
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Hu, JM
   Chang, YL
   Hsieh, CC
   Huang, SM
AF Hu, Je-Ming
   Chang, Yung-Lung
   Hsieh, Cheng-Chih
   Huang, Shih-Ming
TI The Synergistic Cytotoxic Effects of GW5074 and Sorafenib by Impacting
   Mitochondrial Functions in Human Colorectal Cancer Cell Lines
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colorectal cancer; C-RAF inhibitor; multi-kinase inhibitor;
   mitochondrial dysfunction; the combination index
ID C-RAF; HEPATOCELLULAR-CARCINOMA; INHIBITOR; AUTOPHAGY; KINASES;
   ACTIVATION; APOPTOSIS; FISSION; PATHWAY; STRESS
AB Colorectal cancer (CRC) ranks third in the United States for incidence or mortality. Surgical resection is the primary treatment for patients at an early stage, while patients with advanced and metastatic CRC receive combined treatment with chemotherapy, radiotherapy, or targeted therapy. C-RAF plays a key role in maintaining clonogenic and tumorigenic capacity in CRC cells and it might be a potential therapeutic target for CRC. Sorafenib is a popular oral multi-kinase inhibitor, including a B-RAF inhibitor that targets the RAF-MEK-ERK pathway. Sorafenib, as a single agent, has tumor-suppressing efficacy, but its clinical application is limited due to many complex drug resistance mechanisms and side effects. GW5074 is one of the C-RAF inhibitors and has the potential to enhance the efficacy of existing cancer chemotherapies. In this study, we investigated whether the combination of sorafenib with GW5074 could reduce the dosage of sorafenib and enhance its tumor-suppressive effect in two CRC cell lines, HCT116 and LoVo cells. Our findings demonstrate that GW5074 can potentiate the cytotoxicity of sorafenib and dramatically reduce the half-maximal inhibitory concentration (IC50) dose of sorafenib from 17 and 31 mu M to 0.14 and 0.01 mu M in HCT116 and LoVo cells, respectively. GW5074, similar to sorafenib, suppressed the cellular proliferation and induced cellular apoptosis and cytosolic ROS, but had no further enhancement on the above-mentioned effects when combined with sorafenib. The synergistic effects of GW5074 and sorafenib were mainly found in mitochondrial functions, including ROS generation, membrane potential disruption, and fission-fusion dynamics, which were examined by using the flow cytometry analysis. In summary, the C-RAF inhibitor GW5074 might potentiate the cytotoxicity of the B-RAF inhibitor sorafenib mediated through mitochondrial dysfunctions, suggesting that GW5074 potentially serves as a sensitizer for sorafenib application to reduce the risk of drug resistance of CRC treatment. Our findings also provide novel insights on using C-RAF inhibitors combined with sorafenib, the current CRC therapeutic drug choice, in CRC treatment.
C1 [Hu, Je-Ming; Chang, Yung-Lung; Huang, Shih-Ming] Natl Def Med Ctr, Inst Med Sci, Taipei, Taiwan.
   [Hu, Je-Ming] Triserv Gen Hosp, Natl Def Med Ctr, Dept Surg, Div Colorectal Surg, Taipei, Taiwan.
   [Chang, Yung-Lung; Huang, Shih-Ming] Natl Def Med Ctr, Dept Biochem, Taipei, Taiwan.
   [Hsieh, Cheng-Chih] Natl Def Med Ctr, Inst Pharm, Sch Pharm, Taipei, Taiwan.
   [Hsieh, Cheng-Chih] Kaohsiung Vet Gen Hosp, Dept Pharm, Kaohsiung, Taiwan.
C3 National Defense Medical Center; National Defense Medical Center;
   Tri-Service General Hospital; National Defense Medical Center; National
   Defense Medical Center; Kaohsiung Veterans General Hospital
RP Huang, SM (corresponding author), Natl Def Med Ctr, Inst Med Sci, Taipei, Taiwan.; Huang, SM (corresponding author), Natl Def Med Ctr, Dept Biochem, Taipei, Taiwan.
EM shihming@ndmctsgh.edu.tw
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NR 44
TC 5
Z9 5
U1 0
U2 9
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 JUN 7
PY 2022
VL 12
AR 925653
DI 10.3389/fonc.2022.925653
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 2G1IQ
UT WOS:000813352500001
PM 35747833
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Huang, EM
   Ma, T
   Zhou, JJ
   Ma, N
   Yang, WS
   Liu, CX
   Hou, ZH
   Chen, S
   Zong, Z
   Zeng, B
   Li, YR
   Zhou, TC
AF Huang, Enmin
   Ma, Tao
   Zhou, Junji
   Ma, Ning
   Yang, Weisheng
   Liu, Chuangxiong
   Hou, Zehui
   Chen, Shuang
   Zong, Zhen
   Zeng, Bing
   Li, Yingru
   Zhou, Taicheng
TI A novel senescence-associated LncRNA signature predicts the prognosis
   and tumor microenvironment of patients with colorectal cancer: a
   bioinformatics analysis
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article; Early Access
DE Colorectal cancer (CRC); cellular senescence; long non-coding RNA
   (lncRNA); tumor microenvironment (TME); immune response
ID CELLS; SURVIVAL; P53
AB Background: Accumulating evidence suggests that cellular senescence promotes tumor formation and that long non-coding RNAs (lncRNAs) expression predicts tumor prognosis. However, senescence-related variables, particularly lncRNAs, are still largely unknown. Therefore, the present study developed a novel senescence-associated lncRNA signature to predict colorectal cancer (CRC) prognosis.Methods: A co-expression network of senescence-associated mRNAs and lncRNAs was built using RNA sequence data from The Cancer Genome Atlas (TCGA). By using the prognosis outcomes data of overall survival (OS) and disease-free survival (DFS) from TCGA, we constructed a prognostic senescence associated lncRNA signature (SenALSig). The OS and DFS were compared between the low-and high-risk groups defined by SenALSig. A single-sample gene set enrichment analysis (ssGSEA) and CIBERSORT algorithm were used to investigate the relationship between the predictive signature and immune status. Finally, the relationship between SenALSig and drug treatment options was investigated. An independent CRC cohort and three CRC cell lines were recruited to perform real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) analysis to validate the results discovered in silico.Results: A prognostic risk model consisting of six senescence-associated lncRNAs was constructed, including SNHG16, AL590483.1, ZEB1-AS1, AC107375.1, AC068580.3, and AC147067.1. High-risk scores according to the SenALSig were significantly associated with poor OS (hazard ratio =1.218, 95% confidence interval: 1.140-1.301; P<0.001). The model's accuracy was further supported by receiver operating characteristic (ROC) curves (the area under the curve is 0.714) and a principal component analysis (PCA). In univariate and multivariate Cox regression analyses, SenALSig was further found to be a prognostic factor independent of other clinical factors. Furthermore, we discovered that immune checkpoint expression and response to chemotherapy and targeted therapy differed significantly between the SenALSig-stratified high and low-risk groups. Finally, the qPCR results revealed that the expression levels of the six senescence associated lncRNAs differed significantly between tumor and normal tissues and between the CRC cell lines and a normal human colon mucosal epithelial cell line.Conclusions: SenALSig can better predict survival and risk in CRC patients, as well as help develop new anti-cancer treatment strategies for CRC.
C1 [Huang, Enmin; Ma, Tao; Ma, Ning; Yang, Weisheng; Liu, Chuangxiong; Hou, Zehui; Chen, Shuang; Zeng, Bing; Li, Yingru; Zhou, Taicheng] Sun Yat sen Univ, Dept Gastroenterol Surg, Affiliated Hosp 6, Guangzhou, Peoples R China.
   [Huang, Enmin; Ma, Tao; Ma, Ning; Yang, Weisheng; Liu, Chuangxiong; Hou, Zehui; Chen, Shuang; Zeng, Bing; Li, Yingru; Zhou, Taicheng] Sun Yat sen Univ, Affiliated Hosp 6, Hernia Ctr, Guangzhou, Peoples R China.
   [Huang, Enmin; Ma, Tao; Zhou, Junji; Ma, Ning; Yang, Weisheng; Liu, Chuangxiong; Hou, Zehui; Chen, Shuang; Zeng, Bing; Li, Yingru; Zhou, Taicheng] Sun Yat sen Univ, Affiliated Hosp 6, Guangdong Prov Key Lab Colorectal & Pelv Floor Dis, Guangzhou, Peoples R China.
   [Zhou, Junji] Sun Yat sen Univ, Affiliated Hosp 6, Dept Gastrointestinal Surg, Guangzhou, Peoples R China.
   [Zong, Zhen] Nanchang Univ, Affiliated Hosp 2, Dept Gastroenterol Surg, Nanchang, Peoples R China.
   [Zeng, Bing; Li, Yingru; Zhou, Taicheng] Sun Yat sen Univ, Affiliated Hosp 6, Dept Gastroenterol Surg, Guangzhou 510655, Peoples R China.
   [Zeng, Bing; Li, Yingru; Zhou, Taicheng] Sun Yat sen Univ, Affiliated Hosp 6, Hernia Ctr, Guangzhou 510655, Peoples R China.
   [Zeng, Bing; Li, Yingru; Zhou, Taicheng] Sun Yat sen Univ, Affiliated Hosp 6, Guangdong Prov Key Lab Colorectal & Pelv Floor Dis, Guangzhou 510655, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen University;
   Sun Yat Sen University; Nanchang University; Sun Yat Sen University; Sun
   Yat Sen University; Sun Yat Sen University
RP Zeng, B; Li, YR; Zhou, TC (corresponding author), Sun Yat sen Univ, Affiliated Hosp 6, Dept Gastroenterol Surg, Guangzhou 510655, Peoples R China.; Zeng, B; Li, YR; Zhou, TC (corresponding author), Sun Yat sen Univ, Affiliated Hosp 6, Hernia Ctr, Guangzhou 510655, Peoples R China.; Zeng, B; Li, YR; Zhou, TC (corresponding author), Sun Yat sen Univ, Affiliated Hosp 6, Guangdong Prov Key Lab Colorectal & Pelv Floor Dis, Guangzhou 510655, Peoples R China.
EM zengbing3@mail.sysu.edu.cn; liyingru@mail.sysu.edu.cn;
   zhoutch3@mail.sysu.edu.cn
RI zehui, hou/ABD-7065-2020; ma, tao/JTS-7892-2023
FU National Key Clinical Discipline; Basic and Applied Basic Research Fund
   Project of Guangdong Province [2019A1515011200, 2021A1515410004];
   National Natural Science Foundation of China [81973858, 82172790];
   Science and Technology Plan Project of Qingyuan City [2019A028]
FX The work was funded by the National Key Clinical Discipline, the Basic
   and Applied Basic Research Fund Project of Guangdong Province (No.
   2021A1515410004, to Zhou TC) , the National Natural Science Foundation
   of China (No. 81973858, to Zeng B and No. 82172790, to Li YR) , the
   Basic and Applied Basic Research Fund Project of Guangdong Province (No.
   2019A1515011200, to Zeng B) , the Science and Technology Plan Project of
   Qingyuan City (No. 2019A028, to Zeng B) .
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NR 60
TC 9
Z9 9
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 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD 2022 AUG 11
PY 2022
DI 10.21037/jgo-22-721
EA AUG 2022
PG 25
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA 4W6RQ
UT WOS:000860287700001
PM 36092325
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Pfohl, U
   Loskutov, J
   Bashir, S
   Kühn, R
   Herter, P
   Templin, M
   Mamlouk, S
   Belanov, S
   Linnebacher, M
   Bürtin, F
   Vetter, M
   Reinhard, C
   Wedeken, L
   Regenbrecht, CRA
AF Pfohl, Ulrike
   Loskutov, Juergen
   Bashir, Sanum
   Kuhn, Ralf
   Herter, Patrick
   Templin, Markus
   Mamlouk, Soulafa
   Belanov, Sergei
   Linnebacher, Michael
   Buertin, Florian
   Vetter, Marcus
   Reinhard, Christoph
   Wedeken, Lena
   Regenbrecht, Christian R. A.
TI A RAS-Independent Biomarker Panel to Reliably Predict Response to MEK
   Inhibition in Colorectal Cancer
SO CANCERS
LA English
DT Article
DE organoids; biomarker; targeted therapy; colorectal cancer; CRC; SMAD4;
   TGF-beta/BMP-pathway; intra-tumor heterogeneity; MEK inhibition
ID BONE MORPHOGENETIC PROTEIN; 5-FLUOROURACIL-BASED CHEMOTHERAPY; CLINICAL
   DEVELOPMENT; TUMOR-SUPPRESSOR; PIK3CA MUTATION; PROGNOSTIC ROLE;
   OVARIAN-CANCER; RESISTANCE; PATHWAY; ARID1A
AB Background: In colorectal cancer (CRC), mutations of genes associated with the TGF-beta/BMP signaling pathway, particularly affecting SMAD4, are known to correlate with decreased overall survival and it is assumed that this signaling axis plays a key role in chemoresistance. Methods: Using CRISPR technology on syngeneic patient-derived organoids (PDOs), we investigated the role of a loss-of-function of SMAD4 in sensitivity to MEK-inhibitors. CRISPR-engineered SMAD4(R361H) PDOs were subjected to drug screening, RNA-Sequencing, and multiplex protein profiling (DigiWest (R)). Initial observations were validated on an additional set of 62 PDOs with known mutational status. Results: We show that loss-of-function of SMAD4 renders PDOs sensitive to MEK-inhibitors. Multiomics analyses indicate that disruption of the BMP branch within the TGF-beta/BMP pathway is the pivotal mechanism of increased drug sensitivity. Further investigation led to the identification of the SFAB-signature (SMAD4, FBXW7, ARID1A, or BMPR2), coherently predicting sensitivity towards MEK-inhibitors, independent of both RAS and BRAF status. Conclusion: We identified a novel mutational signature that reliably predicts sensitivity towards MEK-inhibitors, regardless of the RAS and BRAF status. This finding poses a significant step towards better-tailored cancer therapies guided by the use of molecular biomarkers.
C1 [Pfohl, Ulrike; Loskutov, Juergen; Reinhard, Christoph; Wedeken, Lena; Regenbrecht, Christian R. A.] CELLphenomics GmbH, Robert Rossle Str 10, D-13125 Berlin, Germany.
   [Pfohl, Ulrike] Goethe Univ Frankfurt Main, Inst Mol Biosci, Max von Laue Str 13, D-60438 Frankfurt, Germany.
   [Bashir, Sanum; Kuhn, Ralf] Max Delbruck Ctr Mol Med, Genome Engn & Dis Models, Robert Rossle Str 10, D-13125 Berlin, Germany.
   [Herter, Patrick; Templin, Markus; Reinhard, Christoph; Wedeken, Lena; Regenbrecht, Christian R. A.] Univ Tubingen, NMI Nat & Med Sci Inst, Markwiesenstr 55, D-72770 Reutlingen, Germany.
   [Templin, Markus] ASC Oncol GmbH, Robert Rossle Str 10, D-13125 Berlin, Germany.
   [Mamlouk, Soulafa] Charite Univ Med Berlin, Inst Pathol, Virchowweg 15,Charitepl 1, D-10117 Berlin, Germany.
   [Belanov, Sergei] Univ Helsinki, Inst Biotechnol, Viikinkaari 5,Bioctr 2, Helsinki 00790, Finland.
   [Linnebacher, Michael] Rostock Univ, Clin Gen Surg Mol Oncol & Immunotherapy, Med Ctr, Schillingallee 35, D-18057 Rostock, Germany.
   [Buertin, Florian] Rostock Univ, Clin Gen Surg, Med Ctr, Schillingallee 35, D-18057 Rostock, Germany.
   [Vetter, Marcus] Univ Hosp Basel, Petersgraben 4, CH-4031 Basel, Switzerland.
   [Vetter, Marcus] Kantonsspital Baselland, Rheinstr 26, CH-4410 Liestal, Switzerland.
   [Regenbrecht, Christian R. A.] Univ Hosp Gottingen, Inst Pathol, Robert Koch Str 40, D-37075 Gottingen, Germany.
C3 Goethe University Frankfurt; Helmholtz Association; Max Delbruck Center
   for Molecular Medicine; Eberhard Karls University of Tubingen; Berlin
   Institute of Health; Free University of Berlin; Humboldt University of
   Berlin; Charite Universitatsmedizin Berlin; University of Helsinki;
   University of Rostock; University of Rostock; University of Basel;
   Kantonsspital Baselland; University of Gottingen; UNIVERSITY GOTTINGEN
   HOSPITAL
RP Regenbrecht, CRA (corresponding author), CELLphenomics GmbH, Robert Rossle Str 10, D-13125 Berlin, Germany.; Regenbrecht, CRA (corresponding author), Univ Tubingen, NMI Nat & Med Sci Inst, Markwiesenstr 55, D-72770 Reutlingen, Germany.; Regenbrecht, CRA (corresponding author), Univ Hosp Gottingen, Inst Pathol, Robert Koch Str 40, D-37075 Gottingen, Germany.
EM ulrike.pfohl@cellphenomics.com; juergen.loskutov@cellphenomics.com;
   sanum.bashir@biontech.de; ralf.kuehn@mdc-berlin.de;
   patrick.herter@boehringer-ingelheim.com; markus.templin@nmi.de;
   soulafa.mamlouk@charite.de; sergei.belanov@helsinki.fi;
   michael.linnebacher@med.uni-rostock.de;
   florian.buertin@med.uni-rostock.de; marcus.vetter@ksbl.ch;
   christoph.reinhard@cellphenomics.com; lena.wedeken@cellphenomics.com;
   christian.regenbrecht@cellphenomics.com
RI Mamlouk, Soulafa/AGU-7570-2022; Linnebacher, Michael/AAT-3763-2021;
   Vetter, Marcus/K-2027-2016; Kuhn, Ralf/U-1278-2017; Regenbrecht,
   Christian/S-7715-2016; Belanov, Sergei/P-9403-2018
OI Kuhn, Ralf/0000-0003-1694-9803; Linnebacher,
   Michael/0000-0001-8054-1402; Vetter, Marcus/0009-0004-1003-1078;
   Regenbrecht, Christian/0000-0001-9494-5977; Belanov,
   Sergei/0000-0003-3419-3659; Mamlouk, Soulafa/0000-0001-7285-1320;
   Templin, Markus Felix/0000-0002-6569-6489
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NR 84
TC 4
Z9 4
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 JUL
PY 2022
VL 14
IS 13
AR 3252
DI 10.3390/cancers14133252
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 2T2ZP
UT WOS:000822346400001
PM 35805024
OA Green Published, gold, Green Accepted
DA 2025-01-04
ER

PT J
AU Meric-Bemstam, F
   Hurwitz, H
   Raghav, KPS
   McWilliams, RR
   Fakih, M
   VanderWalde, A
   Swanton, C
   Kurzrock, R
   Burris, H
   Sweeney, C
   Bose, R
   Spigel, DR
   Beattie, MS
   Blotner, S
   Stone, A
   Schulze, K
   Cuchelkar, V
   Hainsworth, J
AF Meric-Bemstam, Funda
   Hurwitz, Herbert
   Raghav, Kanwal Pratap Singh
   McWilliams, Robert R.
   Fakih, Marwan
   VanderWalde, Ari
   Swanton, Charles
   Kurzrock, Razelle
   Burris, Howard
   Sweeney, Christopher
   Bose, Ron
   Spigel, David R.
   Beattie, Mary S.
   Blotner, Steven
   Stone, Alyssa
   Schulze, Katja
   Cuchelkar, Vaikunth
   Hainsworth, John
TI Pertuzumab plus trastuzumab for <i>HER2</i>-amplified metastatic
   colorectal cancer (MyPathway): an updated report from a multicentre,
   open-label, phase 2a, multiple basket study
SO LANCET ONCOLOGY
LA English
DT Article
ID SOLID TUMORS; GUIDELINE; THERAPY
AB Background Therapies targeting HER2 have improved clinical outcomes in HER2-positive breast and gastric cancers, and are emerging as potential treatments for HER2-positive metastatic colorectal cancer. MyPathway evaluates the activity of targeted therapies in non-indicated tumour types with potentially predictive molecular alterations. We aimed to assess the activity of pertuzumab and trastuzumab in patients with HER2-amplified metastatic colorectal cancer.
   Methods MyPathway is an ongoing, phase 2a, multiple basket study. Patients in this subset analysis were aged 18 years or older and had treatment-refractory, histologically confirmed HER2-amplified metastatic colorectal cancer with measurable or evaluable disease and an Eastern Cooperative Oncology Group performance status score of 2 or less, enrolled from 25 hospitals or clinics in 16 states of the USA. Patients received pertuzumab (840 mg loading dose, then 420 mg every 3 weeks, intravenously) and trastuzumab (8 mg/kg loading dose, then 6 mg/kg every 3 weeks, intravenously). The primary endpoint was the proportion of patients who achieved an objective response based on investigator-reported tumour responses. Analyses were done per protocol. This ongoing trial is registered with ClinicalTrials.gov, number NCT02091141.
   Findings Between Oct 20, 2014, and June 22, 2017, 57 patients with HER2-amplified metastatic colorectal cancer were enrolled in the MyPathway study and deemed eligible for inclusionin this cohort analysis. Among these 57 evaluable patients, as of Aug 1, 2017, one (2%) patient had a complete response and 17 (30%) had partial responses; thus overall 18 of 57 patients achieved an objective response (32%, 95% CI 20-45). The most common treatment-emergent adverse events were diarrhoea (19 [33%] of 57 patients), fatigue (18 [32%] patients), and nausea (17 [30%] patients). Grade 3-4 treatment-emergent adverse events were recorded in 21 (37%) of 57 patients, most commonly hypokalaemia and abdominal pain (each three [5%] patients). Serious treatment-emergent adverse events were reported in ten (18%) patients and two (4%) of these adverse events (ie, chills and infusion-related reaction) were considered treatment related. There were no treatment-related deaths.
   Interpretation Dual HER2-targeted therapy with pertuzumab plus trastuzumab is well tolerated and could represent a therapeutic opportunity for patients with heavily pretreated, HER2-amplified metastatic colorectal cancer. Copyright (C) 2019 Elsevier Ltd. All rights reserved.
C1 [Meric-Bemstam, Funda; Raghav, Kanwal Pratap Singh] Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapeut, Houston, TX 77030 USA.
   [Hurwitz, Herbert] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
   [McWilliams, Robert R.] Mayo Clin, Rochester, MN USA.
   [Fakih, Marwan] City Hope Natl Med Ctr, Dept Med Oncol & Therapeut Res, Duarte, CA 91010 USA.
   [VanderWalde, Ari] West Canc Ctr, Memphis, TN USA.
   [Swanton, Charles] Francis Crick Inst, London, England.
   [Kurzrock, Razelle] Univ Calif San Diego, Div Hematol & Oncol, Moores Canc Ctr, San Diego, CA 92103 USA.
   [Burris, Howard; Spigel, David R.; Hainsworth, John] Sarah Cannon Res Inst, Nashville, TN USA.
   [Burris, Howard; Spigel, David R.; Hainsworth, John] PLLC, Tennessee Oncol, Nashville, TN USA.
   [Sweeney, Christopher] Harvard Med Sch, Dana Farber Canc Inst, Boston, MA 02115 USA.
   [Bose, Ron] Washington Univ, Sch Med, St Louis, MO USA.
   [Beattie, Mary S.; Blotner, Steven; Stone, Alyssa; Schulze, Katja; Cuchelkar, Vaikunth] Genentech Inc, San Francisco, CA 94080 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; Duke
   University; Mayo Clinic; City of Hope; Francis Crick Institute;
   University of California System; University of California San Diego;
   Sarah Cannon Research Institute; Tennessee Oncology; Harvard University;
   Dana-Farber Cancer Institute; Harvard Medical School; Washington
   University (WUSTL); Roche Holding; Genentech
RP Meric-Bemstam, F (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapeut, Houston, TX 77030 USA.
EM fmeric@mdanderson.org
RI VanderWalde, Ari/HLQ-7510-2023; Kurzrock, Razelle/AAU-9782-2020;
   Swanton, Charles/AEY-0113-2022
OI Fakih, Marwan/0000-0002-6554-5488
FU F Hoffmann-La Roche/Genentech; Cancer Prevention and Research Institute
   of Texas [RP1100584]; Sheikh Khalifa Bin Zayed Al Nahyan Institute for
   Personalized Cancer Therapy; NCATS Grant [UL1 TR000371]; MD Anderson
   Cancer Center Support Grant [P30 CA016672]
FX We thank the patients, families, and study teams who participated in
   MyPathway. We also thank Bongin Yoo (Genentech, South San Francisco, CA,
   USA) for his work on the statistical analysis, Yong Wang (Genentech,
   South San Francisco, CA, USA) for her programming support, Rajesh Patel
   (Genentech, South San Francisco, CA, USA) for his assistance with the
   validation of the molecular profiling data, and Hiro Nitta (Ventana,
   Tucson, AZ, USA) and Bryce Portier (Ventana, Tucson, AZ, USA) for the
   performance of the HER2 gene protein assay. The MyPathway study was
   designed by the Sarah Cannon Research Institute and F Hoffmann-La
   Roche/Genentech in collaboration with the study Steering Committee and
   was funded by F Hoffmann-La Roche/Genentech. Third-party writing
   assistance was provided by Sabrina Hom (CodonMedical, Ashfield) and was
   funded by F Hoffmann-La Roche/Genentech. This work was also supported in
   part by The Cancer Prevention and Research Institute of Texas
   (RP1100584), the Sheikh Khalifa Bin Zayed Al Nahyan Institute for
   Personalized Cancer Therapy, NCATS Grant UL1 TR000371 (Center for
   Clinical and Translational Sciences), and the MD Anderson Cancer Center
   Support Grant (P30 CA016672).
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NR 34
TC 370
Z9 392
U1 2
U2 29
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 APR
PY 2019
VL 20
IS 4
BP 518
EP 530
DI 10.1016/S1470-2045(18)30904-5
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HR3AU
UT WOS:000463009600034
PM 30857956
OA Green Submitted, Green Accepted
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Gupta, A
   Ahmad, A
   Singh, H
   Kaur, S
   Neethu, KM
   Ansari, MM
   Jayamurugan, G
   Khan, R
AF Gupta, Anuradha
   Ahmad, Anas
   Singh, Hardeep
   Kaur, Sharanjeet
   Neethu, K. M.
   Ansari, Md. Meraj
   Jayamurugan, Govindasamy
   Khan, Rehan
TI Nanocarrier Composed of Magnetite Core Coated with Three Polymeric
   Shells Mediates LCS-1 Delivery for Synthetic Lethal Therapy of
   BLM-Defective Colorectal Cancer Cells
SO BIOMACROMOLECULES
LA English
DT Article
ID IRON-OXIDE NANOPARTICLES; COMPREHENSIVE GENOMIC CHARACTERIZATION;
   CHROMOSOME INSTABILITY; GENETIC INSTABILITY; MOLECULES; GROWTH; COLON
AB Synthetic lethality is a molecular-targeted therapy for selective killing of cancer cells. We exploited a lethal interaction between superoxide dismutase 1 inhibition and Bloom syndrome gene product (BLM) defect for the treatment of colorectal cancer (CRC) cells (HCT 116) with a customized lung cancer screen-l-loaded nanocarrier (LCS-1-NC). The drug LCS-1 has poor aqueous solubility. To overcome its limitations, a customized NC, composed of a magnetite core coated with three polymeric shells, namely, aminocellulose (AC), branched poly(amidoamine), and paraben-PEG, was developed for encapsulating LCS-1. Encapsulation efficiency and drug loading were found to be 74% and 8.2%, respectively. LCS-1-NC exhibited sustained release, with similar to 85% of drug release in 24 h. Blank NC (0.5 mg/mL) exhibited cytocompatibility toward normal cells, mainly due to the AC layer. LCS-1-NC demonstrated high killing selectivity (104 times) toward BLM-deficient HCT 116 cells over BLM-proficient HCT 116 cells. Due to enhanced efficacy of the drug using NC, the sensitivity difference for BLM-deficient cells increased to 1.7 times in comparison to that with free LCS-1. LCS-1-NC induced persistent DNA damage and apoptosis, which demonstrates that LCS-1-NC effectively and preferentially killed BLM-deficient CRC cells. This is the first report on the development of a potential drug carrier to improve the therapeutic efficacy of LCS-1 for specific killing of CRC cells having BLM defects.
C1 [Gupta, Anuradha; Ahmad, Anas; Singh, Hardeep; Kaur, Sharanjeet; Neethu, K. M.; Ansari, Md. Meraj; Jayamurugan, Govindasamy; Khan, Rehan] Inst Nano Sci & Technol, Mohali 160062, Punjab, India.
C3 Department of Science & Technology (India); Institute of Nano Science &
   Technology (INST)
RP Jayamurugan, G; Khan, R (corresponding author), Inst Nano Sci & Technol, Mohali 160062, Punjab, India.
EM jayamurugan@inst.ac.in; rehankhan@inst.ac.in
RI Jayamurugan, Govindasamy/C-6807-2019; Khan, Rehan/AAR-4803-2020; Ansari,
   Md. Meraj/AAD-8416-2020; Gupta, Anuradha/G-5882-2014
OI Khan, Rehan/0000-0002-2406-1129; Ansari, Md. Meraj/0000-0001-5562-2892;
   Ahmad, Anas/0000-0002-1105-7526; Gupta, Anuradha/0000-0003-3791-4562
FU SERB, Department of Science and Technology (DST) [YSS/2015/001851,
   ECR/2016/000441, SB/S2/RJN-047/2015]; DST-SERB; INST; DST
FX This work is supported by SERB, Department of Science and Technology
   (DST), grant nos. YSS/2015/001851, ECR/2016/000441, and
   SB/S2/RJN-047/2015. G.J. thank DST-SERB for Ramanujan Fellowship. A.G.
   and S.K. thank INST and DST for postdoctoral fellowship. The authors
   thank Panjab University (SAIF facility) for NMR and confocal microscopy,
   DIHAR-DRDO for use of the cell culture facility, and IIT-Madras for
   magnetic measurements. BLM-deficient HCT 116 cells were generously
   provided by Dr. Bert Vogelstein (Johns Hopkins University). We thank Dr.
   Ehesan Ali, INST, for his critical reading of the manuscript. We thank
   Director, INST, for his constant support.
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NR 59
TC 37
Z9 37
U1 1
U2 17
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1525-7797
EI 1526-4602
J9 BIOMACROMOLECULES
JI Biomacromolecules
PD MAR
PY 2018
VL 19
IS 3
BP 803
EP 815
DI 10.1021/acs.biomac.7b01607
PG 13
WC Biochemistry & Molecular Biology; Chemistry, Organic; Polymer Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry; Polymer Science
GA FZ4CU
UT WOS:000427539600011
PM 29451980
DA 2025-01-04
ER

PT J
AU Xu, D
   Li, LJ
   Yu, ZM
AF Xu, Dan
   Li, Linjun
   Yu, Zhaomin
TI Effect and mechanism of curcumin on colon cancer cell senescence through
   early growth response 1 (EGR1)
SO TRANSLATIONAL CANCER RESEARCH
LA English
DT Article
DE Colon cancer (CC); curcumin; cell senescence; transcriptional regulation
ID SIRT6; DNA
AB Background: The expression level of early growth response 1 (EGR1) is elevated in colon cancer (CC) tissues and is closely associated with poor prognosis in colorectal cancer. However, the role of EGR1 as a transcription factor (TF) influencing cell senescence in the progression of CC remains largely unexplored. This study aims to investigate the impact of curcumin on colorectal cancer cell senescence by modulating EGR1. Methods: Genes associated with cell senescence were obtained from a public database, and ChIP-X predicted TFs were utilized. The R2 database was employed to examine the relationship between gene expression and survival. CC cell lines were transfected with plasmids to achieve stable expression. Stable transfected cell lines were screened, and changes in RNA and protein expression were assessed using real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) and Western blot (WB) analysis. Senescence levels were measured by SA-beta-Gal staining. Cell proliferation and invasion capabilities were evaluated through soft agar and Matrigel invasion assays. Molecular docking was used to predict the interaction between curcumin and EGR1. Gene activity changes were detected using a dual luciferase reporter gene assay. Results: The results indicated that EGR1 was overexpressed in CC tissues and correlated with poor prognosis. As a TF, EGR1 negatively regulated the expression of telomerase reverse transcriptase (TERT) and sirtuin 6 (SIRT6) genes associated with cell senescence. Knocking down EGR1 increased the rate of cell senescence and inhibited cell proliferation and invasion. Curcumin inhibited the transcriptional activity of EGR1, thereby promoting cell senescence and inhibiting tumor progression. Conclusions: In conclusion, curcumin hampers the activity of TF EGR1, affecting the transcription and translation of target genes TERT and SIRT6, thus promoting cell senescence and inhibiting CC cell proliferation. These findings provide potential insights for targeted therapy of CC
C1 [Xu, Dan; Li, Linjun] Huazhong Univ Sci & Technol, Maternal & Child Hlth Hosp Hubei Prov, Tongji Med Coll, Dept Oncol, Wuhan, Peoples R China.
   [Yu, Zhaomin] Xinhua Hosp Hubei Univ Chinese Med, Dept Oncol, 11 Lingjiao Lake Rd, Wuhan 430015, Peoples R China.
C3 Huazhong University of Science & Technology
RP Yu, ZM (corresponding author), Xinhua Hosp Hubei Univ Chinese Med, Dept Oncol, 11 Lingjiao Lake Rd, Wuhan 430015, Peoples R China.
EM lk083@163.com
FX Funding: This work was supported by the Hubei Provincial Health
   Commission Project (No. WJ2019M240 to L.L.)
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NR 25
TC 0
Z9 0
U1 5
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 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-24-26
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA E7B2E
UT WOS:001304514400005
PM 39145095
OA gold, Green Published
DA 2025-01-04
ER

PT S
AU Albuquerque, C
   Pereira, LP
AF Albuquerque, Cristina
   Pereira, Lucilia Pebre
BE Jordan, P
TI Wnt Signalling-Targeted Therapy in the CMS2 Tumour Subtype: A New
   Paradigm in CRC Treatment?
SO TARGETED THERAPY OF COLORECTAL CANCER SUBTYPES
SE Advances in Experimental Medicine and Biology
LA English
DT Article; Book Chapter
DE CMS2 therapy; Immunomodulation; Just-right signalling; Nutraceuticals;
   Wnt antagonists/agonists; Wnt signalling
ID CONSENSUS MOLECULAR SUBTYPES; CANCER STEM-CELLS; METASTATIC
   COLORECTAL-CANCER; CETUXIMAB PLUS IRINOTECAN; WNT/BETA-CATENIN PATHWAY;
   COLON-CARCINOMA CELLS; IN-VITRO; BETA-CATENIN; 1ST-LINE TREATMENT;
   MESENCHYMAL TRANSITION
AB Colorectal cancers (CRC) belonging to the consensus molecular subtype 2 (CMS2) have the highest incidence rate, affect mainly the distal colon and rectum, and are characterized by marked Wnt/beta-catenin/Transcription Factor 7-Like 2 (TCF7L2) pathway activation and also by activation of epidermal growth factor receptor (EGFR) signalling. Despite having the highest overall survival, CMS2 tumours are often diagnosed at stage III when an adjuvant chemotherapy-based regimen is recommended. Nevertheless, colorectal cancer stem cells (CSCs) and circulating tumour cells may still evade the current therapeutic options and metastasize, stressing the need to develop more tailored therapeutic strategies. For example, activation of EGFR signalling is being used as a target for tailored therapy, however, therapy resistance is frequently observed. Therefore, targeting the Wnt signalling axis represents an additional therapeutic strategy, considering that CMS2 tumours are "Wnt-addicted". Several efforts have been made to identify Wnt antagonists, either of synthetic or natural origin. However, an inverse gradient of Wnt/beta-catenin/TCF7L2 signalling activity during CRC progression has been suggested, with early stage and metastatic tumours displaying high and low Wnt signalling activities, respectively, which lead us to revisit the "just-right" signalling model. This may pinpoint the use of Wnt signalling agonists instead of antagonists for treatment of metastatic stages, in a context-dependent fashion. Moreover, the poor immunogenicity of these tumours challenges the use of recently emerged immunotherapies. This chapter makes a journey about CMS2 tumour characterization, their conventional treatment, and how modulation of Wnt signalling or immune response may be applied to CRC therapy. It describes the newest findings in this field and indicates where more research is required.
C1 [Albuquerque, Cristina; Pereira, Lucilia Pebre] Portuguese Inst Oncol Lisbon Francisco Gentil, EPE, Mol Pathobiol Res Unit, Lisbon, Portugal.
RP Albuquerque, C (corresponding author), Portuguese Inst Oncol Lisbon Francisco Gentil, EPE, Mol Pathobiol Res Unit, Lisbon, Portugal.
OI Pebre Pereira, Lucilia/0000-0001-7648-7220; Albuquerque,
   Cristina/0000-0002-9707-0317
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NR 182
TC 8
Z9 8
U1 0
U2 8
PU SPRINGER INTERNATIONAL PUBLISHING AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 0065-2598
EI 2214-8019
BN 978-3-0300-2771-1
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 2018
VL 1110
BP 75
EP 100
DI 10.1007/978-3-030-02771-1_6
D2 10.1007/978-3-030-02771-1
PG 26
WC Oncology
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA BL9PR
UT WOS:000458008800006
PM 30623367
DA 2025-01-04
ER

PT J
AU Lee, JW
   Park, YS
   Choi, JY
   Chang, WJ
   Lee, S
   Sung, JS
   Kim, B
   Lee, SB
   Lee, SY
   Choi, J
   Kim, YH
AF Lee, Jong Won
   Park, Young Soo
   Choi, Jung Yoon
   Chang, Won Jin
   Lee, Soohyeon
   Sung, Jae Sook
   Kim, Boyeon
   Lee, Saet Byeol
   Lee, Sung Yong
   Choi, Jungmin
   Kim, Yeul Hong
TI Genetic Characteristics Associated With Drug Resistance in Lung Cancer
   and Colorectal Cancer Using Whole Exome Sequencing of Cell-Free DNA
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE circulating cell-free DNA (cfDNA); whole exome sequencing; drug
   resistance; lung cancer; colorectal cancer
ID CIRCULATING TUMOR DNA; ACQUIRED-RESISTANCE; MUTATIONS; PLASMA;
   HETEROGENEITY; MECHANISMS; LANDSCAPE; THERAPY; LIQUID; GROWTH
AB Circulating cell-free DNA (cfDNA) can be used to characterize tumor genomes through next-generation sequencing (NGS)-based approaches. We aim to identify novel genetic alterations associated with drug resistance in lung cancer and colorectal cancer patients who were treated with EGFR-targeted therapy and cytotoxic chemotherapy through whole exome sequencing (WES) of cfDNA. A cohort of 18 lung cancer patients was treated with EGFR TKI or cytotoxic chemotherapy, and a cohort of 37 colorectal cancer patients was treated with EGFR monoclonal antibody or cytotoxic chemotherapy alone. Serum samples were drawn before and after development of drug resistance, and the genetic mutational profile was analyzed with WES data. For 110 paired cfDNA and matched germline DNA WES samples, mean coverage of 138x (range, 52-208.4x) and 47x (range, 30.5-125.1x) was achieved, respectively. After excluding synonymous variants, mutants identified in more than two patients at the time of acquired resistance were selected. Seven genes in lung cancer and 16 genes in colorectal cancer were found, namely, APC, TP53, KRAS, SMAD4, and EGFR. In addition, the GPR155 I357S mutation in lung cancer and ADAMTS20 S1597P and TTN R7415H mutations in colorectal cancer were frequently detected at the time of acquired resistance, indicating that these mutations have an important function in acquired resistance to chemotherapy. Our data suggest that novel genetic variants associated with drug resistance can be identified using cfDNA WES. Further validation is necessary, but these candidate genes are promising therapeutic targets for overcoming drug resistance in lung cancer and colorectal cancer.
C1 [Lee, Jong Won; Park, Young Soo; Sung, Jae Sook; Kim, Boyeon; Lee, Saet Byeol; Kim, Yeul Hong] Korea Univ, Canc Res Inst, Coll Med, Seoul, South Korea.
   [Lee, Jong Won; Kim, Boyeon; Lee, Saet Byeol; Kim, Yeul Hong] Korea Univ, Brain Korea Plus Project Biomed Sci 21, Coll Med, Seoul, South Korea.
   [Lee, Jong Won; Choi, Jungmin] Korea Univ, Dept Biomed Sci, Coll Med, Seoul, South Korea.
   [Choi, Jung Yoon] Korea Univ, Coll Med, Korea Univ Ansan Hosp, Dept Internal Med,Div Hematol Oncol, Ansan, Gyeonggi, South Korea.
   [Chang, Won Jin; Lee, Soohyeon; Kim, Yeul Hong] Korea Univ, Coll Med, Korea Univ Anam Hosp, Dept Internal Med,Div Hematol Oncol, Seoul, South Korea.
   [Lee, Sung Yong] Korea Univ, Coll Med, Med Ctr, Dept Internal Med,Div Pulm, Seoul, South Korea.
   [Choi, Jungmin] Yale Univ, Sch Med, Dept Genet, New Haven, CT USA.
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); Korea University; Korea University Medicine (KU
   Medicine); Yale University
RP Kim, YH (corresponding author), Korea Univ, Canc Res Inst, Coll Med, Seoul, South Korea.; Kim, YH (corresponding author), Korea Univ, Brain Korea Plus Project Biomed Sci 21, Coll Med, Seoul, South Korea.; Kim, YH (corresponding author), Korea Univ, Coll Med, Korea Univ Anam Hosp, Dept Internal Med,Div Hematol Oncol, Seoul, South Korea.
EM yhk0215@korea.ac.kr
RI Lee, Ju-Seog/X-1786-2018; Lee, Joo Yong/ADE-2110-2022; Kim,
   Tae-You/J-2750-2012; Lee, Soohyeon/AAX-9843-2020; lee, jung/H-8107-2018
OI LEE, SUNG YONG/0000-0002-8693-5792; Choi, Jungmin/0000-0002-8614-0973;
   Park, Young Soo/0000-0003-4481-5415; Kim, Boyeon/0009-0004-1546-3080;
   Lee, Jongwon/0000-0002-2203-3634; Lee, Soohyeon/0000-0001-9665-062X;
   Kim, Yeul Hong/0000-0002-2555-2333
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TC 4
Z9 4
U1 2
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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 24
PY 2022
VL 12
AR 843561
DI 10.3389/fonc.2022.843561
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 0L6RE
UT WOS:000781599000001
PM 35402275
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Park, Y
   Yang, J
   Kim, MS
   Hyun, H
AF Park, Yoonbin
   Yang, Juhui
   Kim, Moon Suk
   Hyun, Hoon
TI A Three-In-One Heptamethine Cyanine Dye Induces Endoplasmic Reticulum
   Stress and Apoptosis in Colorectal Cancer
SO ADVANCED HEALTHCARE MATERIALS
LA English
DT Article; Early Access
DE ER stress; heptamethine cyanine dyes; near-infrared fluorescence
   imaging; reactive oxygen species; tumor targeting
ID INDOCYANINE DYE; FLUOROPHORES
AB One of the most significant challenges for image-guided cancer-targeted therapy is to develop multifunctional optical contrast agents enabling simultaneous targeting and therapy. Herein, a feasible strategy is based on the incorporation of therapeutic moieties into the non-delocalized structure of polymethine indocyanines, known as the "structure-inherent targeting" concept. By possessing a rigid chloro-cyclohexenyl ring in the heptamethine cyanine backbone, a new type of multifunctional near-infrared fluorescent dye, Ph790H, that targets tumor without the need for additional targeting ligands is synthesized. Armed with a phthalimide pharmacophore holding a prominent position in medicinal chemistry, Ph790H simultaneously induces endoplasmic reticulum (ER) stress to exert targeted therapeutic effects on HT-29 colorectal cancer xenografts. In terms of molecular mechanism, the lipophilic cationic Ph790H can be actively internalized into HT-29 cells through clathrin-mediated endocytosis. Consequently, mitochondrial reactive oxygen species (ROS) overproduction further induces activation of ER stress, demonstrated by increased ROS concentration and decreased mitochondrial membrane potential, which contributes to cell apoptosis and inhibition of tumor growth. Overall, Ph790H represents an effective "three-in-one" agent for the integration of cancer targeting, imaging, and therapy, which may provide a practical strategy to develop multifunctional small molecule theranostic agents for simultaneous cancer diagnosis and therapy.
C1 [Park, Yoonbin; Yang, Juhui; Hyun, Hoon] Chonnam Natl Univ, Med Sch, Dept Biomed Sci, Hwasun 58128, South Korea.
   [Park, Yoonbin; Hyun, Hoon] Chonnam Natl Univ, Biomed Sci Grad Program BMSGP, Hwasun 58128, South Korea.
   [Kim, Moon Suk] Ajou Univ, Dept Mol Sci & Technol, Suwon 16499, South Korea.
RP Hyun, H (corresponding author), Chonnam Natl Univ, Med Sch, Dept Biomed Sci, Hwasun 58128, South Korea.; Hyun, H (corresponding author), Chonnam Natl Univ, Biomed Sci Grad Program BMSGP, Hwasun 58128, South Korea.; Kim, MS (corresponding author), Ajou Univ, Dept Mol Sci & Technol, Suwon 16499, South Korea.
EM moonskim@ajou.ac.kr; hhyun@jnu.ac.kr
FU National Research Foundation of Korea [RS-2024-00458419]; National
   Research Foundation of Korea (NRF) - Korea government (MSIT)
FX This study was supported by the National Research Foundation of Korea
   (NRF) grant funded by the Korea government (MSIT) (No.
   RS-2024-00458419).
CR Baig N, 2021, MATER ADV, V2, P1821, DOI 10.1039/d0ma00807a
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NR 29
TC 0
Z9 0
U1 0
U2 0
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 2024 DEC 25
PY 2024
DI 10.1002/adhm.202404027
EA DEC 2024
PG 13
WC Engineering, Biomedical; Nanoscience & Nanotechnology; Materials
   Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Science & Technology - Other Topics; Materials Science
GA Q2A2Q
UT WOS:001382770200001
PM 39722134
DA 2025-01-04
ER

PT J
AU Al-Obeed, O
   El-Obeid, AS
   Matou-Nasri, S
   Vaali-Mohammed, MA
   AlHaidan, Y
   Elwatidy, M
   Al Dosary, H
   Alehaideb, Z
   Alkhayal, K
   Haseeb, A
   McKerrow, J
   Ahmad, R
   Abdulla, MH
AF Al-Obeed, Omar
   El-Obeid, Adila Salih
   Matou-Nasri, Sabine
   Vaali-Mohammed, Mansoor-Ali
   AlHaidan, Yazeid
   Elwatidy, Mohammed
   Al Dosary, Hamad
   Alehaideb, Zeyad
   Alkhayal, Khayal
   Haseeb, Adil
   McKerrow, James
   Ahmad, Rehan
   Abdulla, Maha-Hamadien
TI Herbal melanin inhibits colorectal cancer cell proliferation by altering
   redox balance, inducing apoptosis, and modulating MAPK signaling
SO CANCER CELL INTERNATIONAL
LA English
DT Article
DE Herbal melanin; Colorectal cancer; Proliferation; Apoptosis; Reactive
   oxygen species; TLR4 receptor; Signaling pathways
ID TARGETED THERAPY; NIGELLA-SATIVA; CHEMOTHERAPY; PATHWAYS;
   PHOSPHORYLATION; ACTIVATION; EXPRESSION; GENERATION; PROTEIN; GROWTH
AB Background Colorectal carcinoma is one of the most deadly cancers that requests effective and safe chemotherapy. Evaluation of natural product-based anticancer drugs as adjuvant treatment with fewer side effects is largely unexplored research fields. Herbal melanin (HM) is an extract of the seed coats of Nigella sativa that modulates an inflammatory response through toll-like receptor 4 (TLR4). This TLR4 receptor is also involved in the modulation of apoptosis. We therefore explored the anticancer potential of HM and specifically its effect on the molecular mechanisms underlying adenocarcinoma and metastatic colorectal cancer (mCRC) cell death in vitro. Methods Cell viability was evaluated using the MTT assay. Cellular reactive oxygen species (ROS), glutathione levels, and apoptotic status were assessed using fluorometric and colorimetric detection methods. HM-induced apoptotic and other signaling pathways were investigated using Western blot technology and mitochondrial transition pore assay kit. TLR4 receptor downregulation and blockade were performed using siRNA technology and neutralizing antibody, respectively. Results Our results showed that HM inhibited the proliferation of the colorectal adenocarcinoma HT29 and mCRC SW620 cell lines. Furthermore, HM enhanced ROS production and decreased glutathione levels. HM-induced apoptosis was associated with mitochondrial outer membrane permeability and cytochrome c release, inhibition of the Bcl2 family proteins, and activation of caspase-3/-7. In addition, HM modulated MAPK pathways by activating the JNK pathway and by inhibiting ERK phosphorylation. TLR4 receptor downregulation enhanced HM-induced apoptosis while TLR4 receptor blockade partially alleviated HM-inhibited ERK phosphorylation. Conclusion Altogether, these findings indicate that HM exerts pro-apoptotic effects and inhibits MAPK pathway through TLR4 in mCRC and colorectal adenocarcinoma cells, suggesting HM as a promising natural-based drug for the treatment of colorectal cancer.
C1 [Al-Obeed, Omar; Vaali-Mohammed, Mansoor-Ali; Elwatidy, Mohammed; Al Dosary, Hamad; Alkhayal, Khayal; Ahmad, Rehan; Abdulla, Maha-Hamadien] King Khalid Univ Hosp, Dept Surg, POB 7805 37, Riyadh 11472, Saudi Arabia.
   [Al-Obeed, Omar; Vaali-Mohammed, Mansoor-Ali; Elwatidy, Mohammed; Al Dosary, Hamad; Alkhayal, Khayal; Ahmad, Rehan; Abdulla, Maha-Hamadien] King Saud Univ, Coll Med, POB 7805 37, Riyadh 11472, Saudi Arabia.
   [El-Obeid, Adila Salih] King Saud Bin Abdulaziz Univ Hlth Sci, King Abdullah Int Med Res Ctr, Dept Biobank, Minist Natl Guard Hlth Affairs, POB 22490, Riyadh 11426, Saudi Arabia.
   [El-Obeid, Adila Salih] Ahfad Univ Women, Fac Pharmacol, Khartoum, Sudan.
   [Matou-Nasri, Sabine; AlHaidan, Yazeid; Alehaideb, Zeyad] King Saud Bin Abdulaziz Univ Hlth Sci, Cell & Gene Therapy Grp, Med Genom Res Dept, King Abdullah Int Med Res Ctr,Minist Natl Guard H, POB 22490, Riyadh 11426, Saudi Arabia.
   [Haseeb, Adil] Univ Khartoum, Dept Phys, Fac Sci, Khartoum, Sudan.
   [McKerrow, James] Univ Calif San Diego, Skaggs Sch Pharm & Pharmaceut Chem, La Jolla, CA 92093 USA.
C3 King Saud University; King Saud University; King Saud Bin Abdulaziz
   University for Health Sciences; Ministry of National Guard - Health
   Affairs; King Saud Bin Abdulaziz University for Health Sciences;
   University of Khartoum; University of California System; University of
   California San Diego
RP Abdulla, MH (corresponding author), King Khalid Univ Hosp, Dept Surg, POB 7805 37, Riyadh 11472, Saudi Arabia.; Abdulla, MH (corresponding author), King Saud Univ, Coll Med, POB 7805 37, Riyadh 11472, Saudi Arabia.
EM mabdulla@ksu.edu.sa
RI Alkhayal, Khayal/AAB-6746-2022; Elwetidy, Mohammad/GOV-5329-2022; ,
   Mansoor-Ali Vaali-Mohammed, PhD/G-4772-2012
OI , Mansoor-Ali Vaali-Mohammed, PhD/0000-0002-6437-711X; Alhaidan,
   Yazeid/0000-0002-0569-2988; Ahmad, Rehan/0000-0003-2612-2818; El-Wetidy,
   Mohammad/0000-0003-2725-4708; Al-Khayal, Khayal/0000-0001-8296-808X
FU deanship of scientific research, King Saud University [693540]
FX This work was supported and funded by the deanship of scientific
   research, King Saud University for funding through Vice Deanship of
   Scientific Research Chairs (693540).
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NR 63
TC 26
Z9 28
U1 0
U2 7
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1475-2867
J9 CANCER CELL INT
JI Cancer Cell Int.
PD APR 16
PY 2020
VL 20
IS 1
AR 126
DI 10.1186/s12935-020-01206-x
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LI0WA
UT WOS:000529206100001
PM 32322173
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Wang, T
   Sun, FM
   Wang, Y
   Jiang, JH
   Pan, MZ
   Yuan, MN
   Zhang, H
   Du, XD
   Hezam, K
   Song, K
   Wang, M
   Zhang, J
AF Wang, Tong
   Sun, Fumou
   Wang, Yang
   Jiang, Jiahao
   Pan, Mingzhu
   Yuan, Minne
   Zhang, Hang
   Du, Xiaodian
   Hezam, Kamal
   Song, Kai
   Wang, Min
   Zhang, Juan
TI NKG2D Immunoligand rG7S-MICA Enhances NK Cell-mediated
   Immunosurveillance in Colorectal Carcinoma
SO JOURNAL OF IMMUNOTHERAPY
LA English
DT Article
DE immunosurveillance; NK cells; colorectal carcinoma; rG7S-MICA
ID NATURAL-KILLER-CELLS; HEPATOCELLULAR-CARCINOMA; MONOCLONAL-ANTIBODIES;
   MEMBRANE ANTIGEN; CANCER-THERAPY; IMMUNE-SYSTEM; CD24 GENE; IN-VITRO;
   CETUXIMAB; EXPRESSION
AB Colorectal carcinoma (CRC) is one of the most common malignant cancers worldwide. The poor response of CRC to chemotherapy has whipped up the interest in targeted therapy with monoclonal antibodies for its potential efficiency. However, cetuximab, as one of the first-line targeted drugs in the treatment of CRC, has drug resistance and poor prognosis in clinic. To address this, a novel bispecific protein with CRC targeting and natural killer (NK) cell triggering was used for treatment. NK cell-mediated immunosurveillance is normally activated by the activating receptor natural killer cell receptor NK group 2, member D (NKG2D), which binds its key ligand major histocompatibility complex (MHC) class I-related chain A (MICA) expressed on the tumor cells. To trigger NK cell-mediated cytotoxicity, we fused MICA portion to a single-chain antibody fragment rG7S targeting the tumor-associated antigen CD24. In vitro, flow cytometry, cytotoxicity assay, degranulation, and cytokines release assay revealed that the fusion protein rG7S-MICA could both binds to CD24 and NKG2D which enhances NK cell sensitivity and NKG2D-mediated immunosurveillance against CD24(+) CRC cells. Furthermore, in a CD24(+) CRC-bearing nude mice model, rG7S-MICA effectively recruits NK cell to the tumor site and increase the release of cytokines such as interferon- (IFN-) and tumor necrosis factor- (TNF-), and shows potential antitumor effects. In conclusion, rG7S-MICA provides a novel immunotherapeutic strategy for CRC, which could be further developed against other CD24(+) malignancies.
C1 [Wang, Tong; Sun, Fumou; Wang, Yang; Jiang, Jiahao; Pan, Mingzhu; Yuan, Minne; Zhang, Hang; Du, Xiaodian; Hezam, Kamal; Song, Kai; Wang, Min; Zhang, Juan] China Pharmaceut Univ, Sch Life Sci & Technol, Antibody Engn Lab, State Key Lab Nat Med, Nanjing, Jiangsu, Peoples R China.
   [Song, Kai] Xuzhou Vocat Coll Bioengn, Dept Bioengn, Xuzhou, Peoples R China.
C3 China Pharmaceutical University
RP Zhang, J (corresponding author), China Pharmaceut Univ, 154 Tong Jia Xiang 24, Nanjing 210009, Peoples R China.
EM juancpu@126.com
RI pan, mingzhu/ISB-7589-2023; Zhang, Jiaqi/JDC-4383-2023; Zhang,
   Juan/GRX-2638-2022; Hezam, Kamal/Y-6402-2019; wang, rui/JAC-6240-2023
OI Hezam, Kamal/0000-0001-8551-8383
FU National Natural Science Foundation of China [NSFC81473125]; Natural
   Science Foundation of Jiangsu Province [Jiangsu Province Qinglan Project
   - Priority Academic Program Development of Jiangsu Higher Education
   Institutions] [BK20161459]; Natural Science Foundation of Jiangsu
   Province [Graduate Innovation Program of Jiangsu Province] [BK20161459,
   KYLX15_0670, KYLX 15_0190]
FX Supported by the National Natural Science Foundation of China
   (NSFC81473125). Natural Science Foundation of Jiangsu Province
   (BK20161459) [Jiangsu Province Qinglan Project (2014)-a project funded
   by the Priority Academic Program Development of Jiangsu Higher Education
   Institutions; The Graduate Innovation Program of Jiangsu Province
   (KYLX15_0670 and KYLX 15_0190)].All authors have declared that there are
   no financial conflicts of interest with regard to this work.
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NR 43
TC 14
Z9 15
U1 0
U2 33
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 APR
PY 2018
VL 41
IS 3
BP 109
EP 117
DI 10.1097/CJI.0000000000000215
PG 9
WC Oncology; Immunology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology; Research & Experimental Medicine
GA GA2TW
UT WOS:000428179400002
PM 29528990
DA 2025-01-04
ER

PT J
AU Cai, CJ
   Luo, QQ
   Liu, YH
   Peng, YH
   Zhang, XY
   Jiang, ZH
   Feng, ZY
   Qi, YR
   Gao, Y
   Liu, YT
   Liu, P
   Chen, YH
   Guo, C
   Shen, H
   Zeng, S
   Han, Y
AF Cai, Changjing
   Luo, Qingqing
   Liu, Yihan
   Peng, Yinghui
   Zhang, Xiangyang
   Jiang, Zhaohui
   Feng, Ziyang
   Qi, Yaru
   Gao, Yan
   Liu, Yongting
   Liu, Ping
   Chen, Yihong
   Guo, Cao
   Shen, Hong
   Zeng, Shan
   Han, Ying
TI The optimal first-line treatment for patients with left-sided RAS
   wild-type metastatic colorectal cancer: Double-drug regimen or
   triple-drug regimen therapy
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Article
DE colorectal cancer; cetuximab; panitumumab; bevacizumab; targeted therapy
ID FOLFIRI PLUS BEVACIZUMAB; COLON-CANCER; OPEN-LABEL; FOLFOXIRI;
   CETUXIMAB; SURVIVAL; CHEMOTHERAPY; PANITUMUMAB; TRIAL; BRAF
AB There are many treatments for metastatic colorectal cancer (mCRC). Among them, uncertainty remains especially concerning the clinical benefit of different regimens for left-sided RAS wild-type (WT) mCRC in the triple-drug therapy era. No studies have been conducted to answer this critical clinical issue. We performed a comprehensive analysis of published data and real-world data. First, we conducted analyses of the published trials to show the landscape of efficacy and safety in the treatments of left-sided RAS WT mCRC. Then, we initiated a multicenter real-world study as the validation dataset. This study included six published randomized controlled trials (RCTs) and a total of 1925 patients. The double-drug regimen plus cetuximab/panitumumab (D + C/P) achieved the longest overall survival (OS) in patients with left-sided mCRC (HR = 0.74, 95%CI: 0.57-0.98), while triple-drug regimen with bevacizumab (T + B, HR = 1.1, 95%CI: 0.63-2.0), compared with double-drug with bevacizumab (D + B). The D + C/P had the highest overall response rate (ORR) in patients with left-sided mCRC (OR = 1.8, 95%CI: 0.89-3.8), while T + B (OR = 1.8, 95%CI: 0.70-4.8), compared with D + B. The multicenter real-world cohort showed the double-drug regimen plus cetuximab had longer progression-free survival (PFS) in left-sided mCRC patients than the triple-drug regimen with bevacizumab. The safety analysis showed the incidence of the adverse events (grade & GE;3) in the triple-drug therapy plus bevacizumab was higher than that in the double-drug therapy plus cetuximab/panitumumab. This work demonstrates the ranking of three regimens for therapeutic efficacy and safety in patients with left-sided RAS WT mCRC. The double-drug regimen plus cetuximab/panitumumab appears more effective and safer than double-drug and triple-drug based regimens with bevacizumab. Further trials and cohort analyses on this topic would increase confidence in these results.
C1 [Cai, Changjing; Liu, Yihan; Peng, Yinghui; Zhang, Xiangyang; Jiang, Zhaohui; Feng, Ziyang; Qi, Yaru; Gao, Yan; Liu, Yongting; Liu, Ping; Chen, Yihong; Guo, Cao; Shen, Hong; Zeng, Shan; Han, Ying] Cent South Univ, Xiangya Hosp, Dept Oncol, Changsha, Peoples R China.
   [Cai, Changjing; Liu, Yihan; Peng, Yinghui; Zhang, Xiangyang; Jiang, Zhaohui; Feng, Ziyang; Qi, Yaru; Gao, Yan; Liu, Yongting; Liu, Ping; Chen, Yihong; Guo, Cao; Shen, Hong; Zeng, Shan; Han, Ying] Cent South Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, Changsha, Peoples R China.
   [Luo, Qingqing] Hunan Normal Univ, Affiliated Hosp 1, Hunan Prov Peoples Hosp, Dept Oncol, Changsha, Peoples R China.
C3 Central South University; Central South University; Hunan Normal
   University
RP Zeng, S; Han, Y (corresponding author), Cent South Univ, Xiangya Hosp, Dept Oncol, Changsha, Peoples R China.; Zeng, S; Han, Y (corresponding author), Cent South Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, Changsha, Peoples R China.
EM zengshan2000@csu.edu.cn; yinghan@csu.edu.cn
RI zhang, zheng/KBQ-7815-2024; Shen, Hong/N-9734-2019; Feng,
   Ziyang/HDM-9235-2022; Cai, Changjing/ABA-4542-2021; liu,
   yuchen/GYQ-6286-2022
OI Zeng, Shan/0000-0002-0988-723X
FU National Natural Science Foundation of China; Nature Science Foundation
   of Hunan Province [82203015, 81772627, 81874073, 81974384, 82173342];
   CSCO Cancer Research Foundation [2021JJ31092, 2021JJ31048]; key R & D
   Projects of Hainan Province [Y-HR2019-0182, Y-2019Genecast-043]; 
   [ZDYF2021SHFZ099];  [ZDYF022SHFZ086];  [ZDYF022SHFZ087]
FX This study was supported by grants from the National Natural Science
   Foundation of China (Nos. 82203015, 81772627, 81874073, 81974384 &
   82173342), two projects from the Nature Science Foundation of Hunan
   Province (Nos. 2021JJ31092 & 2021JJ31048), and two projects from CSCO
   Cancer Research Foundation (Nos. Y-HR2019-0182 & Y-2019Genecast-043),
   key R & D Projects of Hainan Province (Nos. ZDYF2021SHFZ099,
   ZDYF022SHFZ086, ZDYF022SHFZ087).
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Z9 2
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U2 9
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 SEP 30
PY 2022
VL 13
AR 1015510
DI 10.3389/fphar.2022.1015510
PG 10
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 5K1GT
UT WOS:000869481700001
PM 36249804
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Michel, M
   Kaps, L
   Maderer, A
   Galle, PR
   Moehler, M
AF Michel, Maurice
   Kaps, Leonard
   Maderer, Annett
   Galle, Peter R.
   Moehler, Markus
TI The Role of p53 Dysfunction in Colorectal Cancer and Its Implication for
   Therapy
SO CANCERS
LA English
DT Review
DE colorectal cancer; p53; systemic therapy; immunotherapy; tumor
   microenvironment (TME); cancer-associated fibroblasts; signaling;
   targeted therapy
ID WILD-TYPE P53; TUMOR-SUPPRESSOR FUNCTION; TP53 MUTATIONS PREDICT;
   FOLFIRI PLUS CETUXIMAB; III COLON-CANCER; MUTANT P53; LIVER METASTASES;
   THYMIDYLATE SYNTHASE; ADJUVANT TREATMENT; MICROSATELLITE INSTABILITY
AB Simple Summary
   Despite remarkable progress being made by preventive medical check-ups in the last decades, colorectal cancer (CRC) remains one of the most frequent and deadliest cancers worldwide. An understanding of the mutational landscape in CRC is needed to develop new mutanome-directed therapies with stronger efficacy and less side-effects than current therapeutic standard regimes. Carcinogenesis in CRC is a multi-gene driven process, where premalignant cells accumulate successively key tumorigenesis-related mutations. Here, inactivation of the tumor suppressor gene p53 is a hallmark event during tumorigenesis. Mutations of p53 impact the prognosis of patients, enabling the use of targeted therapies such as immune therapy. Alterations of p53 affect not only the tumor biology of cancer cells but also the surrounding tumor microenvironment (TME).
   Colorectal cancer (CRC) is one of the most common and fatal cancers worldwide. The carcinogenesis of CRC is based on a stepwise accumulation of mutations, leading either to an activation of oncogenes or a deactivation of suppressor genes. The loss of genetic stability triggers activation of proto-oncogenes (e.g., KRAS) and inactivation of tumor suppression genes, namely TP53 and APC, which together drive the transition from adenoma to adenocarcinoma. On the one hand, p53 mutations confer resistance to classical chemotherapy but, on the other hand, they open the door for immunotherapy, as p53-mutated tumors are rich in neoantigens. Aberrant function of the TP53 gene product, p53, also affects stromal and non-stromal cells in the tumor microenvironment. Cancer-associated fibroblasts together with other immunosuppressive cells become valuable assets for the tumor by p53-mediated tumor signaling. In this review, we address the manifold implications of p53 mutations in CRC regarding therapy, treatment response and personalized medicine.
C1 [Michel, Maurice; Kaps, Leonard; Maderer, Annett; Galle, Peter R.; Moehler, Markus] Univ Med Ctr Mainz, Dept Med 1, D-55131 Mainz, Germany.
   [Kaps, Leonard] Univ Med Ctr Mainz, Inst Translat Immunol, D-55131 Mainz, Germany.
   [Kaps, Leonard] Univ Med Ctr Mainz, Res Ctr Immune Therapy, D-55131 Mainz, Germany.
C3 Johannes Gutenberg University of Mainz; Johannes Gutenberg University of
   Mainz; Johannes Gutenberg University of Mainz
RP Moehler, M (corresponding author), Univ Med Ctr Mainz, Dept Med 1, D-55131 Mainz, Germany.
EM Maurice.Michel@unimedizin-mainz.de; Leonard.Kaps@unimedizin-mainz.de;
   Annett.Maderer@unimedizin-mainz.de; Peter.Galle@unimedizin-mainz.de;
   markus.moehler@unimedizin-mainz.de
RI Galle, Peter/ABE-2872-2021
OI Maderer, Annett/0000-0001-9891-5046; Galle, Peter
   Robert/0000-0001-8294-0992
FU Clinician Scientist Fellowship "Else Kroner Research College"
   [2018_Kolleg.05]; Clinician Scientist Fellowship of the Mainz Research
   School of Translational Biomedicine
FX Maurice Michel is supported by the Clinician Scientist Fellowship "Else
   Kroner Research College: 2018_Kolleg.05". Leonard Kaps is supported by
   the Clinician Scientist Fellowship of the Mainz Research School of
   Translational Biomedicine.
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NR 197
TC 55
Z9 55
U1 1
U2 21
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 10
AR 2296
DI 10.3390/cancers13102296
PG 24
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SI7NI
UT WOS:000655015300001
PM 34064974
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Liu, Q
   Yin, T
   Wang, GP
   Guo, FC
   Ou, YH
   Li, Y
   Wang, YS
AF Liu, Qin
   Yin, Tao
   Wang, Guoping
   Guo, Fuchun
   Ou, Yuhong
   Li, Yi
   Wang, Yongsheng
TI Vascular endothelial growth receptor 1 acts as a stress-associated
   protein in the therapeutic response to thalidomide
SO EXPERIMENTAL AND THERAPEUTIC MEDICINE
LA English
DT Article
DE thalidomide; vascular endothelial growth factor receptor 1; stress
   response; reactive oxygen species; CT26; human umbilical vein
   endothelial cells
ID CELL-CYCLE PROGRESSION; HEAT-SHOCK PROTEINS; TUMOR-GROWTH;
   GASTRIC-CANCER; IN-VIVO; MULTIPLE-MYELOMA; BCL-2 EXPRESSION; METASTASIS;
   APOPTOSIS; VEGF
AB Thalidomide (THD) exhibits antitumor effects in several types of cancer. However, the failure of THD to inhibit tumor growth has also been observed in a number of murine models in vivo. The mechanism involved in the therapeutic failure of THD remains unclear. The present study demonstrated that, accompanied by growth-arresting and apoptosis-inducing effects (P<0.05), THD upregulated vascular endothelial growth factor receptor 1 (VEGFR1) expression levels in CT26 murine colorectal carcinoma cell lines. This in vitro phenomenon was also observed in various other cell lines, including human umbilical vein endothelial cells, SW480, SW620 and HCT116. Reactive oxygen species (ROS) levels were increased compared with those in the untreated control when cells were exposed to THD (P<0.05). Furthermore, results suggested that ROS suppression may have provoked the induction of VEGFR1 expression to some extent. In addition, the results revealed that THD failed to inhibit CT26 tumor growth in vivo and the expression of VEGFR1 protein was elevated by THD treatment compared with the control group in the murine colorectal tumor model (P<0.05). The results of further experiments suggested that VEGFR1 was elevated in response to various stress-associated situations, including chemotherapy, radiotherapy and thermotherapy, which indicate that it may act as a stress-associated protein. The present findings provide a foundation for the future study of VEGFR1-targeted therapy to enhance the efficacy of current therapies.
C1 [Wang, Yongsheng] Sichuan Univ, State Key Lab Biotherapy, Dept Thorac Oncol, 17,Sect 3,South Peoples Rd, Chengdu 610041, Sichuan, Peoples R China.
   [Wang, Yongsheng] Sichuan Univ, West China Hosp, Collaborat Innovat Ctr Biotherapy, Ctr Canc, 17,Sect 3,South Peoples Rd, Chengdu 610041, Sichuan, Peoples R China.
C3 Sichuan University; Sichuan University
RP Wang, YS (corresponding author), Sichuan Univ, State Key Lab Biotherapy, Dept Thorac Oncol, 17,Sect 3,South Peoples Rd, Chengdu 610041, Sichuan, Peoples R China.; Wang, YS (corresponding author), Sichuan Univ, West China Hosp, Collaborat Innovat Ctr Biotherapy, Ctr Canc, 17,Sect 3,South Peoples Rd, Chengdu 610041, Sichuan, Peoples R China.
EM wangys@scu.edu.cn
RI Wang, Yongsheng/IVH-6129-2023; yi, li/KFR-6141-2024; Li,
   Yifan/IAQ-2592-2023
FU National Natural Science Foundation of China [81501609, 81272523]
FX The present study was supported by grants from the National Natural
   Science Foundation of China (grant nos. 81501609 and 81272523).
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NR 53
TC 0
Z9 2
U1 0
U2 14
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-0981
EI 1792-1015
J9 EXP THER MED
JI Exp. Ther. Med.
PD NOV
PY 2017
VL 14
IS 5
BP 4263
EP 4271
DI 10.3892/etm.2017.5028
PG 9
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA FM4GS
UT WOS:000414973100042
PM 29075340
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Holch, JW
   Ricard, I
   Stintzing, S
   Modest, DP
   Heinemann, V
AF Holch, Julian Walter
   Ricard, Ingrid
   Stintzing, Sebastian
   Modest, Dominik Paul
   Heinemann, Volker
TI The relevance of primary tumour location in patients with metastatic
   colorectal cancer: A meta-analysis of first-line clinical trials
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE Metastatic colorectal cancer; Primary tumour location; Sidedness;
   Prognostic biomarker; Predictive biomarker; Cetuximab; Panitumumab;
   Bevacizumab; Anti-EGFR; Anti-VEGF
ID COLON-CANCER; 2 SIDES; CETUXIMAB; DISTAL; EXPRESSION; PREDICTOR;
   BENEFIT; STAGE; SITE
AB Background: Retrospective subgroup analyses suggest that primary tumour location (PTL) has a prognostic importance and relates to response to targeted therapy.
   Methods: We conducted a meta-analysis of first-line clinical trials available up to October 2016, which assessed the relevance of PTL in patients with metastatic colorectal cancer (mCRC). Right- and left-sided colorectal cancers were differentiated (RC and LC).
   Results: In 13 first-line randomised controlled trials and one prospective pharmacogenetic study, RC was associated with a significantly worse prognosis compared with LC (hazard ratio [HR] for overall survival: 1.56; 95% confidence interval [CI]: 1.43-1.70; P < 0.0001). A meta-analysis of PRIME and CRYSTAL study suggests that PTL was predictive of survival benefit from addition of anti-EGFR antibody to standard chemotherapy in patients with RAS wildtype tumour (overall survival, HR for LC: 0.69; 95% CI: 0.58-0.83; P < 0.0001 and HR for RC: 0.96; 95% CI: 0.68-1.35; P = 0.802). A meta-analysis of FIRE-3/AIO KRK0306, CALGB/SWOG 80405 and PEAK study indicates that patients with RAS wild-type LC had a significantly greater survival benefit from anti-EGFR treatment compared with anti-VEGF treatment when added to standard chemotherapy (HR 0.71; 95% CI: 0.58-0.85; P = 0.0003). By contrast, in patients with RC, benefit from standard therapy was poor and bevacizumab-based treatment was numerically associated with longer survival (HR 1.3; 95% CI: 0.97-1.74; P = 0.081).
   Conclusions: The present meta-analysis demonstrates that PTL is prognostic in mCRC. Further, it supports the conclusion that patients with left-sided RAS wild-type mCRC should be preferentially treated with an anti-EGFR antibody. In right-sided mCRC, chemotherapy plus bevacizumab is a treatment option, but optimal treatment has yet to be defined. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [Holch, Julian Walter; Stintzing, Sebastian; Modest, Dominik Paul; Heinemann, Volker] Ludwig Maximilians Univ Munchen, Univ Hosp Grosshadern, Dept Med Oncol, Marchioninistr 15, D-81377 Munich, Germany.
   [Holch, Julian Walter; Stintzing, Sebastian; Modest, Dominik Paul; Heinemann, Volker] Ludwig Maximilians Univ Munchen, Univ Hosp Grosshadern, Ctr Comprehens Canc, Marchioninistr 15, D-81377 Munich, Germany.
   [Ricard, Ingrid] Ludwig Maximilians Univ Munchen, Inst Med Informat Biometry & Epidemiol, Marchioninistr 15, D-81377 Munich, Germany.
C3 University of Munich; University of Munich; University of Munich
RP Holch, JW (corresponding author), Ludwig Maximilians Univ Munchen, Dept Med Oncol, Marchioninistr 15, D-81377 Munich, Germany.; Holch, JW (corresponding author), Ludwig Maximilians Univ Munchen, Ctr Comprehens Canc, Marchioninistr 15, D-81377 Munich, Germany.
EM julian.holch@med.uni-muenchen.de; ricard@ibe.med.uni-muenchen.de;
   sebastian.stintzing@med.uni-muenchen.de;
   dominik.modest@med.uni-muenchen.de; volker.heinemann@med.uni-muenchen.de
RI Modest, Dominik Paul/AAW-9756-2021; Stintzing, Sebastian/I-4538-2016
OI Stintzing, Sebastian/0000-0002-3297-5801
CR [Anonymous], ANN ONCOL S6
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NR 29
TC 410
Z9 438
U1 0
U2 43
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0959-8049
EI 1879-0852
J9 EUR J CANCER
JI Eur. J. Cancer
PD JAN
PY 2017
VL 70
BP 87
EP 98
DI 10.1016/j.ejca.2016.10.007
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EF9MX
UT WOS:000390655400010
PM 27907852
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Inamura, K
AF Inamura, Kentaro
TI Colorectal Cancers: An Update on Their Molecular Pathology
SO CANCERS
LA English
DT Review
DE chromosomal instability; colorectal cancer; microsatellite instability;
   molecular characterization; personalized therapy
ID ISLAND METHYLATOR PHENOTYPE; MICROSATELLITE INSTABILITY;
   MISMATCH-REPAIR; HUMAN COLON; ASPIRIN USE; IMMUNE MICROENVIRONMENT; PD-1
   BLOCKADE; MUTATIONS; CELL; SUBTYPES
AB Colorectal cancers (CRCs) are the third leading cause of cancer-related mortality worldwide. Rather than being a single, uniform disease type, accumulating evidence suggests that CRCs comprise a group of molecularly heterogeneous diseases that are characterized by a range of genomic and epigenomic alterations. This heterogeneity slows the development of molecular-targeted therapy as a form of precision medicine. Recent data regarding comprehensive molecular characterizations and molecular pathological examinations of CRCs have increased our understanding of the genomic and epigenomic landscapes of CRCs, which has enabled CRCs to be reclassified into biologically and clinically meaningful subtypes. The increased knowledge of the molecular pathological epidemiology of CRCs has permitted their evolution from a vaguely understood, heterogeneous group of diseases with variable clinical courses to characteristic molecular subtypes, a development that will allow the implementation of personalized therapies and better management of patients with CRC. This review provides a perspective regarding recent developments in our knowledge of the molecular and epidemiological landscapes of CRCs, including results of comprehensive molecular characterizations obtained from high-throughput analyses and the latest developments regarding their molecular pathologies, immunological biomarkers, and associated gut microbiome. Advances in our understanding of potential personalized therapies for molecularly specific subtypes are also reviewed.
C1 [Inamura, Kentaro] Japanese Fdn Canc Res, Canc Inst, Div Pathol, Koto Ku, 3-8-31 Ariake, Tokyo 1358550, Japan.
C3 Japanese Foundation for Cancer Research
RP Inamura, K (corresponding author), Japanese Fdn Canc Res, Canc Inst, Div Pathol, Koto Ku, 3-8-31 Ariake, Tokyo 1358550, Japan.
EM kentaro.inamura@jfcr.or.jp
RI Inamura, Kentaro/G-4229-2018
OI Inamura, Kentaro/0000-0001-6444-3861
FU JSPS KAKENHI [JP16K08679]; Ministry of the Environment, Japan;
   Grants-in-Aid for Scientific Research [16K08679] Funding Source: KAKEN
FX This study was supported by JSPS KAKENHI Grant Number JP16K08679; and
   the Ministry of the Environment, Japan. The author thanks Yuki Takano
   (Japanese Foundation for Cancer Research, Tokyo, Japan) and Chikako
   Yoshida (Japanese Foundation for Cancer Research, Tokyo, Japan) for
   their secretarial expertise.
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NR 125
TC 111
Z9 120
U1 2
U2 45
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 2072-6694
J9 CANCERS
JI Cancers
PD JAN
PY 2018
VL 10
IS 1
AR 26
DI 10.3390/cancers10010026
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FU8JH
UT WOS:000424098600025
PM 29361689
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Li, WJ
   Gao, T
   Pei, RJ
AF Li, Wenjing
   Gao, Tian
   Pei, Renjun
TI Selection of trophoblast cell surface antigen 2-targeted aptamer for the
   development of cytotoxic aptamer-drug conjugate
SO INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
LA English
DT Article
DE Trop2; Aptamer; SELEX; Aptamer-drug conjugate; Targeted therapy;
   Colorectal cancer
ID BREAST-CANCER; POOR-PROGNOSIS; EXPRESSION; ANTIBODY
AB Trophoblast cell surface antigen 2 expressed in several malignant cancers promotes tumor growth and metastasis via several signal transduction pathways. Trop2 is reputed as a prospective biomarker and therapeutic target. Trophoblast cell surface antigen 2-targeted agents, including antibodies, antibody conjugates and therapeutic combinations, could be utilized to fight cancers. To develop an effective drug targeting strategy, we resorted to a new trophoblast cell surface antigen 2-targeted anticancer treatment through aptamer conjugated with chemotherapeutic drug. This study identified trophoblast cell surface antigen 2-specific ssDNA aptamers using engineered trophoblast cell surface antigen 2 overexpression cells for cell-SELEX. The obtained ssDNA aptamer bound to trophoblast cell surface antigen 2 overexpressed cells with nanomolar affinity and was specific for several tumor cell types which express trophoblast cell surface antigen 2 abundantly. Significant cytotoxicity against HT29 cell by the conjugate of trophoblast cell surface antigen 2 aptamer and Emtansine was observed while resulting negligible therapeutic effect on human normal intestinal epithelial cell line HIEC in vitro, indicating that the conjugate shows potential as a promising therapeutic agent. Furthermore, the isolated aptamer demonstrated the ability for the targeted delivery, resulting excellent therapeutic effectiveness of aptamer-drug conjugate for xenograft tumor model of mice with human colorectal cancer.
C1 [Li, Wenjing; Pei, Renjun] Univ Sci & Technol China, Sch Nanotech & Nanob, Hefei 230026, Peoples R China.
   [Li, Wenjing; Gao, Tian; Pei, Renjun] Chinese Acad Sci, Suzhou Inst Nanotech & Nanob, CAS Key Lab Nanobio Interface, Suzhou 215123, Peoples R China.
C3 Chinese Academy of Sciences; University of Science & Technology of
   China, CAS; Chinese Academy of Sciences
RP Pei, RJ (corresponding author), Univ Sci & Technol China, Sch Nanotech & Nanob, Hefei 230026, Peoples R China.; Gao, T; Pei, RJ (corresponding author), Chinese Acad Sci, Suzhou Inst Nanotech & Nanob, CAS Key Lab Nanobio Interface, Suzhou 215123, Peoples R China.
EM tgao2017@sinano.ac.cn; rjpei2011@sinano.ac.cn
RI Li, Wenjing/ABA-9384-2022
FU National Natural Science Foundation of China [22307137, 22177129];
   Science and Technology Foundation of Jiangsu Province [BK20220099,
   BE2023731]
FX This work was supported by grants from the National Natural Science
   Foundation of China (22307137, 22177129) and the Science and Technology
   Foundation of Jiangsu Province (BK20220099, BE2023731) .
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NR 30
TC 0
Z9 0
U1 6
U2 6
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0141-8130
EI 1879-0003
J9 INT J BIOL MACROMOL
JI Int. J. Biol. Macromol.
PD NOV
PY 2024
VL 279
AR 135456
DI 10.1016/j.ijbiomac.2024.135456
EA SEP 2024
PN 4
PG 9
WC Biochemistry & Molecular Biology; Chemistry, Applied; Polymer Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry; Polymer Science
GA G9K6L
UT WOS:001319746200001
PM 39250993
DA 2025-01-04
ER

PT J
AU Matsuoka, T
   Yashiro, M
AF Matsuoka, Tasuku
   Yashiro, Masakazu
TI Precision medicine for gastrointestinal cancer: Recent progress and
   future perspective
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Gastrointestinal cancer; Esophageal cancer; Gastric cancer; Colorectal
   cancer; Precision medicine; Liquid biopsy; Gene panel; Precision
   surgery; Biomarkers
ID SQUAMOUS-CELL CARCINOMA; CIRCULATING TUMOR-CELLS; COMPREHENSIVE
   MOLECULAR CHARACTERIZATION; MISMATCH REPAIR DEFICIENCY;
   COLORECTAL-CANCER; GASTRIC-CANCER; LIQUID BIOPSY; PROGNOSTIC VALUE;
   MUTATIONAL LANDSCAPE; GENOMIC LANDSCAPE
AB Gastrointestinal (GI) cancer has a high tumor incidence and mortality rate worldwide. Despite significant improvements in radiotherapy, chemotherapy, and targeted therapy for GI cancer over the last decade, GI cancer is characterized by high recurrence rates and a dismal prognosis. There is an urgent need for new diagnostic and therapeutic approaches. Recent technological advances and the accumulation of clinical data are moving toward the use of precision medicine in GI cancer. Here we review the application and status of precision medicine in GI cancer. Analyses of liquid biopsy specimens provide comprehensive real-time data of the tumor-associated changes in an individual GI cancer patient with malignancy. With the introduction of gene panels including next-generation sequencing, it has become possible to identify a variety of mutations and genetic biomarkers in GI cancer. Although the genomic aberration of GI cancer is apparently less actionable compared to other solid tumors, novel informative analyses derived from comprehensive gene profiling may lead to the discovery of precise molecular targeted drugs. These progressions will make it feasible to incorporate clinical, genome-based, and phenotype-based diagnostic and therapeutic approaches and apply them to individual GI cancer patients for precision medicine.
C1 [Matsuoka, Tasuku; Yashiro, Masakazu] Osaka City Univ, Grad Sch Med, Dept Surg Gastroenterol, Osaka 5458585, Japan.
   [Yashiro, Masakazu] Osaka City Univ, Grad Sch Med, Oncol Inst Geriatr & Med Sci, Osaka 5458585, Japan.
C3 Osaka Metropolitan University; Osaka Metropolitan University
RP Yashiro, M (corresponding author), Osaka City Univ, Grad Sch Med, Dept Surg Oncol, Abeno Ku, 1-4-3 Asahi Machi, Osaka 5458585, Japan.
EM m9312510@med.osaka-cu.ac.jp
FU KAKENHI [18H02883]; Grants-in-Aid for Scientific Research [18H02883]
   Funding Source: KAKEN
FX Supported by KAKENHI (Grant-inAid for Scientific Research), No.
   18H02883.
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NR 164
TC 33
Z9 35
U1 0
U2 23
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 JAN 15
PY 2020
VL 12
IS 1
DI 10.4251/wjgo.v12.i1.1
PG 21
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA LS3FH
UT WOS:000536272700001
PM 31966910
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Elekonawo, FMK
   Bos, DL
   Goldenberg, DM
   Boerman, OC
   Rijpkema, M
AF Elekonawo, Fortune M. K.
   Bos, Desiree L.
   Goldenberg, David M.
   Boerman, Otto C.
   Rijpkema, Mark
TI Carcinoembryonic antigen-targeted photodynamic therapy in colorectal
   cancer models
SO EJNMMI RESEARCH
LA English
DT Article
DE Colorectal cancer; Targeted photodynamic therapy; Carcinoembryonic
   antigen; Targeted; IRDye700DX
ID ANTIBODY-DRUG CONJUGATE; PHOTOIMMUNOTHERAPY; GOVITECAN; RESECTION;
   RADIOIMMUNOTHERAPY; METASTASES; SURGERY; TRIAL; HEAD
AB Background: In colorectal cancer, survival of patients is drastically reduced when complete resection is hampered by involvement of critical structures. Targeted photodynamic therapy (tPDT) is a local and targeted therapy which could play a role in eradicating residual tumor cells after incomplete resection. Since carcinoembryonic antigen (CEA; CEACAM5) is abundantly overexpressed in colorectal cancer, it is a potential target for tPDT of colorectal cancer.
   Methods: To address the potential of CEA-targeted PDT, we compared colorectal cancer cell lines with different CEA-expression levels (SW-48, SW-480, SW-620, SW-1222, WiDr, HT-29, DLD-1, LS174T, and LoVo) under identical experimental conditions. We evaluated the susceptibility to tPDT by varying radiant exposure and concentration of our antibody conjugate (DTPA-hMN-14-IRDye700DX). Finally, we assessed the efficacy of tPDT in vivo in 18 mice (BALB/cAnNRj-Foxn1(nu/nu)) with subcutaneously xenografted LoVo tumors.
   Results: In vitro, the treatment effect of tPDT varied per cell line and was dependent on both radiant exposure and antibody concentration. Under standardized conditions (94.5 J/cm(2) and 0.5 mu g/mu L antibody conjugate concentration), the effect of tPDT was higher in cells with higher CEA availability: SW-1222, LS174T, LoVo, and SW-48 (22.8%, 52.8%, 49.9%, and 51.9% reduction of viable cells, respectively) compared to cells with lower CEA availability. Compared to control groups (light or antibody conjugate only), tumor growth rate was reduced in mice with s.c. LoVo tumors receiving tPDT.
   Conclusion: Our findings suggest cells (and tumors) have different levels of susceptibility for tPDT even though they all express CEA. Furthermore, tPDT can effectively reduce tumor growth in vivo.
C1 [Elekonawo, Fortune M. K.; Bos, Desiree L.; Boerman, Otto C.; Rijpkema, Mark] Radboud Univ Nijmegen, Med Ctr, Dept Radiol & Nucl Med, POB 9101, NL-6500 HB Nijmegen, Netherlands.
   [Goldenberg, David M.] Ctr Mol Med & Immunol, Mendham, NJ USA.
   [Goldenberg, David M.] Immunomed Inc, Morris Plains, NJ USA.
   [Goldenberg, David M.] IBC Pharmaceut Inc, Morris Plains, NJ USA.
C3 Radboud University Nijmegen
RP Elekonawo, FMK (corresponding author), Radboud Univ Nijmegen, Med Ctr, Dept Radiol & Nucl Med, POB 9101, NL-6500 HB Nijmegen, Netherlands.
EM fortune.elekonawo@radboudumc.nl
RI Rijpkema, Mark/D-1974-2010; Elekonawo, Fortuné/H-3521-2016
OI Elekonawo, Fortune/0000-0002-1726-186X
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NR 37
TC 8
Z9 9
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 2191-219X
J9 EJNMMI RES
JI EJNMMI Res.
PD DEC 11
PY 2019
VL 9
IS 1
AR 108
DI 10.1186/s13550-019-0580-z
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA KM1IF
UT WOS:000513871000002
PM 31828541
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Sanchez-Ibarra, HE
   Jiang, XL
   Gallegos-Gonzalez, EY
   Cavazos-González, AC
   Chen, YH
   Morcos, F
   Barrera-Saldaña, HA
AF Sanchez-Ibarra, Hector Eduardo
   Jiang, Xianli
   Gallegos-Gonzalez, Elena Yareli
   Cavazos-Gonzalez, Adriana Carolina
   Chen, Yenho
   Morcos, Faruck
   Barrera-Saldana, Hugo Alberto
TI <i>KRAS</i>, <i>NRAS</i>, and <i>BRAF</i> mutation prevalence,
   clinicopathological association, and their application in a predictive
   model in Mexican patients with metastatic colorectal cancer: A
   retrospective cohort study
SO PLOS ONE
LA English
DT Article
ID BREAST-CANCER; RISK; CLASSIFICATION; PROGNOSIS; SURVIVAL
AB Mutations inKRAS,NRAS, andBRAF(RAS/BRAF) genes are the main predictive biomarkers for the response to anti-EGFR monoclonal antibodies (MAbs) targeted therapy in metastatic colorectal cancer (mCRC). This retrospective study aimed to report the mutational status prevalence of these genes, explore their possible associations with clinicopathological features, and build and validate a predictive model. To achieve these objectives, 500 mCRC Mexican patients were screened for clinically relevant mutations inRAS/BRAFgenes. Fifty-two percent of these specimens harbored clinically relevant mutations in at least one screened gene. Among these, 86% had a mutation inKRAS, 7% inNRAS, 6% inBRAF, and 2% in bothNRASandBRAF. Only tumor location in the proximal colon exhibited a significant correlation withKRASandBRAFmutational status (p-value = 0.0414 and 0.0065, respectively). Further t-SNE analyses were made to 191 specimens to reveal patterns among patients with clinical parameters andKRASmutational status. Then, directed by the results from classical statistical tests and t-SNE analysis, neural network models utilized entity embeddings to learn patterns and build predictive models using a minimal number of trainable parameters. This study could be the first step in the prediction forRAS/BRAFmutational status from tumoral features and could lead the way to a more detailed and more diverse dataset that could benefit from machine learning methods.
C1 [Sanchez-Ibarra, Hector Eduardo; Gallegos-Gonzalez, Elena Yareli; Cavazos-Gonzalez, Adriana Carolina; Barrera-Saldana, Hugo Alberto] Vitagenesis SA CV, Genet Lab, Monterrey, Nuevo Leon, Mexico.
   [Jiang, Xianli; Chen, Yenho; Morcos, Faruck] Univ Texas Dallas, Evolutionary Informat Lab, Dept Biol Sci, Richardson, TX 75083 USA.
C3 University of Texas System; University of Texas Dallas
RP Barrera-Saldaña, HA (corresponding author), Vitagenesis SA CV, Genet Lab, Monterrey, Nuevo Leon, Mexico.
EM habarrera@gmail.com
RI ; Jiang, Xianli/AAB-5437-2020
OI Sanchez Ibarra, Hector Eduardo/0000-0002-9991-267X; Barrera Saldana,
   Hugo A./0000-0003-1587-4571; Jiang, Xianli/0000-0003-1697-8575
FU National Council on Science and Technology (CONACyT) [185427,
   ECO-2015C01-260826, 294875, 280114]; National Institute of Health
   [R35GM133631]
FX The experimental laboratory work was carried out with equipment from
   "Laboratorio Nacional de Servicios Especializados de Investigacion,
   Desarrollo e Innovacion (I+D+I) para Farmoquimicos y
   Biotecnologicos,"LANSEIDI-Far BioTec-CONACyT. This research was
   partially funded by the National Council on Science and Technology
   (CONACyT) grants 185427, ECO-2015C01-260826, 294875, and 280114 held by
   HAB (Vitagenesis) and the fund from the National Institute of Health
   Grant R35GM133631 (to XJ and FM) University of Texas at Dallas held by
   FM. Vitagenesis website: https://www.vitagenesis.org/.LANSEIDI website:
   http://www.lanseidi.com/.Vitagenesis provided support in the form of
   salaries for authors HES, EYG, and ACC. Vitagenesis nor the University
   of Texas had not have any additional role in the study design, data
   collection, and analysis, decision to publish, or preparation of the
   manuscript.
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NR 44
TC 26
Z9 27
U1 1
U2 2
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 JUL 6
PY 2020
VL 15
IS 7
AR e0235490
DI 10.1371/journal.pone.0235490
PG 16
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA MM3OG
UT WOS:000550068700016
PM 32628708
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Tang, LX
   Yu, S
   Zhang, QQ
   Cai, YL
   Li, W
   Yao, SB
   Cheng, HD
AF Tang, Lingxue
   Yu, Sheng
   Zhang, Qianqian
   Cai, Yinlian
   Li, Wen
   Yao, Senbang
   Cheng, Huaidong
TI Identification of hub genes related to CD4<SUP>+</SUP> memory T cell
   infiltration with gene co-expression network predicts prognosis and
   immunotherapy effect in colon adenocarcinoma
SO FRONTIERS IN GENETICS
LA English
DT Article
DE colon adenocarcinoma; immunotherapy; CD4+memory T cell; weighted gene
   coexpression network analysis; gene
ID FACTOR-BETA 2; COLORECTAL-CANCER; EXPRESSION; MUTATION; BREAST; KRAS;
   STATISTICS; BIOMARKERS; MECHANISM; INSIGHTS
AB Background: CD4(+) memory T cells (CD4+ MTCs), as an important part of the microenvironment affecting tumorigenesis and progression, have rarely been systematically analyzed. Our purpose was to comprehensively analyze the effect of CD4(+) MTC infiltration on the prognosis of colon adenocarcinoma (COAD).
   Methods: Based on RNA-Seq data, weighted gene co-expression network analysis (WGCNA) was used to screen the CD4(+) MTC infiltration genes most associated with colon cancer and then identify hub genes and construct a prognostic model using the least absolute shrinkage and selection operator algorithm (LASSO). Finally, survival analysis, immune efficacy analysis, and drug sensitivity analysis were performed to evaluate the role of the prognostic model in COAD.
   Results: We identified 929 differentially expressed genes (DEGs) associated with CD4(+) MTCs and constructed a prognosis model based on five hub genes (F2RL2, TGFB2, DTNA, S1PR5, and MPP2) to predict overall survival (OS) in COAD. Kaplan-Meier analysis showed poor prognosis in the high-risk group, and the analysis of the hub gene showed that overexpression of TGFB2, DTNA, S1PR5, or MPP2 was associated with poor prognosis. Clinical prediction nomograms combining CD4(+) MTC-related DEGs and clinical features were constructed to accurately predict OS and had high clinical application value. Immune efficacy and drug sensitivity analysis provide new insights for individualized treatment.
   Conclusion: We constructed a prognostic risk model to predict OS in COAD and analyzed the effects of risk score on immunotherapy efficacy or drug sensitivity. These studies have important clinical significance for individualized targeted therapy and prognosis.
C1 [Tang, Lingxue; Yu, Sheng; Zhang, Qianqian; Cai, Yinlian; Li, Wen; Yao, Senbang; Cheng, Huaidong] Anhui Med Univ, Affiliated Hosp 2, Dept Oncol, Hefei, Peoples R China.
   [Tang, Lingxue; Yu, Sheng; Zhang, Qianqian; Cai, Yinlian; Li, Wen; Yao, Senbang; Cheng, Huaidong] Anhui Med Univ, Dept Oncol, Hefei, Peoples R China.
C3 Anhui Medical University; Anhui Medical University
RP Cheng, HD (corresponding author), Anhui Med Univ, Affiliated Hosp 2, Dept Oncol, Hefei, Peoples R China.; Cheng, HD (corresponding author), Anhui Med Univ, Dept Oncol, Hefei, Peoples R China.
EM chd1975ay@126.com
RI Zhang, Qianqian/GXA-0841-2022; Tang, LX/ISS-0697-2023; cai,
   yinlian/JHT-6487-2023; Yao, Senbang/AGS-2326-2022
OI Cai, Yinlian/0000-0002-8945-8549; Yu, Sheng/0000-0001-9881-8625; Tang,
   Lingxue/0000-0002-3304-5307
FU National Natural Science Foundation of China [81872504]
FX This work was supported by the National Natural Science Foundation of
   China (No. 81872504).
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NR 75
TC 2
Z9 3
U1 1
U2 7
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 AUG 29
PY 2022
VL 13
AR 915282
DI 10.3389/fgene.2022.915282
PG 20
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA P5DX0
UT WOS:001050888900001
PM 36105107
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Bebb, DG
   Banerji, S
   Blais, N
   Desmeules, P
   Gill, S
   Grin, A
   Feilotter, H
   Hansen, AR
   Hyrcza, M
   Krzyzanowska, M
   Melosky, B
   Noujaim, J
   Purgina, B
   Ruether, D
   Simmons, CE
   Soulieres, D
   Torlakovic, EE
   Tsao, MS
AF Bebb, D. Gwyn
   Banerji, Shantanu
   Blais, Normand
   Desmeules, Patrice
   Gill, Sharlene
   Grin, Andrea
   Feilotter, Harriet
   Hansen, Aaron R.
   Hyrcza, Martin
   Krzyzanowska, Monika
   Melosky, Barbara
   Noujaim, Jonathan
   Purgina, Bibiana
   Ruether, Dean
   Simmons, Christine E.
   Soulieres, Denis
   Torlakovic, Emina Emilia
   Tsao, Ming-Sound
TI Canadian Consensus for Biomarker Testing and Treatment of TRK Fusion
   Cancer in Adults
SO CURRENT ONCOLOGY
LA English
DT Article
DE NTRK; larotrectinib; entrectinib; targeted therapy; molecular testing;
   oncogenic drivers; TRK fusion; tumour-agnostic
ID CELL LUNG-CANCER; ANALOG SECRETORY CARCINOMA; SOFT-TISSUE SARCOMA;
   METASTATIC COLORECTAL-CANCER; GASTROINTESTINAL STROMAL TUMORS;
   ETV6-NTRK3 GENE FUSION; POSITIVE SOLID TUMORS; V600E BRAF MUTATIONS;
   PHASE-II TRIAL; OPEN-LABEL
AB The tyrosine receptor kinase (TRK) inhibitors larotrectinib and entrectinib were recently approved in Canada for the treatment of solid tumours harbouring neurotrophic tyrosine receptor kinase (NTRK) gene fusions. These NTRK gene fusions are oncogenic drivers found in most tumour types at a low frequency (<5%), and at a higher frequency (>80%) in a small number of rare tumours (e.g., secretory carcinoma of the salivary gland and of the breast). They are generally mutually exclusive of other common oncogenic drivers. Larotrectinib and entrectinib have demonstrated impressive overall response rates and tolerability in Phase I/II trials in patients with TRK fusion cancer with no other effective treatment options. Given the low frequency of TRK fusion cancer and the heterogeneous molecular testing landscape in Canada, identifying and optimally managing such patients represents a new challenge. We provide a Canadian consensus on when and how to test for NTRK gene fusions and when to consider treatment with a TRK inhibitor. We focus on five tumour types: thyroid carcinoma, colorectal carcinoma, non-small cell lung carcinoma, soft tissue sarcoma, and salivary gland carcinoma. Based on the probability of the tumour harbouring an NTRK gene fusion, we also suggest a tumour-agnostic consensus for NTRK gene fusion testing and treatment. We recommend considering a TRK inhibitor in all patients with TRK fusion cancer with no other effective treatment options.
C1 [Bebb, D. Gwyn] Tom Baker Canc Clin, Calgary, AB T2N 4N2, Canada.
   [Bebb, D. Gwyn] Univ Calgary, Calgary, AB T2N 4N2, Canada.
   [Banerji, Shantanu] Univ Manitoba, Res Inst Oncol & Hematol, CancerCare Manitoba, Winnipeg, MB R3E 0V9, Canada.
   [Blais, Normand; Soulieres, Denis] Univ Montreal, Ctr Hosp Univ Montreal, Dept Med, Montreal, PQ H2X 3E4, Canada.
   [Desmeules, Patrice] Univ Laval, Inst Univ Cardiol & Pneumol Quebec, Serv Anatomopathol & Cytol, Quebec City, PQ G1V 0A6, Canada.
   [Gill, Sharlene; Melosky, Barbara; Simmons, Christine E.] BC Canc, Vancouver, BC V5Z 4E6, Canada.
   [Grin, Andrea; Feilotter, Harriet] Queens Univ, Dept Pathol & Mol Med, Kingston, ON K7L 3N6, Canada.
   [Hansen, Aaron R.; Krzyzanowska, Monika] Univ Hlth Network, Princess Margaret Canc Ctr, Dept Med Oncol & Hematol, Toronto, ON M5G 2C1, Canada.
   [Hyrcza, Martin] Univ Calgary, Arnie Charbonneau Canc Inst, Dept Pathol & Lab Med, Calgary, AB T2N 4Z6, Canada.
   [Noujaim, Jonathan] Hop Maison Neuve Rosemont, Montreal, PQ H1T 2M4, Canada.
   [Purgina, Bibiana] Univ Ottawa, Ottawa Hosp, Dept Pathol & Lab Med, Ottawa, ON K1N 6N5, Canada.
   [Ruether, Dean] Tom Baker Canc Clin, Dept Oncol, Calgary, AB T2N 4N2, Canada.
   [Torlakovic, Emina Emilia] Saskatchewan Hlth Author, Dept Pathol & Lab Med, Saskatoon, SK S7N 5B5, Canada.
   [Torlakovic, Emina Emilia] Univ Saskatchewan, Saskatoon, SK S7N 5B5, Canada.
   [Tsao, Ming-Sound] Univ Hlth Network, Dept Pathol, Lab Med Program, Toronto, ON M5G 2C4, Canada.
C3 University of Calgary; Tom Baker Cancer Clinic; University of Calgary;
   CancerCare Manitoba Foundation; University of Manitoba; Universite de
   Montreal; Laval University; McMaster University; Queens University -
   Canada; University of Toronto; University Health Network Toronto;
   Princess Margaret Cancer Centre; University of Calgary; Universite de
   Montreal; University of Ottawa; Ottawa Hospital Research Institute;
   University of Calgary; Tom Baker Cancer Clinic; University of
   Saskatchewan; University of Toronto; University Health Network Toronto
RP Bebb, DG (corresponding author), Tom Baker Canc Clin, Calgary, AB T2N 4N2, Canada.; Bebb, DG (corresponding author), Univ Calgary, Calgary, AB T2N 4N2, Canada.; Tsao, MS (corresponding author), Univ Hlth Network, Dept Pathol, Lab Med Program, Toronto, ON M5G 2C4, Canada.
EM gwyn.bebb@ahs.ca; sbanerji@cancercare.mb.ca;
   normand.blais.chum@ssss.gouv.qc.ca; patrice.desmeules@criucpq.ulaval.ca;
   sgill@bccancer.bc.ca; andrea.grin@kingstonhsc.ca; hf4@queensu.ca;
   aaron.hansen@uhn.ca; martin.hyrcza@albertaprecisionlabs.ca;
   monika.krzyzanowska@uhn.ca; bmelosky@bccancer.bc.ca;
   john.c.njm@gmail.com; bpurgina@toh.ca;
   dean.ruether@albertahealthservices.ca; christine.simmons@bccancer.bc.ca;
   denis.soulieres.chum@ssss.gouv.qc.ca;
   emina.torlakovic@saskhealthauthority.ca; ming.tsao@uhn.ca
RI Krzyzanowska, Monika/ABG-3505-2020; Tsao, Ming/M-3503-2017
OI Tsao, Ming/0000-0002-9160-5405; Krzyzanowska,
   Monika/0000-0001-5533-7418; Feilotter, Harriet/0000-0002-1388-2183;
   Blais, Normand/0000-0003-2698-4362
FU Bayer Canada Inc.
FX Editorial support was provided by MEDUCOM Health Inc. and sponsored by
   Bayer Canada Inc. Upon request, the sponsor provided data, documents,
   and materials necessary for development of the manuscript. The sponsor
   reviewed the draft publication for scientific and medical accuracy. The
   authors considered any comments made by the sponsor and accepted or
   rejected revisions suggested by the sponsor.
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NR 128
TC 30
Z9 31
U1 1
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1198-0052
EI 1718-7729
J9 CURR ONCOL
JI Curr. Oncol.
PD FEB
PY 2021
VL 28
IS 1
BP 523
EP 548
DI 10.3390/curroncol28010053
PG 26
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QO6VK
UT WOS:000623279100053
PM 33467570
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yuan, Y
   Yang, CX
   Wang, YZ
   Sun, MM
   Bi, CH
   Sun, ST
   Sun, GJ
   Hao, JP
   Li, LL
   Shan, CL
   Zhang, S
   Li, YB
AF Yuan, Yu
   Yang, Chenxin
   Wang, Yingzhi
   Sun, Mingming
   Bi, Chenghao
   Sun, Sitong
   Sun, Guijiang
   Hao, Jingpeng
   Li, Lingling
   Shan, Changliang
   Zhang, Shuai
   Li, Yubo
TI Functional metabolome profiling may improve individual outcomes in
   colorectal cancer management implementing concepts of predictive,
   preventive, and personalized medical approach
SO EPMA JOURNAL
LA English
DT Article
DE Predictive preventive personalized medicine; Metabolomics; UPLC-Q-TOF;
   MS; Colorectal cancer; Serum; Glycodeoxycholic acid; Therapeutic
   targets; Celastrol; Poly(ADP-ribose) polymerase-1
ID PARP-1; ACID; OVEREXPRESSION; INHIBITION; CELASTROL; GROWTH; STAGE
AB Objectives Colorectal cancer (CRC) is one of the most common solid tumors worldwide, but its diagnosis and treatment are limited. The objectives of our study were to compare the metabolic differences between CRC patients and healthy controls (HC), and to identify potential biomarkers in the serum that can be used for early diagnosis and as effective therapeutic targets. The aim was to provide a new direction for CRC predictive, preventive, and personalized medicine (PPPM). Methods In this study, CRC patients (n = 30) and HC (n = 30) were recruited. Serum metabolites were assayed using an ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS) technology. Subsequently, CRC cell lines (HCT116 and HCT8) were treated with metabolites to verify their function. Key targets were identified by molecular docking, thermal shift assay, and protein overexpression/inhibition experiments. The inhibitory effect of celastrol on tumor growth was also assessed, which included IC50 analysis, nude mice xenografting, molecular docking, protein overexpression/inhibition experiments, and network pharmacology technology. Results In the CRC group, 15 serum metabolites were significantly different in comparison with the HC group. The level of glycodeoxycholic acid (GDCA) was positively correlated with CRC and showed high sensitivity and specificity for the clinical diagnostic reference (AUC = 0.825). In vitro findings showed that GDCA promoted the proliferation and migration of CRC cell lines (HCT116 and HCT8), and Poly(ADP-ribose) polymerase-1 (PARP-1) was identified as one of the key targets of GDCA. The IC50 of celastrol in HCT116 cells was 121.1 nM, and the anticancer effect of celastrol was supported by in vivo experiments. Based on the potential of GDCA in PPPM, PARP-1 was found to be significantly correlated with the anticancer functions of celastrol. Conclusion These findings suggest that GDCA is an abnormally produced metabolite of CRC, which may provide an innovative molecular biomarker for the predictive identification and targeted prevention of CRC. In addition, PARP-1 was found to be an important target of GDCA that promotes CRC; therefore, celastrol may be a potential targeted therapy for CRC via its effects on PARP-1. Taken together, the pathophysiology and progress of tumor molecules mediated by changes in metabolite content provide a new perspective for predictive, preventive, and personalized medical of clinical cancer patients based on the target of metabolites in vivo.
C1 [Yuan, Yu; Bi, Chenghao; Sun, Sitong; Li, Yubo] Tianjin Univ Tradit Chinese Med, Sch Chinese Mat Med, Tianjin State Key Lab Modern Chinese Med, Tianjin 301617, Peoples R China.
   [Yang, Chenxin; Li, Lingling; Zhang, Shuai] Tianjin Univ Tradit Chinese Med, Sch Integrat Med, Tianjin 301617, Peoples R China.
   [Wang, Yingzhi; Sun, Mingming; Shan, Changliang] Nankai Univ, Coll Pharm, State Key Lab Med Chem Biol, Tianjin 300350, Peoples R China.
   [Wang, Yingzhi; Sun, Mingming; Shan, Changliang] Nankai Univ, Tianjin Key Lab Mol Drug Res, Tianjin 300350, Peoples R China.
   [Sun, Guijiang] Tianjin Med Univ, Dept Kidney Dis & Blood Purificat, Hosp 2, Tianjin 300211, Peoples R China.
   [Hao, Jingpeng] Tianjin Med Univ, Dept Anorectal Surg, Hosp 2, Tianjin 300211, Peoples R China.
C3 Tianjin University of Traditional Chinese Medicine; Tianjin University
   of Traditional Chinese Medicine; Nankai University; Nankai University;
   Tianjin Medical University; Tianjin Medical University
RP Li, YB (corresponding author), Tianjin Univ Tradit Chinese Med, Sch Chinese Mat Med, Tianjin State Key Lab Modern Chinese Med, Tianjin 301617, Peoples R China.; Zhang, S (corresponding author), Tianjin Univ Tradit Chinese Med, Sch Integrat Med, Tianjin 301617, Peoples R China.
EM shuaizhang@tjutcm.edu.cn; yuboli1@163.com
RI li, lingling/HTR-2760-2023; Shan, changliang/L-9029-2016; Wang,
   Yingzhi/JTV-6945-2023; yang, chenxin/LIF-6361-2024; Chen,
   zihao/HGE-3792-2022
OI Shan, Changliang/0000-0002-4906-1686
FU National Natural Science Foundation of China [81573825, 81902826,
   81672781, 81973356]; Tianjin Development Program for Innovation and
   Entrepreneurship [20190617]; Fundamental Research Funds for the Central
   Universities, Nankai University [3206054, 91923101, 63213082, 92122017];
   National Key R&D Program of China [2018YFC2002000]; Fundamental Research
   Funds for the Central Universities [3206054, 91923101, 63213082,
   ,2018YFC2002000]; Swedish Heart-Lung Foundation [20190617] Funding
   Source: Swedish Heart-Lung Foundation
FX This work was supported by the National Natural Science Foundation of
   China (81573825, 81902826, 81672781 and 81973356) and Tianjin
   Development Program for Innovation and Entrepreneurship (20190617), the
   Fundamental Research Funds for the Central Universities, Nankai
   University (3206054, 91923101, 63213082 and 92122017), and the National
   Key R&D Program of China (No. 2018YFC2002000).National Natural Science
   Foundation of China,81573825,Yubo Li,81902826,Shuai Zhang,81672781,Shuai
   Zhang,81973356,Shuai Zhang, Tianjin Development Program for Innovation
   and Entrepreneurship, 20190617, Yubo Li, Fundamental Research Funds for
   the Central Universities, 3206054, Changliang Shan, 91923101, Changliang
   Shan, 63213082, Changliang Shan,92122017,Changliang Shan,National Key
   R&D Program of China,2018YFC2002000,Changliang Shan
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NR 84
TC 5
Z9 7
U1 5
U2 24
PU SPRINGER INT PUBL AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 1878-5077
EI 1878-5085
J9 EPMA J
JI EPMA J.
PD MAR
PY 2022
VL 13
IS 1
SI SI
BP 39
EP 55
DI 10.1007/s13167-021-00269-8
EA JAN 2022
PG 17
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA ZN1HY
UT WOS:000749027300001
PM 35273658
OA Green Published
DA 2025-01-04
ER

PT J
AU Zhao, S
   Pan, WB
   Jiang, HJ
   Zhang, RJ
   Jiang, H
   Liang, ZH
   Hu, HB
AF Zhao, Sheng
   Pan, Wenbin
   Jiang, Huijie
   Zhang, Rongjun
   Jiang, Hao
   Liang, Zonghui
   Hu, Hongbo
TI Cerenkov luminescence imaging is an effective preclinical tool for
   assessing colorectal cancer PD-L1 levels in vivo
SO EJNMMI RESEARCH
LA English
DT Article
DE Colorectal cancer; Immunotherapy; Cerenkov luminescence imaging;
   Programmed death ligand-1; Preclinical tool
ID MOUSE MODEL; EXPRESSION; CELL; BLOCKADE; ANTIBODY
AB Background Preclinical and clinical studies have demonstrated that immunotherapy has effectively delayed tumor progression, and the clinical outcomes of anti-PD-1/PD-L1 therapy were related to PD-L1 expression level in the tumors. A(131)I-labeled anti-PD-L1 monoclonal antibody tracer,I-131-PD-L1-Mab, was developed to study the target ability of noninvasive Cerenkov luminescence imaging in colorectal cancer xenograft mice. Method Anti-PD-L1 monoclonal antibody labeled with(131)I (I-131-PD-L1-Mab), and in vitro binding assays were used to evaluate the affinity of(131)I-PD-L1-Mab to PD-L1 and their binding level to different colorectal cancer cells, and compared with flow cytometry, Western blot analysis, and immunofluorescence staining. The clinical application value of(131)I-PD-L1-Mab was evaluated through biodistribution and Cerenkov luminescence imaging, and different tumor-bearing models expressing PD-L1 were evaluated. Results I-131-PD-L1-Mab showed high affinity to PD-L1, and the equilibrium dissociation constant was 1.069 x 10(-9) M. The competitive inhibition assay further confirmed the specific binding ability of(131)I-PD-L1-Mab. In four different tumor-bearing models with different PD-L1 expression, the biodistribution and Cerenkov luminescence imaging showed that the RKO tumors demonstrated the highest uptake of the tracer(131)I-PD-L1-Mab, with a maximum uptake of 1.613 +/- 0.738% IA/g at 48 h. Conclusions There is a great potential for(131)I-PD-L1-Mab noninvasive Cerenkov luminescence imaging to assess the status of tumor PD-L1 expression and select patients for anti-PD-L1 targeted therapy.
C1 [Zhao, Sheng; Pan, Wenbin; Jiang, Huijie; Jiang, Hao; Hu, Hongbo] Harbin Med Univ, Affiliated Hosp 2, Dept Radiol, Harbin, Peoples R China.
   [Zhang, Rongjun] Jiangsu Inst Nucl Med, Wuxi, Jiangsu, Peoples R China.
   [Liang, Zonghui] Fudan Univ, Jingan Dist Ctr Hosp Shanghai, Shanghai, Peoples R China.
C3 Harbin Medical University; Fudan University
RP Jiang, HJ (corresponding author), Harbin Med Univ, Affiliated Hosp 2, Dept Radiol, Harbin, Peoples R China.; Zhang, RJ (corresponding author), Jiangsu Inst Nucl Med, Wuxi, Jiangsu, Peoples R China.; Liang, ZH (corresponding author), Fudan Univ, Jingan Dist Ctr Hosp Shanghai, Shanghai, Peoples R China.
EM jianghuijie@hrbmu.edu.cn; zhangrongjun@jsinm.org; liangzhjhj@163.com
RI Zhao, Sheng/AAQ-9304-2020; jiang, hui/KYP-5273-2024; Hongbo,
   Hu/AAC-6933-2021
OI jiang, huijie/0000-0002-8356-9643
FU National Key Research and Development Program of China [2019YFC0118100];
   National Natural Science Foundation of China [81671760, 81871423,
   81873910]; Scientific Research Transformation Special Fund of
   Heilongjiang Academy of Medical Sciences [2018415]; Scientific Research
   Project of Health and Family Planning Commission of Heilong jiang
   Province [201622, 201812]
FX This study was supported by grants from the National Key Research and
   Development Program of China (No. 2019YFC0118100), National Natural
   Science Foundation of China (Nos. 81671760, 81871423, and 81873910),
   Scientific Research Transformation Special Fund of Heilongjiang Academy
   of Medical Sciences (No. 2018415); Scientific Research Project of Health
   and Family Planning Commission of Heilong jiang Province (Nos. 201622
   and 201812).
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PG 11
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA MC0MV
UT WOS:000542993000001
PM 32542442
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

EF